Abstract

Clinical expressions of myocardial ischemia are protean and include angina and symptoms related to ventricular systolic and diastolic dysfunction and arrhythmia. The consequences of ischemia are also variable and range from no immediate adverse effects to sudden death, myocardial infarction and severe impairment of cardiac performance and heart failure. However, myocardial ischemia can occur without any clinical manifestations and can be clinically totally silent. There is a multitude of evidence for the existence of “silent” myocardial ischemia (1). Reversible left ventricular regional wall motion abnormalities, either stress-induced or spontaneous, in the absence of angina, provide evidence for silent myocardial ischemia. Global and regional myocardial lactate production, a metabolic marker of ischemia, has been documented in the absence of angina. Reversible myocardial thallium perfusion defects at rest or during dipyridamole or exercise stress occur rather frequently without associated angina. On the basis of wall motion abnormalities, metabolic dysfunction, reversible scintigraphic perfusion defects and ischemic changes on the stress electrocardiogram (ECG), the incidence rate of silent myocardial ischemia has been estimated to be approximately 34% in patients with coronary artery disease (2). However, recently popularized ambulatory electrocardiography in studies to detect ischemia have revealed a much higher incidence of silent ischemia (3). It has been documented that ST segment shifts, both depression and elevation. on the ambulatory ECG correlate well with other markers of myocardial ischemia (4). Electrocardiographic monitoring has revealed that in patients with stable exertional angina resulting from obstructive coronary artery disease, approximately 70% of episodes of ischemia are asymptomatic. In postinfarction patients and in patients with

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