Sudden death from coronary heart disease. Survival time, frequency of thrombi, and cigarette smoking.
TL;DR: The concept that recent coronary thrombi, when found in these acute events, do not usually trigger the onset of the attack but develop as a secondary phenomenon during the course of the acute event is tended to support.
About: This article is published in Chest.The article was published on 1970-08-01. It has received 127 citations till now. The article focuses on the topics: Sudden death & Population.
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TL;DR: The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present, and these findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.
Abstract: 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.
1,683 citations
TL;DR: Coronary arterial spasm was demonstrated in six of fifteen acute myocardial infarctions associated with coronary artery disease and a dynamic interaction between spasm, platelet aggregates and the atherosclerotic plaque may precede coronary thrombosis.
Abstract: Coronary arteriography was performed before and after the intracoronary injection of nitroglycerin to determine the presence or absence of spasm in patients within the first 12 hours of acute myocardial infarction. Coronary arterial spasm was demonstrated in six of fifteen (40%) acute myocardial infarctions associated with coronary artery disease. In five of the six instances the interval from the onset of symptoms to arteriography was less than 6 hours. Spasm was superimposed on a high-grade atherosclerotic obstruction and was separated from the catheter tip by a segment of normal vessel in each instance. The coronary artery remained patent (following the initial relief of spasm) in two patients maintained on sublingual nitrates and heparin. Spasm, superimposed on an atherosclerotic obstruction, may be the primary event or a secondary occurrence in the pathophysiology of acute myocardial infarction. Catecholamines could play an important role in the early pathophysiology of acute myocardial infarction by producing spasm and/or platelet aggregation at the site of an atherosclerotic obstruction. A dynamic interaction between spasm, platelet aggregates and the atherosclerotic plaque may precede coronary thrombosis.
554 citations
TL;DR: It has become clear that sudden death is not the inexorable culmination of advanced coronary atherosclerosis but instead is the result of ventricular fibrillation and therefore is readily reversible.
Abstract: In the industrially developed countries, sudden cardiac death is the leading cause of death. It was recognized at the dawn of recorded history and even depicted in Egyptian relief sculpture from the tomb of a noble of the Sixth dynasty approximately 4,500 years ago. Sudden cardiac death has left no age untouched. Sparing neither saint nor sinner, it has burdened man with a sense of uncertainty and fragility. The enormity of this problem demands attention. In the United States, sudden cardiac death claims about 1,200 lives daily, or approximately one victim every minute. It is the leading cause of death among men aged 20 to 64 years, accounting for 32 percent of the fatalities in this group. Nearly 25 percent of persons dying suddenly have had no prior recognized symptoms of heart disease.The excess of widows observed in retirement communities is accounted for by the three- to fourfold greater incidence of sudden cardiac death among men. Sudden death in old age might be a blessing rather than a scourge, but instead it frequently explodes a man's life at its prime, at a median age of only 59 years. The medical profession has sensed the issue but has largely ignored sudden death as a problem amenable to solution. This indifference has not been the result of a lack of interest or concern but a reflection of the belief that sudden cardiac death was the inevitable culmination of coronary atherosclerosis. Because sudden death was unpredictable and afflicted the apparently healthy subject outside the hospital, the physician considered it an act of fate before which he was largely helpless. The advent of the coronary care unit has promoted a reassessment of this complex problem. It has become clear that sudden death is not the inexorable culmination of advanced coronary atherosclerosis but instead is the result of ventricular fibrillation and therefore is readily reversible. 7,8 If ventricular fibrillation were only the consequence of severe coronary atherosclerosis, once reversed it would promptly recur. However, patients treated for ventricular fibrillation seldom have recurring episodes, and they usually recover and survive for long periods. 9,10 The new concept that ventricular fibrillation is an electrical accident suggests that its cause is not anatomic and thereby contributes to the growing interest in redefining the basis for sudden death and developing methods for its containment. Until recently our inability to deal with sudden cardiac death has not been due to a gap in the application of knowledge but to a gap in knowledge itself. The purpose of this review is to indicate how much we know and to sketch the path of possible further progress.
447 citations
TL;DR: Acute changes in coronary plaque morphology (thrombus, plaque disruption, or both) were found in 57% of cases of sudden coronary death and Hearts without acute or healed myocardial infarction and without active lesions were similar to hearts with active lesions with respect to heart weight and severity of epicardial coronary disease.
Abstract: Background The reported frequency of active coronary lesions (plaque rupture and coronary thrombosis) in sudden death due to coronary artery atherosclerosis (sudden coronary death) has varied from 80% of cases in previous series. In hearts lacking an active coronary lesion, sudden death has usually been attributed to a healed myocardial infarction. The purpose of the present study was to determine the frequency of active and inactive coronary lesions and myocardial infarction in individuals with sudden coronary death. Methods and Results The hearts of persons who died as a result of sudden coronary death underwent perfusion-fixation and postmortem angiography. An active coronary lesion was defined as a disrupted plaque, luminal fibrin/platelet thrombus, or both. We defined an inactive lesion as having a cross-sectional luminal stenosis of ≥75% with neither plaque disruption nor luminal thrombus. Ninety hearts were examined (from 72 men and 18 women; mean age at the time of death, 51±10 years). Ac...
403 citations
TL;DR: The infrequency of coronary thrombi in patients who died of acute cardiovascular collapse without myocardial necrosis, in those in whom necrosis was limited to the subendocardium, and their occurrence at, or proximal to, sites already severely narrowed by old atherosclerotic plaques suggest that coronaryThrombi are consequences rather than causes of acute myocardIAL infarction.
386 citations
References
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TL;DR: It has been shown perhaps for the first time that the correction of cardiac arrest outside hospital is a practicable proposition and no death has occurred in transit in a fifteen-month period.
593 citations
TL;DR: It was found that in men who report habitual consumption of 20 or more cigarettes per day the risk of myocardial infarction was about three times greater than in nonsmokers, former cigarette smokers, or pipe and cigar smokers.
Abstract: The relationship of smoking habit to total mortality and to the incidence of new manifestations of coronary heart disease (CHD) has been examined in 2,282 middle-aged men under medical surveillance for ten years in Framingham, Mass, and 1,838 middle-aged men followed for eight years in Albany, NY. It was found that in men who report habitual consumption of 20 or more cigarettes per day the risk of myocardial infarction was about three times greater than in nonsmokers, former cigarette smokers, or pipe and cigar smokers. No relationship was shown between smoking habit and angina pectoris when this symptom was the sole manifestation of CHD. The association between heavy cigarette smoking and increased morbidity and mortality from CHD was unexplained, although it appeared to be relatively immediate. It is inferred that stopping cigarette smoking lessens the risk of CHD.
234 citations
TL;DR: Under the support of a feasibility study grant from the Regional Medical Program, St. Vincent’s Hospital and Medical Center of New York undertook a mobile coronary care unit project, indicating that such a project is feasible and considerable good can be done.
78 citations
Journal Article•
38 citations
TL;DR: In this study of 3,000 males the statistical association of coronary artherosclerotic heart disease (CAHD) and smoking habits was most striking under the age of 51, and heavy cigarette smoking was suggested not so much as a factor in atherogenesis, but as afactor in precipitating acute clinical events in individuals with advanced CAHD.
Abstract: In this study of 3,000 males the statistical association of coronary artherosclerotic heart disease (CAHD) and smoking habits was most striking under the age of 51. In this group 21 (11.7%) of 179 heavy cigarette smokers had CAHD, whereas 100 (6.5%) of 1,521 other individuals had CAHD. The ratio of myocardial infarcts to isolated angina pectoris was 1.3:1 in heavy smokers, and 0.5:1 in other categories. Heavy cigarette smoking was also associated with higher serum cholesterol levels. It was suggested not so much as a factor in atherogenesis, but as a factor in precipitating acute clinical events in individuals with advanced CAHD. Cigar, pipe, and light cigarette smoking did not appear to be related to the problem.
31 citations