CMD in Obstructive CAD

Abstract

In 1974, Gould et al. described the effects of progressive coronary artery narrowing on resting and maximal coronary blood flow in a canine model [1]. A reduction in coronary artery diameter of C50 % limited maximal coronary vasodilator capacity and a reduction of C85 % limited resting coronary blood flow. These laboratory findings were soon transposed into the clinical setting, where a stenosis C50 % of luminal diameter was defined as a hemodynamically significant lesion and one C85 % as a critical lesion [2]. The notion of ''critical coronary stenosis'' was then further translated into ''ischemia-causing stenosis.'' Based on this chain of postulates, coronary stenosis gained increasing recognition as a consistent cause of angina.The results of the experimental findings of Gould et al. have been recently confirmed in patients using PET and quantitative coronary angigography [3,4]. Of note, these studies have clearly shown that, in patients with stable CAD, there is no reduction in MBF in resting conditions even with coronary stenosis [90 %, likely due to the presence of an effective collateral circulation.Therefore, when a relatively simple percutaneous technique, such as angioplasty, that could reduce the atherosclerotic obstruction was introduced [5], the cardiology community reacted with enormous enthusiasm and promptly endorsed the methodology.However, following millions of procedures performed worldwide, outcome analysis does not support the initial enthusiasm, at least in a large subset of patients with stable CAD. Several lines of evidence suggest that the direct relationship between chronic obstructive coronary atherosclerosis and angina has been taken for granted and may represent an overly simplified view. Indeed, many patients with angina and evidence of myocardial ischemia do not have detectable coronary atherosclerosis at angiography, as highlighted in the section on MVA (Chap. 4);

Coronary Microvascular Dysfunction, Microvascular Angina, and Management

“…Patients with CMD and obstructive epicardial CAD can present with angina that is prolonged or poorly responsive to sublingual nitrates. Concurrent CMD and MVA can also be suspected in patients with angina that appears to be more severe than expected by the degree of epicardial coronary stenosis [25]. Angina that persists despite successful revascularization may also be due to CMD.…”