digoxin and Coronary-Vasospasm

Topics: Angina Pectoris; Arrhythmias, Cardiac; Calcium Channel Blockers; Coronary Vasospasm; Digoxin; Diltiazem; Heart Block; Heart Diseases; Heart Rate; Humans; Hypertension; Nifedipine; Verapamil

Heart diseases requiring glycoside therapy are often associated with coronary artery disease. This study evaluated quantitatively the effect of an intravenous bolus injection of digoxin (0.8 mg) on diameters of epicardial coronary arteries in 11 patients with coronary artery disease. Coronary angiograms were taken up to 30 min following intravenous administration of glycosides. The maximum decrease in mean diameters of angiographically normal coronary segments was 10.0 +/- 3.5% (p < or = 0.001) compared to control. Maximum reduction in minimal diameters of stenotic segments was 22.1 +/- 13.1% (p < or = 0.001). This vasoconstriction could be reversed with nitroglycerin. Thus, intravenous administration of digoxin induces vasoconstriction of normal and stenotic coronary arteries, which could cause ischemic complications in the presence of high-grade stenoses. Since digoxin-induced vasoconstriction could be reversed with nitroglycerin, concomitant vasodilator therapy is recommended.

Topics: Adult; Aged; Angioplasty, Balloon, Coronary; Coronary Angiography; Coronary Circulation; Coronary Disease; Coronary Vasospasm; Digoxin; Drug Therapy, Combination; Female; Hemodynamics; Humans; Injections, Intravenous; Male; Middle Aged; Nitroglycerin; Recurrence

Calcium antagonists, of which the best known are verapamil, nifedipine and diltiazem, are a powerful group of cardioactive agents with a clinical spectrum of indications rather similar to those of beta-adrenoceptor blockade, including angina of effort, angina at rest, hypertension and supraventricular tachycardias (nifedipine is ineffective for the latter). In angina caused by coronary spasm, calcium antagonists are preferred to beta-blockade. Calcium antagonists have a basically different mode of action from beta-adrenoceptor blockade, although both ultimately act on the free cytoplasmic calcium ion concentration. Critical differences between the calcium antagonists are dependent on the individual properties of the calcium antagonists concerned. Different binding sites on the sarcolemma have been identified for nifedipine-like agents and verapamil, but with a different interaction with the nifedipine site. None of these sites might be relevant to the binding of calcium antagonists to the tissue of their therapeutic site of action (arterial smooth muscle for all; atrioventricular node for verapamil and diltiazem). As a group, calcium antagonists cause vascular dilation and do not cause bronchial constriction, in contrast to the beta-adrenoceptor blocking agents. In many patients, these diverse properties allow safe combination of calcium antagonists and beta-adrenoceptor blockers if due care is observed, especially in the case of nifedipine. The clinical differences between the effects of various calcium antagonists reflect: (i) the greater vasodilator capacity of nifedipine, so that at a given concentration the afterload effect dominates over possible effects on the nodal or myocardial tissue; (ii) the greater inhibition of vagal tone by nifedipine than by verapamil or diltiazem; and (iii) the greater inhibition of the atrioventricular node by verapamil and diltiazem. In angina of effort, calcium antagonists are now becoming the agents of first choice in some centers. Experimental use of calcium antagonists include the possible prevention of ventricular fibrillation, the inhibition of ischemic injury, the prevention of catecholamine mediated injury to the myocardium and decreased arterial calcinosis.

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Animals; Arrhythmias, Cardiac; Calcium; Calcium Channel Blockers; Catecholamines; Coronary Disease; Coronary Vasospasm; Coronary Vessels; Digoxin; Drug Interactions; Heart; Heart Failure; Humans; Hypertension; Myocardial Contraction; Myocardial Infarction; Myocardium; Prazosin; Sinoatrial Node; Structure-Activity Relationship; Ventricular Fibrillation