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Natural and Unnatural Triggers of Myocardial Infarction
Abstract
Previous analyses have suggested that factors that stimulate the sympathetic nervous system and catecholamine release can trigger acute myocardial infarction. The wake-up time, Mondays, winter season, physical exertion, emotional upset, overeating, lack of sleep, cocaine, marijuana, anger, and sexual activity are some of the more common triggers. Certain natural disasters such as earthquakes and blizzards have also been associated with an increase in cardiac events. Certain unnatural triggers may play a role including the Holiday season. Holiday season cardiac events peak on Christmas and New Year. A number of hypotheses have been raised to explain the increase in cardiac events during the holidays, including overeating, excessive use of salt and alcohol, exposure to particulates, from fireplaces, a delay in seeking medical help, anxiety or depression related to the holidays, and poorer staffing of health care facilities at this time. War has been associated with an increase in cardiac events. Data regarding an increase in cardiac events during the 9/11 terrorist attack have been mixed. Understanding the cause of cardiovascular triggers will help in developing potential therapies.
... CV (or an underlying condition) may heighten thrombin generation, triggering coronary thrombosis (34), while CV with or without secondary thrombus formation may result in myocardial necrosis. (46) Additionally, coronary vasoconstriction may promote plaque rupture, especially when it is recurring. AMI may be caused by a ruptured plaque together with CV, but the vasospasm may disappear shortly afterward, leaving the remaining atherosclerotic plaque as the apparent culprit. ...
... (113) AMI's other emotional triggers include Mondays, winter, emotional upset, overeating, lack of sleep, cocaine, sex, Christmas, and New Year. (46) Generally, (only) 18% of AMI patients report that emotional upset preceded the AMI itself. (114) However, this does not include emotional factors that are not consciously perceived, such as suppressed anger, and therefore may be a substantial underestimation. ...
... (119) However, this was not seen in later attacks. (46) The wearing of gas masks and the associated sense of 'suffocation' is suspected of contributing to this situation. (46) Surprisingly, there was no increase in cardiac deaths during the 9/11 attacks in New York (5), perhaps due to the absence of a continued feeling of personal threat following the initial disastrous events. ...
Significant influences of the psyche on coronaries have been robustly observed in patients suffering from angina pectoris, myocardial ischemia, and acute myocardial infarction, with or without coronary atherosclerotic disease (CAD). These patients regularly report a feeling of chest oppression. Rather than being the consequence of ischemia, this specifically oppressive feeling may be part of the underlying cause, being foremost a pattern of stressful constriction/oppression. Evidence comes from clinical and epidemiological studies as well as from basic neurocognitive science. If the mental/environmental pattern translates into a mental/neuronal pattern, then into a pathophysiological pattern, we may gain the means for better causal insight as well as targeted management through in-depth studies. We see the pathophysiological mechanism being coronary vasospasm (of arteries and arterioles), which may be involved in ischemia more frequently than previously thought, with or without CAD. Much is already known about the relevant link between psyche and body. This knowledge may be applied practically through coronary imagery, which, in conjunction with established therapeutic approaches, could save many lives. Such an approach is easy to learn and can be used preventively or in acute situations.
... Dehydration, a deficit in body water content, is prevalent in clinical environments [1][2][3] and associated with increased mortality and morbidity. [3][4][5][6][7][8] However, clinical dehydration is a continuum rather than a binary state and has no internationally-recognised definition. Associated clinical signs can be subtle and unreliable, and there is no objective marker with everyday clinical utility. ...
... -1 ). 3 In 2004, The US National Hospital Discharge Survey reported over 500,000 hospitalisations were primarily due to dehydration, incurring healthcare costs in excess of 5 billion dollars. 2 Furthermore, it has been repeatedly shown that dehydration is associated with increased mortality 1,28-31 and morbidity. [3][4][5][6][7][8]32 Clinical signs of dehydration are variable and non-specific and there remains no reliable objective diagnostic test with everyday utility. 9,11 As such, hydration status is often ineffectively managed in hospitals, with several studies demonstrating that patients become dehydrated during hospital admission. ...
Background:
Dehydration is common in hospitals and is associated with increased mortality and morbidity. Clinical assessment and diagnostic measures of dehydration are unreliable. We sought to investigate the novel concept that individuals might control their own intravenous rehydration, guided by thirst.
Methods:
We performed a single-blind, counterbalanced, randomised cross-over trial. Ten healthy male volunteers of mean age 26 (standard deviation [sd] 10.5) yr were dehydrated by 3-5% of their baseline body mass via exercising in the heat (35°C, 60% humidity). This was followed by a 4 h participant-controlled intravenous rehydration: individuals triggered up to six fluid boluses (4% dextrose in 0.18% sodium chloride) per hour in response to thirst. Participants undertook two blinded rehydration protocols which differed only by bolus volume: 50 ml (low volume [LV]) or 200 ml (high volume [HV]). Each hour during the rehydration phase, plasma osmolality (pOsm) was measured and thirst score recorded. Nude body mass was measured at baseline, after dehydration, and after the rehydration phase.
Results:
In both conditions, the mean dehydration-related body mass loss was 3.9%. Thirst score was strongly associated with pOsm (within-subject r=0.74) and demand for fluid decreased as pOsm corrected. In the HV condition, participants rapidly rehydrated themselves (mean fluid delivered 3060 vs 981 ml in the LV condition) to body mass and pOsm no different to their euhydrated state.
Conclusion:
Healthy individuals appear able to rely on thirst to manage intravenous fluid intake. Future work must now focus on whether patient-controlled intravenous fluids could represent a paradigm shift in the management of hydration in the clinical setting.
Clinical trial registration:
NCT03932890.
... Having not been able to find explicitly-stated criteria to count a heart attack as an earthquake death within the documentation of the earthquake consequences databases used as sources for the present work, it is not clear how the connection between the two is made as the time of death moves further away from the time of the earthquake. & Heart failures can have and be influenced by many causes, such as time of the day, day of the week, season, physical exertion, emotional upset, consumption of psychotropic substances, and sexual activity (Kloner 2006). This implies, for example, that some of the cardiac-related deaths that occur (sufficiently) concurrently with an earthquake might be related to unusual physical exertion, like escaping from a building during the ground shaking or cleaning up earthquake debris, with the question of whether the emotional distress caused by the earthquake had a decisive influence or not over the heart failure left unanswered . ...
... This has been suggested by the observation of increased numbers of cardiac-related deaths after earthquakes followed by smaller-thanaverage such deaths in the period following the earthquake Bazoukis et al. 2018). However, Kloner (2006) ponders as well on the potential effects of ischemic preconditioning 3 on the reduced number of cardiac-related deaths after the earthquake. & Other factors such as limited or delayed access to medical attention due to damage to roads, traffic cutoff after disasters and even damage to hospitals themselves might have an influence on the occurrence of a cardiac-related death on the day of the earthquake, irrespective of whether the earthquake acted as a trigger or not (e.g., Tanaka et al. 2015;Bazoukis et al. 2018). ...
Interest in small-to-medium magnitude earthquakes and their potential consequences has increased significantly in recent years, mostly due to the occurrence of some unusually damaging small events, the development of seismic risk assessment methodologies for existing building stock, and the recognition of the potential risk of induced seismicity. As part of a clear ongoing effort of the earthquake engineering community to develop knowledge on the risk posed by smaller events, a global database of earthquakes with moment magnitudes in the range from 4.0 to 5.5 for which damage and/or casualties have been reported has been compiled and is made publicly available. The two main purposes were to facilitate studies on the potential for earthquakes in this magnitude range to cause material damage and to carry out a statistical study to characterise the frequency with which earthquakes of this size cause damage and/or casualties (published separately). The present paper describes the data sources and process followed for the compilation of the database, while providing critical discussions on the challenges encountered and decisions made, which are of relevance for its interpretation and use. The geographic, temporal, and magnitude distributions of the 1958 earthquakes that make up the database are presented alongside the general statistics on damage and casualties, noting that these stem from a variety of sources of differing reliability. Despite its inherent limitations, we believe it is an important contribution to the understanding of the extent of the consequences that may arise from earthquakes in the magnitude range of study.
... Of 370,758 patients in the 2004 US National Hospital Discharge Survey, there were 518,000 hospitalizations primarily due to dehydration, incurring healthcare costs in excess of 5 billion dollars [2]. The problem is not restricted to hospitalized patients, a recent UK study found one in every five older people living in long-term care to be dehydrated (serum osmolality >300 mOsm/kg) and half to be either dehydrated or at risk of becoming so (!295-300 mOsm/kg) [3]. Furthermore, it has been repeatedly shown that dehydration is associated with increased mortality and morbidity [3][4][5][6][7][8]. ...
... Even mild dehydration may contribute to sudden cardiac death following ACS [149]. ACS demonstrates a circadian oscillation, most typically occurring between the hours of 06:00 and midday [4,150]. A biologically plausible mechanism is that individuals are relatively dehydrated in the mornings following an overnight fast, creating prothrombotic conditions that contribute to infarct development [151]. ...
Background: Dehydration appears prevalent, costly and associated with adverse outcomes. We sought to generate consensus on such key issues and elucidate need for further scientific enquiry.
Materials and methods: A modified Delphi process combined expert opinion and evidence appraisal. Twelve relevant experts addressed dehydration’s definition, objective markers and impact on physiology and outcome.
Results: Fifteen consensus statements and seven research recommendations were generated. Key findings, evidenced in detail, were that there is no universally accepted definition for dehydration; hydration assessment is complex and requires combining physiological and laboratory variables; “dehydration” and “hypovolaemia” are incorrectly used interchangeably; abnormal hydration status includes relative and/or absolute abnormalities in body water and serum/plasma osmolality (pOsm); raised pOsm usually indicates dehydration; direct measurement of pOsm is the gold standard for determining dehydration; pOsm >300 and ≤280 mOsm/kg classifies a person as hyper or hypo-osmolar; outside extremes, signs of adult dehydration are subtle and unreliable; dehydration is common in hospitals and care homes and associated with poorer outcomes.
Discussion: Dehydration poses risk to public health. Dehydration is under-recognized and poorly managed in hospital and community-based care. Further research is required to improve assessment and management of dehydration and the authors have made recommendations to focus academic endeavours.
• Key messages
• Dehydration assessment is a major clinical challenge due to a complex, varying pathophysiology, non-specific clinical presentations and the lack of international consensus on definition and diagnosis.
• Plasma osmolality represents a valuable, objective surrogate marker of hypertonic dehydration which is underutilized in clinical practice.
• Dehydration is prevalent within the healthcare setting and in the community, and appears associated with increased morbidity and mortality.
... p=0.001), and paroxysmal arrhythmias treated with electrocardioversion (0.9% vs. 4.5%, p=0.022) were significantly more common in a subgroup analysis of patients treated in hospitals located within 20 km of the epicenter according to Babić et al. (61). Again, after the 1994 earthquake in California, USA, the number of patients admitted with acute myocardial infarctions increased by 35% in the week following the disaster (62). When compared with the same period in the previous year, the rate of admission for acute myocardial infarction increased considerably in the six weeks following the earthquake in Taiwan (63). ...
... AMI is primarily caused by a blocked coronary artery due to atherothrombosis, leading to heart muscle damage. This can result from a ruptured atherosclerotic lesion triggered by factors such as viral infections, smoking, alcohol, hypertension, exertion, or stress [36][37][38][39]. The immune system's role in AMI is crucial, as a proinflammatory response can accelerate atherosclerosis, causing events such as AMI. ...
Current evidence suggests that recent acute respiratory infections and seasonal influenza may precipitate acute myocardial infarction (AMI). This study examined the potential link between recent clinical respiratory illness (CRI) and influenza, and AMI in Bangladesh. Conducted during the 2018 influenza season at a Dhaka tertiary-level cardiovascular (CV) hospital, it included 150 AMI cases and two control groups: 44 hospitalized cardiac patients without AMI and 90 healthy individuals. Participants were matched by gender and age groups. The study focused on self-reported CRI and laboratory-confirmed influenza ascertained via quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) within the preceding week, analyzed using multivariable logistic regression. Results showed that cases reported CRI, significantly more frequently than healthy controls (27.3% vs. 13.3%, adjusted odds ratio (aOR): 2.21; 95% confidence interval (CI): 1.05–4.06), although this was not significantly different from all controls (27.3% vs. 22.4%; aOR: 1.19; 95% CI: 0.65–2.18). Influenza rates were insignificantly higher among cases than controls. The study suggests that recent respiratory illnesses may precede AMI onset among Bangladeshi patients. Infection prevention and control practices, as well as the uptake of the influenza vaccine, may be advocated for patients at high risk of acute CV events.
... This is primarily driven by an acute end stage of a chronic inflammatory atherosclerotic lesion characterized by abrupt rupturing of the de-stabilized atherosclerotic plaque due to short term exposure of certain triggering factors that may differ from the number of known cardiovascular risk factors (46). Such triggers of plaque rupture can include respiratory viral infections including influenza along with smoking, excessive alcohol, hypertension, heavy physical exertion or any kind of stressful events (47,48). One study showed respiratory viral infections can precipitate both STEMI and NSTEMI and was positively associated with risk of mortality among NSTEMI, but not among STEMI (49). ...
Background: Several studies imply that influenza and other respiratory illness could lead to acute myocardial infarction (AMI), but data from low-income countries are scarce. We investigated the prevalence of recent respiratory illnesses and confirmed influenza in AMI patients, while also exploring their relationship with infarction severity as defined by ST-elevation MI (STEMI) or high troponin levels. Methods: This cross-sectional study, held at a Dhaka tertiary hospital from May 2017 to October 2018, involved AMI inpatients. The study examined self-reported clinical respiratory illnesses (CRI) in the week before AMI onset and confirmed influenza using baseline qRT-PCR. Results: Of 744 patients, 11.3% reported a recent CRI, most prominently during the 2017 influenza season (35.7%). qRT-PCR testing found evidence of influenza in 1.5% of 546 patients, with all positives among STEMI cases. Frequencies of CRI were higher in patients with STEMI and in those with high troponin levels, although these associations were not statistically significant after adjusting for other variables. The risk of STEMI was significantly greater during influenza seasons in unadjusted analysis (RR: 1.09, 95% CI: 1.02- 1.18), however, this relationship was not significant in the adjusted analysis (aRR: 1.03, 95% CI: 0.91- 1.16). Conclusions: In Bangladesh, many AMI patients had a recent respiratory illness history, with some showing evidence of influenza. However, these illnesses showed no significant relationship to AMI severity. Further research is needed to understand these associations better and to investigate the potential benefits of infection control measures and influenza vaccinations in reducing AMI incidence.
... 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. ...
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.
... [43][44][45] Avoidance of potential triggers of cardiac and cerebrovascular events during the acute phase, such as excessive use of alcohol, overeating, lack of sleep, work stress, and long working hours, may be beneficial and is without harm. 46,47 ...
Background:
The excess risk of cardiovascular disease associated with a wide array of infectious diseases is unknown. We quantified the short- and long-term risk of major cardiovascular events in people with severe infection and estimated the population-attributable fraction.
Methods:
We analyzed data from 331 683 UK Biobank participants without cardiovascular disease at baseline (2006-2010) and replicated our main findings in an independent population from 3 prospective cohort studies comprising 271 533 community-dwelling participants from Finland (baseline 1986-2005). Cardiovascular risk factors were measured at baseline. We diagnosed infectious diseases (the exposure) and incident major cardiovascular events after infections, defined as myocardial infarction, cardiac death, or fatal or nonfatal stroke (the outcome) from linkage of participants to hospital and mortality registers. We computed adjusted hazard ratios (HRs) and 95% CIs for infectious diseases as short- and long-term risk factors for incident major cardiovascular events. We also calculated population-attributable fractions for long-term risk.
Results:
In the UK Biobank (mean follow-up, 11.6 years), 54 434 participants were hospitalized for an infection, and 11 649 had an incident major cardiovascular event at follow-up. Relative to participants with no record of infectious disease, those who were hospitalized experienced increased risk of major cardiovascular events, largely irrespective of the subtype of infection. This association was strongest during the first month after infection (HR, 7.87 [95% CI, 6.36-9.73]), but remained elevated during the entire follow-up (HR, 1.47 [95% CI, 1.40-1.54]). The findings were similar in the replication cohort (HR, 7.64 [95% CI, 5.82-10.03] during the first month; HR, 1.41 [95% CI, 1.34-1.48] during mean follow-up of 19.2 years). After controlling for traditional cardiovascular risk factors, the population-attributable fraction for severe infections and major cardiovascular events was 4.4% in the UK Biobank and 6.1% in the replication cohort.
Conclusions:
Infections severe enough to require hospital treatment were associated with increased risks for major cardiovascular disease events immediately after hospitalization. A small excess risk was also observed in the long-term, but residual confounding cannot be excluded.
... We then speculated that the eLOS was a result of the admission of season-related complications. Moreover, the biologically plausible temperature hypothesis has proven that the cold temperature could elevate systemic vascular resistance and fibrinogen levels, resulting in an increase in blood pressure, thrombus formation as well as enhanced fibrinolytic activity, platelet adhesiveness, and lipid levels [42,43], which may make it easier to cause perioperative complications. Although several of the above-mentioned seasonalrelated diseases including hematological complications and cardiac complications were not significantly correlated with eLOS after multivariate adjustment, the trends were observed with significant differences in our univariate analysis. ...
We aimed to identify the risk factors associated with an extended length of hospital stay (eLOS) in older hip-fracture patients and to explore the relationships between eLOS and mortality and functional outcomes. In this retrospective analysis of surgically treated intertrochanteric fracture (IF) patients, all variables were obtained and compared between the eLOS group and the normal LOS group. All participants were followed-up for a minimum of two years and the relation between the eLOS and all-cause mortality and functional outcomes were compared. After adjustment for potential confounders, we identified that patients with high modified Elixhauser’s Comorbidity Measure (mECM) had the highest likelihood of eLOS, followed by obesity, admission in winter, living in urban, pulmonary complications, admission in autumn, and time from injury to surgery. In addition, our results showed no significant difference in the mortality and functional outcomes between the two groups during follow-up. By identifying these risk factors in the Chinese geriatric population, it may be possible to risk-stratify IF patients and subsequently streamline inpatient resource utilization. However, the differences between health care systems must be taken into consideration. Future studies are needed to preemptively target the modifiable risk factors to demonstrate benefits in diminishing eLOS.
... The holiday is traditionally associated with happiness and joy, but, from a public health standpoint, often involves high mortality and morbidity [1]. Hypotheses concerning the source of this phenomenon include overeating, alcohol, anxiety, a decline in medication adherence, depression, and limited access to health care [1][2][3]. ...
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.
... La experiencia de estrés severo aumenta a largo plazo la morbilidad para diversas enfermedades, especialmente las de tipo cardiovascular (Boscarino, 1997). El estrés crónico se ha asociado consistentemente con el desarrollo de arteriosclerosis coronaria, incremento de la masa del ventrículo izquierdo, calcificaciones coronarias, propensión al desarrollo de infarto de miocardio, arritmias malignas y muerte cardiaca súbita (Kloner, 2006;Lanas y cols., 2007;Matthews, Zhu, Tucker y Whooley, 2006;Rosengren, Hawken y cols., 2004;Strike y Steptoe, 2003). La activación crónica del SNS, y los incrementos subsiguientes en catecolaminas y cortisol, se asocian con una mayor tasa cardiaca, output cardiaco, vasoconstricción en el sistema circulatorio y presión arterial. ...
... Coronary Heart Disease Acute coronary syndromes (ACS) are one of the commonest causes of death while travelling abroad. [18][19][20][21] They account for a fifth of all in-flight medical emergencies in some reports. 22,23 Physical and mental stress, weather changes and dehydration represent major precipitating factors. ...
Introduction: Primary care practitioners and travel medicine physicians are primarily responsible for identifying individuals who may be unfit for overseas travel and consulting with them pre-travel. Pre-existing medical conditions such as cardiovascular disease, chronic respiratory conditions and diabetes mellitus (DM) have the potential to complicate travel journeys. A considerable percentage of travel-associated illness may be due to the decompensation of a pre-existing medical condition. This review seeks to address the challenges faced by travellers with each of these conditions, including recently updated and evidence-based practical approaches for travel with comorbidities.
Methods: Sources for this review were identified through searches of PubMed/Google Scholar for materials published between 1st January 2000 and 31st December 2019, using combinations of search terms.
Results: The volume of literature on travelling with a pre-existing condition exploded with more than 865 associated articles indexed on the PubMed alone as of March 2020. After screening titles, abstracts and, in some cases, the full text version of indexed articles, 121 articles were deemed relevant to the subject matter of this review.
Conclusion: Rational approaches to pre-planning for travel with a medical condition will contribute to the prevention of problems while in transit as well as when at the travel destination. It is imperative for health care providers to be aware of the preventative measures and current recommendations that should be taken before and during travel to protect individuals with a chronic illness. Further research and studies should be directed to protect this vulnerable group of travellers.
... The eff ects of earthquakes on cardiovascular events have been studied in diff erent countries with varying results. 47 After the earthquake in Northridge, CA, USA, in 1994, occurrence of acute myocardial infarctions increased by 35% in the week after the earthquake compared with the week before, 48 and the rate of sudden cardiac death also rose. 49 After the earthquake in Taiwan in 1999, the rate of admission due to acute myocardial infarction increased signifi cantly in the 6 weeks after the earthquake compared with the same period in the previous year. ...
... In addition, the decreased fibrinolytic activity and increased ability to activate blood platelets play an important role. All the mentioned processes may lead to the rupture of atherosclerotic plaques and ultimately ACS [24,25]. The lost matches played by Jagiellonia Bialystok at home were found to be associated with a 27% increase in the number of male admissions for ACS. ...
Introduction
Acute coronary syndrome (ACS) could be triggered by emotions that are often associated with watching sport events. The aim of this study was to assess the influence of soccer matches on the frequency of admissions for ACS.
Material and methods
The study was based on the medical records of patients treated at the Clinical Hospital of Medical University of Bialystok from 2007 to 2018. All the official matches of the local team that took place during the study period were included in the analysis. A Poisson regression with a time effect of 0 and +1 day was used to assess the effect of matches.
Results
A total of 10 529 patients admitted due to ACS from Bialystok city and county were included in the analysis. The mean age of the patients was 66.6 ±12 years, and the majority were male (62%). The mean daily number of ACS admissions was 2.4 ±1.7. Since 2007, Jagiellonia Białystok has played 451 matches in total. The comparative analysis of exciting matches showed a higher frequency of admissions due to unstable angina (UA) (1.50 ±1.55 vs. 0.71 ±0.90, p < 0.01). The lost matches played at home were associated with a 27% increase in the number of male admissions for ACS (RR = 1.27, 95% CI: 1.02–1.58, p = 0.03).
Conclusions
The results achieved by the local professional soccer team are related to the incidence of ACS in the male population. Emotions caused by lost games play an important role as a triggering factor for ACS in this group.
... 1-12 A number of factors have been proposed to explain this association between infection and acute cardiovascular disease including activation of various inflammatory molecules and platelets, endothelial dysfunction, and/or augmented sympathetic nervous activity with release of high levels of catecholamines into the circulation. [1][2][3][4][5][6][7][8][9][10][11][12] Indeed, it is possible that all of these elements may be occurring simultaneously leading to atherosclerotic plaque instability and a concomitant hypercoagulable state. ...
... However, increased circulatory mortality may occur during and outside of the typical influenza season. The increase in circulatory mortality may be due to cold temperature during winter months potentially leading to increased blood pressure and thrombus formation [29]. Other respiratory bacterial or viral pathogens such as S. pneumoniae and parainfluenza may also contribute to these deaths [24,30]. ...
Background:
Influenza causes substantial morbidity and mortality worldwide, however, reliable burden estimates from developing countries are limited, including India. We aimed to quantify influenza-associated mortality for India utilizing 2010-2013 nationally representative data sources for influenza virus circulation and deaths.
Methods:
Virological data were obtained from the influenza surveillance network of 10 laboratories led by National Institute of Virology, Pune covering eight states from 2010-2013. Death data were obtained from the nationally representative Sample Registration System for the same time period. Generalized linear regression with negative binomial distribution was used to model weekly respiratory and circulatory deaths by age group and proportion of specimens positive for influenza by subtype; excess deaths above the seasonal baseline were taken as an estimate of influenza-associated mortality counts and rates. Annual excess death rates and the 2011 India Census data were used to estimate national influenza-associated deaths.
Results:
Estimated annual influenza-associated respiratory mortality rates were highest for those ≥65 years (51.1, 95% confidence interval (CI) = 9.2-93.0 deaths/100 000 population) followed by those <5 years (9.8, 95% CI = 0-21.8/100 000). Influenza-associated circulatory death rates were also higher among those ≥65 years (71.8, 95% CI = 7.9-135.8/100 000) as compared to those aged <65 years (1.9, 95% CI = 0-4.6/100 000). Across all age groups, a mean of 127 092 (95% CI = 64 046-190,139) annual influenza-associated respiratory and circulatory deaths may occur in India.
Conclusions:
Estimated influenza-associated mortality in India was high among children <5 years and adults ≥65 years. These estimates may inform strategies for influenza prevention and control in India, such as possible vaccine introduction.
... A drop in temperature increases diuresis with an increase in blood viscosity and haemoconcentration. Cold causes an increase in coagulation factors as fibrinogen and platelets counts which may promote acute thrombosis [8,10,[16][17][18][19]. ...
Cruise tourism to Antarctica is constantly growing. Passengers and crewmembers may experience illnessesor injuries while traveling to remote areas with harsh weather conditions from where prompt evacuationis mostly unavailable. While a small explorer ship was at Wilhelmina bay (64°39' South and 62°08' West)in the Antarctic Peninsula, a 73-year-old male passenger presented with acute chest pain after two shortexcursions off the vessel in cold weather conditions. He was treated on board and remained clinicallystable until the ship reached Ushuaia at the end of the cruise which was 5 days after the symptoms onset.
... 51 Although reciprocal activation between sympathetic (cold shock) and parasympathetic (diving response) systems is commonly adaptive (follow one another), simultaneous activation appears to be associated with ectopic beats or arrhythmias. 51,54,55 Cold waterÀinduced rhythm disturbances are common, albeit frequently asymptomatic. 24,51,56 In most humans, head-out cold-water immersion results in sympathetically driven sinus tachycardia with variable ectopic beats and supraventricular or junctional arrhythmias. ...
Sudden death during whitewater recreation often occurs through understandable mechanisms such as underwater entrapment or trauma, but poorly defined events are common, particularly in colder water. These uncharacterized tragedies are frequently called flush drownings by whitewater enthusiasts. We believe the condition referred to as cold water immersion syndrome may be responsible for some of these deaths. Given this assumption, the physiologic alterations contributing to cold water immersion syndrome are reviewed with an emphasis on those factors pertinent to flush drowning.
... K. pneumoniae is often involved in community-acquired and nosocomial infections [12]. Pneumonia was also found to increase the circulating levels of inflammatory cytokines, which promote thrombogenesis [13] and suppress ventricular function [14,15]. Increased coagulation activity has been observed in pneumonia, including those with mild disease [16,17]. ...
Background:
Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery.
Patients and methods:
We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin.
Results:
Bacterial culture showed different bacteria in 14 samples. Leukocyte infiltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44-50) vs. 55 (47-62) years, P=0.001, respectively], white blood cells, and white blood cells (WBCs) (16670 vs. 7550 cells/µl, P<0.0001, respectively). In hospital-major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not significantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CI: 06-6.3), P=0.5]. Patients with bacteria, heavy infiltration, and pneumolysin had insignificant higher events compared with those without [10/35 (28.6%) vs. 16/105 (15.2%) events, OR 2.2 (95% CI: 0.92-5.43), P=0.13]. However, the difference was not significant. By multivariate analysis, bacteria, leukocyte infiltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were significant predictors of bacterial footprints (P<0.0001 and P=0.04, respectively).
Conclusion:
Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.
... 5 Moreover, the incidence of ischemic heart disease (IHD) is increasing. 6,7 The major factor of IHD is acute myocardial ischemia (AMI), 8 which is one of the most serious health issues in both developed and developing countries. 9,10 AMI is predicted to be the major cause of death by 2020. ...
Here we aimed to observe the effects of total ginsenosides (TG) against isoproterenol (ISO) induced myocardial ischemia (MI) and to explore its underlying mechanisms based on L-type Ca ²⁺ current (I Ca-L ), intracellular Ca ²⁺ ([Ca ²⁺ ] i ) and contraction in isolated rat myocytes. Rat model of MI was induced by subcutaneously injection of ISO (85 mg/kg) for 2 consecutive days. J-point elevation, heart rate, serum levels of creatine kinase (CK) and lactated dehydrogenase (LDH), and heart morphology changes were observed. Influences of TG on I Ca-L , [Ca ²⁺ ] i and contraction in isolated rat myocytes were observed by the patch-clamp technique and IonOptix detection system. TG significantly reduced J-point elevation, heart rate, serum levels of CK and LDH, and improved heart pathologic morphology. TG decreased I Ca-L in concentration-dependent manner with a half-maximal inhibitory concentration (IC 50 ) of 31.65 μg/mL. TG (300 μg/mL) decreased I Ca-L of normal and ischemic ventricular myocytes by 64.33 ± 1.28% and 61.29 ± 1.38% respectively. At 30 μg/mL, TG reduced Ca ²⁺ transient by 21.67 ± 0.94% and cell shortening by 38.43 ± 6.49%. This study showed that TG displayed cardioprotective effects on ISO-induced MI rats and the underlying mechanisms may be related to inhibition of I Ca-L , damping of [Ca ²⁺ ] i and decrease of contractility.
... Medzi faktory, ktoré pôsobia stimulačne na sympatikoadrenálny systém a vedú k zvýšenému uvoľneniu katecholamínov (čím sa môžu podieľať na vzniku akútneho in- farktu myokardu) patria čas vstávania, pondelok, zimné obdobie, fyzická záťaž, emočné rozrušenie, rozčúlenie, nadmerný príjem potravy, nedostatok spánku, užívanie drogy (kokaín, marihuana) a sexuálne aktivity. Vznik infarktu myokardu sa dáva do súvislosti aj s pôsobením ďalších stresorov, medzi ktoré patria prírodné katastrofy, ako sú naprí- klad zemetrasenie a výrazné zmeny počasia (Kloner, 2006;Bhattacharyya a Steptoe, 2007). ...
Stres predstavuje všeobecne prítomný fenomén. Takmer každý jedinec sa denne
stretáva s pôsobením stresorov, podnetov, ktoré vyvolávajú stresovú reakciu. Aj keď
sa môže zdať, že stres predstavuje niečo negatívne, samotná stresová reakcia je veľmi
dôležitá v prípade, že organizmu hrozí nebezpečenstvo. Nebezpečným sa stres stáva
vtedy, keď na organizmus pôsobí dlhodobo.
Čo ale termín stres znamená ? Jednotná a všeobecná definícia stále neexistuje.
A to aj napriek tomu, že od čias Bernarda, ktorý popísal význam vnútorného pro-
stredia, Cannona, ktorý sa venoval štúdiu účasti sympatikového nervového systému
v udržiavaní homeostázy a klasických experimentov Selyeho, ktorý preukázal význam
hypotalamo-hypofýzo-adrenokortikálnej osi pri zvládaní záťažových situácií, sa dosia-
hol výrazný pokrok v štúdiu mechanizmov stresovej reakcie. Podrobne boli popísané
dráhy, podieľajúce sa na prenose signálov súvisiacich s pôsobením stresorov na organiz-
mus, mechanizmy spracovania týchto signálov a mechanizmy centrálnej regulácie sys-
témov stresovej reakcie, a to ako na systémovej, tak celulárnej a molekulárnej úrovni.
Výskum stresu preukázal, na rozdiel od pôvodnej Selyeho doktríny nešpecifickosti stre-
sovej reakcie, že aj keď stresová reakcia vykazuje pri pôsobení rôznych stresorov určité
podobnosti, ide o reakciu špecifickú v závislosti od vyvolávajúceho podnetu. Výrazný
pokrok sa dosiahol aj pri objasňovaní mechanizmov podieľajúcich sa na negatívnom
pôsobení stresovej reakcie na činnosť orgánových systémov, pričom v súčasnosti sa
do popredia dostáva koncept allostatického preťaženia. Zistilo sa, že aj keď chronické
pôsobenie stresorov zväčša priamo nevyvoláva vznik chorôb, ide o permisívny faktor,
ktorý môže mať u predisponovaného jedinca negatívny dopad na jeho zdravotný stav.
Zámerom publikácie je priblížiť súčasné poznatky, týkajúce sa stresovej reakcie
a mechanizmov podieľajúcich sa na negatívnom pôsobení stresorov na organizmus. Pri
príprave textov boli použité viaceré literárne zdroje, medzi iným aj klasické diela, ako
sú An Introduction to the Study of Experimental Medicine, The Wisdom of the Body
a The Stress of Life. Z ďalších monografií je potrebné obzvlášť spomenúť učebnicu
Williams Textbook of Endocrinology; monografiu Stress, Catecholamines, and Cardi-
ovascular Disease, ako aj česko-slovenské knižné publikácie Život, adaptace a stres
a Neuroendokrinná reakcia v strese u človeka. Ďalším podkladom pre prípravu textov
boli časopisecké publikácie dostupné v databáze PubMed do augusta 2011. V textoch
sú zainkorporované aj teoretické a experimentálne poznatky získané počas pôsobenia
v Laboratóriu pre výskum stresu Ústavu experimentálnej endokrinológie SAV v Bra-
tislave.
... (5)(6)(7)(8) Reasons for this phenomenon have not been well elucidated and the hypotheses explored include variation in hormone secretion, exposure to toxic environmental agents, weather variations and different psychosocial factors. (9) So far, there is no evidence in the published literature about the weekly distribution of ACS in Argentina; therefore, it is unknown whether ACS have a specific pattern and which could be the associated variables. ...
Introducción: Una particularidad de los síndromes coronarios agudos (SCA) es que su distribución impresiona tener aspectos cronobiológicos, ya que no se mantiene estable a lo largo del año y varía incluso según el día de la semana y la hora del día. No tenemos conocimiento de evidencia publicada acerca de la distribución de los casos de SCA acorde al día de la semana en nuestro país, por lo que se ignora si sigue un patrón determinado y cuáles podrían ser las variables asociadas.
Objetivo: Analizar la distribución diaria de los casos de SCA y las eventuales diferencias en el tratamiento y la evolución clínica de los pacientes.
Material y métodos: Se estudió el número y la evolución de SCA sin ST elevado (SCA no-STE, n = 6.277) y con ST elevado al ingreso (SCA-STE, n = 4.237) acorde al día de la semana mediante el análisis del registro Epi-Cardio 2006-2012. Resultados: La frecuencia fue mayor en los primeros días de la semana, descendiendo durante el fin de semana (global y SCA no-STE: p < 0,001; SCA-STE: p < 0,01), sin relación con la edad y el sexo. En los SCA-STE, la indicación y el tipo de reper- fusión no tuvieron diferencias según el día de la semana.
Conclusiones: La frecuencia de internaciones por SCA es mayor en los primeros días laborables y menor los fines de semana, sin diferencias en el uso de recursos complejos ni en la evolución inicial.
Background: Acute coronary syndromes (ACS) seem to have a chronobiological distribution with seasonal, weekly and circadian variations. So far, there is no evidence in the published literature about the weekly distribution of ACS in Argentina; thus, we ignore if ACS have a specific pattern and which could be the associated variables.
Objective: The aim of this study was to analyze the weekly distribution of ACS and the differences in treatment and clinical outcome.
Methods: The distribution of cases of non-ST-segment elevation (NSTE) ACS (n=6277) and ST-segment elevation (STE) ACS (n=4237) was retrospectively analyzed according to the day of the week using the Epi-Cardio registry 2006-2012.
Results: The frequency was higher during the first days of the week and descended during the weekend (all ACS and NSTE- ACS p<0.001; STE-ACS p<0.01), and was not related with age or sex. In STE-ACS, the indication and the type reperfusion therapy did not present differences according the day of the week.
Conclusions: The frequency of hospitalization due to ACS is higher within the first days of the workweek and decreases during the weekend, and there are no differences in the use of complex resources and in the initial outcome.
... Many risk factors, such as hypertension, smoking, diabetes mellitus, smoking, dyslipidemia, are widely known [1][2][3]. External triggers, which are exemplified by wake-up time, Mondays, winter season, physical exertion, emotional upset, overeating, lack of sleep, cocaine, marijuana, anger, and sexual activity, can also precipitate myocardial infarction [4]. Natural disasters have also been reported to increase the risk of myocardial infraction [5,6]. ...
Background:
Natural disasters, such as tsunami, hurricanes and earthquakes, may have a negative impact on cardiac health. The aim of our systematic review is to evaluate the impact of earthquakes on the incidence of acute coronary syndromes and cardiac mortality and to examine the impact of the time of earthquakes on the incidence of acute coronary syndromes.
Materials and methods:
MEDLINE and Cochrane databases were searched for studies reporting on the impact of earthquakes on acute coronary syndromes from inception until December 20, 2017. Reference lists of all included studies and relevant review studies were also searched.
Results:
A total of 26 studies on 12 earthquake disasters were included in the systematic review. The existing data show a significant negative impact of Great East Japan, Christchurch, Niigata-Chuetsu, Northridge, Great Hanshin-Awaji, Sichuan, Athens, Armenia and Noto Peninsula earthquakes on the incidence of acute coronary syndromes. By contrast, studies on the Newcastle, Loma Prieta and Thessaloniki earthquakes did not show a significant correlation with myocardial infarction and cardiac mortality.
Conclusions:
Earthquakes may be associated with increased incidence of acute coronary syndromes and cardiac mortality. There are conflicting data about the impact of the time of earthquakes on the incidence of acute coronary syndromes. Measures for the adjustment of the healthcare systems to treat cardiovascular diseases after natural disasters should be immediately implemented particularly in high-risk regions.
... Such dehydration is not benign: its presence is associated with an increased risk of myocardial infarction (Kloner, 2006), renal calculi (Feehally & Khosravi, 2015), venous thromboembolic disease (Saad et al., 2016) and acute kidney injury (Kanagasundaram, 2015). Meanwhile, dehydration increases pain perception (Farrell et al., 2006) and the associated risk of delirium is comparable with that related to opiate administration (Boettger et al., 2015). ...
Background:
Dehydration is highly prevalent and is associated with adverse cardiovascular and renal events. Clinical assessment of dehydration lacks sensitivity. Perhaps a patient's thirst can provide an accurate guide to fluid therapy. This systematic review examines the sensitivity of thirst in responding to changes in plasma osmolality in participants of any age with no condition directly effecting their sense of thirst.
Methods:
Medline and EMBASE were searched up to June 2017. Inclusion criteria were all studies reporting the plasma osmolality threshold for the sensation of thirst.
Results:
A total of 12 trials were included that assessed thirst intensity on a visual analogue scale, as a function of plasma osmolality (pOsm), and employed linear regression to define the thirst threshold. This included 167 participants, both healthy controls and those with a range of pathologies, with a mean age of 41 (20-78) years.The value ±95% CI for the pOsm threshold for thirst sensation was found to be 285.23 ± 1.29 mOsm/kg. Above this threshold, thirst intensity as a function of pOsm had a mean ± SEM slope of 0.54 ± 0.07 cm/mOsm/kg. The mean ± 95% CI vasopressin release threshold was very similar to that of thirst, being 284.3 ± 0.71 mOsm/kg.Heterogeneity across studies can be accounted for by subtle variation in experimental protocol and data handling.
Conclusion:
The thresholds for thirst activation and vasopressin release lie in the middle of the normal range of plasma osmolality. Thirst increases linearly as pOsm rises. Thus, osmotically balanced fluid administered as per a patient's sensation of thirst should result in a plasma osmolality within the normal range. This work received no funding.
Aims
Internal and external triggers affect seasonal and circadian variations of myocardial infarction (MI). We aimed to assess sex differences in common triggers of MI.
Methods
A nationwide, retrospective cross-sectional postal survey study was conducted. Individuals who experienced a MI during holidays and weekdays were identified through the SWEDEHEART registry. 27 potential MI-triggers were rated in regards of occurring more or less than usual during the last 24 hours before the MI. Three areas were covered: activities, emotions and food- or alcohol consumption. A logistic regression model was used to identify sex differences for each trigger and odds ratios (OR) were reported.
Results
451 patients, of whom 317 were men responded. The most common reported triggers were stress (35.3%), worry (26.2 %), depression (21.1%) and insomnia (20.0%). Women reported emotional triggers including sadness (OR 3.52, 95% CI 1,92-6,45), stress (OR 2.38, 95% CI 1.52-3.71), insomnia (OR 2.31, 95% CI 1,39-3,81) and upset (OR 2.69, 95% CI 1.47-4.95) to a greater extent than men. Outdoor activity was less reported by women, OR 0.35, 95% CI 0.14-0.87. No significant sex differences were found in other activities or food and alcohol consumption.
Conclusion
Self-experienced stress and distress were higher among women prior to myocardial infarction compared to men. Understanding sex perspectives in acute triggers may help us find preventive strategies and to reduce the excess numbers of MI.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
The first volume in the new Cambridge Handbooks in Behavioral Genetics series, Behavioral Genetics of the Mouse provides baseline information on normal behaviors, essential in both the design of experiments using genetically modified or pharmacologically treated animals and in the interpretation and analyses of the results obtained. The book offers a comprehensive overview of the genetics of naturally occurring variation in mouse behavior, from perception and spontaneous behaviors such as exploration, aggression, social interactions and motor behaviors, to reinforced behaviors such as the different types of learning. Also included are numerous examples of potential experimental problems, which will aid and guide researchers trying to troubleshoot their own studies. A lasting reference, the thorough and comprehensive reviews offer an easy entrance into the extensive literature in this field, and will prove invaluable to students and specialists alike.
Takotsubo syndrome is an acute heart disease usually triggered by significant emotional or physical stress, very occasionally described in association with natural disasters such as earthquakes. Clinically, it simulates an acute myocardial infarction with similar symptoms, laboratory tests, and electrocardiographic changes. Coronary angiography shows the absence of significant coronary disease. We report two women, aged 71 and 80 years, and who developed a Takotsubo syndrome after an earthquake. In both, the syndrome was diagnosed with cardiac magnetic resonance imaging.
Sudden cardiac death (SCD) accounts for approximately 15%–20% of all deaths worldwide, the causes of which are mainly structural heart diseases. However, SCD also occurs in patients without major cardiac structural abnormalities due to electrophysiological abnormalities or other unexplained causes which account for about 1%–15% cases of SCD, namely sudden unexplained cardiac death (SUCD). The causes of SUCD cannot be explained by routine forensic pathological examination. Hence, identifying the causes of SUCD remains a major challenge in forensic fields. Consequently, it is significant to discover the risk factors and molecular biomarkers for diagnosis and prediction of SUCD. SUCD can be at least partially explained by acute and chronic psychological stress, such as Takotsubo cardiomyopathy (TCM), which is increasingly recognized as a potentially modifiable risk factor for SUCD. Additionally, the inherited lethal cardiac arrhythmia due to ion channelopathies is one of the causes of SUCD. However, SCD resulted from psychological stress or lethal cardiac arrhythmia lacks postmortem observable morphological evidence. Therefore, the postmortem diagnosis of SUCD remains a primary challenge in forensic pathology because of the absence of recognized diagnostic biomarkers. Recent advances in knowledge give us additional possibility in understanding the cause of SUCD. In this review, we summarized the updated risk factors of SUCD including genetics and psychological stress, as well as the potential diagnostic biomarkers of SUCD, such as micro-RNAs, heat shock proteins, Galectin-3 and inflammation factors. Meanwhile, we concluded the ongoing researches on novel measurements including chemical analysis, machine learning and artificial intelligence for predicting the cause of SCD.
Purpose
: To investigate seasonal variation in optic disc hemorrhage (DH) by review of fundus photographs representative of the past two calendar years (2019 and 2020).
Design
: Retrospective, observational trend study.
Methods
: Patients who had visited the Glaucoma Clinic of Seoul National University Hospital and underwent fundus photography were included. All of the available stereo disc photography (SDP) and red-free retinal nerve fiber layer photography (RNFLP) taken between January 1st, 2019 and December 31st, 2020 was retrospectively reviewed. The monthly incidence rate of DH was determined by reference to the photography. Seasonal temperature information and patients’ intraocular pressure (IOP) information were obtained, organized and analyzed.
Results
: Fundus images of 13,514 eyes were reviewed, and 454 eyes were confirmed to have DH. Poisson regression analyses revealed that as the temperature rose by 1°C, the DH risk ratio was reduced to 0.979 (95% CI 0.969-0.989, p<0.01). The DH incidence ratio was 1.53 (95% CI 1.23-1.91, p<0.01) for the T<10°C group relative to the T≥20°C group. The IOP of the patients with DH in winter was significantly higher than that measured in summer.
Conclusion
: DH is affected by temperature, and as such, shows seasonal variability. This variability is believed to be caused by temperature-related factors such as IOP or hematological factors.
Introduction and objectives
Some atmospheric features have been linked to the triggering of myocardial infarction. Because data from the Temperate-Mediterranean is scarce, we sought to study whether meteorological parameters influence the incidence of ST-elevation myocardial infarction (STEMI) as confirmed by primary percutaneous intervention in a city with temperate weather (Porto, Portugal).
Methods
Retrospective analysis of a series of STEMI-patients from January 2010 to December 2017. Temperature (T), relative humidity (RH), precipitation, and atmospheric pressure were obtained from a government-led institute. We utilized a generalized linear model (GLM) with a Poisson distribution, where a series of models with multivariable analysis were computed. The effects (GLM coefficients) are presented as excess relative risk (ERR).
Results
One thousand and four consecutive STEMI-patients were included. The most important predictors of STEMI were Tmin two days before (for 1 °C drop ERR=1.9%, p=0.009) and a 1% increase in RH three days before (EER=0.7%, p=0.006). Conversely, the same increase in RH the day before reduced the relative risk (EER=-0.6%, p=0.023). Temperature range, atmospheric pressure and precipitation had no impact on STEMI incidence.
Conclusion
In a Temperate-Mediterranean city hot or cold temperature extremes, temperature drop and relative humidity had a significant impact on the occurrence of STEMI.
Introduction
FIFA World Cup represent one of the world's greatest phenomena. The spectators watch the matches of national teams with great emotional involvement. It is well documented fact that emotional stress can be a trigger of unwanted cardiovascular (CV) event.
Aim
The aim of this retrospective study was to determine whether there had been an increase in the number of the emergency admissions for CVD in the Emergency Room and Clinic for Cardiovascular Diseases of the Sestre milosrdnice University Hospital Centre during and after the matches that the Croatian national team played in the FIFA World Cup 2018.
Methods
The hospital’s database was examined for the dates when Croatia played its matches, plus two more days after each match. An unexposed period that included the same dates in 2017 and 2019 was formed.
Results
1093 cases were assessed. The incidence of CV admissions during the exposed period was 1.15 (95% confidence interval [CI]; 1.02 to 1.31) times higher than during the unexposed period. There was a 1.30 (95% CI; 1.1 to 1.54) times higher incidence in women compared to the unexposed period. Arrhythmias and angina pectoris were the CVDs that occurred more frequently in the exposed period.
Conclusion
This study showed that watching Croatian national team's matches and cheering represented an additional risk for a CV incident, especially in women.
Although it is widely recognized that environmental factors such as smoking, diet, exercise, and socioeconomic status affect the risk of cardiovascular disease, recent work showing the effects of other environmental factors provides a more complete assessment of the situation. This view has emerged from three developments. Firstly, there has been a sudden explosion in the prevalence of diabetes and obesity which indicates a strong environmental component. Secondly, there is an accumulation of evidence suggesting that most cases of these diseases could be prevented by healthy lifestyle choices. Finally, studies have shown that exposure to environmental pollutants has a significant effect on heart disease risk. This book is the first to provide a comprehensive account of the effects of pollutants on heart disease and to integrate this area of research within the overall theme of environmental cardiology. The introductory chapter outlines the effects of different aspects of the environment on heart disease and provides a context for the discussion that follows. Subsequent chapters give an overview of the effects of particulate matter and discuss the epidemiological studies supporting the link. The book then goes on to cover the effects of pollution on different aspects of cardiovascular disease (hypertension, stroke, heart failure, ischemic heart disease and atherogenesis). Because of a close association between diabetes and heart disease, a discussion of the effects of particulate matter on diabetes is also included. Later chapters discuss the effects of individual pollutants such as vehicular emissions, metals and aldehydes. A review on manufactured nanoparticles is incorporated because these particles represent an important new threat to cardiovascular health. The understanding that emerges from this monograph suggests that we must be more alert to the effects of the environment and develop strategies that target, not only the diseased individual, but also the unhealthy, disease-causing environment. It is essential reading for cardiologists, epidemiologists, urban planners and pollution control specialists.
This brings together mind and body at the subconceptual level, where patterns of neuronal activation and connectivity represent concepts. The individual components of these patterns do not embody concepts – instead, it is the activation of overall patterns and the application of pattern recognition that give rise to conceptual thought. This is also the level of deep meaning, where we are profoundly touched emotionally – the level of poetry and art, empathy and autosuggestion as way of communication of these patterns as patterns, in very complex ways. If the mind influences the body, it is at this subconceptual level – although this may be an arbitrary distinction, since mind and body are two different perspectives of a single entity. However, this does not mean that the psyche can be rationalized away. On the contrary, we see mind and body as art and paint within an accomplished work of art. Without paint, the art does not exist. On the other hand, the value of the painting lies in the art – without this art, there is no meaning and nothing is worthwhile.
We investigate the implications of subconceptual processing for placebo, empathy, double-blind studies, medical causal thinking and other areas. We then show the consequences that arise in medical domains such as psychogenic non-epileptic seizures, peptic ulcer disease and several others. It is our hope that this research will lead to a future where the patient lies at the center of scientific medicine, both at the conceptual and subconceptual level. We believe that this fundamental shift will allow many health-related domains to be managed much more cost-effectively and sustainably. However, the single most important outcome will be a vast increase in humanity – where inner human strength is promoted as an incredibly important component of addressing health issues.
One of the particularly vulnerable groups for adverse weather conditions is people with heart disease. Most of the studies analyzed the association between certain weather conditions and increased mortality, morbidity, hospital admissions, calls, or visits to the emergency department and used as statistical data. This study evaluated associations between daily weather conditions and daily weather-related well-being in patients with coronary artery disease (CAD). From June 2008 to October 2012, a total of 865 consecutive patients with CAD (mean age 60 years; 30% of women) were recruited from the cardiac rehabilitation program at the Hospital Palanga Clinic, Lithuania. To evaluate the well-being, all patients filled in Palanga self-assessment diary for weather sensitivity every day from 8 to 21 days (average 15 ± 3 days) about their well-being (psychological, cardiac, and physical symptoms) on the last day. The weather data was recorded in the database eight times every day with a 3-hour interval using the weather station “Vantage Pro2 Plus” which was located in the same Clinic. The daily averages of the eight time records for weather parameters were calculated and were linked to the same-day diary data. We found that the well-being of patients with CAD was associated with weather parameters; specifically, general well-being was better within the temperature range 9–15 °C and worse on both sides of this range. Worsened general well-being was also associated with higher relative humidity and lower atmospheric pressure. Weather parameters can explain from 3 to 8% of the variance of well-being in patients with CAD.
Objectives:
To investigate whether the depth of the facial nerve from the skin surface as it exits the stylomastoid foramen differs between the paralyzed and unaffected sides in patients with Bell's palsy.
Methods:
Forty-three patients (23 females, 20 males; mean age 43.8 ± 15.2 years) diagnosed with Bell's palsy between January 2014 and June 2017 were retrospectively reviewed and those who had a cranial MR imaging performed within 10 days upon admission to hospital were included in the study. The axial postcontrast CUBE sequence was utilized for the measurement of the facial nerve depth. Age, gender, and body mass index (BMI) as well as concomitant chronic diseases, were also noted. The severity of facial paralysis was graded using the House-Brackmann (HB) scoring system.
Results:
The facial nerve depth was significantly lower on the paralytic side compared to the unaffected side (32.9 ± 5.4 mm vs. 36.9 ± 5.1 mm, respectively; p = 0.007). The facial nerve depth on the paralytic side was not statistically different in the female patients compared to male patients (31.2 ± 4.6 mm vs. 34.7 ± 5.7 mm, respectively; p = 0.270). The facial nerve depth on the paralytic side was not correlated with patients' age (r = 0.288; p = 0.999), BMI (r = 0.215, p = 0.999), and HB scores (r = 0.031; p = 0.999).
Conclusion:
In our study cohort of patients with Bell's palsy, the facial nerve in the paralytic side is located more superficially as it exits the stylomastoid foramen when compared to the contralateral side. Therefore, the depth of the facial nerve may potentially play a key role in the etiology of Bell's palsy, which should be further evaluated.
Background
Cardiovascular disease is the most common cause of morbidity and mortality worldwide, with ischemic heart disease (IHD) accounting for roughly 50% of these events in industrialized nations.
In recent years, the relative importance of IHD in less industrialized countries is also rising at an alarming and steadily-increasing rate.
Objective
Many experimental, observational and epidemiological studies have demonstrated the importance of psychosocial risk factors in the development and clinical manifestations of IHD. They act both indirectly, associated with an unhealthy lifestyle; and directly, through the activation of inflammatory cascades and the sympathetic nervous system. They also cluster with biological risk factors to increase the incidence and clinical manifestations of IHD. From these assumptions, there emerges the potential that an integrated approach that incorporates psychological therapy in various forms might reduce IHD patients’ symptoms and maladaptive behaviors, and thereby enhance their prognosis.
Methods
To date, three psychotherapeutic approaches have been utilized within cardiac psychology practice: (1) cognitive-behavioral psychotherapy; (2) psychodynamic psychotherapy; and (3) ontopsychological psychotherapy. The current article briefly describes these three approaches and how their use might enhance the care of IHD patients.
Results
A range of psychological characteristics influence the development, course and management of cardiac patients’ IHD. Among others, these include patients’ emotions, attitudes, behaviors, relationships, and stressors. State-of- the-art literature suggests that psychological interventions should be considered in much the same way as medical interventions, in terms of their relevance to both patient management and outcomes.
Conclusion
For this reason, it is essential that professional psychological and psychotherapeutic support be rendered available to cardiology patients, as a means to enhance both the effectiveness and efficiency of care.
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.
Recent studies have shown an association between infections, such as influenza, pneumonia, or bacteremia, and acute cardiac events. We studied the association between foot infection and myocardial infarction, arrhythmia, and/or congestive heart failure. We analyzed the records of 318 consecutive episodes of deep soft tissue infection, gangrene, and/or osteomyelitis in 274 patients referred to a vascular surgery service at a tertiary center. We identified 24 acute cardiac events in 21 of 318 (6.6%) episodes of foot infection or foot gangrene. These 24 events included 11 new myocardial infarctions (3.5%), 8 episodes of new onset or worsening congestive heart failure (2.5%), and 5 new arrhythmias (1.6%). Tachycardia and systemic inflammatory response syndrome were associated with acute cardiac events ( P < .05 for each). The 1-year survival of patients with acute cardiac events was 50.4%, significantly lower than the 91.7% 1-year survival of patients without acute cardiac events ( P < .0015). Acute cardiac complications are not uncommon among patients presenting with severe foot infection and are associated with a high 1-year mortality. Primary care physicians, cardiologists, and vascular and orthopedic surgeons must keep a high index of suspicion for the occurrence of an acute cardiac event.
Inability to predict short-term cardiovascular (CV) events and take immediate preemptive actions has long been the Achilles heel of cardiology. However, certain triggers of these events have come to light. Although these triggers are nonspecific and are part of normal life, studying their temporal relationship with the onset of CV events provides an opportunity to alert high-risk atherosclerotic patients who may be most vulnerable to such triggers, the “vulnerable patient”. Herein, we review the literature and shed light on the epidemiology and underlying pathophysiology of different triggers. We describe that certain adrenergic triggers can precipitate a CV event within minutes or hours; whereas triggers that elicit an immune or inflammatory response such as infections may tip an asymptomatic “vulnerable patient” to become symptomatic days and weeks later. In conclusion, healthcare providers should counsel high-risk CV patients (e.g., in secondary prevention clinics or those with coronary artery Calcium >75th percentile) on the topic, advise them to avoid such triggers, take protective measures once exposed, and seek emergency care immediately after becoming symptomatic after such triggers. Furthermore, clinical trials targeting triggers (prevention or intervention) are needed.
Objective To investigate whether an important football match increases stress to such an extent that it triggers acute myocardial infarction and stroke. Design Longitudinal study of mortality around 22 June 1996 (the day the Dutch football team was eliminated from the European football championship). Mortality on 22 June was compared with the five days before and after the match and in the same period in 1995 and 1997. Setting Netherlands. Subjects Dutch population aged 45 years or over in June 1996. Main outcome measures All cause mortality and mortality due to coronary heart disease and stroke. Results Mortality from coronary heart disease and stroke was increased in men on the day of the match (relative risk 1.51, 95% confidence interval 1.08 to 2.09). No clear rise in mortality was observed for women (1.11, 0.80 to 1.56). Among men, about 14 excess cardiovascular deaths occurred on the day of the match. Conclusion Important sporting events may provoke a sufficient level of stress to trigger symptomatic cardiovascular disease. The difference between men and women requires further investigation.
It can now be appreciated that there are two quite different processes encompassed by the term 'plaque haemorrhage.' The fact that the media behind plaques becomes intensely vascularised and that these vessels enter the intima is beyond dispute. Bleeding from such vessels crossing the media causes a limited number of red cells to lie free within the lipid pool of many plaques. No fibrin or platelets are present, and the process is almost ubiquitous in large lipid rich plaques. The second process is the presence of large numbers of red cells, masses of platelets, and considerable amounts of fibrin within the plaque. If serial histological sections are used these elements can be traced to an entry into the lumen via a fissure, although this may be closed by a mass of thrombus. The two processes must be clearly separated and the term intraplaque thrombosis is more applicable to that associated with fissures from the lumen. It is plaque fissuring with related intraintimal thrombosis progressing to the formation of an intraluminal thrombus that is the important dynamic process unifying crescendo agina, acute myocardial infarction, and sudden ischaemic death. It is difficult to escape the conclusion that the failure of pathologists to think in terms of dynamic processes and to believe what was seen at necropsy was an immutable reflection of events in life that occurred days before has seriously hindered the understanding by clinicians of how atheroma produces acute clinical symptoms.
Background: Although it is well known that the acute myocardial infarction can be triggered by events such as physical activity, emotional stress, sexual activity or eating, the observed frequencies of these events preceding the onset of myocardial infarction vary between published reports. Methods: A meta-analysis of 17 seldom population-based studies that included data on frequency of external triggers or onsets during sleep was performed. In each analysis, the data were combined only from the studies reporting on a particular trigger. Results: Of the 10519 patients, heavy physical activity was recorded before the onset of myocardial infarction in 6.1%, whereas mild-to-moderate physical activity was recorded in 28.6% of 7517 patients. Eating preceded the onset in 8.2% of 4785 patients, various kinds of emotional stress in 6.8% of 2565 (particularly anger in 2.1% of 2283), meteorologic stress in 3.7% of 337 1, and sexual activity in 1.1% of 3406 patients. Out of 11778 patients, 20.7% had infarction onset during sleep. Triggers in general (OR = 1.45, 95%CI = 1.21 - 1.76; p < 0.0001), heavy physical activity (OR = 6.21, 95%CI = 3.77 - 10.23; p < 0.0001) and eating (OR = 1.70, 95%CI = 1.14 - 2.53; p = 0.0008) were more likely to precede the infarction onset in men while women were more likely to report emotional stress (OR = 0.66, 95%CI = 0.50 - 0.86; p = 0.002). Conclusions: The present meta-analysis defines the occurrence of possible external triggers before the onset of myocardial infarction in general population, but their actual contribution to the very onset is somewhat less frequent. Future investigation should identify other eventual triggers unrecognized as yet, asses the risk of triggering myocardial infarction among patients with defined levels of ischemic heart disease or plaque vulnerability, and further elucidate the pathophysiologic mechanisms of gender differences and beneficial effect of habitual physical activity. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
Background
Variations in the incidence of acute myocardial infarction during the week may differ between and within communities, according to lifestyle.
Objective
To identify potential triggering factors for acute myocardial infarction by examining variations in incidence in the days of the week within the Osaka area of Japan.
Patients
Of 2511 consecutive patients in this region who were admitted to hospital for acute myocardial infarction between April 1998 and March 2001 and consented to take part, 2400 who had a definitely identified time of onset were enrolled.
Results
For this group as a whole, no significant difference in incidence was noted between days of the week. However, in subgroup analyses women were shown to have significant variation through the week, peaking on Saturday with a 39% increase in relative risk (p = 0.037); working subjects showed a peak on Monday, with a 26% increase in relative risk (p = 0.038). Stratified analyses showed that in working men there was a prominent Monday peak in the onset of infarction, with a 30% increase in relative risk (p = 0.022), while in working women, there was no significant variation through the week.
Conclusions
Earlier findings of a Monday peak linked to increased physical and mental occupational stress are confirmed. There is also an increase in uncertain risk factors on Saturdays for Japanese women, possibly involving a stressful weekend burden for women. Confirmation of this finding in other communities may help identify triggers of acute myocardial infarction and be useful in prevention.
A recent study in Moscow reported higher cardiovascular mortality on Saturdays, Sundays, and Mondays and linked this to the Russian pattern of binge drinking.1 Other studies have reported an increased risk of cardiac events on Mondays, a peak on other days, or no significant weekly variation.2 We investigated the patterns of death from coronary heart disease by day of the week in the Scottish population and explored possible links with patterns of alcohol consumption.
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.
During the past decade, knowledge of the clinical course of coronary artery thrombosis and the pathologic changes associated with it has been increased rapidly. Nevertheless, the actual events which precipitate an attack remain a matter of speculation. Characteristically, an attack of angina pectoris follows physical exertion or emotional stress, and without critical analysis the same factors have been considered responsible for inducing coronary artery thrombosis.Fitzhugh and Hamilton1 and others2 expressed the belief that coronary thrombosis follows unusual exertion. Riesman and Harris3 and Wolff and White4 concurred with them but pointed out that an attack often occurs while the patient is at rest or even in bed. Other authors5 found no definite relationship between physical stress and coronary thrombosis. Luten6 went so far as to state that the attack invariably occurs in the absence of effort.Similarly, the importance of occupation and social status
A circadian variation of sudden cardiac death has been documented, but its relation to individual time of awakening and possible triggering events has not been studied in the general population. By monitoring of mortality records in 4 cities and towns in Massachusetts, 148 potential cases of sudden cardiac death were identified. In 94 cases, the informants listed on the death certificates were contacted, the diagnosis of sudden cardiac death was established, and a telephone interview was completed within a mean of 19 days (range 8 to 28) after the death.The time of day of all 94 cases of sudden cardiac death (mean age 61 ± 9 years, 74% men) demonstrated a circadian variation (p < 0.05) with a peak from 9:00 A.M. to 12:00 noon. An analysis of time of death adjusted for individual wake-times of the decedents demonstrated an increased onset of sudden cardiac death during the initial 3-hour interval after awakening with a relative risk of 2.6 (95% confidence interval 1.6, 4.2) compared with other times of the day.The increased risk of sudden cardiac death soon after awakening suggests specific triggering factors or mechanisms that are particularly likely to occur during this time. The narrowing of the time interval during which the risk of sudden cardiac death is increased should facilitate the study of possible pathogenetic mechanisms and triggering factors of the disease and may aid in the design of more effective preventive strategies.
Background:
Although it is well known that the acute myocardial infarction can be triggered by events such as physical activity, emotional stress, sexual activity or eating, the observed frequencies of these events preceding the onset of myocardial infarction vary between published reports.
Methods:
A meta-analysis of 17 seldom population-based studies that included data on frequency of external triggers or onsets during sleep was performed. In each analysis, the data were combined only from the studies reporting on a particular trigger.
Results:
Of the 10519 patients, heavy physical activity was recorded before the onset of myocardial infarction in 6.1%, whereas mild-to-moderate physical activity was recorded in 28.6% of 7517 patients. Eating preceded the onset in 8.2% of 4785 patients, various kinds of emotional stress in 6.8% of 2565 (particularly anger in 2.1% of 2283), meteorologic stress in 3.7% of 3371, and sexual activity in 1.1% of 3406 patients. Out of 11778 patients, 20.7% had infarction onset during sleep. Triggers in general (OR = 1.45, 95%CI = 1.21-1.76; p < 0.0001), heavy physical activity (OR = 6.21, 95%CI = 3.77-10.23; p < 0.0001) and eating (OR = 1.70, 95%CI = 1.14-2.53; p = 0.0008) were more likely to precede the infarction onset in men while women were more likely to report emotional stress (OR = 0.66, 95%CI = 0.50-0.86; p = 0.002).
Conclusions:
The present meta-analysis defines the occurrence of possible external triggers before the onset of myocardial infarction in general population, but their actual contribution to the very onset is somewhat less frequent. Future investigation should identify other eventual triggers unrecognized as yet, asses the risk of triggering myocardial infarction among patients with defined levels of ischemic heart disease or plaque vulnerability, and further elucidate the pathophysiologic mechanisms of gender differences and beneficial effect of habitual physical activity.
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.
The incidence and natural history of coronary heart disease have varied with time. Mortality has declined over a number of years and, within each year, events are more common in the winter months, at the beginning of the work week, and in the early hours of the morning. As with the overall risk of coronary heart disease, variations by time are due to a combination of behavioral factors, such as cigarette smoking; levels of physical activity; alcohol consumption and diet; physiologic factors, such as catecholamine secretion, sympathetic tone, and hemostatic factors; and environmental factors, such as temperature, exposure to sunlight, and work-related stress. This paper reviews the evidence for an association with time and discusses possible explanations for these findings.
Death certificates in eastern Massachusetts after six blizzards in 1974--78, including the record blizzard of Feb. 6, 1978, were examined to identify the effect on mortality of these storms. The total number of deaths was significantly higher (8%) in a "blizzard week" than in the preceding and subsequent (control) weeks (114.1 vs. 105.3 deaths per day). Deaths from ischaemic heart-disease (I.H.D.), which rose significantly by 22% in the blizzard week from 36.7 to 44.6 deaths per day, accounted for 90% of the excess total deaths. The increase was greater in males than in females (30% vs. 12%), and in both sexes there was no difference in the distribution of deaths by age between the blizzard and control weeks. I.H.D. deaths were increased for 8 days after a snowstorm, suggesting that the effect was related to activities such as snow shovelling rather than the storm itself. The identification of those at increased risk of I.H.D. death after major snowstorms and of the circumstances surrounding such deaths could lead to public-health measures to reduce these weather-related premature deaths.
Continuous intra-arterial blood-pressure and electrocardiogram recordings were obtained in twenty hypertensive and five normotensive ambulant patients. Blood-pressure was highest mid-morning and then fell progressively throughout the remainder of the day. Blood-pressure was lowest at 3 A.M. and began to rise again during the early hours of the morning before waking. These findings may have important consequences with regard to the therapeutic management of hypertension.
Cardiovascular responses to a stream of cold air (0-10degrees C) directed towards the face and abdomen separately were examined in 12 human subjects. Cold air directed at the side of the face produced a 36+/-6 degrees increase in forearm vascular resistance and 22"/-4 degrees reduction in blood flow. Cold air on the abdomen did not produce a significant change in vascular resistance. The results are discussed in relation to angina pectoris evoked by cold wind.
Information obtained during the past decade suggests that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering coronary thrombosis is supported by finding that (1) the frequencies of the onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations, with similar increases in the period from 6 AM to noon; (2) the frequency of transient myocardial ischemia shows a similar increase in the morning, and episodes are often preceded by mental or physical triggers; (3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi; (4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state, or coronary vasoconstriction, are accentuated in the morning; and (5) aspirin and beta-adrenergic blocking agents that affect certain of these processes have been shown to prevent disease onset. The hypothesis presented is that occlusive coronary thrombosis occurs when (1) an atherosclerotic plaque becomes vulnerable to rupture; (2) mental or physical stress causes the plaque to rupture; and (3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of the onset of acute disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.
There is a circadian pattern in the occurrence of cardiac events in patients with coronary artery disease. Whether changes in coronary vascular tone contribute to these phenomena is unknown. We measured the ischemic threshold, defined as either the heart rate or rate-pressure product at 1-mm ST segment depression during treadmill exercise and used it as an index of the lowest coronary vascular resistance; the premise was that when ischemic threshold became lower, coronary vascular resistance was higher, and vice versa.
Fifteen patients (group A) with stable coronary artery disease underwent four identical treadmill exercise tests in 24 hours, and ischemic threshold was measured as the heart rate at the onset of 1-mm ST depression. Before each treadmill test, postischemic forearm vascular resistance was measured after 5 minutes of forearm occlusion, using strain-gauge plethysmography. Sixteen additional patients (group B) underwent two treadmill tests at 8 AM and 1 PM, and ischemic threshold was measured as the heart rate-blood pressure product at 1-mm ST depression. A circadian variation was noted: In group A, the heart rate-derived ischemic threshold was lower at 8 AM and 9 PM compared with noon and 5 PM (p less than 0.03). Also, in group B, the rate-pressure product-derived ischemic threshold was 8 +/- 2% lower at 8 AM compared with 1 PM (p = 0.008). A circadian variation parallel to the observed variation in ischemic threshold was also noted in the postischemic forearm blood flow, which was lower in the morning and at night (p less than 0.004). There was a strong correlation between postischemic forearm blood flow and ischemic threshold (p less than 0.0001), such that ischemic threshold was lower at the time of day when postischemic forearm blood flow was lower, and vice versa.
A lower ischemic threshold in the morning suggests that the ischemia-induced coronary vascular resistance is increased at this time, a finding supported by a similar variation in postischemic forearm vascular resistance. Parallel changes in forearm and coronary resistance suggest that generalized (neural or humoral factors) rather than local factors are responsible for the observed circadian changes. Increased coronary tone in the mornings may not only contribute to the higher incidence of transient ischemia but may help trigger acute cardiac events at this time.
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.
Circadian patterns have been observed for various cardiovascular functions and events including sudden cardiac death. This study examined whether ventricular arrhythmias could be a pathophysiologic explanation for the increase in prevalence of sudden cardiac death observed between 6 A.M. and noon. Hypertensive men 35 to 70 years of age and without a history of symptomatic cardiac disease were withdrawn from diuretic treatment and received 1 month of oral electrolyte repletion with both 40 mmol of potassium chloride and 400 mg of magnesium oxide daily. Then continuous 24-hour Holter monitoring was performed and ventricular arrhythmias were classified by 6-hour time intervals. The interval from 6 A.M. to noon revealed a higher prevalence of complex or frequent ventricular arrhythmias than the interval from midnight to 6 A.M., as well as a higher mean number of ventricular premature complexes per hour. The differences were statistically significant (p less than 0.01) and amounted to increases of about one third. Ventricular arrhythmias during the other two 6-hour periods were intermediary in frequency. It is concluded that the increase in sudden cardiac death noted in the morning might be related, at least in part, to an increase in frequency of ventricular arrhythmias; the implications of this observation for preventive cardiology deserve further investigation.
Increased platelet aggregation in the morning and upon assuming an upright posture may account at least in part for the observed circadian variation in onset of acute myocardial infarction. The Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of alternate-day aspirin intake (325 mg) among 22,071 US male physicians, afforded the opportunity to assess this circadian pattern and examine whether it is altered by aspirin therapy. During a 5-year period of follow-up, 342 cases of nonfatal myocardial infarction were confirmed, of which the time of onset was available in 211 (62%). The placebo group showed a bimodal circadian variation in onset of myocardial infarction with a primary peak between 4:00 AM and 10:00 AM (p less than 0.001). In the aspirin group, however, this circadian variation was minimal (p = 0.16), due primarily to a marked reduction in the morning peak of infarction. Specifically, aspirin was associated with a 59.3% reduction in the incidence of infarction during the morning waking hours, compared with a 34.1% reduction for the remaining hours of the day. The greater reduction was observed during the 3-hour interval immediately after awakening, a period with a risk of infarction twice that of any other comparable time interval (p less than 0.001). Aspirin intake was associated with a mean reduction in the incidence of infarction of 44.8% over the entire 24-hour cycle. These data support the hypothesis that increased platelet aggregability in the morning and upon arising contributes to the occurrence of myocardial infarction and that aspirin reduces the risk of infarction by inhibiting platelet aggregation during these critical periods.
Several studies have observed an increased occurrence of acute myocardial infarction (AMI) in the morning based on subjective self-reports and objective confirmation. Evidence has also been collected to suggest a circadian variation in the onset of sudden cardiac death and silent myocardial ischemia. No published reports have examined the time of onset of AMI in relation to time after awakening. The present study examines the times of onset of AMI in relation to awakening in 137 patients with confirmed AMI. Information concerning time of awakening on the day of AMI revealed a marked increase in the onset of initial AMI symptoms within the first hour after awakening. Of the patients studied, approximately 23% reported onset of the initial symptoms of AMI within 1 hour after awakening. An increased onset of symptoms of AMI soon after awakening was also observed when patients in whom the acute cardiac symptoms were known to or may have caused awakening were excluded from consideration. This was also noted in subgroups of AMI patients classified according to age, order and location of AMI. These results extend previous observations of the circadian morning increase of AMI onset and assist in narrowing the search for potential triggers of the circadian variation of onset of AMI to physiologic changes that may occur soon after awakening.
The time of acute myocardial infarction was determined in all 1,741 patients of the ISAM (Intravenous Streptokinase in Acute Myocardial Infarction) Study, based on onset of clinical symptoms and evaluation of plasma CK-MB enzyme time-activity curves. The incidence of myocardial infarction was markedly increased between 6:00 AM and 12:00 noon compared with other times of day (p less than 0.001). Myocardial infarction occurred 3.8 times more frequently between 8:00 and 9:00 AM (hour of maximum incidence) than between 12:00 midnight and 1:00 AM (hour of minimum incidence). Time of myocardial infarction based on clinical and enzymatic methods correlated well (r = 0.95). Patients with higher or lower left ventricular ejection fraction, higher or lower degree of wall motion abnormalities and residual stenosis of the coronary arteries, and one-, two-, or three-vessel disease exhibited a similar circadian pattern, suggesting that the morning is a risk period for patients with mild as well as severe coronary artery disease. Only the group of patients receiving beta-adrenergic blocking therapy before the event did not show an increased morning incidence of myocardial infarction. This observation may contribute to an understanding of the mechanisms by which beta-blockers reduce the incidence of myocardial infarction. Further investigation of physiologic changes occurring during the morning period of increased risk of myocardial infarction may lead to better understanding of the disorder. Design and timing of cardioprotective medication may play a crucial role in improving prevention of acute myocardial infarction.
Information obtained during the past decade suggests the need to reexamine the possibility that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering onset of coronary thrombosis is supported by the findings that 1) the frequencies of onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations with parallel increases in the period from 6:00 AM to noon, 2) transient myocardial ischemia shows a similar morning increase, and episodes are often preceded by mental or physical triggers, 3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi, 4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state or coronary vasoconstriction, are accentuated in the morning, and 5) aspirin and beta-adrenergic blocking agents, which block certain of these processes, have been shown to prevent disease onset. The hypothesis is presented that occlusive coronary thrombosis occurs when 1) an atherosclerotic plaque becomes vulnerable to rupture, 2) mental or physical stress causes the plaque to rupture, and 3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of onset of acute disease suggests the need for pharmacologic protection of patients during vulnerable periods, and provides clues to mechanism, the investigations of which may lead to improved methods of prevention.
To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P less than 0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB-estimated timing confirmed the existence of a circadian rhythm, with a three-fold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction.
Mortality from acute myocardial infarction (MI) over the 5 year period 1982-1987 in Brown County, Wisconsin, was analyzed to assess the relationship with environmental temperature. Deaths occurring on the day of and the day following a significant snowfall as well as deaths occurring in health care facilities were eliminated from consideration because the focus was upon temperature, not snowfall or events within a hospital. These criteria resulted in the inclusion of 1,802 days and 926 cases of acute MI. The mean temperature on the day of death was obtained from climatological data and were grouped into six categories covering a range of temperatures from less than -17.8 degrees C (0 degrees F) to 16.1 degrees C (61 degrees F). The number of deaths in each category was tabulated. The effect of temperature, sex, and age were analyzed by regression analysis. The results indicated a linear increase in mortality as mean daily temperature decreased over the temperature range. The inverse temperature effect was most pronounced in males over the age of 60. These results indicate that cold temperatures appear to be associated with an increased mortality from myocardial infarction.
Natural inhibitors of endogenous fibrinolysis may displace the hemostatic equilibrium toward thrombosis and favor events such as acute myocardial infarction, sudden cardiac death and stroke, where a thrombotic process is known to occur.1,2 The clinical incidence of these syndromes shows a circadian distribution with highest frequency in the morning.3,5 These observations prompted us to investigate possible circadian changes of blood fibrinolytic activity in normal subjects. Two major components of the fibrinolytic system, tissue-type plasminogen activator (t-PA) and its fast-acting inhibitor (PAI), were measured with specific assays. This study reports markedly reduced fibrinolytic activity during the early morning hours related to increased plasminogen activator inhibition.
We have previously reported that the frequencies of myocardial infarction and of sudden cardiac death are highest during the period from 6 a.m. to noon. Since platelet aggregation may have a role in triggering these disorders, we measured platelet activity at 3-hour intervals for 24 hours in 15 healthy men. In vitro platelet responsiveness to either adenosine diphosphate (ADP) or epinephrine was lower at 6 a.m. (before the subjects arose) than at 9 a.m. (60 minutes after they arose). The lowest concentration of these agents required to produce biphasic platelet aggregation decreased (i.e., aggregability increased) from a mean +/- SEM of 4.7 +/- 0.6 to 3.7 +/- 0.6 microM (P less than 0.01) for ADP and from 3.7 +/- 0.8 to 1.8 +/- 0.5 microM (P less than 0.01) for epinephrine. The period from 6 to 9 a.m. was the only interval in the 24-hour period during which platelet aggregability increased significantly. We subsequently studied 10 subjects on alternate mornings after they arose at the normal time and after delayed arising. The morning increase in platelet aggregability was not observed when the subjects remained supine and inactive. Thus, there is a temporal association between increased platelet aggregability in the morning and an increased frequency of myocardial infarction and of sudden cardiac death. Demonstration of this association does not establish a cause--effect relation, but together with other evidence linking platelets to these disorders, it may provide insight into the mechanisms precipitating myocardial infarction and sudden cardiac death and aid in the design of more effective preventive measures.
We studied 1217 cases of myocardial infarction, admitted to Patna Medical College Hospital, Patna, during the period 1979 to 1983, and correlated the incidence of the disease with air-temperature, seasons and months. There was no monthly variation in the incidence of the disease. The seasons similarly had no influence on incidence. The frequency of myocardial infarction, however, was significantly higher when the minimum air-temperature was 16 degrees C or less (P less than 0.001). This study indicates that drop in atmospheric temperature below a certain level directly increases the incidence of myocardial infarction and suggests simple prevention measures against the adverse effect of cold.
To determine if sudden cardiac death shows circadian variation, the time of day of sudden cardiac deaths in the Framingham Heart Study was analyzed. Analysis was based on mortality data collected in a standardized manner for the past 38 years for each death among the 5,209 persons in the original cohort. The necessary assumptions about the cause and timing of unwitnessed deaths were made in a manner likely to diminish the possibility of detecting an increased incidence of sudden cardiac death during the morning. In the Framingham study, analyses using these assumptions reveal a significant circadian variation (p less than 0.01) in occurrence of sudden cardiac death (n = 429), with a peak incidence from 7 to 9 AM and a decreased incidence from 9 AM to 1 PM. Risk of sudden cardiac death was at least 70% higher during the peak period than was the average risk during other times of the day. Further studies are needed to confirm this finding in other populations, to collect data regarding medications and to determine activity immediately before sudden cardiac death. Investigation of physiologic changes occurring during the period of increased incidence of sudden cardiac death may provide increased insight into its causes and suggest possible means of prevention.
To determine whether sudden cardiac death exhibits a circadian rhythm similar to that recently demonstrated for nonfatal myocardial infarction, we analyzed the time of day of sudden cardiac death as indicated by death certificates of 2203 individuals dying out of the hospital in Massachusetts in 1983. The data reveal a prominent circadian variation of sudden cardiac death, with a low incidence during the night and an increased incidence from 7 to 11 A.M. The pattern is remarkably similar to that reported for nonfatal myocardial infarction and episodes of myocardial ischemia. The finding that the frequency of sudden cardiac death is increased in the morning is compatible with hypotheses that sudden cardiac death results from ischemia or from a primary arrhythmic event. Further study of the physiologic changes occurring in the morning may provide new information supporting or refuting these hypotheses, thereby leading to increased understanding and possible prevention of sudden cardiac death.
To examine whether a significant circadian variation of transient myocardial ischemia exists and to better understand the character of such variation, 32 patients with chronic stable symptoms of coronary artery disease underwent one or more days of ambulatory monitoring of ischemic ST segment changes during daily life. A total of 251 episodes of ischemic ST segment depression occurred in 24 (75%) of the 32 patients with a median duration of 5 min (range 1 to 253). A significant circadian increase in ischemic activity was found with 39% of episodes and 46% of total ischemic time occurring between 6 A.M. and 12 P.M. (p less than .05 and p = .02, respectively). In 21 patients with ST segment depression during the 6 hr after waking and the 6 hr before sleep, 68% of episodes occurred in the morning compared with 32% in the evening. There were no significant differences in heart rate at onset, heart rate at 1 min before onset, and activity score associated with ST segment depression. The proportion of minutes showing ST segment depression when the heart rate was above the lowest rate associated with ST segment depression was significantly greater in the morning compared with the evening (26% vs 15%; p = .03). Thus the early morning increase in ST segment depression does not appear to be explained by differences in extrinsic activity and/or stress measured by physical activity score and heart rate response. More importantly, this phenomenon is often ignored by the usual patterns of drug administration for angina.(ABSTRACT TRUNCATED AT 250 WORDS)
The diurnal rhythms of plasma epinephrine and norepinephrine were investigated in a group of normal young men. Sleep, posture, illumination, and food intake were monitored. Plasma epinephrine demonstrated a statistically significant diurnal rhythm, with a mean amplitude of 14 +/- 1.6 (+/- SE) pg/ml superimposed on a mean level of 43 +/- 5.3 pg/ml. The trough occurred at 03.20 h +/- 35 min. Plasma norepinephrine had a significant diurnal rhythm, with a mean amplitude of 111 +/- 19 pg/ml superimposed on a mean level of 413 +/- 25 pg/ml, with the trough occurring at 02.20 h +/- 30 min. There was a significant correlation between the two rhythms at zero phase shift, with a pooled value for the group of r = 0.49. Epinephrine levels had no direct relationship to sleep or posture, whereas norepinephrine levels were significantly higher with upright posture and higher when the men were awake than when asleep. Our results indicate that circadian variations in the sympathetic-adrenal medullary system are not explained by a single controlling influence and that the norepinephrine rhythm can be accounted for as a direct response to changes in posture and sleep, whereas the epinephrine rhythm is probably controlled by a circadian oscillator.
We studied the time of onset of chest pain in 1099 patients admitted to a coronary care unit with myocardial infarction using a statistical model. Statistical analysis demonstrated an excess of infarcts with time of onset of chest pain at 0700 hours (14%) and at midnight (11%), with the remaining infarct population (75%) forming a background distribution over the 24 hr.
Six hours of mild surface cooling in moving air at 24 degrees C with little fall in core temperature (0.4 degree C) increased the packed cell volume by 7% and increased the platelet count and usually the mean platelet volume to produce a 15% increase in the fraction of plasma volume occupied by platelets. Little of these increases occurred in the first hour. Whole blood viscosity increased by 21%; plasma viscosity usually increased, and arterial pressure rose on average from 126/69 to 138/87 mm Hg. Plasma cholesterol concentration increased, in both high and low density lipoprotein fractions, but values of total lipoprotein and lipoprotein fractions were unchanged. The increases in platelets, red cells, and viscosity associated with normal thermoregulatory adjustments to mild surface cooling provide a probable explanation for rapid increases in coronary and cerebral thrombosis in cold weather. The raised arterial pressure and possibly cholesterol concentration may contribute to slower components of the increased thrombosis.
The nature of the pathologic lesion in sudden cardiac ischemic death is in dispute. Among 100 subjects who died of ischemic heart disease in less than six hours, coronary thrombi were found in 74. There was no difference in incidence between those who died in less than 15 minutes, those who died in 15 to 60 minutes, and those who died after one hour. Among 26 cases without an intraluminal thrombus, plaque fissuring was found in 21; thus, in only 5 cases was no acute arterial lesion demonstrated. No intraluminal thrombi were found in age-matched controls. Forty-eight of the 74 thrombi were found at sites of preexisting high-grade stenosis; 14 were found at points of previous stenosis of less than 50 per cent of the diameter of the lumen. Forty-seven per cent of the thrombi were found in the right coronary artery. Only 30 per cent were found in the left anterior descending coronary artery. The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present. These findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.
A study of vital statistics data from five Minneapolis-St. Paul winters indicates cardiovascular mortality is influenced by winter temperatures and snow. Although air temperature was not statistically implicated in triggering cardiovascular mortality in four of the five study winters, during the winter of 1976-77, about 15 per cent of the variance in daily cardiovascular mortality could be attributed to fluctuations in the daily minimum air temperature. Snow influenced mortality on the day of occurrence as well as the two days following a snowfall. There appear to be some differences in the ability of winter weather to influence mortality from acute myocardial infarction (ICD 410) and old myocardial infarction (ICD 412). The variance in daily ICD 410 mortality attributable to the influence of snow is somewhat less than that in daily ICD 412 mortality. The greatest variance in daily ICD 412 mortality that could be ascribed to snow occurred during the winter of 1974-75, and was 13 per cent. It is likely that rain intermixed with snow may also trigger increased mortality from cardiovascular disease. A combination of rain and snow can produce dramatic increased in mortality from ICD 410. Study of mortality data from five winters indicates that snow is somewhat more important in triggering deaths from heart disease than is air temperature.
Incidence cases of coronary heart disease that occurred in Rochester, Minnesota, during the years 1950 through 1975 were used for a study of the distribution of sudden cardiac death (1,054 cases) by day of the week and season of the year. Overall, sudden cardiac death--that is, death within 24 hours of onset of symptoms--occurred with greater frequency on Saturdays than on other days of the week. The frequency of occurrence of sudden cardiac death by season varied somewhat--the highest frequency was in winter and the lowest in summer-- but no more than expected by chance. Among males, there was a decreasing trend by day of the week from Saturday to Friday, and this was so for those with and those without a history of coronary heart disease (P less than 0.01).
A morning peak in occurrence of sudden cardiac death has been identified in epidemiological studies, but the studies are subject to selection bias, with the exclusion of unwitnessed deaths, which are more likely to occur at night. The recent availability of implantable cardioverter/defibrillators that record the time of ventricular tachyarrhythmias requiring either pacing or shock therapy provides an opportunity to clarify the timing of ventricular tachyarrhythmias predisposing to sudden cardiac death. Analysis of the timing of arrhythmias in different patient subgroups, such as patients with poor left ventricular function, may provide further insight into the mechanism of onset of sudden cardiac death.
We studied patients in whom a cardioverter/defibrillator (Ventak PRx) was implanted between September 1990 and September 1993 in US centers. Events that could be timed occurred in 483 patients. With an RR cycle length of 240 ms as a cutoff, corresponding to a heart rate of 250 beats per minute, episodes were categorized as rapid (n = 1217) or less rapid (n = 9266) ventricular tachyarrhythmias. A higher proportion of both rapid and less rapid ventricular tachyarrhythmias began in the late morning compared with other times of the day. The subgroup of patients with ejection fraction < 20% at the time of implantation demonstrated a more uniform 24-hour distribution of tachycardias < or = 250 beats per minute than patients with higher left ventricular ejection fraction.
Further investigation of the late morning peak and of precipitants of ventricular tachyarrhythmias by use of data from the implantable cardioverter/defibrillator may provide insight into the pathophysiological mechanisms causing sudden cardiac death.
The acute coronary syndromes, including unstable angina and acute myocardial infarction, currently constitute a major preoccupation of clinical cardiology. This century has witnessed a remarkable evolution in our clinical concepts of these syndromes. Herrick1 described the survival of patients with acute coronary thrombosis early in the century. The introduction of the ECG led to major clinical advances in the definition of acute myocardial infarction during the first half of this century and furnished the basis of modern coronary care.
In the latter half of this century, the advent of coronary arteriography permitted definition in the living patient of coronary stenoses due to atherosclerosis. The introduction of this diagnostic technique allowed the development of rational treatment modalities such as coronary artery bypass surgery and, subsequently, percutaneous transluminal coronary angioplasty. Until recently, it seemed that we had achieved a firm understanding of the pathophysiology of human coronary artery disease and had devised appropriate modes of therapy for its major manifestations. Yet, recent clinical data suggest that we still have much to learn about the pathophysiology of the acute coronary syndromes.
Bypass surgery and angioplasty aim to restore blood flow to sites beyond hemodynamically significant stenoses in the coronary arteries. These revascularization therapies effectively relieve angina pectoris in many cases (although often not permanently). Quite naturally, the availability of these modalities led the cardiology community to focus on high-grade coronary stenosis, visible by angiography, as the critical issue in coronary heart disease. Much of the basis of contemporary cardiology and cardiac surgery rests on the axiom: the greater the stenosis, the greater the risk of a clinical event such as myocardial infarction or unstable angina pectoris.
However, data emerging from clinical and pathological studies over the past decade have occasioned a reassessment of this central dogma of clinical cardiology.2 First, the …
This study was carried out to determine the effect of the once-daily calcium channel blocking agent amlodipine (half-life 35 to 50 h) on the circadian pattern of myocardial ischemia in patients with chronic stable angina.
Myocardial ischemia during normal daily life, both symptomatic and asymptomatic, has been associated with increased risk of cardiovascular morbidity and mortality, and the circadian pattern parallels that for myocardial infarction and sudden death.
The Circadian Anti-Ischemia Program in Europe (CAPE) was a large, 10-week international (63 sites), double-blind, parallel study. After a 2-week, single-blind placebo phase, during which stable doses of antianginal treatment were maintained (beta-adrenergic blocking agents in 65% of patients), patients with chronic stable angina with at least three attacks of angina per week, with at least four ischemic episodes or > or = 20 min of ST segment depression in 48 h of Holter monitoring, were randomized to receive treatment with either 5 mg/day of amlodipine or placebo (2:1 randomization). The dose was increased to 10 mg/day after 4 weeks. During week 7 of treatment, 48-h ambulatory ECG monitoring was repeated.
Three hundred fifteen of 1,160 patients screened were eligible, and 250 had complete evaluable data. Compared with placebo, amlodipine significantly reduced both the frequency of ST segment depression episodes (60% for amlodipine vs. 44% for placebo, p = 0.025) and total integrated ST ischemic area (62% mm-min vs. 50% mm-min, p = 0.042). Amlodipine reduced ischemia over the 24 h with the intrinsic circadian pattern maintained. In addition, diary data showed a significant reduction in angina (70% for amlodipine vs. 44% for placebo, p = 0.0001) and in nitroglycerin consumption (67% vs. 22%, respectively, p = 0.0006). Amlodipine and placebo demonstrated similar safety profiles (adverse events 17.3% for amlodipine and 13.3% for placebo; discontinuation rates due to adverse events were 2% vs. 4.4%, respectively).
Once-daily amlodipine, when added to background treatment, significantly reduced both symptomatic and asymptomatic ischemic events over 24 h in patients with chronic stable angina.
Seasonal and circadian variations in the occurrence of myocardial infarction and sudden cardiac death have been documented, suggesting that triggering factors may play a role in the causation of cardiac events. However, there are only sparse and conflicting data on the weekly distribution of the disorders.
To determine the weekly variation of acute myocardial infarction and sudden cardiac death, 5596 consecutive patients (71% men; age, 63 +/- 1 years) were analyzed in a regionally defined population (n = 330,000; age, 25 to 74 years) monitored from 1985 to 1990. The exact time of onset of symptoms was used to determine the day of the event. Patients with myocardial infarction (n = 2636) demonstrated a significant weekly variation (P < .01) with a peak on Monday, whereas patients with sudden cardiac death (n = 2960) were evenly distributed throughout the week. A similar weekly pattern was observed in subgroups of patients with myocardial infarction defined with respect to age, sex, cardiac risk factors, prior cardiac medication, and infarct characteristics. The working population demonstrated a weekly variation of myocardial infarction as opposed to the nonworking population, with a 33% increase in relative risk of disease onset on Monday (P < .05) and a trough on Sunday compared with the expected number of cases, if homogeneity was assumed.
The onset of acute myocardial infarction demonstrates a peak on Monday primarily in the working population. If this finding is confirmed in other communities, it may aid in identifying acute triggering events of myocardial infarction and perhaps in improving prevention of the disease.
Using data from a community-based register of heart disease (the WHO MONICA Project) associations between daily temperature, rainfall and other seasonal effects were investigated in relation to fatal coronary events and non-fatal definite myocardial infarctions in an Australian population. Coronary events, both fatal and non-fatal, were 20-40% more likely to occur in winter and spring than at other times of the year. Coronary deaths were more likely to occur on days of low temperature (and to a much lesser extent, on days of high temperature). No differences were found between patterns of sudden and non-sudden deaths (those occurring later after the onset of symptoms) associated with weather conditions. Statistical models allowing simultaneously for longer-term seasonal effects and daily temperature effects suggested that both exist. These results suggest that avoiding temperature stress could lead to reductions in the annual peaks in coronary events.
1. Six elderly (66-71 years) and six young (20-23 years) subjects (half of each group women) were cooled for 2 h in moving air at 18°C to investigate possible causes of increased mortality from arterial thrombosis among elderly people in cold weather. Compared with thermoneutral control experiments, skin temperature (trunk) fell from 35.5 to 29.5°C, with little change in core temperature.
2. Erythrocyte count rose in the cold from 4.29 to 4.69 × 1012/l, without a change in mean corpuscular volume, indicating a 14% or 438 ml decline in plasma volume; increased excretion of water, Na+ and K+ accounted for loss of only 179 ml of extracellular water.
3. Plasma cholesterol and fibrinogen concentrations rose in the elderly subjects from 4.9 mmol/l and 2.97 g/l (control) to 5.45 mmol/l and 3.39 g/l in the cold, and in the young subjects from 3.33 mmol/l and 1.84 g/l (control) to 3.77 mmol/l and 2.07 g/l in the cold. Increases were significant for the elderly subjects, the young subjects and the group as a whole, except for cholesterol in the young subjects, and all were close to those expected from the fall in plasma volume.
4. Plasma levels of Protein C and factor X did not increase significantly in the cold in the elderly subjects, young subjects, or the group as a whole.
5. The results suggest that loss of plasma fluid in the cold concentrates major risk factors for arterial thrombosis, while small molecules, including protective Protein C, redistribute to interstitial fluid.
Epidemiological studies have identified associations between time of day and risk of sudden cardiac death. The marked peak in the occurrence of sudden cardiac death after awakening suggests that the disease is triggered by changes that occur during this time period. Increased sympathetic stimulation is a likely cause of such triggering. In the light of the circadian variation of sudden cardiac death and the evidence linking physical activity or mental stress (both associated with activation of the sympathetic nervous system) to the disease, the role of potential triggering events should be investigated. Controlled studies are needed to determine the relative risk of activities that may trigger sudden cardiac death. Since such studies must rely on witnesses (or resuscitated patients), data quality must be closely scrutinized, and studies using case-control and case-crossover designs are needed. The epidemiological and pathophysiological data reviewed in the present article suggest a number of pathways through which activities may trigger sudden cardiac death. Different extrinsic stimuli may cause similar physiological changes that subsequently lead to acute pathological events, a decrease in the ventricular fibrillation threshold through a direct myocardial effect, or a harmful effect on the conduction system. Myocardial ischemia induced by plaque rupture and thrombosis may lead directly to myocardial electric instability. The presence of chronic structural abnormalities of the myocardial tissue or the conduction system may further lower the threshold for electric instability and ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine the circadian and seasonal variations in the incidence of acute myocardial infarction and the influence of environmental temperature.
633 consecutive patients with acute myocardial infarction admitted to a coronary care unit over four years.
Coronary care unit in a district general hospital.
An observational study.
The onset of acute myocardial infarction had a circadian rhythm with a peak in the second quarter of the day. A seasonal variation was also found with a significant winter peak. There was, however, an excess of infarctions on colder days in both winter and summer indicating that the effect of environmental temperature on the onset of acute myocardial infarction is independent of the time of year.
Acute myocardial infarction is more common in winter and more common on colder days, independent of season. Environmental temperature may play an important part in the pathogenesis of acute myocardial infarction.
The earthquake that struck the Los Angeles area at 4:31 a.m. on January 17, 1994, was one of the strongest earthquakes ever recorded in a major city in North America. Once the life-threatening situation was over, the Northridge earthquake, so called because its epicenter was near Northridge, California, just north of Los Angeles, provided investigators an unusual opportunity to examine the relation between emotional stress and sudden cardiac death.
We reviewed the records of the Department of Coroner of Los Angeles County for the week before the earthquake, the day of the earthquake, the six days after the earthquake, and corresponding control periods in 1991, 1992, and 1993.
On the day of the earthquake, there was a sharp increase in the number of sudden deaths from cardiac causes that were related to atherosclerotic cardiovascular disease, from a daily average (+/- SD) of 4.6 +/- 2.1 in the preceding week to 24 on the day of the earthquake (z = 4.41, P < 0.001). Sixteen victims of sudden death had symptoms, usually chest pain, or died within the first hour after the initial tremor. Only three sudden deaths occurred during or immediately after unusual physical exertion. During the six days after the earthquake, the number of sudden deaths declined to below the base-line value, to an average of 2.7 +/- 1.2 per day.
The Northridge earthquake was a significant trigger of sudden death due to cardiac causes, independently of physical exertion. This finding, along with the unusually low incidence of such deaths in the week after the earthquake, suggests that emotional stress may precipitate cardiac events in people who are predisposed to such events.
During a record-setting heat wave in Chicago in July 1995, there were at least 700 excess deaths, most of which were classified as heat-related. We sought to determine who was at greatest risk for heat-related death.
We conducted a case-control study in Chicago to identify risk factors associated with heat-related death and death from cardiovascular causes from July 14 through July 17, 1995. Beginning on July 21, we interviewed 339 relatives, neighbors, or friends of those who died and 339 controls matched to the case subjects according to neighborhood and age.
The risk of heat-related death was increased for people with known medical problems who were confined to bed (odds ratio as compared with those who were not confined to bed, 5.5) or who were unable to care for themselves (odds ratio, 4.1). Also at increased risk were those who did not leave home each day (odds ratio, 6.7), who lived alone (odds ratio, 2.3), or who lived on the top floor of a building (odds ratio, 4.7). Having social contacts such as group activities or friends in the area was protective. In a multivariate analysis, the strongest risk factors for heat-related death were being confined to bed (odds ratio, 8.2) and living alone (odds ratio, 2.3); the risk of death was reduced for people with working air conditioners (odds ratio, 0.3) and those with access to transportation (odds ratio, 0.3). Deaths classified as due to cardiovascular causes had risk factors similar to those for heat-related death.
In this study of the 1995 Chicago heat wave, those at greatest risk of dying from the heat were people with medical illnesses who were socially isolated and did not have access to air conditioning. In future heat emergencies, interventions directed to such persons should reduce deaths related to the heat.