Coronary microvascular dysfunction in stable ischaemic heart disease (non-obstructive coronary artery disease and obstructive coronary artery disease)

This article is part of the Spotlight Issue on Coronary Microvascular Dysfunction.

1. Introduction

Recently, it has become increasingly obvious that diffuse and focal epicardial coronary disease and coronary microvascular abnormalities may exist side-by-side. Identifying the contributions of each of these three players in the coronary circulation is a difficult task. However, looking at the problem of coronary microvascular dysfunction (CMD) as an adjunct to diffuse and focal plaque and stenosis formation in the coronary arteries makes sense in the context of the vexing challenges of proving the symptomatic and prognostic value of percutaneous coronary interventions (PCIs). Identifying CMD as an additional player in patients with coronary artery disease (CAD) may provide explanations of why symptoms persist so frequently following PCI and why global coronary flow reserve (CFR) may be more prognostically important than fractional flow reserve (FFR) measured in a single vessel before PCI. The term CMD focuses on the functional aspect of microvascular disease. However, we should not forget that, especially in patients with epicardial coronary plaque formation or stenoses morphological changes, such as occlusive microvascular lesions (Figure 1) or microvascular rarefaction, may also be found in the resistance vessels of the coronary tree.

Figure 1

Intramural arteriole of a 59-year-old male patient with ischaemic cardiomyopathy. Left: haematoxylin–eosin staining. Fibrosis is blue and smooth muscle cells are violet. White spaces represent fat accumulation. There is diffuse narrowing of the vessel by a process which resembles vaguely plaque formation in the larger epicardial vessels. Right: same vessel with actin staining. Actin is a marker of smooth muscle cells and shows the irregular proliferation of these cell in the arteriolar wall. Courtesy of Professor Karin Klingel, MD, Director of Cardiac Pathology, Institute of General and Molecular Pathology and Pathologic Anatomy, University of Tübingen, Germany.

In this review, we take a closer look at the challenges of identifying the presence of CMD in the context of diffuse non-obstructive CAD (NOCAD) and obstructive CAD (OCAD). Furthermore, we are going to discuss the pathophysiology in this complex situation, examine the clinical context in which the interaction of the three components takes place and finally look at the non-invasive diagnostic methods relevant for addressing this question.