Angina vasodilator therapy

Nifedipine (Table 3) is a potent vasodilator that selectively dilates resistance vessels and has fewer effects on venous vessels. It does not cause reflex tachycardia during chronic therapy. Nifedipine is one of the first-line choices for black or elderly patients and patients having concomitant angina pectoris, diabetes, or peripheral vascular diseases. Nifedipine, sublingually, is also suitable for the treatment of hypertensive emergencies. Nifedipine does not impair sexual function or worsen blood Hpid profile. The side effects are flushing, headache, and dizziness. 

DHPs are potent arterial vasodilators. They act on resistance vessels and therefore reduce peripheral vascular resistance, lower arterial blood pressure, and antagonize vasospasms in coronary or peripheral arteries. By reducing afterload, DHPs also reduce cardiac oxygen demand. Together with their vascular spasmolytic effect, this explains most of the beneficial actions of DHPs in angina pectoris. Most DHPs are only licensed for the therapy of hypertension, some of them also for the treatment of angina pectoris and vasospastic (Prinzmetal) angina. 

All patients taking these drugs for long-term hypertension therapy should first receive both a diuretic and a /1-blocker. The diuretic minimizes the side effect of sodium and water retention. Direct vasodilators can precipitate angina in patients with underlying coronary artery disease unless the baroreceptor reflex mechanism is completely blocked with a /3-blocker. Nondihydropyridine CCBs can be used as an alternative to /3-blockers in patients with contraindications to /3-blockers. 

This class of drugs includes the oral vasodilators, hydralazine and minoxidil, which are used for long-term outpatient therapy of hypertension the parenteral vasodilators, nitroprusside, diazoxide, and fenoldopam, which are used to treat hypertensive emergencies the calcium channel blockers, which are used in both circumstances and the nitrates, which are used mainly in angina (Table 11-3). 

Dipyridamole is also a potent coronary arteriolar vasodilator, perhaps by opening of vascular K tp channels (2). However, the Food and Drug Administration withdrew conditional approval for certain drug products containing dipyridamole, because of a lack of sufficient evidence of effectiveness in the long-term therapy of angina pectoris (3). 

Dipyridamole is indicated as an adjunct to therapy with cou-marin anticoagulant in the prevention of postoperative thromboembolic complications of cardiac valve replacement as an alternative to exercise in thaUium myocardial perfusion imaging for the evaluation of coronary artery disease in patients who are unable to exercise and in long-term therapy for angina pectoris. Dipyridamole inhibits platelet adhesion and is a coronary vasodilator. Inappropriate use of dipyridamole has caused MI, ventricular fibrillation, tachycardia, bronchospasm, and transient cerebral ischania (see also Figures 14 and 92). 

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