Coronary microvascular dysfunction: an update

Abstract

Many patients undergoing coronary angiography because of chest pain syndromes, believed to be indicative of obstructive atherosclerosis of the epicardial coronary arteries, are found to have normal angiograms. In the past two decades, a number of studies have reported that abnormalities in the function and structure of the coronary microcirculation may occur in patients without obstructive atherosclerosis, but with risk factors or with myocardial diseases as well as in patients with obstructive atherosclerosis; furthermore, coronary microvascular dysfunction (CMD) can be iatrogenic. In some instances, CMD represents an epiphenomenon, whereas in others it is an important marker of risk or may even contribute to the pathogenesis of cardiovascular and myocardial diseases, thus becoming a therapeutic target. This review article provides an update on the clinical relevance of CMD in different clinical settings and also the implications for therapy.

Keywords: Acute coronary syndromes; Coronary microvascular dysfunction; Coronary microvascular obstruction; Myocardial diseases; Stable angina.

Figure 1

In addition to the ‘classic mechanisms’ (i.e. atherosclerotic disease and vasospastic disease) that lead to myocardial ischaemia, coronary microvascular dysfunction (CMD) has recently emerged as a ‘third’ potential mechanism of myocardial ischaemia. As in the case of the other two mechanisms, coronary microvascular dysfunction (alone or in combination with the other two) can lead to transient myocardial ischaemia as in patients with coronary artery disease (CAD) or cardiomyopathy (CMP) or to severe acute ischaemia as observed in Takotsubo syndrome. CFR, coronary flow reserve.

Figure 2

Scheme of the potential causes and consequences of coronary microvascular dysfunction. HC, hypertrophic cardiomyopathy.

Figure 3

Proposed cascade of events in hypertrophic cardiomyopathy, from abnormal coronary arteriolar remodelling leading to myocardial ischaemia, fibrosis and adverse left ventricular remodelling, and heart failure.

Figure 4

Treatment algorithm for patients with microvascular angina. SCS, spinal cord stimulation; EEC, enhanced external counterpulsation.

Figure 5

Prevention more than treatment has a central role in the management of microvascular angina. It starts before infarction pain occurs by targeting risk factors and by avoiding the blockage of ischaemic pre-conditioning. After the onset of infarction pain and before hospital arrival, the reduction in ischaemic time, an early administration of IIb/IIIa inhibitors, and remote ischaemic pre-conditioning have an important role. In the catheterization laboratory, the use of thrombus aspiration, high doses of intracoronary adenosine, and ischaemic post-conditioning are good opportunities to prevent microvascular obstruction (MVO). No drugs have been shown to reverse established microvascular obstruction (from Ref.). IC, intracoronary; IPC, ischaemic pre-conditioning.