Coronary Microvascular Dysfunction in Cardiomyopathies: Insights on Clinical and Prognostic Roles

Coronary microvascular dysfunction (CMD) is a key driver of ischemia and prognosis across several non-ischemic cardiomyopathies. This review summarizes the main tools for diagnosing microvascular dysfunction and available evidence on CMD incidence and the prognostic role in patients with cardiomyopathies. In dilated cardiomyopathy, CMD is associated with reduced myocardial blood flow, greater fibrosis, adverse remodeling, and worse outcomes. In hypertrophic cardiomyopathy, CMD is highly prevalent and multifactorial (arteriolar remodeling, reduced capillary density, extravascular compression, diastolic dysfunction, and/or left ventricular (LV) outflow obstruction), correlating with fibrosis, heart failure, and arrhythmias/sudden death. In Takotsubo syndrome, CMD appears acute and reversible, with microvascular spasms as a predominant mechanism and plausible pathophysiologic basis of the event. In arrhythmogenic right ventricular cardiomyopathy, preliminary data show a blunted hyperemic response and autonomic abnormalities that may impair microvascular vasodilation. In infiltrative and storage diseases (amyloidosis and Anderson–Fabry disease), CMD is often early, preceding hypertrophy/fibrosis, and contributes to symptoms, contractile dysfunction, and adverse outcomes; in sarcoidosis, microvascular inflammation reduces coronary flow reserve (CFR) and is associated with events. Targeted therapies remain limited; optimization of risk factors and drugs that modulate endothelial/metabolic function (statins, angiotensin converting enzyme (ACE) inhibitors, vasodilating β-blockers, calcium channel blockers, sodium glucose cotransporter 2 (SGLT2) inhibitors) yielded variable signals; device-based and nonpharmacologic strategies are under investigation. In conclusion, integrating microcirculatory assessment improves risk stratification and may furnish future therapeutic targets across cardiomyopathies.