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The aim was to analyze the rate of sudden death in elderly Croatian women in comparison to elderly Croatian men, who died suddenly due to swimming. In the period from 2002 to 2011 one elderly Croatian woman and five elderly men died suddenly during swimming. In the same time, the same number of elderly foreigners died due to swimming at the Croatian Adriatic coast. One Croatian woman aged 66, who suffered of arterial hypertension with left ventricular hyper- trophy of 15 mm, diabetes mellitus and alcoholic liver cirrhosis, drowned in the sea during swimming. She was intoxi- cated with alcohol and had alcohol level in urine of 3.03 per thousand. One foreign woman, aged 82, who suffered coronary heart disease with left ventricular scar after myocardial infarction, arterial hypertension with excessive left ventricular hypertrophy of 22 mm and nephroangiosclerosis, suddenly lost conscionsness during swimming. The death rate in elderly Croatian women due to swimming reached 0.25, and the death rate in men is eight times higher: 1.97 (p = 0.0701), but the difference is not significant probably because of a small observational number.

Resting heart rate has been related to the risk of cardiovascular disease and sudden death in several large prospective studies. To investigate prospectively the association of novel heart rate parameters and of carotid artery stiffness with sudden death and other cardiovascular disease. The Paris Prospective Study III (PPS3) is a new, ongoing French prospective study. From June 2008 to December 2011, 10,000 men and women aged 50-75 years who will have a preventive medical check-up at the Centre d'Investigations Préventives et Cliniques in Paris (France), will be enrolled in the study, after signing an informed consent. In addition to the general health examination, each subject's heart rhythm will be recorded during the course of the health check-up (approximately 2(1/2) h) and an echo-tracking of the right carotid bulb will be performed by trained technicians. A bio bank and DNA bank will be established for further biomarker and genetic analyses. The occurrence of cardiovascular disease including acute coronary syndrome, stroke, peripheral artery disease and sudden death, and of mortality, of the participants will be followed up during 20 years. With an estimated mean annual rate of sudden death of 0.1% and its increasing incidence rate with age, between 250 and 300 sudden deaths are expected. This unique study should provide new insights into the regulation of heart rate and blood pressure and should enable to identify novel heart rate parameters that are associated with sudden death.

Objective: Type 2 diabetic patients have a high risk of coronary heart disease (CHD) and sudden death. This cardiovascular risk can be partly attributed to low levels of HDL cholesterol. The B2 allele of the CETP TaqIB polymorphism has been repeatedly reported to be associated with high HDL cholesterol levels in both healthy and type 2 diabetic subjects, but its association with CHD is unclear. We investigated the association of the CETP TaqIB polymorphism with CHD, and sudden death in particular, in a prospective cohort of type 2 diabetic patients., Research Design and Methods: The CETP TaqIB polymorphism was genotyped in 3,124 type 2 diabetic subjects with high cardiovascular risk: the Noninsulin-Dependent Diabetes, Hypertension, Microalbuminuria, Proteinuria, Cardiovascular Events, and Ramipril (DIABHYCAR) study. We used Cox regression analysis to estimate the impact of the TaqIB single nucleotide polymorphism on the CHD events (myocardial infarction or sudden death) during follow-up., Results: The incidence of CHD was higher in B1B1 homozygotes than in B2 carriers (P = 0.02). This effect was mainly due to sudden death (hazard ratio [B1B1 vs. B2+] = 1.51 [95% CI = 1.05-2.18]). Although the B1 allele was associated in a dose-dependent fashion with lower HDL cholesterol (P < 0.001), the association with sudden death persisted after adjustment for multiple risk factors, including HDL cholesterol levels., Conclusions: In type 2 diabetic patients, the CETP TaqIB polymorphism is a good genetic predictor of cardiac mortality. This association is partly independent of the effect on HDL cholesterol levels.

It is a common practice to perform percutaneous or open coronary artery revascularisation in CHD to prevent sudden or unexpected death. Such a practice assumes that sudden and unexpected death is common in stable patients with uncomplicated CHD. This is a retrospective analysis of 248 patients (199, 80% men, 49, 20% women) who had median age 65.1 when assessed after stabilisation of their CHD and were followed up to 25 years until their death. Myocardial revascularisation was only performed after the patients had stabilised if they developed either progressive clinical disability or acute coronary syndromes. At stabilisation, 181 (73%) were uncomplicated, 59 (24%) had heart failure (HF) and 8 (3%) had other comorbidities. At their last visit before death, 67 (27%) were uncomplicated, 121 (49%) had HF, 41 (17%) had cancer and 19 (8%) had other comorbidities. Their median age at death was 72.4 years. 77 (31%) died suddenly, 47 (19%) of HF, 39 (16%) of cancer, 35 (14%) of acute myocardial infarction (AMI) and 50 (20%) had miscellaneous modes of dying. Unexpected death occurred in 26 (10%) of cases: sudden 12, AMI 7, stroke 3, suicide 2, abdominal aneurysm 1, motor vehicle accident 1. We conclude that the clinical condition of most patients with CHD deteriorates between their initial stabilisation and their final visit before their death-metamorphosis. Only a small proportion of deaths occur in patients with stable CHD and no HF. Intervention in stable patients without CHF is unlikely to reduce sudden or unexpected death in patients with CHD.

Background: Patients at high risk of sudden cardiac death, yet at low risk of nonsudden death, might be ideal candidates for antiarrhythmic drugs or devices. Most previous studies of prognostic markers for sudden cardiac death have ignored the competitive risk of nonsudden cardiac death. The goal of the present study was to evaluate the ability of clinical factors to distinguish the risks of sudden and nonsudden cardiac death., Methods: We identified all deaths during a 3.3-year follow-up of 30,680 patients discharged alive after admission to the cardiac care unit of a Seattle hospital. Detailed chart reviews were conducted on 1093 subsequent out-of-hospital sudden deaths, 973 nonsudden cardiac deaths, and 442 randomly selected control patients., Results: Patients who died in follow-up (suddenly or nonsuddenly) were significantly different for many clinical factors from control patients. In contrast, patients with sudden cardiac death were insignificantly different for most clinical characteristics from patients with nonsudden cardiac death. The mode of death was 20% to 30% less likely to be sudden in women, patients who had angioplasty or bypass surgery, and patients prescribed beta-blockers. The mode of death was 20% to 30% more likely to be sudden in patients with heart failure, frequent ventricular ectopy, or a discharge diagnosis of acute myocardial infarction. A multivariable model had only modest predictive capacity for mode of death (c-index of 0.62)., Conclusion: Standard clinical evaluation is much better at predicting overall risk of death than at predicting the mode of death as sudden or nonsudden.

The aim of this study was to evaluate the causes of death in individuals who died suddenly in Addis Ababa, Ethiopia. The selection of the cases was based on police reports, which contained a description of sudden unexpected or instantaneous death. The study was performed on necropsies of the Medico legal Department of Menelik II Hospital, in Addis Ababa during the years 1998 and 1999. According to the pathological features of the heart, we classified 92 dead bodies in 3 groups: Group A: Hearts showing adequate morphological changes to explain sudden death (n = 63). Group B: Hearts showing some structural changes, but inadequate to explain sudden death (n = 20). Group C: Normal hearts (n = 7). In two bodies the general autopsy revealed an extra cardiac cause of death. The single most relevant cause of death in group A was coronary artery disease (44 cases) followed by excessive myocardial hypertrophy due to post-rheumatic valvular lesions (7 cases). While the high prevalence of rheumatic heart disease in Ethiopia is well known, the proportion of cases who died due to coronary heart disease is surprising. Though during the last years some African authors assumed that coronary atherosclerosis is on the increase in developing countries the percentage is higher than expected and higher than in other countries where similar studies exist.

The retrospective analysis of 1700 forensic autopsies over 17 years (1981-97) following unexpected sudden cardiac death revealed a group of 50 cases that could have been related to surgery and/or anaesthesia. Patients were young with no history of cardiac disease. Surgery was performed for uncomplicated disorders, all classified as ASA 1. Cardiac arrest took place at induction of anaesthesia in 16% of cases, during surgery in 64% and at the end of surgery in 20%. Investigation and expertise reports ordered by the public prosecutor revealed none of the typical causes of death usually associated with surgery or anaesthesia. Pathological examination showed cardiac lesions in 47 cases: arrhythmogenic right ventricular cardiomyopathy in 18 cases, coronary artery disease in 10 cases, cardiomyopathy in eight cases, structural abnormalities of the His bundle in nine cases, mitral valve prolapse in one case, and acute myocarditis in one case. Identification of the cause of death of patients at low risk may provide major relief to the family of the patient and the medical staff.

Background: Accordance of all studies concerning the distribution of causes of cardiovascular sports deaths can only be registered in the dominating role of coronary heart disease and myocardial infarction among athletes > 35 years. In North America a predominance of hypertrophic cardiomyopathy among younger sportsmen (< or = 35 years) is described. This study investigates the conditions in the German speaking countries in central Europe., Patients and Methods: The present prospective and retrospective 1.5-year (July 1996 to December 1997) study is based on post-mortem examinations of 28 institutes of pathology and forensic medicine in Germany, Austria and German speaking Switzerland., Results: Twelve out of 113 cases (10.6%) were females, their age being significantly lower (27.8 years, sd = 15.2) than the age of the males (37.5 years, sd = 16.5). Eighty sports deaths (70.8%) were caused by cardiovascular reasons, 33 sports deaths (29.2%) were traumatic in origin. The main cause of cardiovascular deaths of the older athletes (> 35 years) was the coronary heart disease (84.1%). The main reasons for cardiovascular deaths of younger athletes (< or = 35 years) were the coronary heart disease (36.1%) and myocarditis (30.6%). A case of hypertrophic cardiomyopathy was not registered. Most of sports deaths happened in soccer (28), jogging (15), walking (8), cycling (7) and skiing (7). Most of traumatic sports deaths were registered in aerial sports. Four ball players (soccer n = 3, handball n = 1) and 1 motor cyclist suffered from a thrombosis after an orthopedic injury and died due to a consecutive pulmonary embolism., Conclusions: The distribution of cardiovascular sports deaths displays astonishing regional differences. In contrast to North America anatomical-pathological studies of German speaking countries do not show any dominance of hypertrophic cardiomyopathy among younger athletes, although the pathologists in recent investigations knew the results of Maron. Possible explanations for this phenomenon might be varying selections of patients (top-performance athletes and hobby sportsmen) or a different genetical background.

Background: Sudden and cardiac death (including death from congestive heart failure, myocardial infarction, and sudden death) are common occurrences in hemodialysis patients. The intermittent nature of hemodialysis may lead to an uneven distribution of sudden and cardiac death throughout the week. The purpose of this study was to assess the septadian rhythm of sudden and cardiac death in hemodialysis patients., Methods: Data from the United States Renal Data System (USRDS) were obtained to examine the day of death for United States hemodialysis and peritoneal dialysis patients from 1977 through 1997. The days of death were also determined for patients in the Case Mix Adequacy Study of the USRDS., Results: There was an even distribution of sudden and cardiac deaths for patients on peritoneal dialysis, and hemodialysis patients dying of noncardiac deaths also had an even distribution. For all hemodialysis patients, Monday and Tuesday were the most common days of sudden and cardiac death. For patients in the Case Mix Adequacy Study designated as Monday, Wednesday, and Friday dialysis patients, 20.8% of sudden deaths occurred on Monday compared with the 14.3% expected (P = 0.002). Similarly, 20.2% of cardiac deaths occurred on Monday compared with the 14.3% expected (P = 0.0005). Similar trends were found on Tuesday for Tuesday, Thursday, and Saturday dialysis patients., Conclusions: The intermittent nature of hemodialysis may contribute to an increased sudden and cardiac death rate on Monday and Tuesday for patients enrolled in the USRDS.

Over an 11-year period, autopsies were performed on 957 of 1038 nontraumatic deaths in the Emergency Department of the Central Hospital in Ferrara, Italy. Of these 957 cases, 732 (76.5%) met criteria for sudden death. In 100 (14%) of these cases, the death could be attributed to pulmonary embolism (55 cases), stroke (17), or rupture of aortic aneurysm (28). Acute myocardial infarction accounted for 403 (55%) of all sudden deaths. Severe coronary artery disease was found in 340 (84%) of these 403 deaths, with plaque fissuring or thrombi in 189 or 151 cases, respectively. Among the 229 sudden deaths for whom no immediate cause could be determined (31% of the total population), all had evidence of heart disease: 147 individuals had severe coronary artery disease, with plaque fissuring or thrombi found in 72 or 43, respectively. The remaining cases with no immediate cause of death had evidence of a cardiomyopathy (61) or valvular disease (21). We conclude that acute myocardial infarction accounts for the majority of cases of nontraumatic sudden death in our Emergency Department. Altogether, 84% of these patients had severe coronary artery disease. In approximately one-third of cases for whom no immediate cause of sudden death could be determined, all had evidence of heart disease, and about two-thirds had severe coronary artery disease.

Trends in coronary heart disease mortality and sudden death were studied in 35- to 44-year-old white male residents of Allegheny County, Pennsylvania. Deaths coded as any cardiac or vascular disease, diabetes, unexplained sudden death, and other rubrics were eligible for investigation, and the cause of death was validated by physicians examining multiple data sources about the deaths. During 1970-1990, 1,424 white male deaths were investigated, with 903 validated as coronary heart disease. In that time span, white male coronary heart disease mortality fell from 93.4 to 36.7 per 100,000 population per year, a 60% decline. Little proportionate change was seen in characteristics of the deaths, which were predominantly sudden and out-of-hospital. Diabetes mellitus history increased proportionately over time, largely because diabetics' mortality rates, unlike those of all other subgroups, did not fall. These observations support the contention that the decline in coronary heart disease mortality relates to risk factor modification more than to improvements in the treatment of coronary heart disease. Differences in death certification practices must be considered when interpreting and comparing vital statistics data.

Postmortem blood lipid and lipoprotein analyses were conducted in a case-controlled study of young adults (ages 22-43) who died suddenly and unexpectedly of atherosclerotic coronary artery disease in Allegheny County, Pennsylvania. None of the individuals in the study group (n = 28 cases) had a significant medical or cardiac history except in the immediate antemortem period. The control group (n = 31) consisted of age- and sex-matched cohorts who died of noncardiac related fatalities and who had no evidence of CAD. The results indicated a male-to-female ratio of nearly 30:1 with a marked predominance of young white men. Mean total cholesterol (241 mg/dL), triglycerides (583 mg/dL), and low-density lipoproteins (LDL) (107 mg/dL) were all significantly elevated in the study group as compared to controls (p < 0.001, p < 0.018, and p < 0.001 for the three parameters, respectively). Mean Apolipoprotein B (98.7 mg/dL) was also significantly elevated compared to control values (p < 0.001). By contrast, mean high-density lipoprotein values (36 mg/dL) were not significantly different from control values (p = 0.35), and mean values of Apolipoproteins A1 (121 mg/dL) and A2 (37.6 mg/dL) were essentially identical to control values (p = 0.44 and p = 0.64, respectively). The differences in these biochemical markers between the two groups could not be explained by differences in postmortem interval or by the presence of recently ingested food. These findings indicate that elevations of plasma cholesterol, triglycerides, LDL, and Apolipoprotein B are important biochemical markers for the development of early and apparently clinically silent yet life-threatening coronary artery disease.

Only 30-40% of all victims of sudden cardiac death could so far be classified as risk patients during their lifetime. Risk factors for sudden death have little predictive value in an asymptomatic population: for example, the typical risk profile for the presence of coronary heart disease and changes in the surface-ECG at rest and especially in the surface-ECG under stress. Usually, the victims of sudden cardiac death among top performance athletes have been suffering from a heart disease of which they knew nothing beforehand: below 40 years of age, mostly from hypertrophic cardiomyopathy; beyond 40, predominantly from coronary heart disease. Among the heart diseases, sudden cardiac death is the cause of death most often in hypertrophic cardiomyopathy, in dilatative cardiomyopathy and in certain types of coronary heart disease. Notwithstanding the employment of fully update cardiological diagnostics the risk patients cannot be identified with reliable precision among those suffering from these diseases. It is only clinically manifest persistent ventricular tachycardia or successful reanimation in case of ventricular fibrillation that will definitely pinpoint the patient as being at risk of sudden cardiac death also in the future.

With the lengthening of the human life span, cancer has become an increasingly important medical problem for the aged. It is not uncommon to find multiple primary neoplasms in elderly individuals. We recently investigated the death of an elderly man who had died suddenly and had three incidental malignant neoplasms, including a pleural mesothelioma, first diagnosed at autopsy. The importance of performing a complete medicolegal autopsy for epidemiological and statistical purposes is emphasized.

Acute coronary artery disease (CAD) is the leading cause of death in the Federal Republic of Germany. In spite of major advances in means of acute treatment, more than half of the patients die as a direct consequence of the disease; in the majority they die prior to hospitalization. One important reason appears to be the lack of scientific insight into the acute pathophysiologic mechanisms and, therefore, of specific and effective means of prevention. The present article presents a model of the triggering mechanisms of acute CAD based on findings of recent clinical-epidemiologic, pathological, and physiologic studies, and a discussion of its possible clinical significance. In recent studies a marked circadian variation with a morning peak was observed for onset of myocardial infarction, sudden cardiac death, and other cardiovascular diseases. These findings indicate specific endogenous and/or exogenous triggering factors that are particularly likely to occur, or to be effective, during that time of day. The relative risk of myocardial infarction is at least two-fold within the first 2 to 3 h after awakening. Some subgroups of patients, however, demonstrated no such circadian variation. Similarly, certain infarct types and cardiac medication appears to interfere with the circadian pattern. In most cases of acute CAD, the pathological findings demonstrate an intracoronary thrombus formed over a ruptured atherosclerotic plaque. During the time interval following arising, the thrombotic tendency is increased (due to platelet activation, reduced endogenous fibrinolytic activity, and increased coronary tone), as well as the risk of plaque rupture (due to an increase of heart rate and blood pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

The relation of variables obtained from a baseline examination to death from ischemic heart disease (IHD), cerebro-vascular disease (CVD) and sudden death (SUD) was analyzed in a case-control study. From questionnaire survey of approximately 180,000 subjects who underwent baseline health examinations in 1971-1986 at Aichi prefectural center of health care, 148 deaths were selected for this study. The number of cases on IHD, CVD and SUD was 36, 60, and 52, respectively. Mean age of cases was 54.8 years old and the mean follow up interval between baseline examination and death was 3.7 years. Four controls matched according to year of baseline examination, age and sex were chosen arbitrarily for each case, and odds ratios for the three diseases were estimated. In some of the matched sets, odds ratios at a follow up examination were compared with that at the first examination. The results were as follows: 1) Variables showing positive relationships to death from each of the three diseases were hypertension, high fasting blood sugar, abnormality of cardio-thoracic ratio, ST-T abnormality in ECG, left ventricular hypertrophy in ECG. The odds ratio for ST-T abnormality in ECG was significant for all three causes of death. 2) High total cholesterol showed a significant positive relation only to death from IHD. As to death from CVD and SUD, albuminuria and sclerotic changes in fundus oculi were positively and significantly related. Risk factors differed for deaths from the three diseases. 3) In death from IHD and CVD, odds ratio at the second examination was apt to be higher than that at baseline examination. In death from SUD, however, odds ratios at the first and the second examination showed no significant difference.

Sports-related sudden cardiac deaths were compared with non-sports-related sudden cardiac death in individuals (14 to 40 years old) who were autopsied from 1981 to 1988 at the Maryland Medical Examiner's Office. Thirty-four of 690 total cases of sudden cardiac death were sports-related, which represents 5% of sudden cardiac death in this age group. Causes of death were severe atherosclerosis (nine), hypertrophic cardiomyopathy with asymmetry (eight), coronary artery anomalies (four), idiopathic concentric left ventricular hypertrophy (three), myocarditis (two), arrhythmogenic right ventricle (one), Kawasaki disease (one), and unknown (six); two of the cases with unknown causes had tunnel arteries. Exercise-related deaths were more likely due to hypertrophic cardiomyopathy (p = 0.0007) compared with 102 age-, sex-, and race-matched controls in the non-exercise group; there was no difference in the incidence of severe atherosclerosis (p = 0.4). The mean age of individuals with hypertrophic cardiomyopathy with asymmetry was less than that of those with severe atherosclerosis (24 vs 32 years, p = 0.03). Thus exercise precipitates sudden cardiac death in younger individuals with hypertrophic cardiomyopathy.

The baseline electrocardiograms of 5,125 original subjects of the Framingham Heart Study were measured to examine the relation of the QT interval corrected for heart rate (QTc) to risk of total mortality, sudden cardiac death, and death due to coronary artery disease over a 30-year follow-up period. Quintiles of QTc (seconds) less than or equal to 0.36, 0.36 to 0.38, 0.39 to 0.40, 0.41 to 0.43 and greater than or equal to 0.44 were studied in relation to these outcomes. There were no significant differences in the risk of total mortality, sudden cardiac death or death due to coronary artery disease according to QTc. A similar lack of significant association between QTc and these 3 outcomes was observed among all persons studied and in the 2 sexes after using a multiple regression analysis to control for several potentially confounding characteristics including age, gender, cigarette smoking, serum total cholesterol, systolic systemic blood pressure and Framingham relative weight. The results of this study fail to demonstrate an association between baseline QTc and overall mortality, and deaths due to sudden cardiac events or coronary artery disease in a large population-based cohort of essentially healthy persons in whom pathologic forms of QTc prolongation are uncommon.

A clinicopathological synthesis is presented of the relationship of ischemic heart disease to sudden cardiac death. The immediate pathophysiological process responsible for sudden cardiac death is a lethal arrhythmia, usually ventricular fibrillation. Although significant coronary atherosclerosis is present in most cases of naturally occurring sudden death, available evidence indicates that several mechanisms can be operative in the pathogenesis of the fatal event. These are (1) acute myocardial infarction in a minority of cases; (2) myocardial ischemia, without infarction, which is initiated either by (a) an exertion-induced increase in myocardial oxygen demand or (b) an acute coronary event often involving plaque degeneration and platelet aggregation; and (3) a primary arrhythmia, usually resulting from altered electrical conduction in the setting of a previous myocardial infarction.

Although coronary artery disease is the most frequent cause of sudden cardiac death, it may be caused by a heterogeneous group of disorders. Acute ischaemia is responsible for about half the cases of sudden death after acute myocardial infarction, and is manifested through ventricular fibrillation or polymorphic ventricular tachycardia. Several factors affect the haemodynamic consequences of a ventricular arrhythmia. Re-entry is the mechanism involved in patients with a history of myocardial infarction and therapy should be individualised and directed to the arrhythmia. Simple decision trees are available that can help to find the most appropriate therapy; implantable defibrillators are the most effective modality in certain very high risk subsets.

The heart was studied in 30 persons who died suddenly from natural causes in the driver's seat of an automobile, truck or bus. Twenty had cardiac arrest while driving and the other 10 while sitting in the driver's seat of a parked vehicle. Of the 20 drivers, 16 died from atherosclerotic coronary artery disease (CAD): 12 (75%) had minor collisions and 4 did not. Of the 16 with fatal CAD, an average of 2.3 +/- 0.8 of the 4 major coronary arteries were narrowed greater than 75% in cross-sectional area (CSA) by plaque; of 668 five-mm segments of the 4 major (right, left main, left anterior descending, left circumflex) coronary arteries in 13 of these 16 cases, 27 (4%) were narrowed 96 to 100% and 127 (19%) were narrowed 76 to 95% in CSA by plaque. The remaining 4 drivers died from noncoronary conditions: aortic rupture associated with the Marfan syndrome in 1; cardiac sarcoidosis in 1; thoracic aortic dissection in 1; and severe mitral regurgitation from infective endocarditis, which had healed in 1. The other 10 persons were found dead in the driver's seat of a parked vehicle and 8 of them had fatal CAD. Of the 8 CAD victims, an average of 2.5 +/- 1.2 of the 4 major coronary arteries was narrowed greater than 75% by plaque; of the 283 five-mm segments of coronary arteries in 7 of the 8 cases, 44 (16%) were narrowed 96 to 100% and 69 (24%) were narrowed 76 to 95% in CSA by plaque.(ABSTRACT TRUNCATED AT 250 WORDS)

Sudden coronary death is a major manifestation of clinical coronary artery disease which doubles in incidence with each decade of life after age 45, with women lagging behind men in incidence by 20 years. Some 14% of heart attacks present as sudden death, and 41% of deaths from coronary disease are sudden deaths. Half of all sudden coronary deaths occur in persons without prior overt coronary artery disease. Persons with established coronary disease are at a three- to fourfold increased risk of sudden death, but the proportion of coronary deaths due to sudden death is no higher. This report examines how sudden death evolves over the long term in the general population and in persons with overt coronary artery disease, and attempts to delineate prime candidates and modifiable predisposing factors using the Framingham Heart Study. In asymptomatic persons the risk of sudden death varies over a wide range in relation to risk factors such as systolic blood pressure, serum cholesterol, cigarette smoking, heart rate, electrocardiographic abnormality and relative weight. Multivariate combination of these risk factors identifies 38.6% of sudden deaths in men and 43.8% of sudden deaths in women in the upper quintile of multivariate risk, which are, respectively, 6.0 and 5.8 times greater than the proportion of sudden deaths in the lowest quintile. When overt coronary artery disease is manifest, the major risk factors have less influence on sudden death risk, which becomes determined chiefly by indicators of intrinsic myocardial damage. With cardiac failure there is an eightfold increased risk of sudden death in men, and cardiac failure without concomitant coronary artery disease imposes a 2.7-fold increased risk.(ABSTRACT TRUNCATED AT 250 WORDS)

It is unclear whether sudden or nonsudden death can be predicted independently from other risk factors for coronary artery disease (CAD). Therefore, this investigation was undertaken to measure 12-lead QRS voltage sum, a recently proposed (Am J Cardiol 1985;55:485-494) index of left ventricular (LV) hypertrophy, and its ability to predict either subsequent sudden (less than 2 hours) or nonsudden CAD death during 20 to 23 years of follow-up in 1,588 middle aged men (40 to 61 years old) from 2 cohorts of the Italian section of the Seven Countries Study who were free of demonstrable CAD (at entry examination in 1962). The Sokolow-Lyon and the modified Sokolow-Lyon indexes, 2 standard electrocardiographic methods to detect LV hypertrophy were also measured and compared. During follow-up, 67 patients died suddenly and 87 died a nonsudden CAD death. In the Cox proportional-hazards model, age, mean blood pressure, heart rate, body mass index, cholesterol, physical activity, smoking habit, ST-T alterations (Minnesota codes 4.1 to 4.3 together with 5.1 to 5.3) and the 3 electrocardiographic indexes, all measured at the time of enrollment into the study, were included. The 12-lead QRS voltage sum retained significant and independent relation to sudden death (t = 2.00); Sokolow-Lyon index entered the Cox solution for nonsudden CAD death but the association was inverse (t = -2.10). ST-T alterations were significantly associated only with nonsudden CAD death (t = 2.19). Thus, in addition to several known risk factors, measurement of 12-lead QRS voltage sum in middle-aged men without clinical evidence of heart disease may help identify subjects at an increased risk of sudden death; nonsudden CAD death is predicted by Sokolow-Lyon index and by ST-T alterations. The usefulness of these indexes needs to be tested in different populations.

Because beta-adrenergic blockade has as one of its many effects altered electrophysiological abnormalities after dogs with left ventricular hypertrophy have been subjected to coronary occlusion, we tested the hypothesis that metoprolol (200-400 mg/day) would reduce mortality rates in dogs with one-kidney, one clip left ventricular hypertrophy while a similar reduction in arterial pressure with enalapril (20-40 mg/day) would not. Dogs with left ventricular hypertrophy were given metoprolol or enalapril for 5-7 days before a 3-hour coronary occlusion. Infarct size and risk area were measured with triphenyltetrazolium chloride stain and barium angiography, respectively. For control (n = 15), left ventricular hypertrophy (n = 17), left ventricular hypertrophy plus metoprolol (n = 12), and left ventricular hypertrophy plus enalapril (n = 15) groups, mean arterial pressure, ratio of infarct size to risk area, and dogs experiencing sudden death were 110 +/- 4, 142 +/- 4, 121 +/- 7, and 120 +/- 3 mm Hg; 44 +/- 5%, 65 +/- 5%, 44 +/- 7%, and 30 +/- 4%; and 27%, 65%, 17%, and 53%, respectively. Thus, the excessive increase in early mortality occurring when dogs with hypertension and left ventricular hypertrophy undergo coronary occlusion is interrupted with beta-blockade, possibly via electrophysiological effects rather than by changes in arterial pressure or infarct size.

The activity of human myocardial enzymes in sudden coronary death (SCD) was quantitatively histochemically examined. The activity of succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), beta-oxybutyrate dehydrogenase (beta-OBDH), alpha-glycerolphosphate dehydrogenase (alpha-GPDH), NAD-diaphorase (NAD-ase), and glucose-6-phosphate dehydrogenase (G-6-PDH) was measured on prompt autopsies (up to 3 hours of death onset). beta-OBDH and LDH showed an increase in activity in the myocardium from the subjects who had suddenly died from coronary heart disease without evident changes in the heart. In SCD in the presence of small cardiosclerosis, the activity of the enzymes characterizing the major processes of energy generation was also enhanced, which was caused by moderately severe myocardial hypertrophy. In the myocardium from the subjects who had died from coronary heart disease in the presence of large postinfarction cardiosclerosis, the activity of the enzymes was directly related to the degree of myocardial hypertrophy and the signs of chronic heart failure. As myocardial hypertrophy progressed, the enzymatic activity rose, but there were signs of chronic heart failure, it fell. The findings suggest that the changes in myocardial enzymatic activity in SCD are heterogeneous and associated with the type of prior abnormalities in the cardiovascular system.

Sudden death, defined as the death that occurs naturally, unexpectedly and instantaneously or within the first hour of the onset of premonitory symptoms, is one of the most important challenge of the modern cardiology. This is due to both, its elevated incidence (400,000 to 500,000 cases per year in United States alone) and its dramatic presentation (many of the victims are relatively young and have an acceptable quality of life). We have studied de Holter tapes of 233 patients who died suddenly and we can demonstrate that 80% of cases were due to ventricular tachyarrhythmias (ventricular fibrillation 60% and torsades de pointes 20%) and the rameinens 20% were due to bradyarrhythmias. It is well known that ischemic heart disease is the leading cause of sudden death, being responsible for more than 80% of cases. In the present article we will analyze the relationship between sudden death and the different types of ischemic heart disease: stable angina pectoris, unstable angina pectoris, acute myocardial infarction and postinfarction and silent myocardial ischemia.

An epidemiological study on coronary sudden death (CSD) had been carried out in defined areas of Beijing, covering a population of approximately 700,000, for a period of two years, 1984 to 1985. A total of 201 cases of CSD had been registered. The data showed: 1) half of the coronary death in the population were CSD and the rate of CSD increased with age; 2) the rate of CSD in males was higher than that in females; 3) most cases of CSD had a history of cardiovascular diseases; 4) 85% of CSD cases died within 6 hours after acute onset; 5) about half of the CSD cases had predominant symptoms with lower specificity. Some issues about the diagnostic criteria of CSD and cardiac-pulmonary resuscitation outside hospital in the communities of Beijing were discussed in detail.

To describe geographic variations in an indicator of sudden coronary death, data from the National Center for Health Statistics were examined for deaths occurring out of hospital or in emergency rooms in 1984 to 1986 in 42 states. In white males aged 55 to 64 years, the percent of ischemic heart disease deaths coded as occurring out of hospital or in the ER ranged from 49.6% to 70.4%. The percents tended to be higher in mountain states and around Lake Michigan. However, neighboring states sometimes had very different percents. Within regions, percents were higher in nonmetropolitan than in metropolitan areas. Standard mortality ratios for white males of all ages revealed that several states had relatively high rates of death out of hospital or in the ER. These included New York, Michigan, and Wisconsin. High rates of coronary death out of hospital or in the ER may be due to high overall coronary death rates, high percent of coronary deaths occurring out of hospital or in the ER, or both. Further studies are needed of geographic variation in sudden coronary death and cardiac arrest and factors that might explain the variation such as emergency medical services. Place of death data from death certificates may be useful in monitoring efforts to prevent sudden coronary death.

Sudden cardiac death is most often caused by ventricular dysrhythmias. Although women have an incidence of sudden death lower than that of men, 34% of coronary deaths in women are sudden deaths. The atherogenic risk factors do not predict which women are at the highest risk of sudden cardiac death. Left ventricular hypertrophy is a strong risk factor for sudden cardiac death in women. Asymptomatic ventricular dysrhythmias, a risk factor for death after myocardial infarction in men, do not increase the risk of death in women. This gender difference in the risk of sudden cardiac death deserves further attention, since it affects the evaluation of interventions designed to reduce the rate of sudden cardiac death.

To determine whether sudden versus non-sudden cardiac death could be predicted in high risk patients, 1157 medical patients were followed for an average of 46 months after a diagnostic coronary angiogram and 18 clinical, hemodynamic, and angiographic variables known to be associated with a high risk of mortality were analyzed. The total group of 141 deaths was classified into 3 subgroups: (1) 82 sudden deaths (less than 1 hour after onset of symptoms); (2) 46 deaths due to acute myocardial infarction with or without heart failure, and (3) 13 deaths unrelated to cardiac symptoms. In a subset of 64 patients, the duration of electrical systole (QTc) was calculated before angiography and before death. A comparison was made of QTc measurements at entry with QTc values of subjects with normal coronary arteries and normal left ventricular function. Deaths from cardiac causes could often be predicted from older age, male sex, history of myocardial infarction, unstable angina, congestive heart failure, abnormal cardiothoracic ratio, multivessel disease, abnormal left ventricular contraction, and abnormal ejection fraction. However, these variables did not discriminate between sudden and nonsudden cardiac deaths and both modes of death were characterized by depressed left ventricular function and multivessel coronary disease. During follow-up the incidence of acute myocardial infarction was not different in patients with cardiac and noncardiac deaths and in long-term survivors. However, patients dying from cardiac causes had a higher incidence of heart failure. Patients dying suddenly did not present new infarctions during follow-up whereas patients dying from acute myocardial infarction had a 13% incidence of prior infarction and a higher incidence of heart failure. In addition, QTc at entry was longer in nonsurvivors than in normal subjects (p less than 0.0001) and patients experiencing sudden death exhibited the highest incidence of QTc prolongation (greater than or equal to 440 ms) during follow-up (p less than 0.05). We conclude that: (1) although the severity of coronary disease and left ventricular dysfunction are closely related to cardiac mortality, they do not discriminate between sudden and nonsudden cardiac deaths; (2) patients experiencing sudden death are characterized by a low incidence of new myocardial infarction or congestive heart failure and prolongation of the QTc interval during follow-up.

The present case-control study examined if sudden cardiac death in women is preceded by death of a significant other, change in residence, or change in work. The sample included 81 Caucasian women ages 25-64 years in Allegheny County, Pennsylvania, who died suddenly from arteriosclerotic heart disease (ASHD) within a 11/2 year interval. Each case was matched to a neighborhood control on the basis of race, age, and sex. Results revealed that relative to matched controls, cases were six times as likely to have experienced the death of a significant other within the last months; they were no more likely to have experienced changes in living conditions or in work. These findings raise the issue of whether death of a significant other is an antecedent event of death due to ASHD only or death due to all causes. Possible explanations for the temporal association between sudden death and death of a significant other are discussed.

We performed coronary angiography within 95 minutes of the onset of symptoms in seven patients with an acute coronary event after an exercise stress test. The test was normal in six patients. Previous angiography in four patients revealed no evident or moderate obstructive coronary arterial disease. After the test, unstable angina developed in two patients, acute myocardial infarction in four and ventricular fibrillation in one, who was successfully resuscitated. At acute angiography the coronary artery involved was occluded in four and sub-totally obstructed in three. In three cases, coronary occlusion was due to thrombosis, vasospasm, or both. In six vessels there was an eccentric lesion, which is consistent with a ruptured plaque. These findings show that physical exercise can unexpectedly provoke an acute coronary event with sub-total or total occlusion of a previous angiographically normal or moderately obstructed coronary artery. The mechanism is probably related to exercise-induced plaque rupture which can produce coronary (sub)occlusion by coronary thrombosis, spasm, or both.

A prospective study was made of the morbidity and mortality from ischemic heart disease in 390 patients with focal TIA caused by atherosclerotic vascular disease. The 5-year cumulative rate of myocardial infarction or sudden death in these patients was 21.0%, a rate only slightly less than that of fatal or nonfatal cerebral infarction (22.7%). Risk factors including diabetes, angina, and ECG abnormalities were associated with an increase in morbidity and mortality from ischemic heart disease. A major factor associated with these cardiac events was the presence of atherosclerotic obstructive or ulcerative lesions in the carotid arteries. These observations indicate that focal TIA caused by carotid atherosclerosis is a predictor not only of cerebral infarction, but also of serious cardiac disease and death.

A representative sample of all sudden cardiac deaths occurring in Auckland in one year is reported. Data describing demographic variables, personal characteristics and habits, previous symptoms, prodromal symptoms, the acute phase and post mortem results, is presented. Incidence values are very close to those of other similar communities. The syndrome of "sudden death" probably defines a heterogenous group of cases. Deaths were significantly more common in the cooler months, and in the lowest social class. Some evidence is presented consistent with the hypothesis that a high alcohol intake is associated with sudden death. No differences were found between cases dying within five minutes and those dying later but within 24 hours, considering several variables. Myocardial fibrosis at post mortem was a common finding. The role of the coronary ambulance is briefly discussed.