Beta blockers reduce myocardial oxygen consumption by reducing heart rate, myocardial contractility, and afterload, with attenuation of cardiovascular remodeling by decreasing LV wall tension with long-term use. The reduction in myo- cardial oxygen demand is directly proportional to the level of adrenergic tonic stimulation. Furthermore, the reduction in heart rate also shifts the cardiac cycle, permitting more diastolic time and greater coronary perfusion, thereby im- proving myocardial oxygen supply. Long-term beta-blocker treatment is well tolerated, has proven benefit in SIHD by reducing ischemic burden and threshold, and improves survival in patients with LV dys- function or history of MI.757,765,766 When prescribed in com- bination with agents that block the renin-angiotensin-aldoste- rone system, beta blockers are the preferred agents for the treatment of angina in patients with LV dysfunction after MI and in patients with heart failure, on the basis of documented improvements in survival and ventricular A meta-analysis of comparison trials between beta block- ers and calcium channel blockers (dihydropyridine and non- dihydropyridine agents) showed negligible differences in the rate of death or MI over relatively brief durations of admin- istration (ie, 6 wk to 6 mo), although patients with heart failure, heart block, or significant pulmonary disease were excluded from the meta-analysis.420 Beta blockers were found to exhibit an advantage with regard to control of angina and withdrawals from therapy due to adverse events, a problem that was most pronounced with nifedipine.420 Calcium chan- nel blockers, however, have not been shown to improve survival after MI, as beta blockers have, but have been shown to offer protection against severe angina and to reduce the risk of reinfarction after MI.849 851 Adherence to beta-blocker therapy can be influenced by the occurrence of adverse effects such as fatigue, lethargy, sexual dysfunction, or sleep disturbances. 