STABLE, UNSTABLE, AND ASYMPTOMATIC MYOCARDIAL-ISCHEMIA

Basic and applied investigation of stable and unstable myocardial ischemia continues to provide a physiological basis for treatment and a better understanding of clinical phenomena. The distinction between the more severe forms of unstable angina and myocardial infarction is blurred by new markers of myocardial damage such as troponin-T, the presence of which is associated with a worsened prognosis. Vascular segments with altered endothelial function constrict abnormally to catecholamines, blurring the distinction between demand-related and supply-related ischemia. Endothelin levels, markers of platelet activation, and clotting factors are elevated in unstable angina. Hence, the conversion from stable to unstable coronary disease involves a dynamic interaction between the vessel wall and blood elements. Endothelial function is depressed in patients with hypercholesterolemia, a finding that links traditional risk factors and disease instability. Endothelin production may be stimulated by oxidized low-density lipoprotein. High serum ferritin increases the risk of myocardial infarction in men with elevated low-density lipoprotein, suggesting a link between naturally occurring oxidizing agents, lipids, and acute occlusion. While angioscopic studies showed clots in arteries associated with unstable angina, thrombolytic therapy is ineffective. Studies of ''silent'' ischemia related prognosis to ischemia severity, whereas angina is more closely associated with a patient's sensitivity to symptoms. The question of whether silent ischemia warrants treatment remains unanswered.