CLINICAL PERSPECTIVE ON CELIPROLOL - CARDIOPROTECTIVE POTENTIAL

beta-Adrenergic blockers have had widespread use in the treatment of cardiovascular disease. Some agents of this class have been shown to reduce the incidence of total mortality, cardiovascular mortality, sudden death, and nonfatal reinfarction in survivors of acute myocardial infarction. The mechanism for this cardioprotective action is not known. Antiarrhythmic action and hemodynamic alterations have been suggested as possible mechanisms. An anticoagulant mechanism is another possibility, although the antiplatelet effects of beta-blockers are weak. It is now believed that antithrombotic effects may be related to the prevention of coronary artery plaque rupture and the subsequent propagation of an occlusive arterial thrombus rather than a direct anticoagulant action. The therapeutic ability beta-blockers to attenuate the hemodynamic consequences of catecholamine surgers, as they do in aortic dissection, may protect a vulnerable plaque from fracture, reducing the risk of coronary thrombosis, myocardial infarction, and death. Celiprolol, a third-generation beta-1-selective adrenergic blocker with partial beta-2-agonist activity, is comparable to other beta-blockers in antihypertensive and antianginal activity. It has additional actions that may be beneficial to patients: (1) it does not adversely affect lipids and lipoproteins; (2) it does not appear to depress the myocardium in patients with left ventricular dysfunction; (3) it can lower serum fibrinogen levels; and (4) it can cause regression of myocardial mass in patients with left ventricular hypertrophy.