Panza J A, Laurienzo J M, Curiel R V, Unger E F, Quyyumi A A, Dilsizian V, Cannon R O
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
J Am Coll Cardiol. 1997 Feb;29(2):293-301. doi: 10.1016/s0735-1097(96)00481-0.
The present study sought to determine whether myocardial contractile abnormalities accompany the development of chest pain in patients with normal coronary angiograms.
The mechanism of chest pain in patients with angina despite a normal coronary arteriogram is controversial. Although previous studies postulated the existence of coronary microvascular dysfunction, others failed to find evidence of myocardial ischemia, and recent studies have demonstrated abnormal cardiac sensitivity in these patients that can lead to chest pain on a nonischemic basis.
Seventy patients (26 men and 44 women, mean age 49 +/- 10 years) with angina-like chest pain and angiographically normal coronary arteries underwent exercise treadmill testing, radionuclide angiography at rest and during exercise, thallium stress testing and transesophageal dobutamine stress echocardiography. The results of exercise treadmill testing and stress echocardiography were compared with those obtained in 26 normal control subjects (19 men and 7 women, mean age 56 +/- 7 years).
Abnormalities consistent with myocardial ischemia were noted in 31% of the patients during exercise treadmill testing, in 16% during exercise radionuclide angiography and in 18% during thallium stress testing. The findings of the radionuclide studies were not concordant with one another and were not related to the presence of repolarization changes during exercise testing. During infusion of dobutamine, chest pain developed in 59 patients (84%) and in none of the control subjects (p < 0.0001); repolarization changes occurred in 22 patients (34%) and in 2 control subjects (8%) (p < 0.04). None of the patients or the control subjects developed regional wall motion abnormalities with dobutamine. The quantitative myocardial contractile response to dobutamine was similar in patients and control subjects, with an 80% power to detect a 25% difference in systolic wall thickening at the maximal dose of dobutamine.
There was no agreement in the results of noninvasive tests in our patients. Despite the frequent provocation of chest pain and electrocardiographic abnormalities with dobutamine, the patients demonstrated a quantitatively normal myocardial contractile response without development of wall motion abnormalities. These observations strongly suggest that myocardial ischemia is not the cause of chest pain in patients with a normal coronary arteriogram.
本研究旨在确定冠状动脉造影正常的患者在胸痛发作时是否伴有心肌收缩异常。
尽管冠状动脉造影正常，但心绞痛患者胸痛的机制仍存在争议。虽然先前的研究推测存在冠状动脉微血管功能障碍，但其他研究未能找到心肌缺血的证据，且最近的研究表明这些患者存在心脏敏感性异常，可导致非缺血性胸痛。
70例（26例男性和44例女性，平均年龄49±10岁）有类似心绞痛胸痛且冠状动脉造影正常的患者接受了运动平板试验、静息及运动时的放射性核素血管造影、铊负荷试验和经食管多巴酚丁胺负荷超声心动图检查。将运动平板试验和负荷超声心动图的结果与26例正常对照者（19例男性和7例女性，平均年龄56±7岁）的结果进行比较。
运动平板试验中31%的患者、运动放射性核素血管造影中16%的患者以及铊负荷试验中18%的患者出现了与心肌缺血一致的异常。放射性核素研究结果彼此不一致，且与运动试验期间复极变化的存在无关。多巴酚丁胺输注期间，59例患者（84%）出现胸痛，而对照者均未出现胸痛（p<0.0001）；22例患者（34%）出现复极变化，2例对照者（8%）出现复极变化（p<0.04）。多巴酚丁胺试验中，患者和对照者均未出现节段性室壁运动异常。患者和对照者对多巴酚丁胺的定量心肌收缩反应相似，在多巴酚丁胺最大剂量时，有80%的把握检测到收缩期室壁增厚25%的差异。
我们患者的无创检查结果不一致。尽管多巴酚丁胺频繁诱发胸痛和心电图异常，但患者的心肌收缩反应在数量上正常，未出现室壁运动异常。这些观察结果强烈提示，冠状动脉造影正常的患者胸痛并非由心肌缺血引起。
