Viable Myocardium — the Place of Calcium Antagonists

Abstract

The pathogenetic mechanism of myocardial hibernation has not been fully established. Wall motion abnormalities, occurring early after an acute myocardial infarction, may be reversible or permanent [1]. Thrombolytic therapy increases the probability of early reperfusion and may increase the probability of reversible dysfunction [2]. The infarcted segments may show resting hypoperfusion, despite a preserved viability, and functional recovery once perfusion is restored by bypass grafting or coronary angioplasty [3]. Because enhanced left ventricular function after revascularization is associated with improved survival [4], diagnostic procedures that identify reversible dyssynergy may provide significant prognostic information [5]. Recent studies have shown that the presence of both viable and ischemic myocardium detected by positron emission tomography (PET) is associated with increased incidence of cardiac events at follow-up. PET provides improved imaging capabilities compared with single photon emission computed tomography (SPECT) by correcting for photon attenuation and permitting the noninvasive measurement of regional myocardial blood flow in absolute terms or myocardial substrate utilization. Viable myocardium is identified on the basis of enhanced or preserved metabolic activity in underperfused and dysfunctional myocardial regions [6].