Primary microvascular angina - pathophysiology and therapy

Abstract

Microvascular angina (MVA) is a cardiac condition characterized by clinical and imaging evidence of myocardial ischemia, combined with no obstructive coronary ar-tery stenosis (<50% stenosis of epicardial coronary arteries) and evidence of coronary microvascular dysfunction (CMD). MVA is a prevalent, women-predominant, but sub-diagnosed condition that causes significant morbidity and mortality. Among the structural and functional (endothelium-dependent and independent) mechanisms proposed, a chronic and systemic pro-inflammatory state, likely promot-ed by traditional cardiovascular risk factors, stands out. There is also a vasodilator-vasoconstrictor imbalance with decreased vasodilation to acetylcholine and increased vasoconstriction to endothelin, as well as cardiac autonomic dysfunction. Structural vascular remodelling includes fibromuscular hyperplasia, intimal thickening, peri-vascular fibrosis and capillary rarefaction. In diabetic patients, CMD is also promoted by a chronic state of hyperglycemia. Though there are no straightforward guidelines on MVA management, first line recommended pharmacological therapies include beta-blockers, calcium-channel blockers, statins and angiotensin-converting-enzyme inhibitors. A few different phar-macological principles are being investigated and new therapies are expected.