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Journal ArticleDOI

Sudden cardiac death: the major challenge confronting contemporary cardiology.

Bernard Lown
- 01 Feb 1979 - 
- Vol. 43, Iss: 2, pp 313-328
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TLDR
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.

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Citations
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Journal ArticleDOI

Cardiovascular neural regulation explored in the frequency domain.

TL;DR: It is the opinion that rhythms and neural components always interact, just like flexor and extensor tones or excitatory and inhibitory cardiovascular reflexes, and that it is misleading to separately consider vagal and sympathetic modulations of heart rate.
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Sudden Cardiac Death in the United States, 1989 to 1998

TL;DR: Death rates for SCD increased with age and were higher in men than women, although there was no difference at age ≥85 years, and the increase in death rates forSCD among younger women warrants additional investigation.
Journal ArticleDOI

Circadian variation in the frequency of sudden cardiac death.

TL;DR: The finding that the frequency of sudden cardiac death is increased in the morning is compatible with hypotheses that sudden cardiacDeath results from ischemia or from a primary arrhythmic event, and further study of the physiologic changes occurring in theMorning may provide new information supporting or refuting these hypotheses.
Journal ArticleDOI

Heart Rate Variability: Measurement and Clinical Utility

TL;DR: Electrocardiographic RR intervals fluctuate cyclically, modulated by ventilation, baroreflexes, and other genetic and environmental factors that are mediated through the autonomic nervous system, and are useful for assessing risk of cardiovascular death or arrhythmic events, especially when combined with other tests.
Journal Article

Autonomic nervous system and sudden cardiac death. Experimental basis and clinical observations for post-myocardial infarction risk stratification.

TL;DR: A definitive answer on the role that the analysis of markers of cardiac vagal activity may play in risk stratification of patients with coronary artery disease should be provided by Autonomic Tone and Reflexes After Myocardial Infarction (ATRAMI), an ongoing prospective study.
References
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Journal ArticleDOI

Approaches to Sudden Death from Coronary Heart Disease

TL;DR: Since it is likely that SCD is due to an arrhythmia, drug prophylaxis might prove effective and it is mandatory to preselect a population at highest risk before embarking on a drug trial.
Book

Electrophysiology of the heart

TL;DR: This has been a popular book, which covers the field of symptomatology in a remarkably complete way, in 32 short chapters, and the style is informal, almost chatty, but engaging.
Journal ArticleDOI

Neural activity and ventricular fibrillation.

TL;DR: In this country, ventricular fibrillation is the likely mechanism for sudden death and the leading cause of fatality among patients with coronary heart disease.
Journal ArticleDOI

Ventricular Premature Beats and Mortality after Myocardial Infarction

TL;DR: Analyses of survival taking into account other important prognostic variables establish that the presence of complex premature beats in the monitoring hour is associated with a risk of sudden coronary death three times that of the men free of complex ventricular premature beats.
Journal ArticleDOI

Functional distribution of right and left stellate innervation to the ventricles

TL;DR: The electrocardiographic form changes observed following unilateral alteration of sympathetic tone paralleled those electrocardsiographic abnormalities seen in patients with lesions of the central nervous system, suggesting a possible functional explanation for these clinical findings.
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