Management of Structural Microvascular Angina

Introduction to Microvascular Angina

The European Society of Cardiology recommends that microvascular angina be recognized as a clinical syndrome resulting from both structural and functional changes in the coronary microvasculature, with guideline-directed medical therapy improving coronary flow reserve, reducing symptoms, and modifying disease progression 1, 2

Structural alterations in microvascular angina include capillary rarefaction, arteriolar remodeling, and fixed microvascular obstruction caused by chronic risk factor exposure, such as hypertension, diabetes, dyslipidemia, smoking, and aging 4, 5
Functional abnormalities involve endothelial dysfunction, impaired vasodilation, and abnormal vasoconstriction of coronary arterioles, which are more amenable to therapeutic intervention 1, 3

The CorMiCa trial demonstrated that stratified medical treatment based on invasive coronary functional testing significantly improved angina severity and quality of life, with improvements of 11.7 units on the Seattle Angina Questionnaire, providing Class IIa evidence for targeted therapy in established microvascular disease 2, 6
First-line therapies that directly target microvascular dysfunction include beta-blockers, ACE inhibitors, and statins, which improve coronary flow reserve, reduce symptoms, and modify disease progression 2, 6

Microvascular dysfunction carries a worse prognosis than originally recognized, with increased risk of major adverse cardiac events, myocardial infarction, heart failure with preserved ejection fraction, and death 7, 6
Impaired coronary flow reserve (<2.32) is associated with elevated hazard for major coronary events at 10-year follow-up, making therapeutic intervention to improve CFR a critical goal 6

The European Society of Cardiology recommends confirming the diagnosis of microvascular angina with invasive coronary functional testing or non-invasive PET/CMR assessment, and distinguishing the dominant mechanism using acetylcholine provocation testing 2, 8
Stratified medical therapy should be initiated, targeting the specific endotype, with beta-blockers, ACE inhibitors, statins, and aspirin for impaired CFR/elevated IMR with negative acetylcholine test 2, 6
Aggressive modification of cardiovascular risk factors, including treatment of hypertension, diabetes, dyslipidemia, smoking cessation, and weight loss, is essential for improving outcomes 2, 5