Abstract

With the widespread clinical use of angiography in the 70s of the last century, it became apparent that a sizeable proportion of patients referred for anginal symptoms had angiographically normal coronary arteries. These findings stimulated a hot debate among clinicians and scientists on the mechanisms and significance of this condition that seemed to be by far more frequent in women. For many years, there was uncertainty on the real significance of this condition that was often accompanied by electrocardiographic evidence of ischemia during stress.1 The situation began to unravel when myocardial perfusion studies demonstrated that many of these patients had evidence of abnormal perfusion. Cannon and Epstein2 introduced the term microvascular angina (MVA) for this patient population, in view of what appeared to be heightened sensitivity of the coronary microcirculation to vasoconstrictor stimuli associated with a limited microvascular vasodilator capacity. They proposed that dysfunction of small intramural prearteriolar coronary arteries might be the pathogenetic cause of this syndrome. See Article by Thomson et al In the past 20 years, it has become apparent that symptoms and signs of myocardial ischemia, despite normal coronary angiography, could be demonstrated in several clinical conditions, from subjects with risk factors for coronary artery disease to patients with different types of myocardial diseases. The term coronary microvascular dysfunction (CMD) was coined to provide an overarching definition that would encompass a large number of clinical scenarios characterized by evidence of a reduced coronary flow reserve (CFR) that could not be explained by an …

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