Hemodynamic and electrocardiographic correlates of symptomatic and silent myocardial ischemia: pathophysiologic and therapeutic implications.

Numerous hemodynamic, electrocardiographic, metabolic and radionuclide measurements in various subsets of patients with coronary artery disease (CAD) reveal that ischemia does not always occur on the basis of increases in myocardial oxygen consumption. Continuous hemodynamic monitoring indicates that most episodes of myocardial ischemia are not preceded by increases in such major determinants of oxygen consumption as heart rate or blood pressure, but that these usually increase in response to the development of ischemia. The development of pain during ischemia is a late feature and most episodes are silent. There are no significant differences in the hemodynamic characteristics of symptomatic versus asymptomatic episodes of myocardial ischemia in patients with angina at rest or between those associated with ST-segment depression and those with ST-segment elevation. Continuous Holter recordings analyzed by compact analog technique in hospitalized and ambulatory patients with ischemic heart disease indicate that in both unstable and chronic stable angina, over two-thirds of myocardial ischemic episodes are clinically silent. Symptomatic and silent episodes do not differ significantly with respect to duration. Most symptomatic and asymptomatic episodes are not triggered by increases in the determinants of oxygen demand. Such episodes may arise on the basis of a critical reduction in the lumen of the diseased coronary artery leading to a primary reduction in blood flow. Intermittent obstruction due to changes in coronary vasomobility or possibly formation of thrombi may be a common mechanism for the pathogenesis of myocardial ischemia in patients with a varying spectrum of coronary artery lesions. At present, the precise clinical and prognostic significance of silent ischemia in CAD is not completely defined.(ABSTRACT TRUNCATED AT 250 WORDS)