Functional or structural impairment of flow-mediated epicardial vasodilation may precede coronary microvascular dysfunction

Background: The aim was to investigate whether functional and/or structural impairment of flow-mediated epicardial vasodilation (IEV) may precede coronary microvascular dysfunction (CMD) in a cardiometabolic risk population. Methods: ¹³N-ammonia positron emission tomography/computed tomography evaluated global and longitudinal myocardial blood flow (MBF) during pharmacologically induced hyperemia and at rest. Normal coronary microvascular function (nCMF) was defined by a myocardial flow reserve (MFR = MBFstress/MBFrest) of ≥ 2.0, while an abnormal MFR of < 2.0 (predominantly due to decreases in hyperemic MBF) denoted classical CMD. Normal flow-mediated epicardial vasodilation (NEV) was defined as longitudinal hyperemic MBF gradient < -0.10 mL/g/min, whereas a value ≥ -0.10 mL/g/min signifiedIEV. Patients were grouped as follows: group 1 (G1): nCMF and NEV (n = 93); group 2 (G2): nCMF and IEV (n = 62), and group 3 (G3): CMD and IEV (n = 78). From non-gated CT, a semiquantitative four-point scoring system was used to indicate coronary artery calcifications score (CCS). Results: The prevalence of diffuse coronary artery calcification was highest in G1 with 51 %, followed by G3 with 46 % and G2 with 34 %. The extent of CCS was mild-to-moderate and did not differ significantly among groups (p = 0.222). Overall, IEV was present in 60 %, while there was a comparable prevalence of IEV between G2 and G3 (27 % and 33 %, p = 0.27). The hyperemic MBF gradient was highest in G2, intermediate in G3, and lowest in G1 (−0.22 ± 0.11 and −0.18 ± 0.10 vs. 0.03 ± 0.08 mL/g/min; p < 0.001, respectively). Conclusions: In this cardio-metabolic risk population, in about one third of these symptomatic patients functional and/or structural impairment of flow-mediated epicardial vasodilation may precede coronary microvascular dysfunction.