Treatment of microvascular angina: the need for precision medicine

This editorial refers to ‘A randomized, placebo-controlled trial of late Na current inhibition (ranolazine) in coronary microvascular dysfunction: impact on angina and myocardial perfusion reserve’, by C.N. Bairey Merz et al . on page doi:10.1093/eurheartj/ehv647 Up to half of patients who undergo non-urgent coronary angiography because of chest pain are found to have no obstructive coronary artery disease (NO-CAD).1 The mechanisms responsible for chest pain in these patients are heterogeneous. A large number of studies in the past 30 years have shown that in most of these patients chest pain is caused by myocardial ischaemia resulting from coronary microvascular dysfunction (CMD), a condition defined, in the absence of any other cardiac disease, as primary microvascular angina (MVA).2 A direct demonstration of CMD in these patients can be obtained by documenting abnormalities in coronary blood flow (CBF) response to provocative tests using either invasive or non-invasive methods.3 In keeping with the frequent history of predominantly typical exercise-induced angina, most patients present an impairment of coronary microvascular dilatation, which may involve endothelium-dependent or endothelium-independent mechanisms, or a combination of the two.4 In some patients, however, CMD is characterized by enhanced vasoconstriction, as suggested by a reduction of CBF and ischaemia in response to constrictor stimuli such as acetylcholine,5 as well as by the evidence of increased levels of vasoconstrictor agents, such as endothelin-1.6 While CMD can be detected in most patients with chest pain and NO-CAD, a subset of these patients has consistently been found to present enhanced pain perception in response to stimuli, such as intracardiac saline or contrast medium injection, catheter manipulation, and electrical ventricular stimulation, which usually do not …