Early quantitative stress-perfusion cardiac magnetic resonance reveals perfusion abnormalities consistent with coronary microvascular dysfunction in MINOCA patients with otherwise normal cardiac magnetic resonance findings

Coronary microvascular dysfunction (CMD) is a proposed contributor to myocardial infarction with non-obstructive coronary arteries (MINOCA), but the value of early quantitative stress-perfusion CMR (Q-CMR) in this setting is not fully established. We aimed to determine the prevalence of quantitative perfusion abnormalities consistent with CMD using Q-CMR in patients with a working diagnosis of MINOCA and otherwise normal conventional CMR findings. Of 46 consecutive MINOCA patients referred for CMR between 2021 and 2024, 23 had normal findings on conventional CMR at rest and were included. They were compared with age- and sex-matched healthy controls without coronary artery disease, confirmed by coronary CT angiography. All participants underwent dual-sequence first-pass perfusion CMR at rest and during regadenoson stress. Fully automated quantitative perfusion analysis was used to quantify myocardial blood flow (MBF) and myocardial perfusion reserve (MPR). CMR at rest was considered normal in the absence of edema, late gadolinium enhancement, or other structural abnormalities. The MINOCA patients (mean age 63 ± 10 years, 61% female) were scanned a median of 15 days (IQR 10–37) after admission. Compared with controls, they had lower MPR (1.88 ± 0.59 vs. 2.30 ± 0.55; p = 0.013) and lower stress MBF (2.56 ± 0.81 vs. 2.96 ± 0.53 mL/g/min; p = 0.044), while rest MBF was similar. 43% of MINOCA patients had quantitative perfusion findings consistent with CMD according to previously proposed CMR thresholds, compared with none of the controls. In conclusion, early Q-CMR identifies reduced stress MBF and MPR in MINOCA patients with otherwise normal conventional CMR findings and reveals perfusion abnormalities consistent with CMD in nearly half of these patients, suggesting that microvascular dysfunction may contribute to myocardial injury in a subset of MINOCA patients.