title: Changing concepts in the pathophysiology of myocardial ischemia.
abstract: The principal common pathway for myocardial ischemia is an oxygen supply-demand imbalance; more recently, greater emphasis has been placed on limitations of myocardial blood supply, as well as excessive myocardial oxygen demand. Myocardial ischemia is a metabolic event resulting from inadequate oxygen delivery to local tissues. The physiologic effects of ischemia are observed through abnormalities in left ventricular function, electrocardiographic changes, and often, by angina pectoris. Prognostic and therapeutic outcomes are significantly related to the pathophysiology of the underlying coronary lesion. Because myocardial ischemia often occurs without symptoms, clinical distinctions based on angina stability may more appropriately be represented by stable or unstable ischemic syndromes that incorporate silent ischemia. Stable ischemic syndromes occur secondary to coronary plaques, whereas unstable syndromes are the result of active lesions caused by plaque rupture with local thrombus and vasoreactivity that produce intermittent critical decreases in coronary supply. The prognosis of patients with stable ischemia is related to the extent of myocardium at jeopardy and overall left ventricular function. In contrast, unstable syndromes are associated with a worse short-term prognosis, which may be predictable by the presence of silent ischemia or left ventricular dysfunction or both. Therapeutic decisions based on an improved pathophysiologic understanding of ischemic mechanisms as well as the physiologic impact of therapy on cardiac function can enhance efficacy while avoiding adverse effects. Calcium channel blockers appear to afford certain advantages in the treatment of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Medical College of Virginia, Richmond 23298.
authors.forename: G W
authors.initials: GW
authors.lastname: Vetrovec
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans