Sudden cardiac death: Structure, function, and time-dependence of risk

Robert J Myerburg, Kenneth M. Kessler, Agustin Castellanos

Research output: Contribution to journalArticle

452 Citations (Scopus)

Abstract

Sudden cardiac death (SCD) remains a major unresolved clinical and public health problem, accounting for more than 300,000 of the deaths in the United States annually. The ability to identify potential SCD victims is limited by the large size of the population subgroups that contain the majority of SCD victims and by the apparent time dependence of risk of sudden death The latter refers to the tendency for SCD to follow other cardiovascular events within a high-risk period of 6-18 months after a primary cardiovascular event, with risk decreasing thereafter. The combination of time dependence and denominator pool size provides a basis for future studies to identify the higher risk individuals. Pathophysiologically, SCD can be viewed as an interaction between structural abnormalities of the heart, transient functional disturbances, and the specific electrophysiological events responsible for fatal arrhythmias. Structural abnormalities provide the anatomic substrate for chronic risk and include the myocardial consequences of coronary artery disease, left ventricular hypertrophy, myopathic ventricles and specific electrophysiological anatomic abnormalities such as bypass tracts. The functional factors responsible for destabilizing a chronic electrophysiological abnormality include transient ischemia and reperfusion, systemic factors (e.g., electrolyte disturbances, acidosis, and hemodynamic dysfunction), autonomic fluctuations (both systemic and at a tissue level), and myocardial toxic influences such as proarrhythmic effects of various drugs. Each of these changes is able to destabilize myocardial membrane integrity, some regionally and some globally, making the heart susceptible to an electrical triggering event for ventricular tachycardia or fibrillation. Restated in terms of a biological model, functional modulations condition and activate a common electrogenic pathway, permitting otherwise innocuous electrical events (e.g., chronic premature ventricular contractions) to initiate fatal arrhythmias (ventricular tachycardia and fibrillation).

Original languageEnglish
JournalCirculation
Volume85
Issue number1 SUPPL.
StatePublished - Jan 1 1992

Fingerprint

Sudden Cardiac Death
Ventricular Fibrillation
Ventricular Tachycardia
Cardiac Arrhythmias
Biological Models
Ventricular Premature Complexes
Congenital Heart Defects
Poisons
Left Ventricular Hypertrophy
Sudden Death
Population Density
Acidosis
Electrolytes
Reperfusion
Coronary Artery Disease
Ischemia
Public Health
Hemodynamics
Membranes
Pharmaceutical Preparations

Keywords

  • Arrhythmias
  • Left ventricular hypertrophy
  • Sudden cardiac death

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Sudden cardiac death : Structure, function, and time-dependence of risk. / Myerburg, Robert J; Kessler, Kenneth M.; Castellanos, Agustin.

In: Circulation, Vol. 85, No. 1 SUPPL., 01.01.1992.

Research output: Contribution to journalArticle

Myerburg, RJ, Kessler, KM & Castellanos, A 1992, 'Sudden cardiac death: Structure, function, and time-dependence of risk', Circulation, vol. 85, no. 1 SUPPL..
Myerburg, Robert J ; Kessler, Kenneth M. ; Castellanos, Agustin. / Sudden cardiac death : Structure, function, and time-dependence of risk. In: Circulation. 1992 ; Vol. 85, No. 1 SUPPL.
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