These effects reduce angina by improving coronary blood flow. 14 They act as vasodilators by entering vascular smooth muscle, where they are metabolized to nitric oxide, which relaxes vascular smooth muscle, including in coronary arteries. Nitrates ( Table 62-14) continue to be widely prescribed for antianginal treatment and are effective when they are administered sublingually, orally, or topically. When calcium-channel blockers are used alone, diltiazem is often preferred because dihydropyridine calcium-channel blockers can increase the heart rate. When calcium-channel blockers are used with β-blockers, care must be taken not to cause symptomatic bradycardia with verapamil and diltiazem. Because calcium-channel blockers have not been shown to reduce death or MI in patients with stable or previously unstable ischemic heart disease, these agents are usually used in patients who cannot tolerate β-blockers or who require additional pharmacotherapy to control their symptoms. In randomized clinical trials, calcium-channel blockers and β-blockers are generally equally effective in relieving angina, improving time to onset of angina, and improving time to ischemic ST depression during exercise. Conversely, dihydropyridine calcium-channel antagonists, such as amlodipine, have greater effect on vascular smooth muscle, are better peripheral and coronary vasodilators, and hence may have advantages for use in the hypertensive patient with angina. Non-dihydropyridine calcium-channel blockers, such as verapamil and diltiazem, also reduce heart rate. This favorable reduction in myocardial oxygen demand, coupled with an increase in myocardial oxygen supply, results in a reduction in angina and ischemia. Calcium-channel blockers also reduce coronary vascular resistance and inhibit coronary vasospasm by preventing coronary arterial smooth muscle contraction. The β-blocker dose should be titrated to a target resting heart rate of 50 to 60 beats per minute as tolerated by the patient.Ĭalcium-channel blockers ( Table 62-13) reduce afterload by their peripheral vasodilatory effects and thus lower myocardial workload and myocardial oxygen demand. All β-blockers appear to be equally effective in patients with chronic stable angina ( Table 62-12).
β-Blockers also reduce the rate of secondary cardiac events and sudden cardiac death in post-MI patients, but to date there have been no placebo-controlled outcome trials in angina patients. β-Blockers raise the ischemic threshold and delay or prevent the onset of angina with exercise. 12, 13 β-Blockers, which prevent the binding of catecholamines to the β-adrenergic receptor, lower heart rate and myocardial contractility, thereby reducing myocardial workload, myocardial oxygen demand, and ischemia and anginal symptoms. The goal of antianginal therapy is to reduce symptoms of cardiac ischemia and to improve quality of life.
Lee Goldman MD, in Goldman-Cecil Medicine, 2020 Therapeutic Agents to Reduce Angina and Ischemia The combination of organic nitrates and calcium channel blockers may cause orthostatic hypotension. The combination of vardenafil and isosorbide mononitrate may therefore produce excessive hypotension.Īlcohol and other vasodilators may intensify the hypotensive effects of isosorbide mononitrate. Organic nitrates activate guanylate cyclase, which increases cyclic GM P. Vardenafil inhibits phosphodiesterase type 5, the enzyme responsible for the metabolic degradation of cyclic GM P. The combination of tadalafil and isosorbide mononitrate may therefore produce excessive hypotension. Tadalafil inhibits phosphodiesterase type 5, the enzyme responsible for the metabolic degradation of cyclic GM P. The combination of sildenafil and isosorbide mononitrate may therefore produce excessive hypotension.
Sildenafil inhibits phosphodiesterase type 5, the enzyme responsible for the metabolic degradation of cyclic GM P.