No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Behavioral and Emotional Triggers of Acute Coronary Syndromes: A Systematic Review and Critique
Abstract
The objective of this study was to review the evidence that behavioral and emotional factors are triggers of acute coronary syndromes.
Systematic review of the published literature from 1970 to 2004 of trigger events, defined as stimuli or activities occurring within 24 hours of the onset of acute coronary syndromes.
There is consistent evidence that physical exertion (particularly by people who are not normally active), emotional stress, anger, and extreme excitement can trigger acute myocardial infarction and sudden cardiac death in susceptible individuals. Many triggers operate within 1 to 2 hours of symptom onset. There are methodologic limitations to the current literature, including sampling, retrospective reporting, and presentation biases, the role of memory decay and salience, and reverse causation because of silent prodromal events.
Behavioral and emotional factors are probable triggers of acute coronary syndromes in vulnerable individuals, and the pathophysiological processes elicited by these stimuli are being increasingly understood. The benefits to patients of knowledge to these processes have yet to accrue.
... This chapter will present an illustrative, rather than exhaustive, review of the epidemiologic literature on acute precipitating factors for MI. More extensive reviews of acute triggers have been published [18,21,40,51,67,74,76,83]. First, we explain the pathophysiology of MI, specifically, the role of unstable plaque in the development of MI. ...
... Previous reviews (e.g., [76] have commented on the lack of direct evidence of cigarette smoking acutely triggering MI. Though we do not review any large-scale reports of cigarette smoking as a MI trigger, evidence indicates that smoking can acutely precipitate myocardial ischemia in patients with coronary artery disease [6,26]. ...
... In this regard, emotional triggers may be particularly salient and therefore over-emphasized in the patients' explanations. Strike and Steptoe [76] present a thorough discussion of potential methodological issues relating to psychological processes that must be considered in evaluating case-crossover studies. These include reverse causation (e.g., triggers such as emotional distress may be the product of an early phase of MI that triggered a large increase in inflammatory cytokines that subsequently elicits negative affect; see [9]), sampling bias, presentation bias (individuals with MI who present to the hospital may be different than those who do not present due to silent MI or fatal MI), memory decay, and salience (control periods further back in time may not be accurately recalled). ...
Of the numerous causes of myocardial infarction (MI), a salient group of triggers
are acute and occur within 24 h of the onset of MI. After presenting the
pathophysiology of MI, this chapter then provides an illustrative account of the
literature that reports on the risk of MI attributable to these acute triggers.
Behavioral triggers include physical activity, sexual activity, alcohol use, cigarette
smoking, substance use, and sleep disturbances; psychological triggers are
divided into environmental factors (natural disasters, sporting events, and war)
and psychological triggers (acute emotional distress, bereavement, work stress,
and anger). Finally, we examine methodological considerations in the interpretation
of these results; asymptomatic, silent MI may not even be measured, and
recall bias may make attributing a specific trigger to the MI difficult. To better
understand this phenomenon, further research can provide new perspectives on
how triggers are measured, such as gauging the intensity of the trigger.
... To keep this review relevant to the clinician, our focus will be selective and provide a broad overview of mechanisms of disease and their associations with psychosocial factors. For more comprehensive analyses, the reader is referred to Fuster, Badimon, Chesebro, and Fallon (1996); Ross (1999); Rozanski, Blumenthal, Davidson, Saab, and Kubzansky (2005); Strike and Steptoe (2005); and Bhattacharyya and Steptoe (2007). ...
... anger, mental stress, sexual activity, cocaine and marijuana use, Monday mornings (presumably due to the stress of starting the work week), and/or when patients are asleep (Mittleman et al., 1995;Strike & Steptoe, 2005;Verrier & Mittleman, 1996). Because of the complex pathophysiology of CHD, psychosocial and behavioral variables are potentially involved with several different aspects of the atherosclerotic disease process and the transition to clinical events. ...
... Epidemiologic studies suggest that acute stress and emotions such as anger can act as potent triggers of MI and sudden cardiac death (Dimsdale, 2008;Holmes et al., 2006;Strike & Steptoe, 2005). Evidence continues to emerge from laboratory and ambulatory monitoring studies that mental stress and negative emotions are associated with the onset of malignant arrhythmias and elicitation of markers of arrhythmic vulnerability (Strike & Steptoe, 2005). ...
... Acute triggers are classified into four categories: emotional, environmental, physical and chemical [13][14][15][16][17][18]. Among these, emotional triggers can cause MI by affecting the emotional stressors such as anger and anxiety, depression [12,13,19], earthquake, war [18], work-related stress [17], unexpected news [20], and watching sport games [21]. ...
... Acute triggers are classified into four categories: emotional, environmental, physical and chemical [13][14][15][16][17][18]. Among these, emotional triggers can cause MI by affecting the emotional stressors such as anger and anxiety, depression [12,13,19], earthquake, war [18], work-related stress [17], unexpected news [20], and watching sport games [21]. Emotional triggers also reduce sleep, appetite and rest and increase cortisol levels and are associated with cardiovascular diseases [22]. ...
... Hazard period ranges from a few minutes to 24 hours before the onset of MI [18]. At this period, a disease can occur which is immediately before the onset of symptoms [24]. ...
... 6,7 Prior research has demonstrated that MSIMI possesses the capacity to incite angina, myocardial infarction, arrhythmia, and left ventricular dysfunction. [8][9][10][11] There exists evidence that obstructive sleep apnea (OSA) is autonomously linked to obstructive coronary heart disease, hypertension, and sudden cardiac death. [12][13][14][15][16] OSA is typified by recurrent upper airway blockage during sleep, leading to reduced arterial oxygen saturation, and apnea/hypopnea events are frequently terminated by micro arousals. ...
Purpose
Mental stress induced myocardial ischemia (MSIMI) is regarded as the primary cause of the angina with no obstructive coronary artery disease (ANOCA). Obstructive sleep apnea (OSA) is autonomously linked to obstructive coronary heart disease, hypertension, and sudden cardiac death. Similar to the impact of psychological stress on the cardiovascular system, individuals with OSA experience periodic nocturnal hypoxia, resulting in the activation of systemic inflammation, oxidative stress, endothelial dysfunction, and sympathetic hyperactivity. The contribution of OSA to MSIMI in ANOCA patients is unclear. To explore the prevalence of OSA in ANOCA patients and the correlation between OSA and MSIMI, a prospective cohort of female ANOCA patients was recruited.
Patients and Methods
We recruited female patients aged 18 to 75 years old with ANOCA and evaluated MSIMI using positron emission tomography-computed tomography. Subsequently, Level III portable monitors was performed to compare the relationship between OSA and MSIMI.
Results
There is higher REI (7.8 vs 2.6, P=0.019), ODI (4.7 vs 9.2, P=0.028) and percentage of OSA (67.74% vs 33.33%, P=0.004) in MSIMI patients. The patients diagnosed with OSA demonstrated higher myocardial perfusion imaging scores (SSS: 1.5 vs 3, P = 0.005, SDS: 1 vs 3, P = 0.007). Adjusted covariates, the risk of developing MSIMI remained 3.6 times higher in OSA patients (β=1.226, OR = 3.408 (1.200–9.681), P = 0.021).
Conclusion
Patients with MSIMI exhibit a greater prevalence of OSA. Furthermore, the myocardial blood flow perfusion in patients with OSA is reduced during mental stress.
... Through the study of appraisal theory, people can better identify their own and others' emotions. Appraisal theory emphasizes that individuals' representations of emotions vary, indicating that individuals may have different cognitions and expressions of the same emotion [50]. In summary, both emotional elicitation and appraisal theory make significant contributions to emotion recognition. ...
Emotion analysis, an integral aspect of human–machine interactions, has witnessed significant advancements in recent years. With the rise of multimodal data sources such as speech, text, and images, there is a profound need for a comprehensive review of pivotal elements within this domain. Our paper delves deep into the realm of emotion analysis, examining multimodal data sources encompassing speech, text, images, and physiological signals. We provide a curated overview of relevant literature, academic forums, and competitions. Emphasis is laid on dissecting unimodal processing methods, including preprocessing, feature extraction, and tools across speech, text, images, and physiological signals. We further discuss the nuances of multimodal data fusion techniques, spotlighting early, late, model, and hybrid fusion strategies. Key findings indicate the essentiality of analyzing emotions across multiple modalities. Detailed discussions on emotion elicitation, expression, and representation models are presented. Moreover, we uncover challenges such as dataset creation, modality synchronization, model efficiency, limited data scenarios, cross-domain applicability, and the handling of missing modalities. Practical solutions and suggestions are provided to address these challenges. The realm of multimodal emotion analysis is vast, with numerous applications ranging from driver sentiment detection to medical evaluations. Our comprehensive review serves as a valuable resource for both scholars and industry professionals. It not only sheds light on the current state of research but also highlights potential directions for future innovations. The insights garnered from this paper are expected to pave the way for subsequent advancements in deep multimodal emotion analysis tailored for real-world deployments.
... Under the influence of extreme stimuli, the processes of biological oxidation and lipoperoxidation are naturally enhanced, and there is a significant inhibition of the functional activity of the enzyme and non-enzyme chains of the antioxidant system [10]. Particularly, oxidative stress and an increase in the concentration of lipid peroxidation products above the stationary level are considered as a universal mechanism of cell damage in various pathological conditions, including the pathology of the cardiovascular system [11][12]. Consequently, the correction of the level of intermediate products of lipoperoxidation and normalization of the activity of antioxidant systems of the blood are pathogenetically justified. ...
The aim of this scientific research is to study the effect of electromagnetic waves of the terahertz range on the frequency of molecular oxygen (129.0 GHz) on the processes of lipid peroxidation in experimental animals under chronic stress. Overtraining is a psychological and/or physiological condition that manifests itself as impairment in athletic performance. This condition may be based on prolonged competitive stress and stressful psychological factors that can lead to the activation of lipid peroxidation processes (LPO). Moreover, the activation of the processes of lipoperoxidation is the main pathogenetic link of many socially significant diseases, especially cardiovascular disease. These circumstances require the development of modern and relevant methods of prevention and treatment of post-stress disorders. In the last ten years, a new method has been used to assess the effect of stress on the pro-oxidant activity of blood plasma and the concentration of antioxidants by exposure to electromagnetic radiation. In this paper electromagnetic waves of terahertz range, at frequencies of active cellular metabolites, were used to correct the processes of lipoperoxidation (LPO) changes at chronic stress. The innovative device "Оrbit" was used to emit Terahertz (THz) radiation at frequencies of molecular oxygen 129,0 GHz in fractional mode. From the marked activation of lipid peroxidation processes and inhibition of antioxidant activity of blood, it is possible to observe a partial normalization, in the conditions of long-term immobilization or through cold water swimming of animals (rats), by using THz waves 5 days for 15 minutes; moreover, if the same procedure was applied for 30 minutes, a complete normalization of lipid peroxidation and antioxidant levels in the blood of stressed animals occurred. The study shows the high efficiency and expediency of using the device for terahertz therapy "Orbit" in the correction of altered processes of lipid peroxidation and it encourages future application for humans. DOI: https://doi.org/10.52783/pst.289
... 17,18 Similar study by Strike PC and study by Sheps et al found that, there is consistent evidence that emotional distress, anger and extreme excitement can trigger acute coronary syndrome (ACS) and sudden cardiac death in susceptible individuals with both immediate and long-lasting impact. 19,20 Similar findings had also been Rosengren et al that stressful life events in the year preceding the index MI were more common in cardiac patients compared to the control group. 21 Stressors of study by Theorell T and study by Job PR who found that job strain has been associated with increased CVD prevalence. ...
Background: Cardiovascular diseases (CVDs) are common in India, yet there is a lack of comprehensive studies on the specific risk factors for the Indian population. Our research aimed to identify CVD risk factors in individuals under 50 and compare them with healthy controls, offering insights into preventing CVDs in this younger demographic. Methods: This study focused on newly diagnosed cases of CVDs in males under 50 and matched controls with same demographic parameters. Data on personal, medical, lifestyle and biochemical parameters was compared to identify and understand the key risk factors associated with CVDs in this specific population group. Results: Elevated body mass index (BMI) and waist-hip ratio were linked to CVD, with BMI showing a significant association. High triglyceride (TGL) levels (>150 mg/dl) and LDL cholesterol levels (>130 mg/dl) were significantly associated with CVD. The total cholesterol to HDL cholesterol ratio (>4.5) and low HDL cholesterol (<40 mg/dl) were also linked to CVD risk. Diabetes mellitus was strongly associated with CVD (OR-14.04). Stress, as assessed by a stress score >12, was associated with CVD, although the association was not very strong (OR 1.39). Physical exercise was associated with a protective effect against CVD (OR-0.28). These findings emphasize the critical role of lifestyle factors, such as diet, exercise and stress management in CVD prevention and highlight the importance of managing conditions like obesity and diabetes. Conclusions: This study not only deepens our comprehension of CVD prevention but also provides actionable guidance for fostering heart health, both within the studied population and in broader contexts.
... [45][46][47][48][49][50][51][52][53] Mental stress can be measured in daily life as well as modelled in the laboratory using mental stress tasks like public speaking and mental arithmetic, and these studies showed that acute psychological stress can induce myocardial ischemia in some patients with CHD. 17,46,[54][55][56][57][58][59][60][61][62][63][64][65][66][67] CHD is linked to both depression [7][8][9][10][11][12][13][14][15][16][17]68 and PTSD, 9,17,[28][29][30][31][32][33] and stress may mediate its effects either directly, 2-6 through these psychiatric disorders 34,44,49,55,[69][70][71] or via a common genetic link. [72][73][74][75] Mental Stress Ischemia (MSI) can occur in CHD patients without exercise-induced myocardial ischemia MSI is not necessarily associated with atherosclerotic CHD 56,59,60,[62][63][64][76][77][78][79][80][81] , is twice as common in women under 50 than similar aged men, 62 and is associated with increased long-term risk for adverse cardiac events compared to conventional exercise-induced myocardial ischemia. ...
Objective:
Coronary heart disease is a leading cause of death and disability. Although psychological stress has been identified as an important potential contributor, mechanisms by which stress increases risk of heart disease and mortality are not fully understood. The purpose of this study was to assess mechanisms by which stress acts through the brain and heart to confer increased CHD risk.
Methods:
Coronary Heart Disease patients (N=10) underwent cardiac imaging with [Tc-99m] sestamibi single photon emission tomography at rest and during a public speaking mental stress task. Patients returned for a second day and underwent positron emission tomography imaging of the brain, heart, bone marrow, aorta (indicating inflammation) and subcutaneous adipose tissue, after injection of [18F]2-fluoro-2-deoxyglucose for assessment of glucose uptake followed mental stress. Patients with (N=4) and without (N=6) mental stress-induced myocardial ischemia were compared for glucose uptake in brain, heart, adipose tissue and aorta with mental stress.
Results:
Patients with mental stress-induced ischemia showed a pattern of increased uptake in the heart, medial prefrontal cortex, and adipose tissue with stress. In the heart disease group as a whole, activity increase with stress in the medial prefrontal brain and amygdala correlated with stress-induced increases in spleen (r=0.69, p=0.038; and r=0.69, p=0.04 respectfully). Stress-induced frontal lobe increased uptake correlated with stress-induced aorta uptake (r=0.71, p=0.016). Activity in insula and medial prefrontal cortex was correlated with post-stress activity in bone marrow and adipose tissue. Activity in other brain areas not implicated in stress did not show similar correlations. Increases in medial prefrontal activity with stress correlated with increased cardiac glucose uptake with stress, suggestive of myocardial ischemia (r=0.85, p=0.004).
Conclusions:
These findings suggest a link between brain response to stress in key areas mediating emotion and peripheral organs involved in inflammation and hematopoietic activity, as well as myocardial ischemia, in Coronary Heart Disease patients.
... Physical and mental triggers didn't impact differently the self-care ability and emotional regulation: CVD patients seemed overcome the onset of disease being focused on the pathology. Some studies highlighted the relevance of mental triggers in vulnerable individuals, referring to stress, anxiety and depression as mechanisms for acute triggers in CVD onset [4,21] but the topic is controversial: according to opposite point of view, the absolute impact of acute emotional triggers will be greater among individuals with an elevated baseline CVD risk, such that the effect of two episodes of anger daily would vary from approximately one excess cardiovascular event per 1000 person-years in a low-risk population [5]. ...
Background
Cardiovascular disease is a chronic non-communicable illness that causes more than half of all deaths across Europe. Unhealthy lifestyle, inadequate adherence to medical prescriptions, themselves associated with psycho-emotional disorders are considered risk factors for reduced quality of life as well physical condition.
Objective
Aim of our study was to understand predictive factors for disease management by evaluating psychological aspects, self-care processes and emotional regilati0on in CVD outpatients.
Methods
An observational study was conducted. Sixty-one patients, age 18–75 years (M 56.4 ± sd 12.0), diagnosed with CVD participated in the study. The psychological battery was administered during clinical follow-up oriented to detect emotional and psychological dimensions as well adaptive behavioral and quality of life by standardized questionnaire/scales.
Results
Finding showed that emotional dysregulation might influence QoL, particularly significant effect of awareness (β= 0.022; SE = 1.826; p < 0.002), goals (β = - 0.54; SE = 1.48; p < 0.001) and clarity (β = - 0.211; SE = 2.087; p < 0.003). The results also suggest that the mediated effect accounted for awareness index was 18.7% (R² = 0.187) of the variance; goals index 62.8% (R² = 0.628) of the variance and, then significant mediated effect of clarity was 58.8% (R² = 0.588) of the variance. This evidence suggests that the relationship between triggers and QoL is mediated by emotional dysregulation indexes.
Conclusion
In clinical practice psychological screening can be an effective tool for detecting predictive factors in the management of the CVD patient's health and adherence to medical treatment: the screening of predictive psychological factors for allowing a good clinical condition management and a self-care empowerment aimed at increasing psychological well-being and the Quality of Life by planning adequate integrated and multidisciplinary support.
... The effects of stress on cardiac function are expressed by a transient myocardial ischemic response, analogous to exercise stress-induced ischemia, in which the stress is psychological rather than physical [26]. MSIMI is a potential trigger for angina, myocardial infarction, arrhythmias, and left ventricular dysfunction [24,[27][28][29]. The relationship between mental stress and MSIMI varies according to the individual's CV risk level but is unrelated to severity of coronary obstruction or previous revascularization [30]. ...
Epidemiological studies have shown that a substantial proportion of acute coronary events occur in individuals who lack the traditional high-risk cardiovascular (CV) profile. Mental stress is an emerging risk and prognostic factor for coronary artery disease and stroke, independently of conventional risk factors. It is associated with an increased rate of CV events. Acute mental stress may develop as a result of anger, fear, or job strain, as well as consequence of earthquakes or hurricanes. Chronic stress may develop as a result of long-term or repetitive stress exposure, such as job-related stress, low socioeconomic status, financial problems, depression, and type A and type D personality. While the response to acute mental stress may result in acute coronary events, the relationship of chronic stress with increased risk of coronary artery disease (CAD) is mainly due to acceleration of atherosclerosis. Emotionally stressful stimuli are processed by a network of cortical and subcortical brain regions, including the prefrontal cortex, insula, amygdala, hypothalamus, and hippocampus. This system is involved in the interpretation of relevance of environmental stimuli, according to individual’s memory, past experience, and current context. The brain transduces the cognitive process of emotional stimuli into hemodynamic, neuroendocrine, and immune changes, called fight or flight response, through the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. These changes may induce transient myocardial ischemia, defined as mental stress-induced myocardial ischemia (MSIMI) in patients with and without significant coronary obstruction. The clinical consequences may be angina, myocardial infarction, arrhythmias, and left ventricular dysfunction. Although MSIMI is associated with a substantial increase in CV mortality, it is usually underestimated because it arises without pain in most cases. MSIMI occurs at lower levels of cardiac work than exercise-induced ischemia, suggesting that the impairment of myocardial blood flow is mainly due to paradoxical coronary vasoconstriction and microvascular dysfunction.
... Physical and mental triggers didn't impact differently the self-care ability and emotional regulation: CVD patients seemed overcome the onset of disease being focused on the pathology. Some studies highlighted the relevance of mental triggers in vulnerable individuals, referring to stress, anxiety and depression as mechanisms for acute triggers in CVD onset [17,18] but the topic is controversial: according to opposite point of view, the absolute impact of acute emotional triggers will be greater among individuals with an elevated baseline CVD risk, such that the effect of two episodes of anger daily would vary from approximately one excess cardiovascular event per 1000 person-years in a low-risk population [19]. ...
Background. Cardiovascular disease is a chronic non-communicable illness that causes more than half of all deaths across Europe. Unhealthy lifestyle, inadequate adherence to medical prescriptions, themselves associated with psycho-emotional disorders are considered risk factors for reduced quality of life as well physical condition.
Objective. Aim of our study was to understand predictive factors for management by evaluating psychological aspects, self-care processes and emotional regilati0on in CVD outpatients.
Methods. An observational study was conducted. 61 patients, age 18–75 years (M 56.4 ± sd 12.0), diagnosed with CVD participated in the study. The psychological battery was administered during clinical follow-up oriented to detect emotional and psychological dimensions as well adaptive behavioral and quality of life.
Results. Finding showed that emotional dysregulation might influence QoL, particularly significant effect of awareness (β = 0.022; SE = 1.826; p < 0.002), goals (β = - 0.54; SE = 1.48; p < 0.001) and clarity (β = - 0.211; SE = 2.087; p < 0.003). The results also suggest that the mediated effect accounted for awareness index was 18.7% (R² = 0.187) of the variance; goals index 62.8% (R² = 0.628) of the variance and, then significant mediated effect of clarity was 58.8% (R² = 0.588) of the variance. This evidence suggests that the relationship between triggers and QoL is mediated by emotional dysregulation indexes.
Conclusion. Poor adherence to CVD pharmacological therapy could be addressed by identifying the emotional characteristics, subjective emotion ability, and self-care process of patients who are or may be at risk of non-persistence.
... 77 A substantial body of evidence indicates a positive relationship between anger and hostility with increased CVD events in healthy populations, as well as in patients with existing CVD. 78,79 Excessive (and in some instances, paradoxical) vasoconstriction mediated by endothelial dysfunction, 80 pronounced adrenocorticotropic responses to socially salient stress, 81 and increased intima media thickness, 82 are some of the mechanisms linking anger and hostility with potential CVD. ...
Traditional risk factors for cardiovascular disease (CVD) have long been the focus of preventive strategies. The impact of family stress, depression, anxiety, hostility, pessimism, job strain, social isolation, lack of purpose in life and social support, are well recognized risks for CVD development, however they are under-appreciated in clinical practice guidelines. The purpose of this article is to review the impact of acute and chronic stress on CVD risk, elaborate repositioning in guidelines, with emphasis to approaches for stress reduction. Regular exercise, both aerobic and resistance, leads to better adaptiveness to other types of stress, however, it remains unknown whether the total amount of stress one can receive before negative health effects is unlimited. Evidently, marked reductions in stress related disorders are shown following formal cardiac rehabilitation programs. Attendance of cardiac rehabilitation is highly recommended for the stress-related mortality risk reduction. Innovative approaches to offset the broad challenges that CVD pose, augmented by sustained exposure to stress, are desperately needed, but hindered by a lack of successful population-level interventions that promote lasting change.
... The link between anxiety symptoms and symptoms of mental stress and SCA has been studied in various systematic reviews. For example, Strike and Steptoe concluded that mental stress caused by the experience of stressful public events such as earthquakes or emotionally challenging sporting occasions are probable triggers or precipitating factors for acute coronary syndromes, which in turn may lead to VF and subsequently to SCA and SCD (13). Likewise, in a previous meta-analysis, we have shown that anxiety symptoms are a predisposing factor for CVD mortality (including SCA), increasing the risk by 61% (14). ...
Sudden cardiac arrest (SCA) is a leading cause of mortality and morbidity in affluent societies, which underscores the need to identify persons at risk. The etiology of SCA is however complex, with predisposing and precipitating factors interacting. Although anxiety and mental stress have been linked to SCA for decades, their precise role and impact remain unclear and the biological underpinnings are insufficiently understood. In this paper, we systematically reviewed various types of observational studies (total n = 20) examining the association between anxiety or mental stress and SCA. Multiple methodological considerations challenged the summarizing and interpretation of the findings. For anxiety, the overall picture suggests that it predisposes for SCA in physically healthy populations (unadjusted OR = 2.44; 95% CI: 1.06–5.59; n = 3). However, in populations at risk for SCA (n = 4), associations were heterogeneous but not significant. Anxiety may partly predispose to SCA by contributing to other risk factors such as cardiovascular disease and diabetes mellitus via mechanisms such as unhealthy lifestyle and metabolic abnormalities. Mental stress appears to precipitate SCA, presumably by more directly impacting on the cardiac ion channels that control the heart's electrical properties. This may lead to ventricular fibrillation, the arrhythmia that underlies SCA. To advance this field of research, experimental studies that unravel the underlying biological mechanisms are deemed important, and most easily designed for mental stress as a precipitating factor because of the short timeframe. These proof-of-concept studies should examine the whole pathway from the brain to the autonomic nervous system, and eventually to cardiac ion channels. Ultimately, such studies may facilitate the identification of persons at risk and the development of novel preventive strategies.
... Emotional stress has been reported in earlier studies to precede cardiac events [9][10][11]. This was confirmed in our study. ...
Objectives: Christmas holidays have been associated with the highest incidence of myocardial infarction (MI). We wanted to assess possible triggers of MI during Christmas. Design: A nationwide, retrospective postal survey with case-control design. All individuals suffering an MI during the Christmas holidays 2018 and 2019 in Sweden were identified through the SWEDEHEART registry and a control group matched in age and gender with chronic coronary syndrome who did not seek medical attention during Christmas were asked for participation. Subjects completed a questionnaire asking them to rate 27 potential MI-triggers as having occurred more or less than usual. Results: A total of 189 patients suffering an MI on Christmas Eve, Christmas Day, or Boxing Day, and 157 patients in the control group responded to the questionnaire, representing response rates of 66% and 62%, respectively. Patients with MI on Christmas experienced more stress (37% vs. 21%, p = .002), depression (21% vs. 11%, p = .024), and worry (26% vs. 10%, p < .001) compared to the control group. The food and sweets consumption was increased in both groups, but to a greater extent in the control group (33% vs. 50%, p = .002 and 32% vs. 43%, p = .031). There were no increases in quarrels, anger, economic worries, or reduced compliance with medication. Conclusions: Patients suffering MI on Christmas holiday experienced higher levels of stress and emotional distress compared to patients with chronic coronary syndrome, possibly contributing to the phenomenon of holiday heart attack. Understanding what factors increase the number of MI on Christmas may help reduce the excess number of MIs and cardiovascular burden.
... The association between acute emotions and ischemia during MPI is likely [20][21][22][23][24][25] , but evidence to date is based on self-reported emotions only. The unique aspect of this study is the measurement of acute emotions using facial expression recognition software during cardiac stress testing as part of MPI 26 . ...
Background:
Patients with myocardial ischemia in the absence of obstructive coronary artery disease (CAD) often experience anginal complaints and are at risk of cardiac events. Stress-related psychological factors and acute negative emotions might play a role in these patients with suspect coronary microvascular dysfunction (CMD).
Methods and results:
295 Patients (66.9 ± 8.7 years, 46% women) undergoing myocardial perfusion single-photon-emission computed tomography (MPI-SPECT), were divided as follows: (1) a non-ischemic reference group (n = 136); (2) patients without inducible ischemia, but with a history of CAD (n = 62); (3) ischemia and documented CAD (n = 52); and (4) ischemia and suspect CMD (n = 45). These four groups were compared with regard to psychological factors and acute emotions. Results revealed no differences between the groups in psychological factors (all P > .646, all effect sizes d < .015). State sadness was higher for patients with suspect CMD (16%) versus the other groups (P = .029). The groups did not differ in the association of psychological factors or emotions with anginal complaints (all P values > .448).
Conclusion:
Suspect CMD was not associated with more negative psychological factors compared to other groups. State sadness was significantly higher for patients with suspect CMD, whereas no differences in state anxiety and other psychological factors were found.
... All of these factors contribute to the fact that an increased risk for CVD is seen in both depression (Carney and Freedland, 2003;Evans et al., 2005) and PTSD . Behaviors such as stress-induced anger were also associated with increased CVD risk (Boltwood et al., 1993;Burg et al., 1993;Gabbay et al., 1996;Mittleman et al., 1995;Strike et al., 2006;Strike and Steptoe, 2005). Anger and irritability, symptoms of PTSD, could therefore contribute to increased risk of CVD. ...
Da Costa originally described Soldier's Heart in the 19th Century as a syndrome that occurred on the battlefield in soldiers of the American Civil War. Soldier's Heart involved symptoms similar to modern day posttraumatic stress disorder (PTSD) as well as exaggerated cardiovascular reactivity felt to be related to an abnormality of the heart. Interventions were appropriately focused on the cardiovascular system. With the advent of modern psychoanalysis, psychiatric symptoms became divorced from the body and were relegated to the unconscious. Later, the physiology of PTSD and other psychiatric disorders was conceived as solely residing in the brain. More recently, advances in psychosomatic medicine led to the recognition of mind-body relationships and the involvement of multiple physiological systems in the etiology of disorders, including stress, depression, PTSD, and cardiovascular disease, has moved to the fore, and has renewed interest in the validity of the original model of the Soldier's Heart syndrome.
... 10 A range of factors, such as pollution, infections, emotional stress and physical exertion, can also trigger acute CV events particularly in those with pre-existing cardiovascular disease (CVD). [11][12][13] Electronic health record (EHR) databases are derived from clinical care records and contain longitudinal patient data on diagnoses, treatment and other clinically relevant variables, such as smoking. Administrative databases were developed for financial and management purposes to allocate funding or billing of insurance claims. ...
Introduction
Cardiovascular diseases (CVDs) are among the leading causes of death globally. Electronic health records (EHRs) provide a rich data source for research on CVD risk factors, treatments and outcomes. Researchers must be confident in the validity of diagnoses in EHRs, particularly when diagnosis definitions and use of EHRs change over time. Our systematic review provides an up-to-date appraisal of the validity of stroke, acute coronary syndrome (ACS) and heart failure (HF) diagnoses in European primary and secondary care EHRs.
Methods and analysis
We will systematically review the published and grey literature to identify studies validating diagnoses of stroke, ACS and HF in European EHRs. MEDLINE, EMBASE, SCOPUS, Web of Science, Cochrane Library, OpenGrey and EThOS will be searched from the dates of inception to April 2019. A prespecified search strategy of subject headings and free-text terms in the title and abstract will be used. Two reviewers will independently screen titles and abstracts to identify eligible studies, followed by full-text review. We require studies to compare clinical codes with a suitable reference standard. Additionally, at least one validation measure (sensitivity, specificity, positive predictive value or negative predictive value) or raw data, for the calculation of a validation measure, is necessary. We will then extract data from the eligible studies using standardised tables and assess risk of bias in individual studies using the Quality Assessment of Diagnostic Accuracy Studies 2 tool. Data will be synthesised into a narrative format and heterogeneity assessed. Meta-analysis will be considered when a sufficient number of homogeneous studies are available. The overall quality of evidence will be assessed using the Grading of Recommendations, Assessment, Development and Evaluation tool.
Ethics and dissemination
This is a systematic review, so it does not require ethical approval. Our results will be submitted for peer-review publication.
PROSPERO registration number
CRD42019123898
... In addition, a variety of triggers have been associated with the onset of an acute ischemic episode and may contribute to an individual's perception of symptoms. Physical activity, behaviors, and emotional upset occurring within 1-2 h of symptom onset have been reported as precursors to ACS. [24][25][26] Whether physical exertion or emotions trigger variations in symptom onset is unknown. Differences in pathophysiology or in risk factors may influence the development and outcomes of symptoms during ACS. ...
Background
A decision to delay seeking treatment for symptoms of acute coronary syndrome increases the risk of serious complications, disability, and death.
Aims
The purpose of this study was to determine if there was an association between gradual vs abrupt symptom onset and prehospital delay for patients with acute coronary syndrome and to examine the relationship between activities at symptom onset and gradual vs abrupt symptom onset.
Methods
This was a secondary analysis of a large prospective multi-center study. Altogether, 474 patients presenting to the emergency department with symptoms of acute coronary syndrome were included in the study. Symptom characteristics, activity at symptom onset, and prehospital delay were measured with the ACS Patient Questionnaire.
Results
Median prehospital delay time was four hours. Being uninsured (β=0.120, p=0.031) and having a gradual onset of symptoms (β=0.138, p=0.003) were associated with longer delay. A diagnosis of ST-elevation myocardial infarction (β=−0.205, p=0.001) and arrival by ambulance (β=−0.317, p<0.001) were associated with shorter delay. Delay times were shorter for patients who experienced an abrupt vs gradual symptom onset (2.57 h vs 8 h, p<0.001). Among men with an abrupt onset of symptoms and a ST-elevation myocardial infarction diagnosis, 54% reported that symptoms were triggered by exertion ( p=0.046).
Conclusion
Patients should be counselled that a gradual onset of symptoms for potential acute coronary syndrome is an emergency and that they should call 911. Men with ischemic heart disease or with multiple risk factors should be cautioned that symptom onset following exertion may represent acute coronary syndrome.
... Affective science includes a similarly wide variety of constructs, ranging from short-term moods and time-limited episodes of specific emotions to more enduring affective characteristics within normal personality and emotional disorders (19). Brief emotional episodes have been implicated as precipitants of major health outcomes such as cardiovascular events, sudden death, and underlying pathogenic mechanisms (20)(21)(22)(23)(24). However, effects of emotions on the development and course of the major chronic diseases presumably accrue over longer periods, and studies of more enduring emotional characteristics are consistent with this view. ...
Emotional characteristics and processes are robust predictors of the development and course of major medical illnesses and premature mortality, as are a variety of indicators of the presence and quality of personal relationships. Despite clear evidence of close interconnection between these two domains of risk and protection, affective characteristics and relationships have largely been studied separately as influences on health. Following a recent conference on integrative perspectives on emotions, relationships and health co-sponsored by the American Psychosomatic Society and the Society for Affective Science, the present review builds on prior calls for integration, related theory, and current research to outline what is known about the interconnection of these domains as it specifically relates to their overlapping influences on health. Areas of interest include: their interconnected roles over the course of development, which may inform current efforts to understand the influence of early life events on adult health; the parallel positive and negative factors in both domains that could have distinct influences on health; the role of emotion regulation in relationship contexts; and measurement, design, and analysis approaches to capture the dyadic and dynamic aspects of these interconnected influences on health. We conclude with a discussion of an emerging research agenda that includes: common biological foundations of affective and relationship processes; the cultural embeddedness of affective and relationship processes; the potential contribution of affective-relational processes to health disparities; and implications for intervention research.
... Therefore, our data suggest that, within participants with CAD, early childhood trauma elicits activity within brain areas which mediate stress following mental arithmetic and public speaking. That early childhood trauma upregulates the stress responses during these challenges is an important finding, as emotional factors (including moderate to severe stress) increases risk for adverse cardiovascular events (Strike and Steptoe, 2005) including mental stress-induced myocardial ischemia . ...
Background:
Early childhood trauma is known to independently increase adverse outcome risk in coronary artery disease (CAD) patients, although the neurological correlates are not well understood. The purpose of this study was to examine whether early childhood trauma alters neural responses to acute mental stress in CAD patients.
Methods:
Participants (n = 152) with CAD underwent brain imaging with High Resolution Positron Emission Tomography and radiolabeled water during control (verbal counting, neutral speaking) and mental stress (mental arithmetic, public speaking). Traumatic events in childhood were assessed with the Early Trauma Inventory (ETI-SR-SF) and participants were separated by presence (ETI+) or absence (ETI-) of early childhood trauma. Brain activity during mental stress was compared between ETI+ and ETI-.
Results:
Compared to ETI-, ETI+ experienced greater (p < 0.005) activations during mental stress within the left anterior cingulate, bilateral frontal lobe and deactivations (p < 0.005) within the left insula, left parahippocampal gyrus, right dorsal anterior cingulate, bilateral cerebellum, bilateral fusiform gyrus, left inferior temporal gyrus, and right parietal lobe. Significant (p < 0.005) positive correlations between brain activation and ETI-SR-SF scores were observed within the left hippocampus, bilateral frontal lobe, left occipital cuneus, and bilateral temporal lobe.
Limitations:
Results in non-CAD samples may differ and ETI may be subject to recall bias.
Conclusion:
Early childhood trauma exacerbated activations in stress-responsive limbic and cognitive brain areas with direct and indirect connections to the heart, potentially contributing to adverse outcomes in CAD patients.
... For example, people who are more resilient in stressful conditions use more problem-focused coping strategies, and those with less resilience use emotion-focused coping strategies [42]. People with less capable coping abilities, in the long run, suffer from coronary disease and hypertension [43]. Similarly, in a study by Ford, a cognitive model and stress coping were used as ways to predict post-traumatic stress symptoms [44,45], but the sensitivity and specificity of stresscoping were not determined. ...
Objectives
The aim of this study was to investigate the diagnostic value of a stress coping scale for predicting perceived psychological traumatic childbirth in mothers.
Methods
This cross-sectional study was performed on 400 new mothers (within 48 hours of childbirth). Psychological traumatic childbirth was evaluated using the 4 diagnostic criteria of Diagnostic and Statistical Manual of Mental Disorders. Coping was measured using Moss and Billings’ Stress Coping Strategies Scale.
Results
The overall mean score of stress coping was 29 ± 14.2. There were 193 (43.8%) mothers that had experienced a psychological traumatic childbirth. A stress coping score ≤ 30, with a sensitivity of 90.16 (95% CI = 85.1–94.0), and a specificity of 87.44 (95% CI = 82.1–91.6), was determined as a predictor of psychological traumatic childbirth. So that among mothers with stress coping scores ≤ 30, 87% had experienced a psychological traumatic childbirth.
Conclusion
Investigating the degree of coping with stress can be used as an accurate diagnostic tool for psychological traumatic childbirth. It is recommended that during pregnancy, problem-solving and stress management training programs be used as psychological interventions for mothers with low levels of stress control. This will ensure that they can better cope with traumatic childbirth and post-traumatic stress in the postpartum stage.
... Triggers start the attack during a timeframe of some minutes or hours and this attack might differ based on the severity if trigger mechanism (7). Indeed, triggers start the action some minutes to 24 hours before ACS and this time period is called as risk period, and recently 1-2 hours before symptoms initiation has been emphasized (12). The presence of plaques susceptible to atherosclerosis, disturbance in the conductive system of the heart, and small arteries diseases along with physical and emotional trigger stressors, could transiently cause vasoconstriction and prothrombic effects which all finally lead into plaque rupture and thrombosis. ...
Objective: Acute triggers are external stimuli that produce acute pathophysiologic changes directly leading to the onset of myocardial infarction (MI). Acute myocardial infarction (AMI) is one of the main causes of mortality. Recent studies have confirmed the impact of acute triggers on the occurrence of AMI, but have not evaluated their differences in terms of demographic characteristics. This study was conducted to investigate the impact of acute triggers on AMI in various demographic groups. Methods: This is an analytical cross-sectional study on 269 patients affected by AMI in two hospitals in 2015 and 2016 in Iran. To attain the goals of the study, acute triggers were divided into four groups of emotional, environmental, physical, and chemical. A researcher-developed questionnaire and interview were used to collect data. The risk and control periods were also evaluated for each trigger. The data were analyzed by descriptive statistics and inferential statistics such as statistical logistic regression and McNemar's test using SPSS 21. The P-value was set at 0.05. Results: The results showed that sudden exposure to hot/cold weather in men (P=0.03, OR=3.4), underlying diseases (P=0.03, OR=1.8), heavy activities (P=0.03, OR=1.6) and consuming tea/coffee in men (P=0.01, OR=1.8) increased the chance of AMI. It was also discovered that triggers such as pulmonary infections, overeating and/or eating high-fat foods that are not dependent on demographic variables promoted the chance of AMI (P<0.05). Conclusion: All people - regardless of age, sex, and the presence/lack of underlying illness -Are at risk of developing MI in the face of respiratory infections, overeating, and intake of high-fat foods. Also, sudden exposure to hot and / or cold weather, heavy activity and high consumption of coffee and/or tea, can increase the risk of MI in men. � 2017 by Gazi University Medical Faculty.
... Acute coronary syndrome (ACS) is a traumatic event and a common cause for emergency hospital admission [1,2]. The term ACS refers to a series of acute myocardial ischemic states ranging from unstable angina to non-ST-segment elevation myocardial infarction to ST-segment elevation myocardial infarction [3]. ...
Purpose
Perceived social support is known to be an important predictor of health outcomes in patients with acute coronary syndrome (ACS). This study investigates patterns of longitudinal trajectories of patient-reported perceived social support in individuals with ACS.
Methods
Data are from 3013 patients from the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease registry who had their first cardiac catheterization between 2004 and 2011. Perceived social support was assessed using the 19-item Medical Outcomes Study Social Support Survey (MOS) 2 weeks, 1 year, and 3 years post catheterization. Group-based trajectory analysis based on longitudinal multiple imputation model was used to identify distinct subgroups of trajectories of perceived social support over a 3-year follow-up period.
Results
Three distinct social support trajectory subgroups were identified, namely: “High” social support group (60%), “Intermediate” social support group (30%), and “Low” social support subgroup (10%). Being female (OR = 1.67; 95% CI = [1.18–2.36]), depression (OR = 8.10; 95% CI = [4.27–15.36]) and smoking (OR = 1.70; 95% CI = [1.23–2.35]) were predictors of the differences among these trajectory subgroups.
Conclusion
Although the majority of ACS patients showed increased or fairly stable trajectories of social support, about 10% of the cohort reported declining social support. These findings can inform targeted psycho-social interventions to improve their perceived social support and health outcomes.
... Emotional factors, such as anger and stress sensitivity, are increasingly recognized as potential contributors to CAD (2)(3)(4)(5)(6)(7)(8)(9)(10). For example, anger can trigger acute episodes of acute coronary syndrome (ACS) secondary to increased hemodynamic responses (11)(12)(13)(14). ...
Introduction:
Major depression is associated with an increased risk for and mortality from coronary artery disease (CAD), however the mechanisms by which this occurs are not clear. Depression, which is linked to stress, is associated with changes in brain areas involved in memory and the stress response, and it is likely that these regions play an important role in this increased risk. This study assessed the effects of stress on brain and cardiac function in patients with CAD with and without depression.
Methods:
CAD patients with (N = 17) and without (N = 21) major depression based on the Structured Clinical Interview for DSM-IV (DSM-IV) and/or a Hamilton Depression Scale score of nine or greater underwent imaging of the brain with high resolution positron emission tomography (HR-PET) and [O-15] water and imaging of the heart with single photon emission tomography (SPECT) and [Tc-99 m] sestamibi during mental stress (mental arithmetic) and control conditions.
Results:
Patients with CAD and major depression showed increased parietal cortex activation and a relative failure of medial prefrontal/anterior cingulate activation during mental stress compared to CAD patients without depression. Depressed CAD patients with stress-induced myocardial ischemia, however, when compared to depressed CAD patients without showed increased activation in rostral portions of the anterior cingulate.
Conclusions:
These findings are consistent with a role for brain areas implicated in stress and depression in the mechanism of increased risk for CAD morbidity and mortality in CAD patients with the diagnosis of major depression.
... Traditional risk factors such as smoking, age, diabetes, serum cholesterol, serum hypercholesterolemia, and systemic hypertension do not account for all of the risk for CAD (DeFilippis et al., 2015). The influence of acute psychological stress on cardiovascular disease is an emerging public health concern (Rosengren et al., 2004;Steptoe & Kivimaki, 2013;Strike & Steptoe, 2005;Vaccarino & Bremner, 2017). The population attributable risk of CAD due to chronic stress has been estimated at 33%, which suggests a major contributory role (Rosengren et al., 2004). ...
The influence of acute psychological stress on cardiovascular disease is an emerging public health concern. Identification of brain mechanisms underlying this may aid in the discovery of possible treatments. Acute psychological stress may induce arteriolar vasoconstriction and reduce blood flow to vital organs. We hypothesized that functional changes in brain regions involved with memory and autonomic/emotional regulation are implicated in the vasoconstrictive stress response, including the medial prefrontal cortex (anterior cingulate), insula, and dorsolateral prefrontal cortex. Subjects with a history of coronary artery disease (N = 59) underwent measurement of microvascular vasomotor tone with the EndoPAT device and O–15 positron emission tomography (PET) imaging of the brain during exposure to mental stress and control conditions. The peripheral arterial tonometry (PAT) ratio was calculated as the mean peripheral vasomotor tone during stress divided by the mean tone during rest. Whole brain contrasts were performed between groups above and below the median PAT ratio, and significant contrasts were defined with cutoff p < 0.005. Stress‐induced peripheral vasoconstriction (below median PAT ratio) was associated with increased stress activation in insula and parietal cortex, and decreased activation in the medial prefrontal cortex with stress tasks compared to control tasks. These findings demonstrate that stress‐induced vasoreactivity is associated with changes in brain responses to stress in areas involved in emotion and autonomic regulation. These findings have important implications on possible treatments for mental stress‐induced vascular toxicity.
... При парных сравнениях средних величин в четырех и более независимых группах для Согласно Европейским рекомендациям по профилактике сердечно-сосудистых заболеваний (ССЗ), эмоциональный стресс может вызывать различные нарушения системы кровообращения, определяя кардиоваскулярный риск и прогноз [1]. Частые повторные эпизоды эмоциональных стресс-реакций или их хроническое течение играют существенную роль в патогенезе ССЗ [2,3]. ...
Aim. Revealing of the associations of various cardiovascular psychosocial risk factors prevalence — vital exhaustion (VE) and hostility — with arterial hypertension (AH) in open male population, age 25-64 y. o., of moderately urbanized Siberian city. Material and methods. One stage epidemiological study was conducted on representative selection, shaped from election lists of males 25-64 y. o., from one of Tymen city districts. For the analysis of AH the data from cardiological screening was used, and surveying by psychosocial methods in algorithms of MONICA-MOPSY. Results. The prevalence of psychocosical risk factors was found as following: VI — 54,5%, hostility — 46,4%. With the age, higher levels of VE and hostility become more prevalent, achieving maximum at 55-64 y. o. Populational variation of systolic and diastolic blood pressure in males 25-64 y. o. is shifted to the right, with high prevalence of AH. In AH groups there are low and moderate levels of VE and high hostility. Conclusion. The data points on high demand on AH prevention in economically active citizens that have psychosocial risk factors; this requires interventions from the healthcare institutions of the region.
... An extensive review has implicated anger and hostility in the aetiology of acute coronary syndrome (ACS), with even experimentally-evoked anger (e.g. recall and discussion of anger-arousing events), triggering myocardial ischemia in some patients (Strike and Steptoe, 2005). ...
Despite the 60-year history of attempting to understand the relationship between personality and cardiovascular disease (CVD), individual dispositions that affect the manner in which people think, feel and act are not typically considered in cardiac clinical settings. To identify how persistent negative emotional states and behavioural traits impacted cardiovascular health, early studies focused on the Type A personality (competitive, aggressive) and, later on, the Type D personality (‘distressed’). Recent evidence on other personality types or behaviours, such as borderline personality disorder, alexithymia and neuroticism, suggest that it may be the core elements of these, alongside hostility and proneness to anger, that lead to atherosclerosis, endothelial dysfunction, coronary artery calcification, and inflammation. The current paper, and part 2 of the Psychology in Cardiology series, explores the evidence supporting different interventions for people with health-compromising personality factors, to assist in planning lifestyle modification.
... Emotional factors, such as anger and stress sensitivity, are increasingly recognized as potential contributors to CAD (2)(3)(4)(5)(6)(7)(8)(9)(10). For example, anger can trigger acute episodes of acute coronary syndrome (ACS) secondary to increased hemodynamic responses (11)(12)(13)(14). ...
Objective:
Coronary artery disease (CAD) is a major cause of morbidity and mortality, and despite important advances in our understanding of this disorder, the underlying mechanisms remain under investigation. Recently, increased attention has been placed to the role of behavioral factors like emotional stress on CAD risk. Brain areas involved in memory and the stress response, including medial prefrontal cortex, insula and parietal cortex, also have outputs to the peripheral cardiovascular system. The purpose of this study was to assess the effects of mental stress on brain and cardiac function in patients with CAD.
Methods:
CAD patients (N=170) underwent cardiac imaging with [Tc-99m] sestamibi single photon emission tomography (SPECT) at rest and during a public speaking mental stress task. On another day they underwent imaging of the brain with [O-15] water positron emission tomography (PET) during mental stress (arithmetic and public speaking) and control conditions.
Results:
Patients with mental stress-induced myocardial ischemia (MSI) showed increased activation with stress in anterior cingulate, inferior frontal gyrus, and parietal cortex (p<0.005). This was seen with both arithmetic stress and public speaking stress. Arithmetic stress was additionally associated with left insula activation, and public speaking with right pre/post-central gyrus and middle temporal gyrus activation (p<0.005).
Conclusions:
These findings suggest that mental stress-induced myocardial ischemia is associated with activation in brain areas involved in the stress response and autonomic regulation of the cardiovascular system. Altered brain reactivity to stress could possibly represent a mechanism through which stress leads to increased risk of CAD-related morbidity and mortality.
... In rare occasions, exhilaration and laughter may cause serious harms such as cardiac arrhythmias or heart failure (Ferner and Aronson 2013). In patients with coronary artery disease, even short periods of (also positive) intense emotional arousal may trigger the onset of acute coronary syndromes (Mittleman et al. 1995;Samuels 2007;Strike and Steptoe 2005). Amusement accompanied by laughter may also worsen pulmonary functioning in patients with lung disease (Lebowitz et al. 2011). ...
Paul McGhee, one of the most influential pioneers in the field of humor research has been engaged for decades in exploring how humor can be used for the maintenance or improvement of well-being in the face of adversity. The present paper reviews recent empirical research corroborating several of his propositions. Undeniably, the benefits of humor can be much greater when one generates his or her own humor compared to just passively consuming humor. The active use of humor can be a potent tool to successfully cope with and appropriately recover from stressful situations, especially if it becomes a habitual response to adverse circumstances. While the ice is thin with regard to any beneficial effects of humor on physical health, it certainly may enhance the quality of life of patients. The paper concludes with the general evaluation that the documented potential of humor for the maintenance of well-being is impressive, thereby rendering exaggerations and insufficiently substantiated claims of additional effects unnecessary.
Paul McGhee, one of the most influential pioneers in the field of humor research, as well as of structured humor training, has been insisting for decades that using humor can have many benefits beyond being fun, and many followed his lead. Moreover, he had always taken care to systematically collect relevant empirical, scientific evidence and to expertly evaluate it. Not all of his followers took his lead on this matter.
... Nevertheless, despite the above associations, patients without any triggering event (eg, gradual onset of heart failure symptoms, typically over the course of days to weeks) are also frequently encountered. Although there is evidence that physical activity and other specific behaviors are associated with the occurrence of myocardial infarction, 6,7 sudden cardiac death, 8 and stroke, 9,10 no data are available on the correlation between these events and the occurrence of acute heart failure. Further, little information is available about the impact of the triggering events on prognosis. ...
Background:
The onset of acute heart failure is known to be associated with increased physical activity and other specific behaviors that can trigger hemodynamic deterioration. This analysis aimed to describe the distribution of triggers in patients hospitalized for acute heart failure, and investigate their effects on in-hospital outcomes.
Methods:
Consecutive patients hospitalized for acute heart failure between 2010-2014 were registered in a multicenter data registration system (72 institutions within Tokyo, Japan). Baseline demographics and in-hospital mortality were extracted from 17,473 patients. Patients with a trigger were grouped based on their triggering event: those with onset during (a) physical activity; (b) sleeping; (c) eating or watching television; (d) bathing or excretion (using of restrooms); and (e) engaging in other activities; these patients were compared with patients without identifiable triggers. Multiple imputation was used for missing data.
Results:
Patients were predominantly men (57.1%) with a mean age of 76.0 ± 13.0 years; a triggering event was present in 49.1%. No significant difference in baseline characteristics was noted between groups except for younger age, higher blood pressure, and prevalence of signs of congestion in the trigger-positive group. In-hospital mortality rate was 7.9%. Presence of triggers was positively associated with a reduced risk of in-hospital mortality (adjusted OR 0.79; 95% CI 0.70-0.90; p = 0.0003). In a delta-adjusted pattern mixture model, the effect of a triggering event on in-hospital mortality remained consistently significant.
Conclusion:
Triggering events for acute heart failure can provide additional information for risk prediction. Efforts to identify the triggers should be made to classify patients according to risk group.
... In sensitive individuals, suddenly developed emotional states can be a significant causative factor for acute coronary event shortly after the stress, provoking a rapid pathophysiological responses in hemodynamic, hemostatic and neuroendocrine system (Kop 1999). On the other hand, exposure to "chronic" risk factors such as anxiety, depression, stress at workplace, social isolation, smoking and physical inactivity favor the development and gradual progression of the existing CAD (Strike & Steptoe 2005). Emotional responses in patients with AMI differ in coping with one's disease. ...
Background:
The aim of this study was to define the level of patient exposure to stress in the previous 5 years before acute myocardial infarction (AMI), personality type A assessment, ways of coping with stressful situations, health locus of control and the grade of anxiety (as state and personality trait).
Subjects and methods:
118 patients who were consecutively hospitalized during 8 months in our Coronary care unit due to AMI, took part in the study. As controls we examined 103 healthy male volunteers (mean age 60.8±2.93 years).
Results:
AMI patients presented with higher degree of behavior corresponding to type A personality (F=18.756, p=0.000), and also showed higher degree of anxiety, as state and personality trait (F=23.634, p=0.001; F=19.253, p=0.000), in comparison to healthy controls. Also, AMI patients were significantly more often coping emotionally in stressful situations than control subjects (F=21.354, p=0.000), and they had significantly higher external locus of control compared to healthy subjects (F=13.284, p=0.001). They often considered that they were not able to control their health, namely they evaluated their ability to control their health as weak and were much more often directed to cope with intense emotions (r=0.24, p=0.002).
Conclusions:
The study showed that AMI patients psychologically differed from the healthy controls, indicating that they were prone to maladaptive behavioral patterns which could favor development and complicate course of coronary artery disease.
... Episodes of anger can also precipitate or "trigger" acute cardiac events, such as myocardial infarction (Mostofsky et al. 2013(Mostofsky et al. , 2014. Among patients with advanced coronary atherosclerosis, experimentally evoked anger (e.g., recall and discussion of anger-arousing events) can evoke myocardial ischemia (Strike and Steptoe 2005). Thus, anger and hostility most likely predict the development of CHD morbidity and mortality because they promote the initial development and progression of the underlying atherosclerosis but also because these traits can contribute to the precipitation of ischemia and acute coronary crises among persons with advanced disease. ...
Anger and hostility are described with special attention to their cognitive-motivational properties. Varying operational definitions related to anger self-report and behavioral observation are presented. The idea that anger can be maladaptive is now widely accepted as in DSM and alternative classifications of dysfunctional anger. The idea that maladaptive anger raises risks for hypertension and coronary heart disease is reviewed with reference to empirical findings on mediators such as atherosclerosis, cardiovascular reactivity, immune system changes, and unhealthy lifestyles. Given that anger is a relational emotion, it is not surprising that it befalls many interpersonal relations including close/intimate relationships. Dimensions of affiliation and control in relationships are presented as a framework for understanding how anger and hostility can develop and persist in these contexts. The further connection between such anger and cardiovascular function is illustrated. Fortunately, maladaptive anger is treatable, as explained with meta-analytic evidence on cognitive behavioral therapy (CBT). Also available are recent enhancements like CBAT that involve sequencing multiple cognitive, behavioral, and affective strategies appropriate to the process of anger from onset, through progression, to offset. Finally, traditional interpersonal therapies and newer therapeutic formulations such as acceptance and commitment therapy may address major themes in interpersonal conflict underlying the onset and maintenance of cardiovascular disease. Yet, many of these potential applications still await research and implementation in the field of psychocardiology.
Sudden cardiac death (SCD) can be defined as ‘death resulting from abrupt cessation of cardiac function due to sudden cardiac arrest’. This chapter identifies the inherited primary arrhythmia syndromes and lists the key aspects of patient assessment and risk stratification and strategies to reduce the risk of SCD. Increasing age is a strong predictor of risk for SCD, but the relationship between advancing age and incidence of SCD is not linear. Myocarditis results from myocardial infection and/or an autoimmune response that causes active destruction of myocytes. Optimal medical therapy including angiotensin‐converting enzyme inhibitors, beta‐blockers and aldosterone receptor antagonists is recommended in patients with Dilated cardiomyopathy to reduce the risk of sudden death and progressive heart failure. Family screening of first‐degree relatives of victims of Sudden unexpected death (SUD) is important to identify individuals at risk, advise on available treatment and adequately prevent SUD.
According to economists, saving the life of a single American is just as beneficial to society as saving the lives of 2 Saudis, 5 Romanians, 10 Macedonians, 35 Indians, 69 Haitians, 90 Sierra Leoneans, or 148 Liberians. Why do economists think that, to judge if your life is worth saving, they must first check your pocketbook? Why do so many organizations, from the United States Government and the World Bank to the Gates Foundation and the United Nations (many of whom claim to hold the equality of life as sacrosanct) agree that when you check the numbers, rich lives are just worth more?
Are All Lives Equal? investigates how economics has come unbound from its philosophical and ethical foundations. It explores why economists support policy frameworks that would let hundreds of poor people die to save a single rich person. Unlike many philosophical treatises on economics, this book does not advocate blindly discarding the useful tools of Cost-Benefit Analysis and the Value of a Statistical Life. Instead, it strives to thread the needle between economics and philosophy, advocating for reforming the way governments measure benefit by making the system both more accurate and more just.
With over 40 new, original, thought experiments, this book is engaging and accessible to everyone, from economists that know nothing of philosophy, to philosophers that know nothing of economics, to all of us skeptics in between that know nothing of either.
Aim: Myocardial infarction (MI) is one of the most important cardiovascular diseases. A trigger is an external stimulus, potential to create a pathological change leading to a clinical event. In addition to classic risk factors of ischemic heart disease and myocardial infarction, MI triggers play critical roles in the incidence of acute MI.
Methods and Results: This is a cross-sectional study of 254 patients with the first acute myocardial infarction referring to Seyedoshohada heart center of Urmia, Iran were enrolled in the study within one year of study. After 48h of hospitalization and, treatment, and cardiac caring, the patients were provided with the questionnaire to collecting the history of the disease ad triggers. In addition to laboratory and paraclinical data, the analysis of the study was performed. Out of 220 (86.4%) patients with STEMI and 34 (13.6%) patients with NSTEMI, there were significant differences (P-value <0.05) in AMI triggers with LVEF (0.03), gender (0.027), residency and living area (0.039), occupation (0.002), smoking (0.008), abnormal serum TG levels (0.018) and the season of AMI occurrence (0.013). The mean age for AMI patients was 60.4±12.97 years old with a mean BMI of 26.65±4.35 kg/m2.
Conclusion: In addition to classic risk factors of ischemic heart disease and myocardial infarction, health care systems and physicians must pay more attention to triggers that may induce an acute myocardial infarction in people with predisposing factors especially in the male sex, stressful and hand working jobs, and psychological and mental tension patients.
Patients with severe mental illness (SMI) have 13 to 30 years shortened life expectancy when compared to the general population, and 60% of this excess mortality is caused by physical illnesses. Behavioral and social risk factors, as well as a poor quality of physical healthcare offer, contribute to higher rates of medical illness in this population. Sex and gender are individual risk factors, and both account for the expression of disorders. Sex is biological and determines reproductive function, sexual hormones, and gene expression. On the other hand, gender is associated with behavior and life experience. When considering women’s health, some medical conditions, as, for example, thyroid disorders, are more prevalent and can affect women’s mental health. This chapter aims to describe the relationship between the main clinical disorders affecting females and their mental health.
Forgiveness as a procedure has been gaining prominence. The objective of this article is to provide the basics of forgiveness as an intervention so primary care clinicians can facilitate its use. These clinicians include but are not limited to physicians, nurses, medical assistants, pharmacy professionals, physical therapists, social workers, psychologists, case managers, and clergy. This narrative explains the rationale for understanding forgiveness as a procedure and ways to explain it. To assist clinicians and patients in making informed decisions, samples of forgiveness research are included that describe its positive relationship to specific physical health situations. The article also describes an evidence-based forgiveness therapy, circumstances in which it is harmful to forgive oneself or others, describes the limitations of this article, and suggests future directions.
Background:
Cannabis use is associated with an increased risk of stress-related adverse cardiovascular events. Because brain regions of the central autonomic network largely overlap with brain regions related to the neural response to emotion and stress, the central autonomic network may mediate the autonomic response to negative emotional stimuli. We aimed to obtain evidence to determine whether neural connectivity of the central autonomic network is altered in individuals with cannabis use disorder (CUD) when they are exposed to negative emotional stimuli.
Methods:
Effective (directional) connectivity (EC) analysis using dynamic causal modeling was applied to functional magnetic resonance imaging data acquired from 23 subjects with CUD and 23 control subjects of the Human Connectome Project while they performed an emotional face-matching task with interleaving periods of negative-face (fearful/angry) and neutral-shape stimuli. The EC difference (modulatory change) was measured during the negative-face trials relative to the neutral-shape trials.
Results:
The CUD group was similar to the control group in nonimaging measures and brain activations but showed greater modulatory changes in left amygdala to hypothalamus EC (positively associated with Perceived Stress Scale score), right amygdala to bilateral fusiform gyri ECs (positively associated with Perceived Stress Scale score), and left ventrolateral prefrontal cortex to bilateral fusiform gyri ECs (negatively associated with Perceived Stress Scale score).
Conclusions:
Left amygdala to hypothalamus EC and right amygdala to bilateral fusiform gyri ECs are possibly part of circuits underlying the risk of individuals with CUD to stress-related disorders. Correspondingly, left ventrolateral prefrontal cortex to bilateral fusiform gyri ECs are possibly part of circuits reflecting a protective mechanism.
The previous chapter introduced the ImmunoEmotional Regulatory System (IMMERS). Also, there was a brief discussion about psychological states/psychiatric disorders that so far have been linked to the IMMERS. The present chapter considers another aspect of the IMMERS in which physiological states/physical diseases can be fit to the IMMERS.KeywordsAllergic rhinitisAsthmaAutoimmune diseasesCancerCardiovascular diseasesEmotion regulationEmotion dysregulationHemodialysisHuman immunodeficiency virusImmunoemotional regulatory systemInfectionInflammatory bowel diseasemetabolic syndromeNeurological diseasesPhysical diseasesPhysiological statesSkin diseasesSleep disordersStrokeTraumaVaccination
Background
Major incidents affecting large numbers of people may increase the rate of acute cardiovascular events, even among those who are not directly involved in the incident. It is hypothesized that the MV Sewol ferry disaster (South Korea) would increase the incidence of cardiovascular events nation-wide.
Methods
Data on all adult patients (>18 years) who were diagnosed with acute cardiovascular events, including acute myocardial infarction (MI), angina, and cardiac arrhythmias, were extracted from the National Emergency Department Information System (NEDIS) from March 15 through June 17, during the years 2011-2014 (four weeks before to eight weeks after the event date). Poisson regression models were used to calculate the incidence rate ratios (IRRs) comparing the weekly changes in the occurrences of cardiovascular events from the week of the Sewol event (April 16-22, 2014) to eight weeks after the disaster (June 11-17, 2014), using the one-month period before Sewol as a reference period (March 15-April 15), adjusting for calendar years (years 2011-2014) and environmental factors.
Results
During the study periods, cardiovascular events were identified in 73,823 patients. Compared to the reference period, the week of the Sewol disaster and the three weeks after the disaster showed a significant increase in the number of acute cardiovascular events, IRRs of 1.09 (95% CI, 1.03-1.15) and 1.08 (95% CI, 1.02-1.15), respectively (P <.01 for both). In particular, there was 21% increase in incidence of arrhythmia (IRR = 1.21; 95% CI, 1.02-1.44; P = .03) during the week of the Sewol disaster compared with the reference period.
Conclusion
This study showed a significant increase in the incidence of acute cardiovascular events during the week of, and the three weeks after, the Sewol ferry disaster in 2014. These additional cardiac emergencies may be triggered by emotional stressors related to the event, highlighting the public health importance of indirect exposure to a tragic catastrophe.
Background:
Hajj is the largest human gathering with over 2 million people. We evaluated the effect of bundle care intervention on mortality.
Methods:
A population-based, before and after study compared the effect of an intervention on mortality. The intervention included recruitment of cardiac team, introducing 24/7 catheterization service, cardiac coordination, standardized cardiac care pathways, and establishment of an effective transportation system.
Results:
Cardiac mortality accounted for about 52% of all in-hospital deaths before intervention in 2009. This decreased significantly to 43.3%, 32.5%, and 19.7% in 2009, 2010, and 2011, respectively. In-hospital mortality of acute coronary syndromes was 4.7%, 4.6%, and 3.0%, in the years 2009, 2010, and 2011, respectively. Mortality due to other causes remained largely unaffected. There was no significant change in the national mortality due to cardiac causes over the same period provided a reassurance that the observed improvement in in-hospital acute coronary syndrome mortality was not due to overall improvement in health care. The numbers of cardiac catheterization procedures increased 3-fold and cardiac surgical procedures increased 5-fold between 2009 and 2011.
Conclusions:
In this study, we found that an evidence-based intensive bundle care intervention substantially reduced the cardiac mortality among the pilgrims assembling for Hajj in Makkah.
The history of psychosomatic research and current studies of psychological influences on cardiometabolic risk are reviewed. Personality, psychopathological, situational and cognitive-behavioural risk factors are considered. Shortages of current studies are pointed out, the necessity of integration of different psychosomatic approaches as well as the need for individually-oriented investigations are stressed.
Not commonly seen, the risk of sudden death after significant emotional stress has been reported since antiquity and incorporated into folk wisdom, reflected by phrases such as “scared to death” and “broken heart.” A typical “victim” suffers from significant and often life-threatening natural diseases, making determination of the manner of death complicated, and at times controversial. The present study is designed to assess inter-rater variability and nonuniformity and controversy seen in manner of death certification in certain cases of death with significant stress involved in the circumstances of death.
Members of the National Association of Medical Examiner (NAME) were surveyed to assess differences in manner of death certification for eight sudden unexpected death scenarios in middle-aged men and women with underlying cardiac disease after significant stressful events including: being chased down a lonely road followed by a verbal confrontation, a roll-over motor vehicle collision (MVC) without injuries, a fall from a wheelchair in a MVC, an alleged armed robbery, an involuntary commitment, an arrest by police, sexual intercourse, and a severe panic attack with breathing problems. In all cases, the autopsy examination revealed hypertensive and arteriosclerotic cardiovascular disease. In all cases, natural diseases were identified as significant contributing condtions, including emphysema in six cases and diabetes mellitus in three.
Eighty-six responses were collected. The results show wide inter-rater variability, ranging from very good to poor (Kappa ranges from 0.16 to 0.94). One hundred fifty-five comments were collected. Most of the comments addressed more than one topic and were followed by discussions, open questions, and responders’ experiences with previous cases and legal proceedings.
Our data show that cases of sudden death after significant stress have almost complete agreement in four cases and very high inter-rater variability in the other four. We propose that a detailed analysis of each case and an algorithmic approach could improve the predictability of the outcomes of death investigations for the legal system and for families.
Background and aims:
Sleep characteristics are associated with incident cardiovascular diseases (CVD), but there is a lack of studies on the association between sleep characteristics and incidence/progression of coronary artery calcification (CAC).
Methods:
In the Heinz Nixdorf Recall Study, a population-based cohort study in Germany, CAC was assessed by electron-beam tomography at baseline and at 5-year follow-up. In an analysis set of 3043 subjects (age at baseline 45-74 years; 47% men), we fitted logistic and linear regression models to assess associations between self-rated sleep characteristics (nocturnal and total sleep duration; napping; various sleep disorders) and CAC incidence/CAC progression. Progression was measured as 5-year progression factor, as categories of absolute CAC change, and additionally characterized as rapid or slow compared to an extrapolation of baseline CAC values.
Results:
We observed barely any association between sleep characteristics and CAC progression regardless of the chosen statistical approach; associations between sleep and CAC incidence were slightly larger, e.g., the geometric mean of the 5-year CAC progression factor was 6.8% (95% confidence interval: -9.5; 25.9) larger for ≤5 h, 2.9% (-7.3; 14.3) larger for 5.1-6.9 h and 7.1% (-2.4; 15.7) smaller for ≥7.5 h total sleep compared to 7- <7.5 h total sleep. For subjects with any regular sleep disorder, the geometric mean of the 5-year CAC progression was 3.5% (-4.7; 11.2) smaller compared to subjects without any regular sleep disorder.
Conclusions:
In this German cohort study, sleep characteristics were barely associated with CAC progression.
Objective:
Psychological stress in chronic heart failure (CHF) is associated with systemic neurohormonal and immune system responses and increased mortality. Autophagy refers to the biological process of degradation and recycling of dysfunctional cellular components. We investigated the role of psychological stress on autophagy function in CHF mice.
Results:
A one-week stress exposure significantly increased serum levels of corticosterone and Ang II (P= .000), increased levels of oxidative stress, induced overt heart failure, and increased mortality (P =. 002). Furthermore, stress exposure unregulated mRNA expression of beclin-1 (10.891±3.029 versus 4.754±1.713,P = .001), Rubicon (6.403±1.813 versus 3.653±.441,P = .006), and Atg7 (111.696±4.049 versus 6.189±1.931,P = .017), increased expression of autophagosomal, and decreased clearance of autophagosomes. In vitro, Ang II significantly increased autophagy flux in cultured cardiomyocytes, which could be partly inhibited by N-acetylcysteine.
Conclusions:
Psychological stress may contribute to the development of CHF by enhancing heart oxidative stress and impairing autophagy flux.
This work presents data about the adjustment disorder often referred to as emotional stress, it presents the modern concepts about stress, discusses the classifications most used, and offers information on its epidemiology in Brazil. It also discusses the consequences of stress not only to the individual, but to society, as well.
Background: Acute myocardial infarction (AMI) is one of the most preventable non-communicable diseases in human. Identifying triggers of myocardial infarction (MI) and prevention ways of exposure-induced complications can reduce morbidity and mortality in people at risk.
Aim: The aim of this study was to identify the emotional, environmental, physical and chemical dimensions of acute triggers in patients with AMI.
Methods: This case-crossover study was conducted on 269 patients with AMI, hospitalized at two remedial centers in Rasht in 2015. The study samples were selected by convenient sampling method. Data were collected using researcher-made questionnaire through interviews. Hazard and control periods for each trigger and its effects on the development of MI were studied. The collected data were analyzed using descriptive and analytical statistical methods, Cochran test, and generalized estimating equation (GEE) model with logistics function default in SPSS version 21, and p
This chapter will provide a definition of anxiety and describe methods for assessing it within cardiac practice. Next the epidemiology of anxiety disorders and prevalence of anxiety disorders in cardiovascular disease will be reviewed followed by literature on anxiety and cardiovascular disease. Subsequently, different treatment options including pharmacotherapy and different psychological approaches will be evaluated. Other treatment measures discussed in this chapter include breathing retraining, relaxation, and exercise therapy. The chapter concludes with recommendations for treatment of anxiety in heart disease along with future directions for research.
Objective: To identify the trigger points for pain in patients with Acute Coronary Syndrome (ACS) admitted to two hospitals in southern Brazil and to verify the recognition frequency of pain as a cardiac event. Methods: Cross sectional study using secondary database and a 105 patients sample. Results: From the sample, 47 (45%) patients had symptoms at rest; 20 (19%) woke up in pain; 19 (18%) did practice physical exercises; 10 (9.5%) were under stress situations; and 9 (9%) were performing another activity. None of the patients reported sexual activity as a trigger for pain; 67 (64%) related the symptoms to the cardiac event. Conclusion: Pain in patients with ACS occurred in patients at rest. Although the sample reported pain as a cardiac event, there is still a lack of nursing assistance related to health education aimed at early arrivals to the emergency services
Vigorous physical exertion transiently increases the risk of acute myocardial infarction (MI), but little is known about the clinical characteristics of exertion-related MI.
To compare the clinical and angiographic characteristics of patients who had an exertion-related acute MI vs those who experienced an MI not related to exertion.
Prospective observational cohort study of patients with an acute MI referred to a tertiary care hospital for primary angioplasty.
Of 1048 patients with acute MI, 640 (64 who experienced an exertion-related MI and 576 who did not) were selected for treatment with primary angioplasty and admitted between August 1995 and November 1998.
Clinical characteristics of the patients, including their habitual physical activity (determined by the Framingham Physical Activity Index and the Lipid Research Clinic Physical Activity Questionnaire), angiographic findings during coronary angiography, and the relative risk (RR) of MI during exertion.
Patients who experienced exertion-related MI were more frequently men (86% vs 68%), hyperlipidemic (62% vs 40%), and smokers (59% vs 37%), were more likely to present with ventricular fibrillation (20% vs 11%), Killip classification III or IV heart failure (44% vs 22%), single-vessel disease (50% vs 28%), and a large thrombus in the infarct artery (64% vs 35%) and were more likely to be classified as having very low or low activity (84% vs 66%). The RR of experiencing an MI during exertion was 10.1 times greater than the risk at other times (95% confidence interval [CI], 1.6-65.6), with the highest risk among patients classified as very low active (RR, 30.5; 95% CI, 4.4-209.9) and low active (RR, 20.9; 95% CI, 3.1-142.1).
These results show that exertion-related MIs occur in habitually inactive people with multiple cardiac risk factors. These individuals may benefit from modest exercise training and aggressive risk-factor modification before they perform vigorous physical activity.
To examine the combined influence of workplace demands and changes in blood pressure induced by stress on the progression of carotid atherosclerosis.
Population based follow up study of unestablished as well as traditional risk factors for carotid atherosclerosis, ischaemic heart disease, and other outcomes.
Eastern Finland.
591 men aged 42-60 who were fully employed at baseline and had complete data on the measures of carotid atherosclerosis, job demands, blood pressure reactivity, and covariates.
Change in ultrasonographically assessed intima-media thickness of the right and left common carotid arteries from baseline to 4 year follow up.
Significant interactions between workplace demands and stress induced reactivity were observed for all measures of progression (P < 0.04). Men with large changes in systolic blood pressure (20 mm Hg or greater) in anticipation of a maximal exercise test and with high job demands had 10-40% greater progression of mean (0.138 v 0.123 mm) and maximum (0.320 v 0.261 mm) intima-media thickness and plaque height (0.347 v 0.264) than men who were less reactive and had fewer job demands. Similar results were obtained after excluding men with prevalent ischaemic heart disease at baseline. Findings were strongest among men with at least 20% stenosis or non-stenotic plaque at baseline. In this subgroup reactive men with high job demands had more than 46% greater atherosclerotic progression than the others. Adjustment for atherosclerotic risk factors did not alter the results.
Men who showed stress induced blood pressure reactivity and who reported high job demands experienced the greatest atherosclerotic progression, showing the association between dispositional risk characteristics and contextual determinants of disease and suggesting that behaviourally evoked cardiovascular reactivity may have a role in atherogenesis.
Moderate regular alcohol intake has been found to be associated with a decreased risk for coronary heart disease and stroke. We investigated the effects of acute intake of red wine (60 g ethanol) and a standard dinner under controlled conditions on haemostatic factors. Shear-induced platelet aggregation (SIPA) decreased after the intake of alcohol irrespective of whether the subjects were fasting or not, and also after the intake of food. The intake of alcohol inhibited the postprandial increase of von Willebrand factor multimers. Plasma levels of plasminogen activator inhibitor 1 activity (PAI-1) and serum triglycerides were increased by alcohol. Excretion of the platelet thromboxane A 2 metabolites 11-dehydrothromboxane B 2 and 2,3-dinorthromboxane B 2 , as well as the endothelial prostacyclin metabolite 2,3-dinor-6-ketoprostaglandin F 1 &agr;, into urine was not influenced by either alcohol or food. We conclude that eating a dinner together with red wine has no untoward effect on SIPA and that the decrease of SIPA is not specific for alcohol.
Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.
Editor—Witte et al found a significant increase in mortality from coronary heart disease and stroke in Dutch men aged ⩾45 on the day that the Dutch team was eliminated by the French from the 1996 European football championship compared with the five days before and after the match (relative risk 1.51; 95% confidence interval 1.08 to 2.09).1 We reassessed this hypothesis using corresponding French data.
The match had an audience of 4.7 million television viewers in France (around 8% of the French population). We performed the same time series analysis as Witte et al on French mortality data for the periods and personal characteristics corresponding to the Dutch data, the cause of death being classified according to ICD-9 (international classification of diseases, ninth revision, codes 410; 430-434; 436-438).
The table shows that, on the day of the match, mortality from all causes did not increase among French men or women compared with that on the five days before and after the match. In particular, mortality from myocardial infarction or stroke did not increase. On the day of the match 61 deaths from myocardial infarction or stroke were reported; on the day after the match 104 such deaths were reported.
The Dutch results were not confirmed by the French data, and we therefore question Witte et al's conclusion; they might have reached another conclusion had they used larger time windows. Furthermore, how many of the 41 people reported dead from myocardial infarction or stroke actually watched the match?
During and after the World Football Cup held in France from June 10 to July 12 1998 we set up electronic sentinel disease surveillance to estimate the incidence of various conditions in the French population. The incidence of the conditions we looked at might be affected by increased stress, possibly caused by an important football match.
Analysis of our data showed no relevant variation in the disorders surveyed. At the population level the effects of stress induced by important sporting events on health are probably minor.2 The level of population exposure to the risk factor (watching the match on television) was not the same in the French and Dutch populations (8% v 60%); this may have affected people's behaviour as regards alcohol consumption, smoking, and collective excitement. In addition, the match resulted in a nil-nil draw, and France won on penalty kicks. The result of a match may also have its effects.
Further studies are needed to establish whether the findings in the Dutch population are the result of chance or whether this is another French paradox.3
Despite anecdotal evidence suggesting that heavy physical exertion can trigger the onset of acute myocardial infarction, there have been no controlled studies of the risk of myocardial infarction during and after heavy exertion, the length of time between heavy exertion and the onset of symptoms (induction time), and whether the risk can be modified by regular physical exertion. To address these questions, we collected data from patients with confirmed myocardial infarction on their activities one hour before the onset of myocardial infarction and during control periods.
Interviews with 1228 patients conducted an average of four days after myocardial infarction provided data on their usual annual frequency of physical activity and the time, type, and intensity of physical exertion in the 26 hours before the onset of myocardial infarction. We compared the observed frequency of heavy exertion (6 or more metabolic equivalents) with the expected values using two types of self-matched analyses based on a new case-crossover study design. The low frequency of heavy exertion during the control periods was validated by data from a population-based control group of 218 subjects.
Of the patients, 4.4 percent reported heavy exertion within one hour before the onset of myocardial infarction. The estimated relative risk of myocardial infarction in the hour after heavy physical exertion, as compared with less strenuous physical exertion or none, was 5.9 (95 percent confidence interval, 4.6 to 7.7), Among people who usually exercised less than one, one to two, three to four, or five or more times per week, the respective relative risks were 107 (95 percent confidence interval, 67 to 171), 19.4 (9.9 to 38.1), 8.6 (3.6 to 20.5), and 2.4 (1.5 to 3.7). Thus, increasing levels of habitual physical activity were associated with progressively lower relative risks. The induction time from heavy exertion to the onset of myocardial infarction was less than one hour, and symptoms usually began during the activity.
Heavy physical exertion can trigger the onset of acute myocardial infarction, particularly in people who are habitually sedentary. Improved understanding of the mechanisms by which heavy physical exertion triggers the onset of myocardial infarction and the manner in which regular exertion protects against it would facilitate the design of new preventive approaches.
PURPOSE: To determine whether a circadian pattern in onset of symptoms existed and possible external triggers were implicated in the precipitation of acute myocardial infarction (AMI). PATIENTS AND METHODS: One thousand eight hundred eighteen consecutive patients with AMI hospitalized in 14 of the 21 existing coronary care units in Israel during the study period were assessed. RESULTS: The frequency of onset of symptoms by 6-hour intervals showed a predominant morning peak (6 AM to noon) (32%, p < 0.01) in comparison with the other three 6-hour intervals of the day. The preponderance of the morning peak persisted for subgroup analysis by gender (males 32%, females 31%); age (less than or equal to 65 years-32%; greater than 65 years-33%); diabetes mellitus (present or absent, 32%). However, patients with peripheral vascular disease and those with stroke in the past had a predominant evening peak. Possible external triggers of onset of AMI were present in 10% of patients. Exceptional heavy physical work, violent quarrel at work or at home, and unusual mental stress were the three most frequent possible external triggers reported immediately before or within the 24 hours preceding pain onset. Patients with possible external triggers were more likely to be males (85%) and were somewhat but not significantly younger (63.1 years) in comparison with patients without external triggers (73% and 64.3 years respectively). CONCLUSIONS: In a large group of consecutive patients with AMI, a predominant cyclic morning peak of pain onset was found in comparison with the other hours of the day. Possible external triggers precipitating AMI were involved in a minority of cases, suggesting that endogenous changes occurring in the morning hours are generally responsible for the increased rate of myocardial infarction occurring after awakening.
Context:
Studies have found that individuals who consume 1 alcoholic drink every 1 to 2 days have a lower risk of a first acute myocardial infarction (AMI) than abstainers or heavy drinkers, but the effect of prior drinking on mortality after AMI is uncertain.
Objective:
To determine the effect of prior alcohol consumption on long-term mortality among early survivors of AMI.
Design and setting:
Prospective inception cohort study conducted at 45 US community and tertiary care hospitals between August 1989 and September 1994, with a median follow-up of 3.8 years.
Patients:
A total of 1913 adults hospitalized with AMI between 1989 and 1994.
Main outcome measure:
All-cause mortality, compared by self-reported average weekly consumption of beer, wine, and liquor during the year prior to AMI.
Results:
Of the 1913 patients, 896 (47%) abstained from alcohol, 696 (36%) consumed less than 7 alcoholic drinks/wk, and 321 (17%) consumed 7 or more alcoholic drinks/wk. Compared with abstainers, patients who consumed less than 7 drinks/wk had a lower all-cause mortality rate (3.4 vs 6.3 deaths per 100 person-years; hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.43-0.71) as did those who consumed 7 or more drinks/wk (2.4 vs 6.3 deaths per 100 person-years; HR, 0.38; 95% CI, 0.25-0.55; P<.001 for trend). After adjusting for propensity to drink and other potential confounders, increasing alcohol consumption remained predictive of lower mortality for less than 7 drinks/wk, with an adjusted HR of 0.79 (95% CI, 0.60-1.03), and for 7 or more drinks/wk, with an adjusted HR of 0.68 (95% CI, 0.45-1.05; P =.01 for trend). The association was similar for total and cardiovascular mortality, among both men and women, and among different types of alcoholic beverages.
Conclusion:
Self-reported moderate alcohol consumption in the year prior to AMI is associated with reduced mortality following infarction.
Objective.
—The imminent deadline for the 1991 Persian Gulf War and, subsequently, the 18 missile attacks by Iraq on Israel represented an unusual, short-term, life-threatening stressor for an entire nation. We studied mortality in Israel in January and February 1991 to determine whether excess deaths were precipitated on days of missile attacks.
Background Many anecdotes and several uncontrolled case series have suggested that emotionally stressful events, and more specifically, anger, immediately precede and appear to trigger the onset of acute myocardial infarction. However, controlled studies to determine the relative risk of myocardial infarction after episodes of anger have not been reported.
Methods and Results We interviewed 1623 patients (501 women) an average of 4 days after myocardial infarction. The interview identified the time, place, and quality of myocardial infarction pain and other symptoms, the estimated usual frequency of anger during the previous year, and the intensity and timing of anger and other potentially triggering factors during the 26 hours before the onset of myocardial infarction. Anger was assessed by the onset anger scale, a single-item, seven-level, self-report scale, and the state anger subscale of the State-Trait Personality Inventory. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using two types of self-matched control data based on the case-crossover study design. The onset anger scale identified 39 patients with episodes of anger in the 2 hours before the onset of myocardial infarction. The relative risk of myocardial infarction in the 2 hours after an episode of anger was 2.3 (95% confidence interval, 1.7 to 3.2). The state anger subscale corroborated these findings with a relative risk of 1.9 (95% confidence interval, 1.3 to 2.7). Regular users of aspirin had a significantly lower relative risk (1.4; 95% confidence interval, 0.8 to 2.6) than nonusers (2.9; 95% confidence interval, 2.0 to 4.1) (P<.05).
Conclusions Episodes of anger are capable of triggering the onset of acute myocardial infarction, but aspirin may reduce this risk. A better understanding of the manner in which external events trigger the onset of acute cardiovascular events may lead to innovative preventive strategies aimed at severing the link between these external stressors and their pathological consequences.
The aims of this systematic literature review are to describe the pattern of attributions made for the causes of heart disease, and to determine how this pattern varies with the method by which attributions are elicited, and the respondent group.A search yielded 47 papers and reports, containing 54 datasets. Lifestyle factors and chronic stress were the most common causes cited across all datasets. Attributions to stressors and fate or luck were more likely to be reported in studies that used interval rating scales than in studies that used dichotomous ratings. Cardiac patients were more likely to mention stressors and fate or luck as causes of heart disease; non-patients rated being overweight and hypertensive as more importantThe differences observed between the responses of patients and non-patients may be due to actor - observer differences, or to a methodological difference: patients are often asked to report their own experiences whereas non-patients are asked about the general case.
Strategies for tobacco controlEvidence of benefits from smoking cessationThe nature of tobacco smokingThe evidence basis for smoking cessationCommunity interventionsIndividual adviceNicotine replacement therapy (NRT)Bupropion (Zyban)Review of cessation studiesSpecialist smoking cessation clinicsPractical aspects of smoking cessation in clinical practice
LIN, L.-Y., et al.: Derangement of Heart Rate Variability During a Catastrophic Earthquake: A Possible Mechanism for Increased Heart Attacks. At 1:47 AM on September 21, 1999, the middle part of Taiwan was struck by a major earthquake measuring 7.3 on the Richter scale. It has been shown that the mental stress caused by an earthquake could lead to a short- or long-term increase in frequency of cardiac death probably through activation of the sympathetic nervous system. The aim of this study was to investigate the effects of emotional stress on the autonomic system during an actual earthquake. Fifteen patients receiving a 24-hour Holter ECG study starting from 10 ± 4 hours before the onset of the earthquake were included for the analysis of time- and frequency-domains of heart rate variability (HRV) at several time periods. A 24-hour Holter study recorded 2–6 months before the earthquake in 30 age- and sex-matched subjects served as the control group. Heart rate and the low frequency (LF) to high frequency (HF) ratio increased significantly after the earthquake and were attributed mainly to the withdrawal of the high frequency component (parasympathetic activity) of HRV. Sympathetic activation was blunted in elderly subjects > 60 years old. The concomitant ST-T depression observed in the Holter study correlated with a higher increment of LF as compared to HF components. The changes observed in HRV recovered completely 40 minutes following the earthquake. The derangement of HRV results from the withdrawal of the parasympathetic component and the arousal of sympathetic activity by the stressful earthquake. However, this autonomic derangement returned towards normal 40 minutes following the earthquake.
A neglected area of cardiovascular research—study of the mechanisms of acute disease onset—is receiving increased attention. The new interest is based on the undisputed findings that onset of myocardial infarction and sudden cardiac death are more likely soon after awakening, indicating that activities of the patient frequently trigger the diseases. Triggering may occur when stressors produce hemodynamic, vasoconstrictive and prothrombotic forces—acute risk factors—that, in the presence of a vulnerable atherosclerotic plaque, cause plaque disruption and thrombosis. Triggering research may clarify mechanisms and suggest measures to sever the linkage between a potential trigger and its pathologic consequence.
Objectives:
This study sought to compare the clinical features and outcome of a first myocardial infarction with onset of symptoms during or within 30 min of exercise, at rest and in bed.
Background:
It is not known whether activity at onset influences outcome of acute myocardial infarction.
Methods:
Information collected using a standard questionnaire was used to relate activity at the onset of symptoms to in-hospital outcome in 2,468 consecutive patients admitted to a coronary care unit with a first myocardial infarction between 1975 and 1993.
Results:
Patients with exercise-related onset were more likely to be younger and male. Those with onset in bed were more likely to be older and have a history of stable or unstable angina. Compared with patients whose symptoms began at rest, those with exercise-related onset had a lower in-hospital mortality rate after adjusting for age, gender and year of admission (odds ratio [OR] 0.60, 95% confidence interval [CI] 0.40 to 0.89), and patients with onset in bed had a higher mortality rate (OR 1.38, 95% CI 1.03 to 1.85). The incidence of cardiac failure requiring diuretic therapy was also lower for exercise-related onset (OR 0.83, 95% CI 0.67 to 1.04) and higher when onset was in bed (OR 1.36, 95% CI 1.11 to 1.66).
Conclusions:
There is an association between activity at onset and outcome of acute myocardial infarction. Differences in pathophysiology or in the population at risk could explain this observation.
Objective: To quantify the effects of quantity and frequency of alcohol consumption on risk of acute myocardial infarction and coronary death. Design: Case-control study. Setting: Lower Hunter region of New South Wales, Australia, 1983-94. Subjects: Men and women aged 35-69 years. Main outcome measure: Acute myocardial infarction or coronary death. Results: Alcohol consumption patterns were compared between 11 511 cases of acute myocardial infarction or coronary death and 6077 controls randomly selected from the same study population. After adjusting for the effects of age, smoking, and medical history, men and women who consumed one or two drinks of alcohol on five or six days a week had a reduction in risk of a major coronary event compared with men and women who were non-drinkers (odds ratios: men 0.31 (95% confidence interval 0.22 to 0.45); women 0.33 (0.18 to 0.59)). A similar reduction in risk was found after excluding non-drinkers who were formerly moderate to heavy drinkers. An acute protective effect of alcohol consumption was also found for regular drinkers who consumed one or two drinks in the 24 hours preceding the onset of symptoms (odds ratios: men 0.74 (0.51 to 1.09); women 0.43 (0.20 to 0.95)). Conclusions: Frequency and quantity of alcohol consumption are important in assessing the risk of a major coronary event Risk is lowest among men who report one to four drinks daily on five or six days a week and among women who report one or two drinks daily on five or six days a week.
. Premonitory symptoms as well as acute and long-standing stress preceding death were studied in 118 cases of prehospital sudden death, 62% of whom had shown premonitory symptoms. Prodromes were found in 94% of those whose fatal attack lasted longer than 2 hours. Premonitory symptoms seemed often to be unspecific in nature in cases of sudden death compared with those experienced by survivors of acute myocardial infarction. The occurrence of prodromes correlated with normal heart weight but not with the severity of the coronary artery disease or the presence of coronary thrombosis. Heavy smoking and a definite myocardial infarction revealed at autopsy were more frequent in those who had prodromes classifiable as unstable angina than in those with unspecific symptoms or without prodromes. The significance of acute and long-standing stress was most evident in the fatality of subjects with no long history of clinical disease. Although stress factors seemed to modify the course of the attack, a basic factor in the fatality was the coronary artery disease of critical severity. Stress factors did not play a major role in the precipitation of premonitory symptoms. Stress in patients with triple vessel disease in the coronaries was, however, more frequently (88%) conductive to prodromes than in those with double or single vessel disease (50%).
The effect of alcohol on cardiac rhythm was examined in ten male volunteers with a history of acute myocardial infarction. ECG monitoring with a portable ECG recorder was carried out for a period of 48 hours. After a control period of 15-18 hours an exercise test was performed and repeated after a standard dose (0.5 g/kg b.wt.) of alcohol. Then the patients were allowed to drink alcohol freely for two and half hours. The third exercise test was performed on the second morning. Heart rate at rest and sitting on a bicycle was highest in the third test, during the "hangover" period (p less than 0.05). With a submaximal work load heart rate, and also the heart rate-blood pressure pressure product, were highest after a standard dose of alcohol in the second test (p less than 0.05 and less than 0.01 respectively). The number of ectopic beats showed no significant difference in repeated exercise tests. On tape recordings, however, five of the ten patients experienced changes in cardiac rhythm after alcohol. In two patients the number of ectopic beats increased, the third patient had three successive ventricular ectopic beats after alcohol ingestion and in the fourth patient multiple sinus arrests occurred. In one patient a higher heart rate after alcohol ingestion abolished the ventricular ectopic focus seen during the control period.
The deaths of 100 men due to coronary artery disease which occurred so suddenly and unexpectedly as to merit a coroner's necropsy have been studied, with special reference to the exact circumstances of their occurrence. The most significant relationship of sudden death was with acute psychological stress. Moderate physical activity, the time of day, the day of the week, and a recent meal, especially if accompanied by alcohol, were also significantly related. Very strenuous exercise, the season of the year, the environmental temperature or recent change of it, and chronic psychological stress were not so related. Neither were the actual smoking of a cigarette nor the composition of the meal immediately preceding death. Compared with previous series of proved acute myocardial infarction the necropsies in these cases showed that the right coronary artery had been recently occluded by a thrombus more often than the left anterior descending. Stenosis or occlusion of the right coronary artery bore a significant relation to the suddenness of death. Special analysis of the 52 cases in which neither recent thrombus nor infarction were found did not disclose any circumstances attending death which differed from the remainder. Some comparisons are made with the circumstances attending the onset of symptoms in 100 men studied while recovering from an acute myocardial infarct.
The aim of this study was to provide insight into the mechanism of acute myocardial infarction by determining the modifiers of timing and possible triggers of onset of infarction.
A higher frequency of onset of acute myocardial infarction has been reported in the morning with a peak in the 1st 3 h after awakening. This observation suggests that the onset of infarction may be triggered by activity in the morning and at other times of the day.
The clinical history of the 3,339 patients entered into the Thrombolysis in Myocardial Infarction phase II study was analyzed to determine characteristics predicting a higher frequency of infarction between 6 AM and noon, and onset of infarction during exertion.
A higher proportion (34.4%) of infarctions began in the morning (6 AM to noon) compared with other times of the day. Characteristics independently predicting a higher frequency between 6 AM to noon were no beta-adrenergic blocking agent use in the 24 h before infarction, no discomfort other than the index pain in the preceding 48 h, occurrence of the infarction on a weekday and no history of current smoking. In 18.7% of patients, infarction occurred during moderate or marked physical activity. Independent predictors of exertion-related infarction included male gender, no history of current smoking, white race, no use of calcium channel blocking agents or nitrates in the preceding 24 h, the absence of either chest pain at rest in the 3 weeks before infarction or any pain in the preceding 48 h, the absence of new onset angina and the presence of exertional pain in the preceding 3 weeks. Compared with patients whose infarction occurred at rest or during mild activity, those with exertion-related infarction had fewer coronary vessels with > or = 60% stenosis (p = 0.002) and were more likely to have an occluded infarct-related vessel after thrombolytic therapy (p = 0.01).
Further study of the timing and activity at onset of infarction may provide insight into the pathophysiologic mechanisms causing acute myocardial infarction and provide clues to preventive measures.
This study, conducted in Auckland, New Zealand, over 2 years from March 1986, used a case-control design to investigate the hypothesis that alcohol acutely increases the risk of both nonfatal myocardial infarction and coronary death in the 24 hours after drinking, among regular drinkers. The nonfatal myocardial infarction analyses included 278 male and 60 female cases identified from a population-based coronary heart disease surveillance program and 458 male and 266 female controls randomly selected from the same population matched by age and sex. In the coronary death analyses, 172 male and 16 female coronary death cases from the same surveillance program and a population-based sample of 294 males and 165 females who were age and sex matched were examined. Information on alcohol consumption in the 24 hours before the coronary event in cases and a comparable 24-hour period in controls was collected. Study subjects all drank alcohol regularly at least once per month and were aged 25-64 years. Controls were more likely than cases to report a drinking episode in the 24-hour period examined in both sexes and for fatal and nonfatal disease. After controlling for possible confounding, the authors found that drinkers had a consistently lower estimated risk of both fatal and nonfatal coronary heart disease than participants reporting no alcohol in the previous 24 hours. The odds ratios ranged from 0.75 (95% confidence interval 0.62-0.90) for nonfatal myocardial infarction in men to 0.46 (95% confidence interval 0.19-1.10) for coronary death in women. There were no clear differences in estimated acute risk among those who drank one or two drinks, three or four drinks, or more than four drinks in the 24-hour period. These findings suggest that, contrary to previous speculation, alcohol consumption may acutely reduce coronary heart disease risk.
The Iraqi missile attack on Israel provided a unique opportunity to study the effects of fright due to a perceived threat of annihilation on the incidence of acute myocardial infarction (MI) and sudden death among the civilian population. During the first days of the Gulf war we noted a sharp rise in the incidence of acute MI and sudden death in our area compared with five control periods. Patient population in the various study periods did not differ significantly in age, sex ratio, hospital mortality, or proportion of patients in whom the acute event was the first presentation of coronary disease. However, during the first period of the war there were more cases of anterior wall MI and more patients received thrombolytic therapy than during control periods. Despite the continuing missile threat, the incidence of acute MI reverted to normal after the initial phase of the Gulf war.
A morning increase in onset of acute myocardial infarction (MI) has been documented, but its association with wake time and possible triggering events is unclear. The community-based, ongoing Triggers and Mechanisms of Myocardial Infarction (TRIMM) study was designed to investigate the factors associated with the transition from chronic coronary artery disease to acute MI. During the pilot phase in 1989, 224 consecutive hospitalized MI patients (176 men and 48 women, aged 60.3 +/- 9.2 years) of the prospectively defined Monitoring of Trends and Determinates of Cardiovascular Disease (MONICA) Augsburg MI register were interviewed 16.8 +/- 6.5 days after the event. The frequency of onset of MI was significantly higher (p less than 0.01) during the morning from 6 to 9 AM compared with other times of day. After adjustment for individual wake times, the peak of onset of MI was markedly sharper; the relative risk of MI during the 3-hour peak interval (the 3 hours after awakening) compared with other times of day increased from 1.8 (95% confidence interval, 1.3-2.4) to 2.4 (95% confidence interval, 1.8-3.1). Sixty-seven percent of the patients reported possible acute triggers of MI and/or unusual life events; among those, 52% reported stress or emotional upset. The TRIMM pilot study demonstrated the feasibility of a community-based study of possible triggering events of MI. The circadian variation of MI appears to result primarily from increased onset after awakening. This narrowing of the time frame of increased risk of MI should facilitate study of pathogenic mechanisms and aid in the design of more effective preventive regimens.
To test the hypothesis that stress generated by the Newcastle earthquake led to increased risk of heart attack and coronary death.
A natural experiment.
People living in the Newcastle and Lake Macquarie local government areas of New South Wales, Australia.
At 10.27 a.m. on 28 December 1989 Newcastle was struck by an earthquake measuring 5.6 on the Richter scale.
Myocardial infarction and coronary death defined by the criteria of the WHO MONICA Project and hospital admissions for coronary disease before and after the earthquake and in corresponding periods in previous years. Well established, concurrent data collection systems were used.
There were six fatal myocardial infarctions and coronary deaths among people aged under 70 years after the earthquake in the period 28-31 December 1989. Compared with the average number of deaths at this time of year this was unusually high (P = 0.016). Relative risks for this four-day period were: fatal myocardial infarction and coronary death, 1.67 (95% confidence interval [Cl]: 0.72, 3.17); non-fatal definite myocardial infarction, 1.05 (95% Cl: 0.05, 2.22); non-fatal possible myocardial infarction, 1.34 (95% Cl: 0.67, 1.91); hospital admissions for myocardial infarction or other ischaemic heart disease, 1.27 (95% Cl: 0.83, 1.66). There was no evidence of increased risk during the following four months.
The magnitude of increased risk of death was slightly less than that previously reported after earthquakes in Greece. The data provide weak evidence that acute emotional and physical stress may trigger myocardial infarction and coronary death.
A case-control design involving only cases may be used when brief exposure causes a transient change in risk of a rare acute-onset disease. The design resembles a retrospective nonrandomized crossover study but differs in having only a sample of the base population-time. The average incidence rate ratio for a hypothesized effect period following the exposure is estimable using the Mantel-Haenszel estimator. The duration of the effect period is assumed to be that which maximizes the rate ratio estimate. Self-matching of cases eliminates the threat of control-selection bias and increases efficiency. Pilot data from a study of myocardial infarction onset illustrate the control of within-individual confounding due to temporal association of exposures.
Recent documentation of a circadian variation in acute myocardial infarction (AMI) suggests that AMI is not a random event, but may frequently result from identifiable triggering activities. The possible triggers reported by 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size were analyzed. Possible triggers were identified by 48.5% of the population; the most common were emotional upset (18.4%) and moderate physical activity (14.1%). Multiple possible triggers were reported by 13% of the population. Younger patients, men and those without diabetes mellitus were more likely to report a possible trigger than were older patients, women and those with diabetes. The likelihood of reporting a trigger was not affected by infarct size. This study suggests that potentially identifiable triggers may play an important role in AMI. Because potential triggering activities are common in persons with coronary artery disease, yet infrequently result in AMI, further studies are needed to identify (1) the circumstances in which a potential trigger may cause an event, (2) the specific nature of potential triggering activites, (3) the frequency of such activities in individuals who do not develop AMI and (4) the presence or absence of identifiable triggers in various subgroups of patients with infarction.
MI is frequently unrecognized for reasons that are unknown, comprising approximately 40 percent of all MIs that occur. Although many unrecognized MIs are accompanied by symptoms of some sort, probably half are totally asymptomatic. Patients with unrecognized MI seem to be similar to those with typical presentations, with similar risk factors and other characteristics. It appears that MI carries the same prognosis whether clinically apparent or not and, therefore, warrants management in both cases. Therapy for silent MI should be aimed at (1) identification and modification of risk factors, (2) identification and treatment of residual ischemia, and (3) attempts at reducing the risk of reinfarction with subsequent morbidity and mortality. As we develop a better understanding of silent ischemic heart disease, hopefully the optimal management strategy for these patients will emerge.
Ethanol produces in vitro vasoconstriction of coronary arteries and can precipitate angina in patients with coronary obstructive disease. To demonstrate the in vivo effect of ethanol on coronary dynamics, baseline measurements of left anterior descending (LAD) coronary artery dimension by quantitative angiography, hemodynamics, arterial and coronary sinus blood gases, and blood ethanol levels were obtained in 14 closed-chest mongrel dogs. Three ethanol levels were established by intravenous bolus followed by 1-hour maintenance infusions. All measurements made at baseline were recorded every 30 minutes. Phentolamine (5 mg i.v.) and nicardipine (0.15 mg/kg i.v.) were given to evaluate constrictor mechanisms. Blood ethanol levels achieved at 60, 120, and 180 minutes were 649 +/- 48, 1,285 +/- 81, and 2,546 +/- 130 micrograms/ml, respectively. LAD cross-sectional area was reduced significantly from control at the end of each of the three dosing periods (-24 +/- 5%, -40 +/- 3%, and -53 +/- 3%; p less than 0.004). alpha-Adrenergic blockade had no effect on LAD cross-sectional area, while nicardipine partially reversed the ethanol-induced vasoconstriction. No significant change in vessel cross-sectional area took place in control dogs. These data suggest that ethanol induces epicardial coronary artery vasoconstriction in dogs at clinically important blood levels. alpha-Adrenergic blockade does not alter or reverse ethanol-induced vasoconstriction, while calcium channel blockade appears to be an effective vasodilator of ethanol-constricted vessels.
Cigarette smoking is strongly associated with ischemic heart disease and acute coronary events. The effect of smoking a single cigarette on regional myocardial perfusion was studied in 13 chronic smokers with typical stable angina pectoris using positron emission tomography and rubidium-82 (82Rb). Findings were compared with the effects of physical exercise. After exercise, 8 patients (61%) had angina, ST depression and abnormal regional myocardial perfusion. Uptake of 82Rb increased from 49 +/- 8 to 60 +/- 7 in remote myocardium, but decreased from 46 +/- 3 to 37 +/- 5 in an ischemic area. The remaining 5 patients (39%) had homogeneous increases in 82Rb uptake without angina or ST depression. After smoking, 6 of the 8 patients with positive exercise test responses had a decrease in 82Rb uptake, from 47 +/- 3 to 35 +/- 6 in the same segment of myocardium affected during exercise. However, in contrast to exercise, the events during smoking were largely silent. The absolute decreases in regional 82Rb uptake after smoking occurred at significantly lower levels of myocardial oxygen demand than after exercise. This suggests that an impairment of coronary blood supply is responsible. Thus, in smokers with coronary artery disease, each cigarette can cause profound silent disturbances of regional myocardial perfusion that are likely to occur frequently during daily life. Such repeated insults may represent an important mechanism linking smoking with coronary events.
This article has no abstract; the first 100 words appear below.
PATIENTS often recognize symptoms for which they seek medical assistance, but, on the basis of a history and physical and laboratory examination, the physician cannot obtain evidence to account for or justify the patients' complaints.¹ Such patients conform in part to Gillespie's concept of hypochondria, which he viewed as "a persistent preoccupation with the bodily health, out of proportion to any existing justification and with a conviction of disease."² There is considerable disagreement, however, on the appropriate formal definition of hypochondria,³ and it may be incorrect to apply the same designation to profound and persistent hypochondrical syndromes associated with psychiatric . . .
Address reprint requests to Professor Mechanic at the Department of Sociology, University of Wisconsin, Madison, Wisc. 53706.
Supported in part by Public Health Services grant 5 RO1 MH 14835, National Institute of Mental Health.
Meaningful information was available on 26 patients who died suddenly in a 44,000 industrial population. The data, past illnesses, prodromal symptoms, and psychosocial information were obtained from the plant medical records, the private physicians, and mainly from direct interviews with the surviving next-of-kin, usually the wife. The data suggest that the majority of these patients, all men, had been depressed for a week up to several months. The sudden death then occurred in a setting of acute arousal engendered by increased work and activity or circumstances precipitating reactions of anxiety or anger. The findings suggest that the combination of depressive and arousal psychological states or abrupt transition from one such state to another may produce disharmonious responses in the hormonal and autonomic nervous systems, as well as central nervous system mediated behavior, which are conducive to the sudden death.
The effects of acute and subacute psychological stress caused by a sudden general disaster on mortality from atherosclerotic heart disease (underlying cause) and cardiac events (proximate cause) were investigated by comparing total and cause-specific mortality during the days after a major earthquake in Athens in 1981 with the mortality during the surrounding month and the corresponding periods of 1980 and 1982. There was an excess of deaths from cardiac and external causes on the days after the major earthquake, but no excess of deaths from cancer and little, if any, excess of deaths from other causes. The excess mortality was more evident when atherosclerotic heart disease was considered as the underlying cause (5, 7, and 8 deaths on the first three days, respectively; background mean deaths per day 2.6; upper 95th centile 5) than when cardiac events in general were considered as the proximate cause (9, 11, and 14 deaths on the first three days, respectively; background mean 7.1, upper 95th centile 12).
During the period of air-raid alarms in Zagreb (September 1991), the influence of war-induced stress on the incidence and mortality of acute coronary artery disease was investigated. Control periods were September 1989 and September 1990. Among 2903 patients admitted to Emergency Care Units, 369 (13%) were examined for suspect acute coronary artery disease. During the same periods in 1989 and 1990, 10% and 11% of acute coronary artery disease patients were recorded, respectively. The percentage of patients with myocardial infarction or unstable angina, admitted to Coronary Care Units during September 1989, 1990 and 1991, was 49%, 50% and 55%, respectively. The number of Q myocardial patients admitted during September 1991 was significantly higher than that recorded during the same period in 1990. The incidence and mortality patterns in acute coronary artery disease patients were also examined during August, September and October 1991. The peak incidence of acute coronary artery disease was found in the first half of September, while the peak mortality in these patients was found during the second half of September. During the second half of September of 1989, 1990 and 1991, the mortality in Q myocardial patients in Coronary Care Units, was 16.7%, 15.2% and 23.8%, respectively. Besides the war-induced stress, transportation of our patients to shelters or inner parts of the hospital caused additional stress, probably contributing to the development of refractory malignant arrhythmia or heart failure.
Many anecdotes and several uncontrolled case series have suggested that emotionally stressful events, and more specifically, anger, immediately precede and appear to trigger the onset of acute myocardial infarction. However, controlled studies to determine the relative risk of myocardial infarction after episodes of anger have not been reported.
We interviewed 1623 patients (501 women) an average of 4 days after myocardial infarction. The interview identified the time, place, and quality of myocardial infarction pain and other symptoms, the estimated usual frequency of anger during the previous year, and the intensity and timing of anger and other potentially triggering factors during the 26 hours before the onset of myocardial infarction. Anger was assessed by the onset anger scale, a single-item, seven-level, self-report scale, and the state anger subscale of the State-Trait Personality Inventory. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using two types of self-matched control data based on the case-crossover study design. The onset anger scale identified 39 patients with episodes of anger in the 2 hours before the onset of myocardial infarction. The relative risk of myocardial infarction in the 2 hours after an episode of anger was 2.3 (95% confidence interval, 1.7 to 3.2). The state anger subscale corroborated these findings with a relative risk of 1.9 (95% confidence interval, 1.3 to 2.7). Regular users of aspirin had a significantly lower relative risk (1.4; 95% confidence interval, 0.8 to 2.6) than nonusers (2.9; 95% confidence interval, 2.0 to 4.1) (P < .05).
Episodes of anger are capable of triggering the onset of acute myocardial infarction, but aspirin may reduce this risk. A better understanding of the manner in which external events trigger the onset of acute cardiovascular events may lead to innovative preventive strategies aimed at severing the link between these external stressors and their pathological consequences.
The imminent deadline for the 1991 Persian Gulf War and, subsequently, the 18 missile attacks by Iraq on Israel represented an unusual, short-term, life-threatening stressor for an entire nation. We studied mortality in Israel in January and February 1991 to determine whether excess deaths were precipitated on days of missile attacks.
A time-series mortality study.
The state of Israel.
All Israelis aged 25 years and older.
Daily mortality by sex, age, region, underlying cause, and place of death.
On January 18, 1991, the day of the first strike on Israeli cities, a 58% increment in total mortality occurred in the Israeli population (95% confidence interval [CI], 34% to 86%; P < .0001), a 77% excess (95% CI, 40% to 120%) in women and a 41% excess (95% CI, 10% to 79%) in men. This excess mortality occurred largely in the targeted Tel Aviv-central coastal plain and Haifa regions from cardiovascular causes and mainly out of hospital, significantly more so (P < .01) in women than men. Subsequently, on 16 attack days no overall excess was noted, yet a 10% increase in out-of-hospital deaths occurred.
Likely explanations for the initial increase in mortality include acute emotional stress coupled with breathing difficulties induced by gas masks and extended stay in sealed rooms with resultant hypoxia in susceptible individuals. Women were more vulnerable than men. The absence of elevated total mortality in the subsequent attacks suggests a rapid adaptation to the circumstances surrounding the war. The policy of an unventilated sealed room may have been detrimental.
The case-crossover study design is a method to assess the effect of transient exposures on the risk of onset of acute events. Control information for each case is based on his/her past exposure experience, and a self-matched analysis is conducted. Empiric evaluation of five approaches to the analysis of case-crossover data from a study of heavy physical exertion and acute myocardial infarction onset is shown. The data presented are from the Onset Study, a case-crossover study of the determinants of myocardial infarction onset conducted in 45 centers from August 1989 to October 1992. In model 1, exactly one control period (matched on clock-time) was sampled per case. In models 2-4, up to 25 control periods were sampled, and the effect of clock-time on the baseline hazard of infarction was modeled. In model 5, a census of the person-time experienced by each subject over the year preceding the infarction was sampled. The 95% confidence interval for model 1 was 2.7 times wider, and the relative efficiency, defined as v infinity/vM, where vM represents the asymptotic variance estimate of the estimated log relative risk with M control periods sampled per case, was only about 14% of model 5. In models 2-4, the efficiency increased with the number of control periods, regardless of the modeling assumptions. Even with many control periods sampled, models 2-4 achieved only half the efficiency of model 5. The control sampling strategy in any given case-crossover study should be selected with the trade-offs between precision and potential biases of the estimates in mind.
Several studies have suggested an increased risk of fatal coronary heart disease (CHD) among patients with panic disorder, phobic anxiety, and other anxiety disorders. We prospectively examined this association in the Normative Aging Study.
An anxiety symptoms scale was constructed out of five items from the Cornell Medical Index, which was administered to the cohort at baseline. During 32 years of follow-up, we observed 402 cases of incident coronary heart disease (137 cases of nonfatal myocardial infarction, 134 cases of angina pectoris, and 131 cases of fatal CHD: made up of 26 cases of sudden cardiac death and 105 cases of nonsudden death). A nested case-control design (involving 1869 control subjects who remained free of diagnosed CHD) was used to assess the association between anxiety and risk of CHD. Compared with men reporting no symptoms of anxiety, men reporting two or more anxiety symptoms had elevated risks of fatal CHD (age-adjusted odds ratio [OR] = 3.20, 95% confidence interval [CI]: 1.27 to 8.09), and sudden death (age-adjusted OR = 5.73, 95% CI: 1.26 to 26.1). The multivariate OR after adjusting for a range of potential confounding variables was 1.94 (95% CI: 0.70-5.41) for fatal CHD and 4.46 (95% CI: 0.92-21.6) for sudden death. No excess risks were found for nonfatal myocardial infarction or angina.
These data suggest an association between anxiety and fatal coronary heart disease, in particular, sudden cardiac death.
The pressor and tachycardic effects of cigarette smoking are associated with an increase in plasma catecholamines, suggesting the dependence of these effects on adrenergic stimulation. Whether the stimulation occurs at a central or a peripheral level and whether reflex mechanisms are involved is unknown.
In nine normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we measured blood pressure (Finapres device), heart rate (ECG), calf blood flow and vascular resistance (venous occlusion plethysmography), plasma norepinephrine and epinephrine (high-performance liquid chromatography assay), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) while subjects were smoking a filter cigarette (nicotine content, 1.1 mg) or were in control condition. Cigarette smoking (which raised plasma nicotine measured by high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1 ng/mL) markedly and significantly increased mean arterial pressure (+13.2 +/- 2.3%), heart rate (+30.3 +/- 4.7%), calf vascular resistance (+12.1 +/- 4.9%), plasma norepinephrine (+34.8 +/- 7.0%), and plasma epinephrine (+90.5 +/- 39.0%). In contrast, muscle sympathetic nerve activity showed a marked reduction (integrated activity -31.8 +/- 5.1%, P < .01). The reduction was inversely related to the increase in mean arterial pressure (r = -.67, P < .05), but the slope of the relation was markedly less (-54.1 +/- 7.5%, P < .05) than that obtained by intravenous infusion of phenylephrine in absence of smoking. The hemodynamic and neurohumoral changes were still visible 30 minutes after smoking and occurred again on smoking a second cigarette. Sham smoking was devoid of any hemodynamic and neurohumoral effect.
These data support the hypothesis that in humans the sympathetic activation induced by smoking depends on an increased release and/or a reduced clearance of catecholamines at the neuroeffector junctions. Central sympathetic activity is inhibited by smoking, presumably via a baroreceptor stimulation triggered by the smoking-related pressor response. The baroreflex is impaired by smoking, however, indicating that partial inability to reflexly counteract the effect of sympathetic activation is also responsible for the pressor response.
To examine prospectively the association between self-reported symptoms of phobic anxiety and subsequent risk of coronary heart disease, a 2-year follow-up study was conducted of a cohort of 33,999 US male health professionals, aged 42 to 77 years in 1988, who were free of diagnosed cardiovascular disease at baseline. Levels of phobic anxiety were assessed using the Crown-Crisp index, a short, diagnostic self-rating scale used for common phobias. Main outcomes were incidents of coronary heart disease consisting of nonfatal myocardial infarction (MI) and fatal coronary heart disease (CHD).
One hundred sixty-eight incident cases of CHD occurred during 2 years of follow-up (128 cases of nonfatal MI and 40 cases of fatal CHD). The age-adjusted relative risk of fatal CHD among men with highest levels of phobic anxiety (scoring 4 or higher on the Crown-Crisp index) was 3.01 (95% confidence interval, 1.31 to 6.90) compared with men with the lowest levels of anxiety (scoring 0 or 1 on the phobia index). Risk of fatal CHD increased with levels of phobic anxiety (P trend = .002). When fatal CHD was further categorized into sudden and nonsudden coronary death, the excess risk was confined to sudden death (relative risk among men scoring 3 or higher on the phobia index was 6.08; 95% confidence interval, 2.35 to 15.73). No association was found between phobic anxiety and risk of nonfatal MI. These findings remained essentially unchanged after adjusting for a broad range of cardiovascular risk factors.
The specificity, strength, and dose-response gradient of the association, together with the consistency and biological plausibility of the experimental and epidemiologic evidence, support a strong causal association between phobic anxiety and fatal CHD.
It is controversial whether the onset of myocardial infarction occurs randomly or is precipitated by identifiable stimuli. Previous studies have suggested a higher risk of cardiac events in association with exertion.
Consecutive patients with acute myocardial infarction were identified by recording all admissions to our hospital in Berlin and by monitoring a general population of 330,000 residents in Augsburg, Germany. Information on the circumstances of each infarction was obtained by means of standardized interviews. The data analysis included a comparison of patients with matched controls and a case-crossover comparison (one in which each patient serves as his or her own control) of the patient's usual frequency of exertion with the last episode of exertion before the onset of myocardial infarction.
From January 1989 through December 1991, 1194 patients (74 percent of whom were men; mean age [+/- SD], 61 +/- 9 years) completed the interview 13 +/- 6 days after infarction. We found that 7.1 percent of the case patients had engaged in physical exertion (> or = 6 metabolic equivalents) at the onset of infarction, as compared with 3.9 percent of the controls at the onset of the control event. For the patients as compared with the matched controls, the adjusted relative risk of having engaged in strenuous physical activity at the onset of infarction or the control event was 2.1 (95 percent confidence interval, 1.1 to 3.6). The case-crossover comparison yielded a similar relative risk of 2.1 (95 percent confidence interval, 1.6 to 3.1) for having engaged in strenuous physical activity within one hour before myocardial infarction. Patients whose frequency of regular exercise was less than four and four or more times per week had relative risks of 6.9 and 1.3, respectively (P < 0.01).
A period of strenuous physical activity is associated with a temporary increase in the risk of having a myocardial infarction, particularly among patients who exercise infrequently. These findings should aid in the identification of the triggering mechanisms for myocardial infarction and improve prevention of this common and serious disorder.
This study was performed to determine the acute effect of cigarette smoking on proximal and distal epicardial conduit and coronary resistance vessels.
Cigarette smoking causes constriction of epicardial arteries and a decrease in coronary blood flow in patients with coronary artery disease, despite an increase in myocardial oxygen demand. The role of changes in resistance vessel tone in the acute coronary hemodynamic effect of smoking has not been examined.
Twenty-four long-term smokers were studied during cardiac catheterization after vasoactive medications had been discontinued. The effect of smoking one cigarette 10 to 15 mm long on proximal and distal conduit vessel segments was assessed before and immediately after smoking and at 5, 15 and 30 min after smoking (n = 8). To determine the effect of smoking on resistance vessels, coronary flow velocity was measured in a nonobstructed artery with a 3F intracoronary Doppler catheter before and for 5 min after smoking (n = 8). Eight patients were studied without smoking to control for spontaneous changes in conduit arterial diameter (n = 5) and resistance vessel tone (n = 3).
The average diameter of proximal coronary artery segments decreased from 2.56 +/- 0.12 mm (mean +/- SEM) before smoking to 2.41 +/- 0.09 mm 5 min after smoking (-5 +/- 2%, p < 0.05). Distal coronary diameter decreased from 1.51 +/- 0.07 to 1.39 +/- 0.06 mm (-8 +/- 2%, p < 0.01). Marked focal vasoconstriction after smoking was observed in two patients. Coronary diameter returned to baseline by 30 min after smoking. There was no change in vessel diameter in control patients. Despite a significant increase in the heart rate-mean arterial pressure product, coronary flow velocity decreased by 7 +/- 4% (p < 0.05) and coronary vascular resistance increased by 21 +/- 4% (p < 0.01) 5 min after smoking. There was no change in these variables in the control subjects.
Smoking causes immediate constriction of proximal and distal epicardial coronary arteries and an increase in coronary resistance vessel tone, despite an increase in myocardial oxygen demand. These acute coronary hemodynamic effects may contribute to the adverse cardiovascular consequences of cigarette smoking.
The cardiovascular system may react to stress either by coronary events, such as angina pectoris or myocardial infarction, or by non-coronary responses, such as rises in blood pressure or non-specific circulatory disorders and chest pain. There is contradictory information about the cardiovascular reactions to war stress. The aim of this study was to investigate the effects of stress produced by the uprising of December 1989 in Romania on the cardiovascular system. Cases referred from 21 to 31 December 1989 to the emergency department of the largest university clinic of the Cluj district, and those admitted there, were analysed and compared with cases referred in the same periods in 1988, 1990 and 1991 and from 1 to 10 January 1990. There was a significant increase in non-coronary cardiovascular complaints referred for consultation in the first 10 days from the beginning of the uprising in Cluj and a non-significant increase in the following 10 days, but no increase in consultations for complaints of coronary origin due to unstable angina and acute myocardial infarction or changes in hospital admissions. In conclusion, the stress produced by the uprising in Romania was correlated with a higher incidence of non-coronary cardiovascular complaints but no alteration in coronary events (unstable angina, acute myocardial infarction), or in hospital admissions for cardiovascular complaints.