Reis S E, Holubkov R, Lee J S, Sharaf B, Reichek N, Rogers W J, Walsh E G, Fuisz A R, Kerensky R, Detre K M, Sopko G, Pepine C J
Department of Medicine, University of Pittsburgh, Pennsylvania, USA.
J Am Coll Cardiol. 1999 May;33(6):1469-75. doi: 10.1016/s0735-1097(99)00072-8.
We sought to develop and validate a definition of coronary microvascular dysfunction in women with chest pain and no significant epicardial obstruction based on adenosine-induced changes in coronary flow velocity (i.e., coronary velocity reserve).
Chest pain is frequently not caused by fixed obstructive coronary artery disease (CAD) of large vessels in women. Coronary microvascular dysfunction is an alternative mechanism of chest pain that is more prevalent in women and is associated with attenuated coronary volumetric flow augmentation in response to hyperemic stimuli (i.e., abnormal coronary flow reserve). However, traditional assessment of coronary volumetric flow reserve is time-consuming and not uniformly available.
As part of the Women's Ischemia Syndrome Evaluation (WISE) study, 48 women with chest pain and normal coronary arteries or minimal coronary luminal irregularities (mean stenosis = 7%) underwent assessment of coronary blood flow reserve and coronary flow velocity reserve. Blood flow responses to intracoronary adenosine were measured using intracoronary Doppler ultrasonography and quantitative angiography.
Coronary volumetric flow reserve correlated with coronary velocity reserve (Pearson correlation = 0.87, p < 0.001). In 29 (60%) women with abnormal coronary microcirculation (mean coronary flow reserve = 1.84), adenosine increased coronary velocity by 89% (p < 0.001) but did not change coronary cross-sectional area. In 19 (40%) women with normal microcirculation (mean flow reserve = 3.24), adenosine increased coronary velocity and area by 179% (p < 0.001) and 17% (p < 0.001), respectively. A coronary velocity reserve threshold of 2.24 provided the best balance between sensitivity and specificity (90% and 89%, respectively) for the diagnosis of microvascular dysfunction. In addition, failure of the epicardial coronary to dilate at least 9% was found to be a sensitive (79%) and specific (79%) surrogate marker of microvascular dysfunction.
Coronary flow velocity response to intracoronary adenosine characterizes coronary microvascular function in women with chest pain in the absence of obstructive CAD. Attenuated epicardial coronary dilation response to adenosine may be a surrogate marker of microvascular dysfunction in women with chest pain and no obstructive CAD.
我们试图基于腺苷诱导的冠状动脉血流速度变化(即冠状动脉血流储备),制定并验证一种适用于胸痛且无明显心外膜阻塞的女性冠状动脉微血管功能障碍的定义。
女性胸痛通常并非由大血管的固定性阻塞性冠状动脉疾病(CAD)引起。冠状动脉微血管功能障碍是胸痛的另一种机制,在女性中更为普遍,且与充血刺激后冠状动脉容积流量增加减弱(即异常冠状动脉血流储备)相关。然而,传统的冠状动脉容积血流储备评估耗时且并非普遍可用。
作为女性缺血综合征评估(WISE)研究的一部分,48名胸痛且冠状动脉正常或冠状动脉管腔轻度不规则(平均狭窄率 = 7%)的女性接受了冠状动脉血流储备和冠状动脉血流速度储备评估。使用冠状动脉内多普勒超声和定量血管造影测量冠状动脉内腺苷的血流反应。
冠状动脉容积血流储备与冠状动脉血流速度储备相关(Pearson相关系数 = 0.87,p < 0.001)。在29名(60%)冠状动脉微循环异常的女性中(平均冠状动脉血流储备 = 1.84),腺苷使冠状动脉血流速度增加了89%(p < 0.001),但未改变冠状动脉横截面积。在19名(40%)微循环正常的女性中(平均血流储备 = 3.24),腺苷使冠状动脉血流速度和面积分别增加了179%(p < 0.001)和17%(p < 0.001)。冠状动脉血流速度储备阈值为2.24时,对微血管功能障碍诊断的敏感性和特异性之间达到最佳平衡(分别为90%和89%)。此外,发现心外膜冠状动脉扩张至少9%失败是微血管功能障碍的一个敏感(79%)且特异(79%)的替代标志物。
冠状动脉内腺苷引起的冠状动脉血流速度反应可表征无阻塞性CAD的胸痛女性的冠状动脉微血管功能。心外膜冠状动脉对腺苷的扩张反应减弱可能是无阻塞性CAD的胸痛女性微血管功能障碍的替代标志物。