Medical Treatment of Stable Angina

Therapy is directed at reducing heart rate, blood pressure, and contractile responses to exercise and stress, so that myocardial oxygen demand for any given activity is reduced. Medication and interventions that increase coronary blood flow and oxygen delivery may also be useful. The heart rate-systolic blood pressure product provides an estimate of myocardial oxygen demand. Stable angina can usually be relieved promptly by rest and nitroglycerin. Exogenously administered nitrates increase oxygen delivery to the subendocardial region supplied by a severely narrowed coronary artery. One should not use nitrates and erectile dysfunction medications (sildenafil, vardenafil, or tadalafil) within 24 hours of one another as the combination may cause profound hypotension. β-adrenergic antagonists attenuate heart rate, systolic blood pressure, and contractile responses at rest and during exercise. Selected beta-blockers reduce mortality and repeated hospitalization risks in patients with prior myocardial infarctions, heart failure, and hypertension. Beta-blockers may cause bradycardia, bronchospasm, hypotension, atrioventricular (AV) block, and depression of myocardial contractility. They may also exacerbate coronary artery spasm and make it more frequent and severe. Slow calcium channel antagonists relax vascular smooth muscle and increase coronary blood flow. They are divided into two major classes: dihydropyridines (nifedipine and amlodipine) and the nondihydropyridines (diltiazem and verapamil). The nondihydropyridine calcium antagonists decrease AV conduction and sinus node impulse formation while increasing coronary blood flow. The dihydropyridine calcium antagonists do not decrease AV conduction and sinus impulse formation but do increase coronary blood flow. The nondihydropyridines have significant negative inotropic effects and should not be given to patients with clinically significant congestive heart failure (CHF). Angiotensin-converting enzyme (ACE) inhibitors may improve endothelial function in patients with stable coronary heart disease. The risk of myocardial infarction in patients with coronary heart disease is reduced with aspirin. Meta-analysis in various clinical studies have suggested 75 to 150 mg of aspirin daily in patients at high risk for myocardial infarction. Clopidogrel in combination with aspirin may be bene- ficial in those patients with established coronary disease. To date, oral IIb/IIIa platelet antagonists have not been protective, and some studies show possible harm. Chronic oral anticoagulation therapy after myocardial infarction reduces the combined end points of mortality and nonfatal reinfarction while increasing bleeding risks. Patients with known or suspected coronary heart disease should avoid smoking, rigorously control their serum cholesterol with the lowest low-density lipoprotein (LDL) possible, reduce their triglycerides, control their blood pressure and hyperglycemia, and get regular exercise. Evidence suggests that estrogen and progestin do not prevent clinically significant coronary heart disease. The cyclooxygenase (COX-2) inhibitors that increase blood pressure appear to slightly increase the risk of future vascular events (i.e., valdecoxib). Other COX-2 inhibitors used in low dose, such as celecoxib probably do not signifi cantly increase the risk of future vascular events.