In some clinical situations, an abnormal Q wave may represent intense but reversible ischemia, but the point at which irreversible myocardial damage occurs is seldom known in the acute phase. Unfortunately, the correct diagnosis is presently too cumbersome and takes far too long by means of serial ECGs and enzyme determinations. This delay may preclude rapid therapeutic interventions such as angioplasty, thrombolysis, and emergency coronary bypass surgery to provide myocardial salvage. The remarkable progress in the treatment of unstable coronary artery disease has created the need for more reliable markers of cell death so as to exclude patients from aggressive therapy or to terminate aggressive therapy to salvage what is considered ischemic myocardium. Transient Q waves are being reported far more frequently and have assumed far greater clinical importance because of the current aggressive therapy of MI (and ischemia) with thrombolytic agents, angioplasty, and coronary bypass surgery. A Q-wave deflection associated with ST-segment elevation or depression does not invariably indicate MI. The pronouncement of myocardial death has become more complicated than in the past because Q waves are not pathognomonic of myocardial necrosis. Transient ischemic electrical silence with Q waves in the absence of MI is a rare phenomenon and affects the anterior leads much more commonly than the inferior leads. Such Q waves may appear acutely or may be present chronically with the potential of disappearing when coronary perfusion is restored. A transient intraventricular conduction disorder induced by ischemia should always be ruled out before making the diagnosis of a transient ischemic Q wave or electrical silence. Some workers believe that all transient Q waves represent an unstable intraventricular conduction disorder, but recent developments suggest that most transient Q waves in coronary artery disease are engendered by ischemia. Edema and inflammation may play a part in rendering the myocardium electrically inert, and their disappearance may explain the loss of Q waves. The presence of a small MI should not detract from the importance of associated transient Q waves due to potentially salvageable, severely ischemic myocardium, that is, the zone of so-called concussion around the area of necrosis. In evolving Q-wave MI, a new Q wave may reverse acutely if coronary perfusion is restored very early. Disappearance of Q waves several days after MI suggests return of myocardial viability and does not represent a factitious electrical change. Electrical stunning may be associated with myocardial stunning.(ABSTRACT TRUNCATED AT 400 WORDS)