Hemodynamic Effects of Isosorbide-5-Mononitrate in Patients with Coronary Artery Disease, at Rest and Under Exercise

The long-term treatment of angina pectoris (AP) with isosorbide dinitrate (ISDN), in slow-release and rapid-release form, has become accepted practice [13, 18, 20, 21], in spite of the first-pass effect [27, 28]. The action of this organic nitrate, like that of nitroglycerin, is to decrease the tone of both venous and arterial vessels. The resulting reduction of both the preload and the afterload leads to a reduction of the left ventricular (LV) oxygen requirement [1, 9, 11, 12, 15, 22, 23, 24]. It has been shown that ISDN, as well as isosorbide-2-mononitrate (IS-2-MN) and isosorbide-5-mononitrate (IS-5-MN) are to be regarded as effective vasodilating agents, although of different potency [6, 8, 10, 14, 16, 17, 30, 32, 33, 35]. The major problem in therapeutic use of ISDN is that its rate of metabolism is subject to large individual variations, so that the amount of metabolites produced and the amount of unmetab-olized substance remaining are difficult to predict. Thus, the magnitude and duration of the effect of ISDN are linked with the presence of three substances exhibiting different pharmacodynamics [3, 4, 5, 26, 27, 28, 29, 31, 34].