Abstract
Molsidomine, a predominantly venous vasodilator, has been coronary disease. The basic mechanism of its anti-anginal effect is a reduction in myocardial oxygen consumption due to a fall in left ventricular end-diastolic pressure resulting from the vasodilator action of the drug. To this may be added direct dilatation of the main coronary vessels on the surface of the heart, which may account for part in its therapeutic effects in unstable and vasospastic angina. The effectiveness of molsidomine has been evaluated by controlled drug versus placebo or drug versus reference anti-anginal drug studies in 3 types of angina pectoris: exertion, unstable and vasospastic. The usefulness of the drug has also been established in acute and chronic left ventricular failure of ischaemic origin. Because of its high bioavailability when administered orally, molsidomine shows little inter-individual variations in its pharmacodynamic effects. Unlike nitrates, it can be administered for long period without gradual loss of activity with time. Finally, on several experimental models molsidomine has been shown to exert an antiplatelet effect, but the therapeutic implications of this finding have yet to be evaluated.
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