Cannon R O, Curiel R V, Prasad A, Quyyumi A A, Panza J A
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1650, USA.
Am J Cardiol. 1998 Sep 15;82(6):710-4. doi: 10.1016/s0002-9149(98)00456-1.
Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 microg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 microg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5+/-13% vs +1+/-13%, p=0.386) and flow (+179+/-90% vs +169+/-96%, p=0.756), or in the systolic wall thickening responses (+134+/-65% vs +118+/-57%, p=0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121+/-73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129+/-48%, p=0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.
冠状动脉内皮功能障碍被认为是尽管冠状动脉造影正常，但仍出现心肌缺血和心绞痛样胸痛症状患者的病因，尤其是那些运动时出现缺血样ST段压低的患者（X综合征）。我们测量了42例（27例女性和15例男性）有劳力性胸痛且冠状动脉造影正常、静息心电图和超声心动图也正常的患者对乙酰胆碱（3至300微克/分钟）的冠状动脉血管舒缩反应。所有患者均接受平板运动试验，并在经食管超声心动图检查期间测量对多巴酚丁胺（40微克/千克/分钟）的收缩期室壁增厚反应。与30例运动试验结果阴性的患者相比，12例X综合征患者的乙酰胆碱刺激的心外膜冠状动脉直径（分别为+5±13%和+1±13%，p=0.386）和血流量（分别为+179±90%和+169±96%，p=0.756），或收缩期室壁增厚反应（分别为+134±65%和+118±57%，p=0.445）与基线值相比无差异。在乙酰胆碱冠状动脉血流反应处于最低四分位数的患者中，多巴酚丁胺使收缩期室壁增厚增加了121±73%；其中3例在这种应激状态下出现缺血样ST段压低。这种对多巴酚丁胺的收缩反应与冠状动脉血流反应处于最高四分位数的患者中收缩期室壁增厚的增加（129±48%，p=0.777）没有差异，其中3例在这种应激状态下也出现缺血样ST段压低。因此，在无冠状动脉疾病的情况下，冠状动脉内皮功能障碍并不能解释尽管冠状动脉造影正常但仍有胸痛的患者出现的缺血样ST段压低。此外，冠状动脉内皮功能障碍与与心肌缺血一致的应激状态下的心肌收缩反应无关。
