Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; and.
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; and
Am J Physiol Heart Circ Physiol. 2015 Mar 1;308(5):H478-84. doi: 10.1152/ajpheart.00593.2014. Epub 2014 Dec 19.
Endothelial and vascular smooth muscle dysfunction of epicardial coronary arteries play a pivotal role in the pathogenesis of vasospastic angina (VSA). However, coronary microvascular (MV) function in patients with VSA is not fully understood. In the present study, subjects without coronary obstruction were divided into two groups according to the acetylcholine provocation test: VSA group (n = 29) and non-VSA group (n = 21). Hyperemic MV resistance (hMR) was measured using a dual-sensor (Doppler velocity and pressure)-equipped guidewire, and guidewire-derived hemodynamic parameters were compared. There were no between-group differences in clinical demographics, including potential factors affecting MV function (e.g., diabetes). Although coronary flow velocity reserve was similar between the two groups [2.4 ± 1.0 (VSA group) vs. 2.4 ± 0.9 (non-VSA group); P = 0.8], coronary vessel resistance and hMR were significantly elevated in the VSA group compared with the non-VSA group (2.6 ± 3.1 vs. 1.2 ± 0.8, P = 0.04; 1.9 ± 0.6 vs. 1.6 ± 0.5, P = 0.03, respectively). Coronary vasospasm, older age, E/e', and estimated glomerular filtration rate were significantly associated with MV dysfunction [defined as ≥ median value of hMR (1.6)] in univariate analysis. Coronary vasospasm most strongly predicted higher hMR in multivariate logistic regression analysis (odds ratio, 4.61; 95% confidence interval, 0.98-21.60; P = 0.053). In conclusion, coronary MV resistance is impaired in patients with VSA compared with non-VSA patients, whereas coronary flow velocity reserve is maintained at normal levels in both groups. In vivo assessment of hMR might be a promising index of coronary MV dysfunction in patients with VSA.
心外膜冠状动脉的内皮和血管平滑肌功能障碍在痉挛性心绞痛(VSA)的发病机制中起关键作用。然而,VSA 患者的冠状动脉微血管(MV)功能尚不完全清楚。在本研究中,根据乙酰胆碱激发试验将无冠状动脉阻塞的受试者分为 VSA 组(n = 29)和非 VSA 组(n = 21)。使用配备双传感器(多普勒速度和压力)的导丝测量充血性 MV 阻力(hMR),并比较导丝衍生的血流动力学参数。两组之间在临床人口统计学方面没有差异,包括可能影响 MV 功能的潜在因素(例如糖尿病)。尽管两组之间的冠状动脉血流速度储备相似[2.4 ± 1.0(VSA 组)与 2.4 ± 0.9(非 VSA 组);P = 0.8],但 VSA 组的冠状动脉血管阻力和 hMR 明显高于非 VSA 组[2.6 ± 3.1 与 1.2 ± 0.8,P = 0.04;1.9 ± 0.6 与 1.6 ± 0.5,P = 0.03]。单因素分析显示,冠状动脉痉挛、年龄较大、E/e'和估算肾小球滤过率与 MV 功能障碍[定义为 hMR 的中位数以上(1.6)]显著相关。多因素逻辑回归分析显示,冠状动脉痉挛最强预测 hMR 升高(优势比,4.61;95%置信区间,0.98-21.60;P = 0.053)。总之,与非 VSA 患者相比,VSA 患者的冠状动脉 MV 阻力受损,而两组的冠状动脉血流速度储备均保持在正常水平。hMR 的体内评估可能是 VSA 患者冠状动脉 MV 功能障碍的有前途的指标。