Effects of Systemic Nitroglycerin on Perfusion of Ischemic Myocardium in Clinical Coronary Artery Disease

Abstract

In the consideration of the antianginal actions of nitrates in patients with ischemic heart disease, it is acknowledged that the agents improve the imbalance between cardiac oxygen demand and restricted ventricular perfusion by directly dilating diseased coronary arteries [15, 23, 27] and/or by diminishing myocardial energetic requirements through reduction of external work [20–22, 28]. The conventional and paramount concept is that this therapeutic effect of the nitrates in the relief of effort angina predominantly results from their property of systemic venodilation [8, 21, 22, 28, 29], which causes peripheral pooling of blood and decrease of heart size (preload reduction), thereby diminishing systolic wall tension (after-load) and oxygen consumption of the ischemic left ventricle [19]. However, the possibility remains that these agents may also increase hindered segmental perfusion by dilating even diseased vessels and/or by enhancing blood flow through the collateral network. Accordingly, in patients with angiographically defined fixed coronary obstruction without vasospasm, the influence of systemic nitroglycerin on regional coronary circulatory dynamics was directly assessed by the objective means of metered antegrade blood flow through intact saphenous vein grafts.