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 language | English |
|---|---|
| Journal | Circulation |
| Volume | 85 |
| Issue number | 1 SUPPL. |
| State | Published - Jan 1 1992 |
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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 journal › Article
}
TY - JOUR
T1 - Sudden cardiac death
T2 - Structure, function, and time-dependence of risk
AU - Myerburg, Robert J
AU - Kessler, Kenneth M.
AU - Castellanos, Agustin
PY - 1992/1/1
Y1 - 1992/1/1
N2 - 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).
AB - 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).
KW - Arrhythmias
KW - Left ventricular hypertrophy
KW - Sudden cardiac death
UR - http://www.scopus.com/inward/record.url?scp=0026565763&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026565763&partnerID=8YFLogxK
M3 - Article
C2 - 1728501
AN - SCOPUS:0026565763
VL - 85
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 1 SUPPL.
ER -