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Triggering of Acute Myocardial Infarction Onset by Episodes of Anger
Abstract
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.
... Desde hace más de una década, el PCTA se considera como un claro indicador de riesgo coronario (Mittleman et al., 1995;Muller, Adela, Nes-to y Tofler, 1994; Willich, Maclure, Mittleman, Arntz y Muller, 1993). Diversos investigadores (Barefoot, Larsen, Bonderleith y Schroll, 1995;Everson et al., 1997; Kawachi, Sparrow, Spiro, Vokonas y Weiss et al., 1996) han mostrado que los altos niveles de ira y hostilidad se relacionan de un modo importante con el aumento en la morbilidad debida a ECV. ...
Introducción: La sintomatología de ansiedad, depresión y conducta tipo A son aspectos psicológicos prevalentes en población con enfermedades cardiovasculares. Objetivo: validar el Inventario de Ansiedad y Depresión (HADS) y la Escala de Retiro de Patrón de Conducta tipo A (ERCTA) en una población de pacientes con enfermedades cardiovasculares. Método: Se empleó un diseño transversal, con un muestreo no probabilístico, por disponibilidad. Se incluyó a 200 pacientes diagnosticados con enfermedades cardiovasculares, con una media de edad de 59.7 años, de los cuales 59% eran hombres. Los criterios de inclusión fueron ser pacientes con enfermedades cardiovasculares con diagnóstico médico confirmado, en cualquier tratamiento médico, y saber leer y escribir. Los criterios de exclusión fueron sufrir limitaciones visuales o auditivas severas y afectaciones cognitivas, y como criterios de eliminación no concluir la investigación o llenar incorrectamente los cuestionarios. Resultados: El análisis factorial del HADS identificó un solo factor, con un coeficiente alfa de la escala global de 0.94 y una varianza explicada de 59.6%. La estructura factorial del ERCTA, ajustada a un solo factor, mostró un coeficiente alfa de la escala global de 0.93 y una varianza explicada de 67.3%. La validez concurrente entre ambos instrumentos por medio de correlación mostró resultados significativos. Discusión: Los inventarios HADS y ERCTA mostraron ser instrumentos válidos y confiables para su uso en la atención clínica y la investigación de pacientes con enfermedades cardiovasculares. Esta población puede requerir atención psicosocial, además de la que se le brinde a su salud.
Background
Provoked anger is associated with an increased risk of cardiovascular disease events. The underlying mechanism linking provoked anger as well as other core negative emotions including anxiety and sadness to cardiovascular disease remain unknown. The study objective was to examine the acute effects of provoked anger, and secondarily, anxiety and sadness on endothelial cell health.
Methods and Results
Apparently healthy adult participants (n=280) were randomized to an 8‐minute anger recall task, a depressed mood recall task, an anxiety recall task, or an emotionally neutral condition. Pre−/post‐assessments of endothelial health including endothelium‐dependent vasodilation (reactive hyperemia index), circulating endothelial cell‐derived microparticles (CD62E+, CD31+/CD42−, and CD31+/Annexin V+) and circulating bone marrow‐derived endothelial progenitor cells (CD34+/CD133+/kinase insert domain receptor+ endothelial progenitor cells and CD34+/kinase insert domain receptor+ endothelial progenitor cells) were measured. There was a group×time interaction for the anger versus neutral condition on the change in reactive hyperemia index score from baseline to 40 minutes ( P =0.007) with a mean±SD change in reactive hyperemia index score of 0.20±0.67 and 0.50±0.60 in the anger and neutral conditions, respectively. For the change in reactive hyperemia index score, the anxiety versus neutral condition group by time interaction approached but did not reach statistical significance ( P =0.054), and the sadness versus neutral condition group by time interaction was not statistically significant ( P =0.160). There were no consistent statistically significant group×time interactions for the anger, anxiety, and sadness versus neutral condition on endothelial cell‐derived microparticles and endothelial progenitor cells from baseline to 40 minutes.
Conclusions
In this randomized controlled experimental study, a brief provocation of anger adversely affected endothelial cell health by impairing endothelium‐dependent vasodilation.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
The reason why stable atherosclerotic plaques rupture or erode leading to atherothrombosis remains a conundrum. While occasionally myocardial infarction follows an “acute external triggering event,” most appear to occur at random.
The concept of a “vulnerable plaque primed to rupture” was based on post-mortem studies that found atherothrombosis was frequently associated with ruptured plaques that had a thin fibrous cap, a large lipid core, and inflammatory infiltration in its shoulder regions. However, these morphologic descriptors do not explain the processes that occurred within the plaque prior to rupture, and do not explain why in up to one third of cases atherothrombosis is associated with plaque erosion in the absence of inflammation.
Although non-invasive imaging has been able to identify that plaques with a large lipid rich core associated with inflammation are at somewhat higher risk of future injury, most such plaques remain stable.
Together these observations indicate that the vulnerability of plaques is dynamic and raises the possibly that instability relates to ongoing changes in the physiochemistry of the lipid core that at times favors the formation of cholesterol crystals that can “change the destiny of a plaque” by causing traumatic injury and changing the trajectory of the inflammatory milieu in the plaque bed so that it begins to favor persistent inflammatory injury rather than healing.
In the interview, Prof. Barry A. Franklin discussed his perspectives on physical activity, cardiorespiratory fitness, and cardiovascular health. He also unraveled how soft skills can empower superachievers. His major viewpoints are: (a) exercise benefits cardiac patients; yet, too much exercise may be risky, (b) exercise prescription should be scientifically based and varies by different objectives for each individual, (c) patients' motivation to change their behaviors matters during cardiac rehabilitation, (d) physical activities could play a protective role for dementia prevention, (e) technology and virtual approaches enable more patients to participate in cardiac rehab programs, (f) patients with heart failure may benefit even more from exercise training than other patient populations, (g) psychosocial stressors may partially explain some cardiac events, (h) novel risk factors help identify people at increased risk of cardiovascular disease, such as genetics, coronary calcium score, air pollution, and inflammation, and (i) soft skills are needed by all people, regardless of their field.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Liaison psychiatry, the recognition and management of psychiatric problems in the general medical setting, is an essential component of many doctors' work. Depression, anxiety and somatization disorders occur in about 50% of cases presented to primary care physicians. The Handbook of Liaison Psychiatry was first published in 2007 and is a comprehensive reference book for this fast-growing subspecialty. A team of experts in the field cover the full range of issues, from establishing a service and outlining the commonest problems encountered in general hospitals and primary care, to assessment and treatment guidelines, working with specific units within the hospital setting, disaster planning and legal-ethical considerations. It will be essential reading for doctors and other professionals concerned with the psychological health of patients in acute general hospitals and in primary care.
Background
Most deaths from coronary artery disease (CAD) are due to acute myocardial infarction (AMI). There is an urgent need for early AMI detection, particularly in patients with stable CAD. 5-methylcytosine (5mC) regulatory genes have been demonstrated to involve in the progression and prognosis of cardiovascular diseases, while little research examined 5mC regulators in CAD to AMI progression.
Method
Two datasets (GSE59867 and GSE62646) were downloaded from Gene Expression Omnibus (GEO) database, and 21 m5C regulators were extracted from previous literature. Dysregulated 5mC regulators were screened out by “limma.” The least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE) algorithm were employed to identify hub 5mC regulators in CAD to AMI progression, and 43 clinical samples (Quantitative real-time PCR) were performed for expression validation. Then a logistic model was built to construct 5mC regulator signatures, and a series of bioinformatics algorithms were performed for model validation. Besides, 5mC-associated molecular clusters were studied via unsupervised clustering analysis, and correlation analysis between immunocyte and 5mC regulators in each cluster was conducted.
Results
Nine hub 5mC regulators were identified. A robust model was constructed, and its prominent classification accuracy was verified via ROC curve analysis (area under the curve [AUC] = 0.936 in the training cohort and AUC = 0.888 in the external validation cohort). Besides, the clinical effect of the model was validated by decision curve analysis. Then, 5mC modification clusters in AMI patients were identified, along with the immunocyte infiltration levels of each cluster. The correlation analysis found the strongest correlations were TET3—Mast cell in cluster-1 and TET3-MDSC in cluster-2.
Conclusion
Nine hub 5mC regulators ( DNMT3B , MBD3 , UHRF1 , UHRF2 , NTHL1 , SMUG1 , ZBTB33 , TET1 , and TET3 ) formed a diagnostic model, and concomitant results unraveled the critical impact of 5mC regulators, providing interesting epigenetics findings in AMI population vs. stable CAD.
Much of biology is rhythmical and comprises oscillators that can couple. These have optimized energy efficiency and have been preserved during evolution. The respiratory and cardiovascular systems contain numerous oscillators, and importantly, they couple. This coupling is dynamic but essential for an efficient transmission of neural information critical for the precise linking of breathing and oxygen delivery while permitting adaptive responses to changes in state. The respiratory pattern generator and the neural network responsible for sympathetic and cardiovagal (parasympathetic) tone generation interact at many levels ensuring that cardiac output and regional blood flow match oxygen delivery to the lungs and tissues efficiently. The most classic manifestations of these interactions are respiratory sinus arrhythmia and the respiratory modulation of sympathetic nerve activity. These interactions derive from shared somatic and cardiopulmonary afferent inputs, reciprocal interactions between brainstem networks and inputs from supra-pontine regions. Disrupted respiratory–cardiovascular coupling can result in disease, where it may further the pathophysiological sequelae and be a harbinger of poor outcomes. This has been well documented by diminished respiratory sinus arrhythmia and altered respiratory sympathetic coupling in animal models and/or patients with myocardial infarction, heart failure, diabetes mellitus, and neurological disorders as stroke, brain trauma, Parkinson disease, or epilepsy. Future research needs to assess the therapeutic potential for ameliorating respiratory–cardiovascular coupling in disease.
Importance:
Prior studies found a higher risk of acute cardiovascular disease (CVD) around population-wide psychosocial or environmental stressors. Less is known about acute CVD risk in relation to political events.
Objective:
To examine acute CVD hospitalizations following the 2020 presidential election.
Design, setting, and participants:
This retrospective cohort study examined acute CVD hospitalizations following the 2020 presidential election. Participants were adult members aged 18 years or older at Kaiser Permanente Southern California and Kaiser Permanente Northern California, 2 large, integrated health care delivery systems. Statistical analysis was performed from March to July 2021.
Exposure:
2020 US presidential election.
Main outcomes and measures:
Hospitalizations for acute CVD around the 2020 presidential election were examined. CVD was defined as hospitalizations for acute myocardial infarction (AMI), heart failure (HF), or stroke. Rate ratios (RR) and 95% CIs were calculated comparing rates of CVD hospitalization in the 5 days following the 2020 election with the same 5-day period 2 weeks prior.
Results:
Among 6 396 830 adults (3 970 077 [62.1%] aged 18 to 54 years; 3 422 479 [53.5%] female; 1 083 128 [16.9%] Asian/Pacific Islander, 2 101 367 [32.9%] Hispanic, and 2 641 897 [41.3%] White), rates of hospitalization for CVD following the election (666 hospitalizations; rate = 760.5 per 100 000 person-years [PY]) were 1.17 times higher (95% CI, 1.05-1.31) compared with the same 5-day period 2 weeks prior (569 hospitalizations; rate = 648.0 per 100 000 PY). Rates of AMI were significantly higher following the election (RR, 1.42; 95% CI, 1.13-1.79). No significant difference was found for stroke (RR, 1.02; 95% CI, 0.86-1.21) or HF (RR, 1.18; 95% CI, 0.98-1.42).
Conclusions and relevance:
Higher rates of acute CVD hospitalization were observed following the 2020 presidential election. Awareness of the heightened risk of CVD and strategies to mitigate risk during notable political events are needed.
Objective:
Negative emotional states, such as anger and anxiety, are associated with the onset of myocardial infarction and other acute clinical manifestations of ischemic heart disease. The likelihood of experiencing these short-term negative emotions has been associated with long-term psychological background factors such as depression, generalized anxiety, and personality factors. We examined the association of acute emotional states preceding cardiac stress testing (CST) with inducibility of myocardial ischemia and to what extent psychological background factors account for this association.
Methods:
Emotional states were assessed in patients undergoing CST (N = 210; mean age 66.9 years (standard deviation (±) =8.2 years); 91 (43%) women) using self-report measures and video recordings of facial emotion expression. Video recordings were analyzed for expressed anxiety, anger, sadness, and happiness prior to CST. Psychological background factors were assessed with validated questionnaires. Single-photon emission computed tomography was used to evaluate inducibility of ischemia.
Results:
Ischemia occurred in 72 (34%) patients. Emotional states were not associated with subsequent inducibility of ischemia during CST (OR between 0.93 and 1.04; p-values >0.50). Psychological background factors were also not associated with ischemia (OR between 0.96 and 1.06 per scale unit; p values >0.20), and did not account for the associations of emotional states with ischemia.
Conclusions:
Emotional states immediately before CST and psychological background factors were not associated with the inducibility of ischemia. These findings indicate that the well-documented association between negative emotions with acute clinical manifestations of ischemic heart disease requires a different explanation than a reduced threshold for inducible ischemia.
This study aimed to determine early diagnosis genes of acute myocardial infarction (AMI) and then validate their association with ferroptosis, immune checkpoints, and N6-methyladenosine (m6A), which may provide a potential method for the early diagnosis of AMI. Firstly, we downloaded microarray data from NCBI (GSE61144, GSE60993, and GSE42148) and identified differentially expressed genes (DEGs) in samples from healthy subjects and patients with AMI. Also, we performed systematic gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses and used STRING to predict protein interactions. Moreover, MCC and MCODE algorithms in the cytoHubba plug-in were used to screen nine key genes in the network. We then determined the diagnostic significance of the nine obtained DEGs by plotting receiver operating characteristic curves using a multiscale curvature classification algorithm. Meanwhile, we investigated the relationship between AMI and immune checkpoints, ferroptosis, and m6A. In addition, we further validated the key genes through the GSE66360 dataset and consequently obtained nine specific genes that can be used as early diagnosis biomarkers for AMI. Through screening, we identified 210 DEGs, including 53 downregulated and 157 upregulated genes. According to GO, KEGG, and key gene screening results, FPR1, CXCR1, ELANE, TLR2, S100A12, TLR4, CXCL8, FPR2 and CAMP could be used for early prediction of AMI. Finally, we found that AMI was associated with ferroptosis, immune checkpoints, and m6A and FPR1, CXCR1, ELANE, TLR2, S100A12, TLR4, CXCL8, FPR2 and CAMP are effective markers for the diagnosis of AMI, which can provide new prospects for future studies on the pathogenesis of AMI.
Background and purpose:
Whether certain activities can trigger spontaneous intracerebral hemorrhage (ICH) remains unknown. Insights into factors that trigger vessel rupture resulting in ICH improves knowledge on the pathophysiology of ICH. We assessed potential trigger factors and their risk for ICH onset.
Methods:
We included consecutive patients diagnosed with ICH between July 1, 2013, and December 31, 2019. We interviewed patients on their exposure to 12 potential trigger factors (eg, Valsalva maneuvers) in the (hazard) period soon before onset of ICH and their normal exposure to these trigger factors in the year before the ICH. We used the case-crossover design to calculate relative risks (RR) for potential trigger factors.
Results:
We interviewed 149 patients (mean age 64, 66% male) with ICH. Sixty-seven (45%) had a lobar hemorrhage, 60 (40%) had a deep hemorrhage, 19 (13%) had a cerebellar hemorrhage, and 3 (2%) had an intraventricular hemorrhage. For ICH in general, there was an increased risk within an hour after caffeine consumption (RR=2.5 [95% CI=1.8-3.6]), within an hour after coffee consumption alone (RR=4.8 [95% CI=3.3-6.9]), within an hour after lifting >25 kg (RR=6.6 [95% CI=2.2-19.9]), within an hour after minor head trauma (RR=10.1 [95% CI=1.7-60.2]), within an hour after sexual activity (RR=30.4 [95% CI=16.8-55.0]), within an hour after straining for defecation (RR=37.6 [95% CI=22.4-63.4]), and within an hour after vigorous exercise (RR=21.8 [95% CI=12.6-37.8]). Within 24 hours after flu-like disease or fever, the risk for ICH was also increased (RR=50.7 [95% CI=27.1-95.1]). Within an hour after Valsalva maneuvers, the RR for deep ICH was 3.5 (95% CI=1.7-6.9) and for lobar ICH the RR was 2.0 (95% CI=0.9-4.2).
Conclusions:
We identified one infection and several blood pressure related trigger factors for ICH onset, providing new insights into the pathophysiology of vessel rupture resulting in ICH.
Aims
In INTERSTROKE, we explored the association of anger or emotional upset and heavy physical exertion with acute stroke, to determine the importance of triggers in a large, international population.
Methods and results
INTERSTROKE was a case–control study of first stroke in 32 countries. Using 13 462 cases of acute stroke we adopted a case-crossover approach to determine whether a trigger within 1 hour of symptom onset (case period), vs. the same time on the previous day (control period), was associated with acute stroke. A total of 9.2% (n = 1233) were angry or emotional upset and 5.3% (n = 708) engaged in heavy physical exertion during the case period. Anger or emotional upset in the case period was associated with increased odds of all stroke [odds ratio (OR) 1.37, 99% confidence interval (CI), 1.15–1.64], ischaemic stroke (OR 1.22, 99% CI, 1.00–1.49), and intracerebral haemorrhage (ICH) (OR 2.05, 99% CI 1.40–2.99). Heavy physical exertion in the case period was associated with increased odds of ICH (OR 1.62, 99% CI 1.03–2.55) but not with all stroke or ischaemic stroke. There was no modifying effect by region, prior cardiovascular disease, risk factors, cardiovascular medications, time, or day of symptom onset. Compared with exposure to neither trigger during the control period, the odds of stroke associated with exposure to both triggers were not additive.
Conclusion
Acute anger or emotional upset was associated with the onset of all stroke, ischaemic stroke, and ICH, while acute heavy physical exertion was associated with ICH only.
The number of complex infrastructures in an industrial setting is growing and is not immune to unexplained recurring events such as breakdowns or failure that can have an economic and environmental impact. To understand these phenomena, sensors have been placed on the different infrastructures to track, monitor, and control the dynamics of the systems. The causal study of these data allows predictive and prescriptive maintenance to be carried out. It helps to understand the appearance of a problem and find counterfactual outcomes to better operate and defuse the event. In this paper, we introduce a novel approach combining the case-crossover design which is used to investigate acute triggers of diseases in epidemiology, and the Apriori algorithm which is a data mining technique allowing to find relevant rules in a dataset. The resulting time series causal algorithm extracts interesting rules in our application case which is a non-linear time series dataset. In addition, a predictive rule-based algorithm demonstrates the potential of the proposed method.
Psychological and social factors are thought to influence risk for a range of physical illnesses including coronary heart disease, high blood pressure, type 2 diabetes, infectious illness, bronchial asthma and musculoskeletal pain. These associations are underpinned by the impact of psychological stress and other biobehavioral stimuli on the systemic biological responses implicated in disease risk. Several systems are involved, with cardiovascular, neuroendocrine, immune, inflammatory, metabolic and musculoskeletal responses all being relevant. The nature and extent of influence on health outcomes varies across diseases, and different types of study design are needed to evaluate these processes in different health conditions.
Nearly a century ago it was reported that stimulation of the hypothalamus could evoke profound behavioral state changes coupled with altered autonomic function. Since these initial observations, further studies in animals have revealed that two hypothalamic regions-the dorsomedial and ventromedial hypothalamic nuclei-are critical for numerous behaviors, including those in response to psychological stressors. These behaviors are coupled with changes in autonomic functions, such as altered blood pressure, heart rate, sympathetic nerve activity, resetting of the baroreflex and changes in pituitary function. There is also growing evidence that these two hypothalamic regions play a critical role in thermogenesis, and suggestions they could also be responsible for the hypertension associated with obesity. The aim of this chapter is to review the anatomy, projection patterns, and function of the dorsomedial and ventromedial hypothalamus with a particular focus on their role in autonomic regulation. While most of what is known about these two hypothalamic regions is derived from laboratory animal experiments, recent human studies will also be explored. Finally, we will describe recent human brain imaging studies that provide evidence of a role for these hypothalamic regions in setting resting sympathetic drive and their potential role in conditions such as hypertension.
Bereavement due to loss of a partner is one of the most stressful life events, often leading to adverse physiological responses. Spousal loss has been associated with an increased morbidity and mortality, particularly from cardiovascular disease. Use of aspirin and/or beta adrenergic blockers have previously been suggested to play a role in cardiovascular risk associated with early bereavement. However, the available literature regarding this topic is limited. In this review article, we explore the potential beneficial role of aspirin and beta blockers in early bereavement. Our systematic review suggests that most studies have found aspirin and beta blockers to be beneficial in preventing adverse cardiovascular outcomes associated with early bereavement. Further randomized controlled long-term studies are warranted with adequate sample size to clearly establish the role of these medications on cardiovascular disease in late bereavement.
Background:
Anger is a common problem in society, and anger's relationship with mortality, in particular with cardiovascular mortality, has been studied mainly in male western population. There are no prospective studies in Japan, about the association between anger and mortality.
Methods:
This study examined the association of anger with all-cause and cause-specific mortality in a Japanese community. Data came from the Takayama Study, which recruited residents aged ≥35 years in 1992 from Takayama City in Gifu, Japan. The current study used information on anger that was obtained from the second survey in 2002. A total of 11,902 healthy participants aged ≥45 years completed a self-administered questionnaire. Anger was assessed using the Spielberger Trait Anger Scale.
Results:
The main causes of deaths during the follow-up period from 2002 to 2013 were 460 for neoplasm, 254 for cardiovascular, and 435 for other causes. After adjusting for potential confounders, we found a significant positive association between the trait anger score and the risk of cardiovascular mortality for women, with a hazard ratio for high versus low score of trait anger of 1.81 (95% confidence interval 0.91-3.63, p for trend = 0.04), but not for men.
Conclusions:
Data suggest that for Japanese women, high trait anger score may be associated with an increased risk of cardiovascular mortality. Potential gender differences in the association between trait anger and mortality should be further studied from the cultural context.
Background
Psychosocial factors predict heart disease risk, but our understanding of underlying mechanisms is limited. We sought to evaluate the physiologic correlates of psychosocial factors by measuring their relationships with heart rate variability (HRV), a measure of autonomic health, in the ARIC (Atherosclerosis Risk in Communities) study. We hypothesize that increased psychosocial stress associates with lower HRV.
Methods and Results
We studied 9331 participants in ARIC with short‐term HRV data at visits 2 and 4. The mean (SD) age was 54.4 (5.7) years, 55% were women, and 25% were Black. Psychosocial factors included: (1) vital exhaustion (VE), (2) anger proneness, a personality trait, and (3) perceived social support. Linear models adjusted for sociodemographic and cardiovascular risk factors. Low frequency HRV (ln ms ² ) was significantly lower in the highest versus lowest quartiles of VE (B=−0.14, 95% CI, −0.24 to −0.05). When comparing this effect to age (B=−0.04, 95% CI, −0.05 to −0.04), the difference was equivalent to 3.8 years of accelerated aging. Perceived social support associated with lower time‐domain HRV. High VE (versus low VE) also associated with greater decreases in low frequency over time, and both anger and VE associated with greater increases in resting heart rate over time. Survival analyses were performed with Cox models, and no evidence was found that HRV explains the excess risk found with high VE and low perceived social support.
Conclusions
Vital exhaustion, and to a lesser extent anger and social support, were associated with worse autonomic function and greater adverse changes over time.
Arterial thrombosis is the primary cause of death worldwide, with the most important risk factors being smoking, unhealthy diet, and physical inactivity. However, although there are clear indications in the literature of beneficial effects of physical activity in lowering the risk of cardiovascular events, exercise can be considered a double-edged sword in that physical exertion can induce an immediate pro-thrombotic environment. Epidemiological studies show an increased risk of cardiovascular events after acute exercise, a risk, which appear to be particularly apparent in individuals with lifestyle-related disease. Factors that cause the increased susceptibility to arterial thrombosis with exercise are both chemical and mechanical in nature and include circulating catecholamines and vascular shear stress. Exercise intensity plays a marked role on such parameters, and evidence in the literature accordingly points at a greater susceptibility to thrombus formation at high compared to light and moderate intensity exercise. Of importance is, however, that the susceptibility to arterial thrombosis appears to be lower in exercise-conditioned individuals compared to sedentary individuals. There is currently limited data on the role of acute and chronic exercise on the susceptibility to arterial thrombosis, and many studies include incomplete assessments of thrombogenic clotting profile. Thus, further studies on the role of exercise, involving valid biomarkers, are clearly warranted.
Stress-related disorders are diverse and they may be mental and physical. Often, several body systems and organs are involved simultaneously. The pathophysiology of stress-related disorders involves many factors: an observable or perceived stressor, an individual dynamically evolving vulnerability and maladaptation leading to imbalance, as well as environmental, cultural, gender and life-cycle variables. There is a need to develop a comprehensive quantifiable stress assessment instrument. It would be based on the ‘stress factor’, a dimension that would integrate biological, psychological, social, economic and spiritual parameters and would allow for cultural sensitivity. It would contribute to clinical operational sophistication and would illuminate treatment options and multidimensional well-being interventions. Hopefully, it would facilitate development of culturally sensitive pharmaceutical or biophysiological adaptogens and homeostatic interventions.
Background
Acute myocardial infarction (AMI), characterized by an event of myocardial necrosis, is a common cardiac emergency worldwide. However, the genetic mechanisms of AMI remain largely elusive.
Methods
A genome-wide association study dataset of AMI was obtained from the CARDIoGRAMplusC4D project. A transcriptome-wide association study (TWAS) was conducted using the FUSION tool with gene expression references of the left ventricle and whole blood. Significant genes detected by TWAS were subjected to Gene Ontology (GO) enrichment analysis. Then the TWAS results of AMI were integrated with mRNA expression profiling to identify common genes and biological processes. Finally, the identified common genes were validated by RT-qPCR analysis.
Results
TWAS identified 1,050 genes for the left ventricle and 1,079 genes for whole blood. Upon comparison with the mRNA expression profile, 4 common genes were detected, including HP (PTWAS = 1.22 × 10–3, PGEO = 4.98 × 10–2); CAMP (PTWAS = 2.48 × 10–2, PGEO = 2.36 × 10–5); TNFAIP6 (PTWAS = 1.90 × 10–2, PGEO = 3.46 × 10–2); and ARG1 (PTWAS = 8.35 × 10–3, PGEO = 4.93 × 10–2). Functional enrichment analysis of the genes identified by TWAS detected multiple AMI-associated biological processes, including autophagy of mitochondrion (GO: 0000422) and mitochondrion disassembly (GO: 0061726).
Conclusion
This integrative study of TWAS and mRNA expression profiling identified multiple candidate genes and biological processes for AMI. Our results may provide a fundamental clue for understanding the genetic mechanisms of AMI.
Significance
Previous studies have shown a transiently higher risk of acute cardiovascular disease (CVD) events within minutes to hours after behavioral, psychosocial, and environmental triggers. Research is limited examining acute CVD surrounding sociopolitical events. We compared hospitalization rates for acute CVD before and immediately after the date of the 2016 presidential election among patients in an integrated healthcare delivery system. The rate of CVD hospitalizations in the 2 d after the 2016 presidential election was 1.62 times higher compared to the rate in the same 2 d the week prior. Transiently heightened cardiovascular risk around the 2016 election may be attributable to sociopolitical stress. Further research is needed to understand the intersection between major sociopolitical events, perceived stress, and acute CVD.
Central activation in response to emotion and cognitive stress induces perturbations in the heart and the peripheral vasculature that differ in physiology and clinical manifestations when compared with exercise-induced changes. While our conventional framework of epicardial coronary artery disease is foundational in cardiology, an expanded paradigm is required to address the cardiovascular response to mental stress (MS) and its associated risks, thus addressing the intersection of the patient’s ecological and psychosocial experience with cardiovascular biology. To advance the field of MS in cardiovascular health, certain core challenges must be addressed. These include differences in the trigger activation between exercise and emotion, identification and interpretation of imaging cues as measures of pathophysiologic changes, characterization of the vascular response, and identification of central and peripheral treatment targets. Sex and psychosocial determinants of health are important in understanding the emerging overlap of MS–induced myocardial ischemia with microvascular dysfunction and symptoms in the absence of obstructive disease. In overcoming these critical knowledge gaps, integration of the field of MS will require implementation studies to guide use of MS testing, to support diagnosis of MS induced cardiac and vascular pathophysiology, to assess prognosis, and understand the role of endotying to direct therapy.
Background
In ischemic stroke and subarachnoid hemorrhage, there are known preceding triggering events that predispose to the stroke by, for example, abruptly raising blood pressure. We explored, whether triggering events can be identified in non-traumatic intracerebral hemorrhage (ICH).
Methods
We used structured questionnaires to interview consented patients with ICH treated in a tertiary teaching hospital, between 2014 and 2016. We asked of possible trigger factors, including Valsalva-inducing activity, heavy physical exertion, sexual activity, abrupt change in position, a heavy meal, a sudden change in temperature, exposure to traffic jam, and the combination of the first three (any physical trigger) during the hazard period of 0–2 h prior to ICH. The ratio of the reported trigger during the hazard period was compared to the same 2-h period the previous day (control period) to calculate the relative risks for each factor (case-crossover design).
Results
Of our 216 consented ICH patients, 97 (35.0%) could be interviewed for trigger questions. Reasons for not able to provide consistent and reliable responses included lowered level of consciousness, delirium, impaired memory, and aphasia. None of the studied possible triggers alone were more frequent during the hazard period compared to the control period. However, when all physical triggers were combined, we found an association with the triggering event and onset of ICH (risk ratio 1.32, 95% confidence interval 1.01–1.73).
Conclusions
Obtaining reliable information on the preceding events before ICH onset was challenging. However, we found that physical triggers as a group were associated with the onset of ICH.
Cardiovascular diseases are the worldwide leading cause of mortality. Cardiovascular diseases are noncommunicable conditions with a complex pathogenesis, and their clinical manifestations include major cardiovascular events such as myocardial infarction and stroke. Epidemiologic evidence suggests a consistent association between periodontitis and increased risk of cardiovascular diseases. Some evidence supports a beneficial effect of the treatment of periodontitis on both surrogate and hard cardiovascular outcomes. This narrative review has been conducted as an update of the most recent evidence on the effects of periodontitis treatment on cardiovascular outcomes since the last commissioned review of the European Federation of Periodontology‐American Academy of Periodontology World Workshop in 2012. Newer evidence originating from published randomized controlled trials confirms a positive effect of periodontal treatment on surrogate measures of cardiovascular diseases, whereas there have been no randomized controlled trials investigating the effect of periodontal treatment on the incidence of cardiovascular disease events such as myocardial infarction and stroke. In conclusion, there is sufficient evidence from observational and experimental studies on surrogate cardiovascular measures to justify the design and conduct of appropriately powered randomized controlled trials investigating the effect of effective periodontal interventions on cardiovascular disease outcomes (ie, myocardial infarction and stroke) with adequate control of traditional cardiovascular risk factors.
Background
Conventional risk factors for stroke that have been identified are mostly chronic diseases that explain much of the variation as to who develops stroke. However, these risk factors do not equip us with the means to predict when an event like stroke will occur. It has been observed that acute events like stroke and coronary heart disease are preceded by episodes of acute stress. The present study was undertaken to determine whether acute psychological stress is a potential triggering factor for the occurrence of stroke.
Methods
In accordance with the case-crossover study design, patients or Legally Authorized Representative (LAR) were asked to report psychological stress during the two-hour hazard period before the event and during the control period, which was the same 2-hour time period the day before the event. Conditional logistic regression was used to compare each person's exposure during the hazard period to their exposure during the control period.
Results
A total of 151 stroke patients were interviewed. Acute psychological stress was associated with transient increased odds of stroke in the subsequent 2 hours that was 3.4 times higher than the odds during periods with no exposure to these triggers (95% confidence interval 1.55-7.50).
Conclusions
Acute psychological stress is a potential independent triggering factor for the occurrence of stroke. Further confirmatory studies are required to help corroborate these findings and elucidate the mechanisms underlying this short-term increase in risk.
Purpose
Law enforcement is a dangerous profession not only due to assaults, accidents and homicides but also due to health risks. This study examined trends in the national frequency and rate of law enforcement job-related illness deaths in the United States over a 22-year period (1997–2018).
Design/methodology/approach
Data were obtained from the National Law Enforcement Officers Memorial Fund (NLEOMF) on death frequencies related to health issues at work. Death rates were based on the total number of police officers in the United States [rate = (frequency/population at risk) × 100,000]. Trends were examined using standardized regression.
Findings
A total of 646 deaths were attributed to job-related illness. There was a significant upward trend in overall job-related illness deaths (frequency analyses: β = 0.88, p < 0.0001; rate analyses: β = 0.82, p ≤ 0.0001) mainly driven by a significant increase in 911 cancer deaths (frequency analyses: β = 0.88, p < 0.0001; rate analyses: β = 0.88, p ≤ 0.0001). Nearly 82 percent of circulatory deaths were from a heart attack, with an average death age of 46.5 years.
Research limitations/implications
Deaths were not included if they failed to meet medical requirements of the NLEOMF. The data are descriptive, do not estimate risk and should be interpreted cautiously.
Practical implications
Police wellness programs may help to reduce the danger of deaths associated with job-related illness.
Originality/value
This is among the first studies to examine frequency and rate of police health–related deaths due to job exposures.
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.
Background:
Psychological factors such as hostility and depression have been associated with cardiovascular disease. However, their role in predicting incident cardiac events independently one of another is not clear.
Methods:
Among 10,304 GAZEL middle-aged workers free of cardiovascular diseases in 1993, 581 incident cardiac events were validated from 1994-2014. Hostile traits (cognitive hostility, behavioral hostility, irritability and negativism) were assessed with the Buss and Durkee Hostility Inventory at baseline. Depressive symptoms were assessed at baseline and every three years with the Center for Epidemiological Studies Depression scale. We used Cox proportional hazards models to calculate hazard ratios (HR) of hostile traits for incident cardiac events adjusting for baseline self-reported socio-demographics and family history of coronary heart diseases (model 1), then additionally for time-dependent depressive symptoms (either as a binary or continuous variable) (model 2) and for yearly self-reported modifiable cardiovascular risk factors (physical activity, smoking, body mass index, diabetes, dyslipidemia and hypertension) (model 3).
Results:
In Model 1, the only hostile trait associated with incident cardiac events was irritability (HR for one interquartile range: 1.16, 95% confidence interval: 1.02-1.32). This association was no longer statistically significant when further adjusting for depressive symptoms. Depressive symptoms, in turn, remained significant predictors of cardiac events with HRs ranging from 1.40-1.49 (binary).
Limitations:
Hostility traits were measured only once.
Conclusions:
Depressive symptoms might explain the association between irritability and cardiac events and should therefore be prioritized in interventions aiming to prevent cardiovascular disease. Further research is needed to identify the mechanisms underlying this association.
Objective: People with multiple sclerosis (pwMS) who experience higher levels of anger also report poorer quality of life (QoL). This qualitative study explored the subjective experience of anger amongst pwMS, and how anger influenced their lives.
Methods: A series of semi-structured, face-to-face interviews were conducted with 20 pwMS. Interviews were recorded, transcribed and then Interpretative Phenomenological Analysis was used to analyse the emerging themes.
Results: The most common experience of anger was frustration that MS-related symptoms restricted participation in everyday activities. Also, some experiences of anger-with-self were focused on frustration at the inability to overcome symptom-related activity limitations. Participants reported frustration with others’ insensitivity to the effects of the disease process, as well as usual daily irritations with family and colleagues. Some of the participants reported the use of coping strategies to deal with anger episodes.
Conclusion: Many pwMS experience frustration at the restrictions that the disease places on them, self-directed anger, and irritation with others’ attitude towards them. Much research in MS focuses on physical symptoms, but current results indicate that there is a need to better understand the emotional challenges faces by pwMS, and to provide more support for those who are experiencing frustration.
Aims:
Arrhythmogenesis of chronic myocardial infarction (MI) is associated with the prolongation of action potential, reduction of inward rectifier potassium (IK1, Kir) channels and hyper-activity of Calcium/calmodulin-dependent kinase II (CaMKII) in cardiomyocytes. Zacopride, a selective IK1 agonist, was applied to clarify the cardioprotection of IK1 agonism via a CaMKII signaling on arrhythmias post-MI.
Methods:
Male SD rats were implanted wireless transmitter in the abdominal cavity and subjected to left main coronary artery ligation or sham operation. The telemetric ECGs were monitored per day throughout 4 weeks. At the endpoint, isoproterenol (1.28 mg/kg, i.v.) was administered for provocation test. The expressions of Kir2.1 (dominant subunit of IK1 in ventricle) and CaMKII were detected by Western-blotting.
Key findings:
In the telemetric rats' post-MI, zacopride significantly reduced the episodes of atrioventricular conduction block (AVB), premature ventricular contraction (PVC), ventricular tachycardia (VT) and ventricular fibrillation (VF), without significant effect on superventricular premature contraction (SPVC). In provocation test, zacopride suppressed the onset of ventricular arrhythmias in conscious PMI or sham rats. The expression of Kir2.1 was significantly downregulated and p-CaMKII was upregulated post-MI, whereas both were restored by zacopride treatment.
Significance:
IK1/Kir2.1 might be an attractive target for pharmacological controlling of lethal arrhythmias post MI.
Background:
Bereavement is associated with an increased risk of cardiovascular disease; however, no reports exist of interventions to reduce risk. In a randomized, double-blind, placebo-controlled trial of 85 recently bereaved participants, we determined whether β-blocker (metoprolol 25 mg) and aspirin (100 mg) reduce cardiovascular risk markers and anxiety, without adversely affecting bereavement intensity.
Methods:
Participants were spouses (n = 73) or parents (n = 12) of deceased from 5 hospitals in Sydney, Australia, 55 females, 30 males, aged 66.1 ± 9.4 years. After assessment within 2 weeks of bereavement, subjects were randomized to 6 weeks of daily treatment or placebo, and the effect evaluated using ANCOVA, adjusted for baseline values (primary analysis).
Results:
Participants on metoprolol and aspirin had lower levels of home systolic pressure (P = .03), 24-hour average heart rate (P < .001) and anxiety (P = .01) platelet response to arachidonic acid (P < .001) and depression symptoms (P = .046) than placebo with no difference in standard deviation of NN intervals index (SDNNi), von Willebrand Factor antigen, platelet-granulocyte aggregates or bereavement intensity. No significant adverse safety impact was observed.
Conclusions:
In early bereavement, low dose metoprolol and aspirin for 6 weeks reduces physiological and psychological surrogate measures of cardiovascular risk. Although further research is needed, results suggest a potential preventive benefit of this approach during heightened cardiovascular risk associated with early bereavement.
Background:
Roughly, a fourth of all placental abruption cases have an acute aetiologic underpinning, but the causes of acute abruption are poorly understood. Studies indicate that symptoms of stress, depression, and anxiety during pregnancy may be associated with a higher risk of abruption.
Objective:
We examined the rate of abruption in the 2 hours immediately following outbursts of anger.
Methods:
In a multicentre case-crossover study, we interviewed 663 women diagnosed with placental abruption admitted to one of the seven Peruvian hospitals between January 2013 and August 2015. We asked women about outbursts of anger before symptom onset and compared this with their usual frequency of anger during the week before abruption.
Results:
The rate of abruption was 2.83-fold (95% confidence interval [CI] 1.85, 4.33) higher in the 2 hours following an outburst of anger compared with other times. The rate ratio (RR) was lower for women who completed technical school or university (RR 1.38, 95% CI 0.52, 3.69) compared to women with secondary school education or less (RR 3.73, 95% CI 2.32, 5.99, P-homogeneity = .07). There was no evidence that the association between anger episodes and abruption varied by hypertensive disorders of pregnancy (ie preeclampsia/ eclampsia) or antepartum depressive symptoms.
Conclusion:
There was a higher rate of abruption in the 2 hours following outbursts of anger compared with other times, providing potential clues to the aetiologic mechanisms of abruption of acute onset.
Aim: This study is aimed to comparison between left ventricular (LV) function for people with and without type D personality hospitalized for the first time of myocardial infarction (MI). Materials and Methods: In a descriptive-analytical study, 150 patient hospitalized in heart care centers in Isfahan with definite MI diagnosis were selected by simple available sampling method. Data regarding the determination of D and non-D type of personality were collected by a 14-item questionnaire (DS14) and the results from LV performance evaluation using echocardiograph after 1st time heart attack and before clearance from hospital. Collected data were analyzed using SPSS software and t-test, Chi-square, linear and multiple regression tests. Results: The average of ejection fraction (EF) index in total patient was 43 ± 9.47 with the range of 15–60, 14 people (9.3%) normal EF and 136 people (90.7%) had abnormal EF. The average of EF index in 2 groups with D and non-D type of personality were 43.2 ± 10.5 and 42.9 ± 9, respectively, and based on t-test, the average of EF index in 2 groups had no significant difference (P = 0.86). Furthermore, 7 people (12.7%) in group D and 7 people (7.4%) in non-D group had normal EF, and in these two groups, 48 and 88 people had abnormal EF, respectively (87.3% vs. 92.6%), but according to Chi-square test, EF distribution in 2 personality types had no significant difference (P = 0.28). Conclusion: There is no significant relationship of type D personality with LVEF in people with first-time MI.
Background: Psychosocial stress and anger trigger cardiovascular events, but their relationship to heart failure (HF) exacerbations is unclear. We investigated perceived stress and anger associations with HF functional status and symptoms.
Methods and Results: In a prospective cohort study (BETRHEART), 144 patients with HF (77% male; 57.5 ± 11.5 years) were evaluated for perceived stress (Perceived Stress Scale; PSS) and state anger (STAXI) at baseline and every 2 weeks for 3 months. Objective functional status (6-min walk test; 6MWT) and health status (Kansas City Cardiomyopathy Questionnaire; KCCQ) were also measured biweekly. Linear mixed model analyses indicated that average PSS and greater than usual increases in PSS were associated with worsened KCCQ scores. Greater than usual increases in PSS were associated with worsened 6MWT. Average anger levels were associated with worsened KCCQ, and increases in anger were associated with worsened 6MWT. Adjusting for PSS, anger associations were no longer statistically significant. Adjusting for anger, PSS associations with KCCQ and 6MWT remained significant.
Conclusion: In patients with HF, both perceived stress and anger are associated with poorer functional and health status, but perceived stress is a stronger predictor. Negative effects of anger on HF functional status and health status may partly operate through psychological stress.
Autonomic nervous system control of the heart is a dynamic process in both health and disease. A multilevel neural network is responsible for control of chronotropy, lusitropy, dromotropy, and inotropy. Intrinsic autonomic dysfunction arises from diseases that directly affect the autonomic nerves, such as diabetes mellitus and the syndromes of primary autonomic failure. Extrinsic autonomic dysfunction reflects the changes in autonomic function that are secondarily induced by cardiac or other disease. An array of tests interrogate various aspects of cardiac autonomic control in either resting conditions or with physiological perturbations from resting conditions. The prognostic significance of these assessments have been well established. Clinical usefulness has not been established, and the precise mechanistic link to mortality is less well established. Further efforts are required to develop optimal approaches to delineate cardiac autonomic dysfunction and its adverse effects to develop tools that can be used to guide clinical decision-making.
To review what we have covered so far, Chap. 2 proposed a model of how psychosocial factors can activate myriad neurological, neuroendocrine, and endocrine response axes. Similarly, Chap. 2 reviewed the physiological constituents of these stress axes in considerable detail. Chapter 5 reviewed the link from stress arousal to disease by summarizing several noteworthy models constructed to elucidate how stress arousal can lead to disease and dysfunction, that is, mechanisms of pathogenesis that link causally stress arousal to target-organ pathology. The goal of this chapter is to review some of the most common clinical manifestations of excessive stress and, more specifically, to familiarize the reader with some of the most frequently encountered target-organ disorders believed to be related to excessive stress arousal.
Background:
Physical exertion and caffeine consumption are associated with acute myocardial infarction (MI). However, physical exertion and caffeine consumption have not been examined as immediate triggers of MI in low and middle-income countries.
Objective:
Using a self-matched case-crossover design, we examined the acute risk of MI in the hour following episodes of physical exertion, caffeinated coffee, and tea consumption among MI survivors in Thailand.
Methods:
A total of 506 Thai participants (women = 191, men = 315) were interviewed between 2014 and 2017 after sustaining an acute MI. We compared each subject's exposure to physical exertion and consumption of caffeine- containing beverages in the hour preceding the onset of MI with the subject's expected usual frequency in the prior year to calculate relative risks (RRs) and 95% confidence intervals (95%CIs).
Results:
Of the 506 participants, 47 (9.3%) engaged in moderate or heavy physical exertion, 6 (1.2%) consumed tea, and 21 (4.2%) consumed coffee within the hour before MI. The relative risk of MI after moderate or heavy physical exertion was 3.0 (95% CI 2.2-4.2) compared to periods of no exertion, with a higher risk among more sedentary participants compared to active participants. Compared to times with no caffeinated beverage consumption, there was a higher risk of MI in the hour following consumption of caffeinated tea (RR = 3.7; 95%CI: 1.5-9.3) and coffee (RR = 2.3; 95%CI: 1.4-3.6).
Conclusion:
Physical exertion, coffee and tea consumption were associated with a higher risk of MI in the subsequent hour compared to times when the participants were sedentary or did not consume caffeinated beverages. Our study identifies high-risk populations for targeted screening and intervention to prevent acute MI.
Interventional radiology plays a critical role in offering minimally invasive procedures, resulting in increased patient comfort. However, of the millions of patients undergoing interventional procedures each year, many suffer from pre-procedural psychological stressors related to fear of discomfort and diagnostic uncertainty. We describe a case of Takotsubo cardiomyopathy, also called broken heart syndrome or stress cardiomyopathy, following ultrasound-guided renal cyst aspiration in a patient with severe anxiety in anticipation of the interventional radiology procedure.
In this article, the authors evaluate the possible roles of negative emotions and cognitions in the association between socioeconomic status (SES) and physical health, focusing on the outcomes of cardiovascular diseases and all-cause mortality. After reviewing the limited direct evidence, the authors examine indirect evidence showing that (a) SES relates to the targeted health outcomes, (b) SES relates to negative emotions and cognitions, and (c) negative emotions and cognitions relate to the targeted health outcomes. The authors present a general framework for understanding the roles of cognitiveemotional factors, suggesting that low-SES environments are stressful and reduce individuals' reserve capacity to manage stress, thereby increasing vulnerability to negative emotions and cognitions. The article concludes with suggestions for future research to better evaluate the proposed model.
Recent research has renewed interest in the potential influence of hostility on physical health. This review indicates that the evidence available from prospective studies, although not entirely consistent, suggests that hostile persons may be at increased risk for subsequent coronary heart disease and other life-threatening illnesses. Further, several plausible mechanisms possibly linking hostility and health have been articulated and subjected to initial evaluation. Hostile individuals display heightened physiological reactivity in some situations, report greater degrees of interpersonal conflict and less social support, and may have more unhealthy daily habits. Additional research is needed, and it must address a variety of past conceptual and methodological limitations. Perhaps the most central of these concerns are the assessment of individual differences in hostility and the role of social contexts in the psychosomatic process.
Key words: hostility, coronary heart disease (CHD), personality, physiological reactivity, psychosomatics
This study examined the comparative potency of several psychological stressors and exercise in eliciting myocardial ischemia as measured by left ventricular (LV) ejection fraction (EF) changes using radionuclide ventriculography. Twenty-seven subjects underwent both exercise (bicycle) and psychological stressors (mental arithmetic, recall of an incident that elicited anger, giving a short speech defending oneself against a charge of shoplifting) during which EF, blood pressure, heart rate and ST segment were measured. Eighteen subjects had 1-vessel coronary artery disease (CAD), defined by greater than 50% diameter stenosis in 1 artery as assessed by arteriography. Nine subjects served as healthy control subjects. Anger recall reduced EF more than exercise and the other psychological stressors (overall F [3.51] = 2.87, p = .05). Respective changes in EF for the CAD patients were -5% during anger recall, +2% during exercise, 0% during mental arithmetic and 0% during the speech stressor. More patients with CAD had significant reduction in EF (greater than or equal to 7%) during anger (7 of 18) than during exercise (4 of 18). The difference in EF change between patients with CAD and healthy control subjects was significant for both anger (t25 = 2.23, p = 0.04) and exercise (t25 = 2.63, p = 0.01) stressors. In this group of patients with CAD, anger appeared to be a particularly potent psychological stressor.
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.
From among 250 MMPI items that discriminated significantly between teachers scoring high and teachers scoring low on the Minnesota Teacher Attitude Inventory, two sets of 50 items were selected (principally on the basis of content) to form a Hostility (Ho) Scale and a Pharisaic virtue (Pv) scale. "The Ho scale… reveals a type of individual characterized by a dislike for and distrust of others. The Pv scale… reveals a type of person who described himself as preoccupied with morality and ridden with fears and tensions." (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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.
Myocardial infarction has been shown to have a circadian pattern of occurrence, with a significantly increased incidence in the early morning hours.1 Recognition that onset of acute coronary syndromes may not occur as a random event has led investigators to search for triggers of myocardial infarction.2 Both psychological and physical stresses have been implicated as possible triggers. However, thus far only excessive physical exertion has been temporally linked to onset of pathologically documented acute myocardial infarction.3 We report the first case of an acute myocardial infarction associated with extreme emotional upset, which resulted in cardiogenic shock and was successfully reversed by rapid treatment with thrombolytic therapy.
A synthesis of classical and recent thinking on the issues involved in selecting controls for case-control studies is presented in this and two companion papers (S. Wacholder et al. Am J Epidemiol 1992;135:1029-50). In this paper, a theoretical framework for selecting controls in case-control studies is developed. Three principles of comparability are described: 1) study base, that all comparisons be made within the study base; 2) deconfounding, that comparisons of the effects of the levels of exposure on disease risk not be distorted by the effects of other factors; and 3) comparable accuracy, that any errors in measurement of exposure be nondifferential between cases and controls. These principles, if adhered to in a study, can reduce selection, confounding, and information bias, respectively. The principles, however, are constrained by an additional efficiency principle regarding resources and time. Most problems and controversies in control selection reflect trade-offs among these four principles.
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.
To study the effects of standardized mental stress (arithmetic and the Stroop color word test) on plasma coagulation and fibrinolysis, blood samples were obtained before, during, and after 20 minutes of mental stress from 10 healthy, non-smoking young males aged 22 to 30 years. Reactions were compared with those observed during physical exercise and infusion of adrenaline. Both von Willebrand factor antigen and factor VIII coagulant activity increased significantly in response to mental stress (95 +/- 28 vs 123 +/- 56%; p less than 0.05 and 125 +/- 54 vs 217 +/- 170%; p less than 0.05, respectively). There was also a significant increase of factor VII coagulant activity (86 +/- 31 vs 108 +/- 51%; p less than 0.05). Furthermore, mental stress caused an activation of the fibrinolytic system with an elevation of tissue plasminogen activator activity and tissue plasminogen activator antigen (0.80 +/- 0.48 vs 1.23 +/- 0.96 IU/ml; p = 0.076 and 4.38 +/- 1.87 vs 5.78 +/- 2.58 IU/ml; p less than 0.01). Fibrinogen concentration increased during stress (1.95 +/- 0.29 vs 2.11 +/- 0.27 g/l; p less than 0.05). Similar but more pronounced responses were observed during exercise and adrenaline infusion. Parallel to the increases in coagulation and fibrinolytic factors there were significant increases in heart rate, and systolic and diastolic blood pressure. It is concluded that mental stress has significant effects on plasma coagulation and fibrinolysis, and that it could thus affect important risk factors for cardiovascular disease.
This article reviews the epidemiologic evidence linking psychological factors and various indexes of coronary heart disease (CHD) that has been gathered since the Amelia Island Conference in 1978. In general, studies of populations not selected according to CHD risk support the conclusion that the global type A construct is predictive of increased risk of coronary events. In high-risk groups, including patients undergoing coronary angiography, the evidence with respect to global type A is much less clear. This stems from the fact that most of these studies, although generally failing to find statistically significant relationships between coronary events and type A behavior, are flawed in a number of ways, including inadequate statistical power of results, use of less than adequate instruments, and failure to take an apparent interaction between type A behavior and age into account. Nevertheless, taken together, these findings suggest that it may be possible to identify measures of coronary-prone behavior that are more powerful than the global type A measure. Extensive evidence suggests that such measures may be found in the domain of hostility and anger. Measures of hostility and anger coping styles have been found to be associated with coronary atherosclerosis in populations in which global type A was not related to disease, and measures of hostility have predicted increased coronary events and total mortality in prospective population samples followed for from 20 to 25 years. Preliminary evidence suggests that hostility/anger characteristics may account for the increased coronary risk associated with global type A behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
Breslow (1981, Biometrika 68, 73-84) has shown that the Mantel-Haenszel odds ratio is a consistent estimator of a common odds ratio in sparse stratifications. For cohort studies, however, estimation of a common risk ratio or risk difference can be of greater interest. Under a binomial sparse-data model, the Mantel-Haenszel risk ratio and risk difference estimators are consistent in sparse stratifications, while the maximum likelihood and weighted least squares estimators are biased. Under Poisson sparse-data models, the Mantel-Haenszel and maximum likelihood rate ratio estimators have equal asymptotic variances under the null hypothesis and are consistent, while the weighted least squares estimators are again biased; similarly, of the common rate difference estimators the weighted least squares estimators are biased, while the estimator employing "Mantel-Haenszel" weights is consistent in sparse data. Variance estimators that are consistent in both sparse data and large strata can be derived for all the Mantel-Haenszel estimators.
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).
High levels of hostility as assessed by a MMPI scale (Ho) have been found associated with increased levels of arteriographically documented coronary atherosclerosis. In this study we examined the relationship between hostility and subsequent health status in a 25-year follow-up of 255 medical students who completed the MMPI while in medical school. High Ho scores were found to be predictive of both clinical coronary disease incidence and total mortality.
Level of hostility (Ho) was assessed by a 50-item subscale of the Minnesota Multiphasic Personality Inventory at the initial examination of 1877 employed middle-aged men who were free of coronary heart disease (CHD). Ten-year incidence of major CHD events (myocardial infarction and CHD death) was lowest in the first quintile of the Ho scale's distribution, highest in the middle quintile, and intermediate in the other three quintiles. After adjustment for age, blood pressure, serum cholesterol level, cigarette smoking, and intake of ethanol, the relative odds of a major CHD event was 0.68 for men with Ho scores less than or equal to 10 points in comparison to men with higher scores. The Ho scale was positively associated with crude 20-year mortality from CHD, malignant neoplasms, and causes other than cardiovascular--renal diseases and malignant neoplasms. After adjustment for the risk factors listed above, the Ho scale had a statistically significant, positive, monotonic association with 20-year risk of death from all causes combined. A difference of 23 points on the Ho scale, i.e., the difference between the means of the first and the fifth quintiles, was associated with a 42% increase in the risk of death. These results support the previous findings of Williams et al. with respect to the Ho scale and coronary atherosclerosis, and also suggest that the Ho scale may be associated with factors having broad effects on survival.
Induction and latent periods are distinguishable concepts referring respectively to the period between causal action and disease initiation, and the period between disease initiation and detection. A disease cannot be characterized as having a long or short induction period, except in relation to a specific etiologic component. Inappropriate assumptions, explicit or implicit, about the length of the combined induction and latent period (the "empirical induction period") in an analytic study result in nondifferential misclassification and bias toward the null. Repeated analyses, varying the assumptions about the length of the empirical induction period, can be used to minimize such misclassification, thereby providing estimates for an undiluted measure of effect and the mode of the empirical induction period.
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.
At one time or another, most physicians have encountered a patient -- perhaps even a friend or family member -- who suffered a heart attack during strenuous physical exertion. Some familiar examples include shoveling snow, recreational jogging, and sexual activity. Until now, however, a link between heavy exertion and the onset of myocardial infarction has been suggested mainly by temporal associations, anecdotal reports, and everyday experience. In this issue of the Journal, the commonly held notion that vigorous exercise can trigger heart attacks has been buttressed by solid evidence. The two new reports by Mittleman et al.1 in the United . . .
To determine the effects of anger on coronary artery vasoconstriction, 12 patients with symptomatic myocardial ischemia were studied during cardiac catheterization. During catheterization, the patients were asked to recall a recent event that had produced anger. One narrowed and 2 non-narrowed arterial segments were selected using predetermined criteria. Patients also completed various self-report measurements upon entering the catheterization laboratory before any procedures, after completion of the clinical angiogram and after the anger recall stressor. There was a significant increase in subject reports of anger (F[1,6] = 21.94, p < 0.01) and arousal (F [2,6] = 5.49, p < 0.05) during the anger stressor. There were no significant changes in heart rate, systolic or diastolic blood pressure, or heart rate x systolic blood pressure product during the anger stressor. A total of 27 arterial segments (9 narrowed and 18 non-narrowed) were selected and analyzed using quantitative angiographic techniques. Repeated-measures analysis of variance (baseline vs anger stressor) found no significant group differences with regard to changes in arterial diameter between conditions or among segments. Reported anger was significantly correlated with a decrease in both mean (r = -0.76, p < 0.05) and minimal (r = -0.82, p < 0.05) diameter changes in narrowed arteries. Vasoconstriction only occurred with high levels of anger. There were no significant correlations between anger report and diameter change in non-narrowed arteries. Thus, anger may produce coronary vasoconstriction in previously narrowed coronary arteries.
The symptomatology and diagnosis of coronary thrombosis
- Obraztsov
- N D Strazhesko