title: Silent myocardial ischemia. Mechanisms and rationale for therapy.
abstract: The widespread use of Holter monitoring has demonstrated that the majority of ischemic episodes occur during activities that do not require exertion. These episodes tend to occur at only minimal increases in heart rate above resting levels, well below the level of myocardial oxygen demand required to produce ischemia on formal exercise tolerance testing. In all likelihood, therefore, most ischemic events in ambulatory patients are due to a combination of flow-limiting coronary stenosis and superimposed vasoactive or thrombotic elements. Asymptomatic ischemic events are common in subsets of patients with angina pectoris. Traditionally, treatment with calcium channel blockers, beta-blockers, and long-acting nitrates has been aimed at reducing episodes of angina pectoris. Despite a reduction in anginal symptoms, however, it is likely that patients continue to experience silent ischemia, particularly at rest and during activities of daily living. The strategy for treatment in such patients should include the abolition of the patients' "total ischemic activity." It is conceivable that more aggressive anti-ischemic therapy may improve prognosis, as patients with ambulatory ST-segment depression experience frequent cardiac events. Other potential benefits of more aggressive treatment include the prevention of myocardial hibernation, which occurs as a result of a chronic ischemic state, and a reduction in episodes of myocardial stunning. This approach may lead to protection against transient and chronic left ventricular dysfunction, which is associated with a poor prognosis in patients with symptomatic coronary artery disease.
authors.affiliation: Department of Medicine, Cardiology Section, Harvard Medical School, Boston, Massachusetts.
authors.forename: G J
authors.initials: GJ
authors.lastname: Kowalchuk
authors.forename: R W
authors.initials: RW
authors.lastname: Nesto
mesh_terms: D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology; D002637:Chest Pain; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology; D006801:Humans; D009543:Nifedipine / Q000627:therapeutic use; D011379:Prognosis; D011433:Propranolol / Q000627:therapeutic use
chemical_list: D011433:Propranolol; D009543:Nifedipine