[Sudden cardiac death: its definition and mechanisms].

Sudden cardiac death (SD) is reviewed concerning its definition and mechanisms. About the syndrome definition, one concludes that the most suitable way to discriminate arrhythmic death, is to consider both the time since the beginning of the symptoms and the clinical condition before circulatory arrest. During several years the "arrhythmic hypothesis" prevailed to explain SD mechanism. It postulates that, by a fortuitous association, a ventricular ectopic beat activated a re-entry circuit, unchaining the lethal tachycardia. From that hypothesis, a lot of antiarrhythmic clinical trials were conducted in myocardial infarction survivors, recepting that the ventricular ectopic beats suppression would reduce the probability of lethal arrhythmias. Nevertheless no trial confirmed that hypothesis and CAST showed an increase in mortality in patients treated with antiarrhythmic drugs able to suppress ventricular premature beats. From that observation resulted a reinforcement of the "ischemic hypothesis", supported by several arguments. Today we believe that both factors (ischemic and arrhythmic) are important in SD. It was proposed a SD description as a disfunction of a biological system resulting from the interaction between a "pathological structure" and "functional events". The electrogenic component remains central in that model, but is integrated into a structure/function scheme. Under most conditions, the system requires both abnormal structural components (usually chronic) and functional factors (often transient). The structural pathology is most related to old myocardial infarction scars, and the functional factors are ischemia/reperfusion, metabolic alterations (electrolyte imbalance, hypoxemia, acidosis), hemodynamic failure, neurophysiological fluctuations and toxic effects (like proarrhythmia).(ABSTRACT TRUNCATED AT 250 WORDS)