Abstract 11882: Comprehensive Hemodynamic Analysis of Coronary Arterial Responses to Acetylcholine Provocation Test in Patients With Coronary Vasospastic Angina

Abstract

Introduction: Whereas our prior study showed diffuse coronary intimal thickening in pts with coronary vasospastic angina (VSA), coronary epicardial and microvascular (MV) hemodynamic and vessel response during coronary vasospasm has not been well studied. Hypothesis: We hypothesized that coronary pathogenic abnormalities responsible for coronary vasospasm may not be confined to coronary epicardial spastic segments, but the hemodynamic abnormalities may exist in the entire coronary bed. Methods: According to acetylcholine (ACh) provocation tests, excluding pts with atherosclerotic coronary obstruction (stenosis >50% diameter) and possible heart failure (left ventricular ejection fraction <50%), 41 pts were divided into 2 groups; VSA group (n=20) and non-VSA group (n=21). To evaluate hemodynamic parameters comprehensively, average peak velocity (APV), coronary blood flow (CBF: π (APV/2)(vessel diameter/2) 2 ), hyperemic MV resistance (hMR), coronary vascular resistance (CVR: Pd/CBF) and coronary distal pressure (Pd) were measured continuously utilizing a dual-sensor (Doppler velocity and pressure)-equipped guidewire (Combowire, Volcano Therapeutics, Inc.) during ACh provocation test. Results: There were no differences between the 2 groups in baseline characteristics. In spite of absence of between-group differences at baseline in CBF (55±26 vs. 51±29, p=0.5) and CVR (2.4±1.5 vs. 2.6±1.4, p=0.7), intracoronary ACh 100μg provocation significantly increased CVR (2.1±2.2 vs. 0.8±0.7; p=0.001), and then attenuated CBF (77±54 vs. 188±129, p=0.001) in VSA group than in non-VSA group. Furthermore, although coronary flow reserve was identical between the groups (2.2±0.9 [VSA] vs. 2.4±0.9 [non-VSA], p=0.5), hMR was significantly augmented in VSA group (2.0±0.7 vs. 1.6±0.6, p=0.046). Also, there was significantly negative correlation between hMR and estimated glomerular filtration rate, which presumably reflect the integrity of renal MV bed (r=-0.522; p=0.0009). Conclusions: Compared with non-VSA pts, coronary and systemic MV function was impaired in pts with VSA. In vivo assessment using Combowire clarified dynamic entire coronary alteration during ACh provocation test, including coronary MV dysfunction, in pts with VSA.