Circumstances attending 100 sudden deaths from coronary artery disease with coroner's necropsies.

Myers, A; Dewar, H. A.

doi:10.1136/hrt.37.11.1133

Cited by 214 publications

(51 citation statements)

References 11 publications

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“…9−11 Of particular note, a retrospective study of 100 sudden deaths in Newcastle upon Tyne, England, compared with 100 non-fatal myocardial infarctions, showed that a higher proportion of men who died had taken alcohol three hours before deaths and that sudden deaths were most common on Saturdays whereas this was not the case for non-fatal myocardial infarction. 12 There is also supporting evidence from several studies undertaken in Finland, where the pattern of drinking has traditionally resembled that seen in Russia. In one Finnish study, the authors argue that "in cases of sudden death, the aetiological role of coronary heart diseases might have been overestimated among alcohol consumers, because there is evidence that alcohol in itself can injure the myocardium and cause a dangerous arrhythmia or myocardial infarction".…”

Section: Discussionsupporting

confidence: 56%

Alcohol and cardiovascular mortality in Moscow; new evidence of a causal association

Chenet

McKee

Leon

et al. 1998

Journal of Epidemiology & Community Health

157

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Background-In explaining recent trends in Russian mortality, alcohol drinking has often been put forward as a major factor. However, cardiovascular disease remains the major cause of death in Russia and alcohol is currently viewed as having a protective eVect on heart disease. This study explores this apparent paradox by examining daily trends in deaths from cardiovascular disease in Moscow. Subjects-Those dying in Moscow in the years 1993-1995. Methods-Analysis of daily variation in deaths based on data from Moscow City death certificates. Results-There is a significant increase in deaths from alcohol poisoning, accidents, and violence and cardiovascular diseases on Saturdays, Sundays, and Mondays. This is especially marked for sudden deaths. This pattern is consistent with the known pattern of drinking in Russia, which is more likely to take place in binges than is the case in other countries. Conclusion-A possible causative role for alcohol in sudden cardiovascular death is suggested as there are no other obvious explanations for this pattern, which cannot be accounted for by daily variations in traditional risk factors such as smoking or lipids. Although this is inconsistent with the prevailing view in the West that alcohol is seen as cardioprotective, there is considerable supporting evidence from a necropsy study and from studies in other places with a similar pattern of drinking. In countries such as Russia, where patterns of drinking diVer considerably from that in the West, binge drinking can be an important cause of sudden cardiac death. This has important implications for estimates of the amount of mortality worldwide attributable to specific risk factors and thus for national and international policy. (J Epidemiol Community Health 1998;52:772-774) The Russian mortality crisis in the 1990s has attracted much interest but is still poorly understood. Since the mid-1980s, Russian life expectancy at birth displayed unprecedented fluctuations: first rising rapidly during Gorbachev anti-alcohol campaign, then decreasing by 6.5 years for men and 3.5 years for women. Young adults (35-49) have been most severely hit by this mortality crisis. Deaths from accidents and violence as well as alcohol related deaths seem to play a major part, 1 with death rates from accidents and violence increasing fivefold for men in their 40s between 1987 and 1994, and alcohol related mortality increasing sevenfold. 2 These increases, as well as the substantial but short lived decline in mortality coinciding with the anti-alcohol campaign of the mid-1980s, point to alcohol consumption as a major factor in the present mortality crisis. However, the main cause of death contributing to these overall mortality trends is cardiovascular diseases. The most frequent single cause of death is "coronary atherosclerosis" (code 093 in the Soviet classification of diseases). Deaths from this cause have contributed substantially to the recent fluctuation in mortality, exhibiting a sharp fall in the years after 1985, coinciding with Go...

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Section: Discussionsupporting

confidence: 56%

Alcohol and cardiovascular mortality in Moscow; new evidence of a causal association

Chenet

McKee

Leon

et al. 1998

Journal of Epidemiology & Community Health

157

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“…Anecdotal reports and case studies [187][188][189] have long reported a relationship between acute stress and the development of cardiac disease. In addition, the effects of acute stress on heart disease are well supported by epidemiological studies regarding natural life stressors.…”

Section: Acute Life Stressmentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

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“…Numerous studies of cardiac arrest victims and survivors of aborted cardiac arrests have identified several potential causes of cardiac arrest, the most common of which is ventricular tachycardia (VT) or fibrillation (VF) due to either acute ischemia or reentry in a healed myocardial scar. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] These studies have focused primarily on the patient with coronary artery disease, including patients with and without heart failure, and may not accurately indicate the frequency of various causes of death in the heart failure population. Heart failure is associated with activation of the sympathetic nervous system and electrolyte abnormalities that could affect arrhythmogenesis.122,24 In addition, heart failure patients are predisposed to systemic and venous thromboemboli that could precipitate cardiac arrest.…”

mentioning

confidence: 99%

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure.

Luu¹,

Stevenson²,

Stevenson³

et al. 1989

Circulation

484

154

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To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

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Circumstances attending 100 sudden deaths from coronary artery disease with coroner's necropsies.

Cited by 214 publications

References 11 publications

Alcohol and cardiovascular mortality in Moscow; new evidence of a causal association

Alcohol and cardiovascular mortality in Moscow; new evidence of a causal association

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure.

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