Letac B, Berland J, Cribier A, Cazor J L, Hecketsweiler B
Arch Mal Coeur Vaiss. 1983 Feb;76 Spec No:211-22.
Sixty patients without organic heart disease presenting with chest pain suggestive of angina pectoris and angiographically normal coronary arteries underwent clinical, hemodynamic and metabolic investigation. The study of myocardial lactate metabolism during atrial pacing (168 +/- 14 bpm) allowed identification of two groups: --40 patients with a normal coefficient of lactate extraction (K greater than or equal to 9 per cent); --20 patients with a pathologically low coefficient of lactate extraction (K less than 9 per cent) reflecting myocardial ischemia. In the first group, chest pain was often atypical (75 per cent of cases). Hemodynamic investigation showed minor abnormalities of the left ventricle in 48 per cent of cases. The diagnosis of angina was rejected in these patients. In the second group, the majority of patients developed chest pain (85 per cent of cases) at the maximal heart rate with significant ST depression (80 per cent of cases). The chest pain was typical of angina pectoris in 50 per cent of cases. Hemodynamic and angiographic investigation of the left ventricle was completely normal in nearly all cases. Only these patients with clinical, electrocardiographic and metabolic signs of myocardial ischemia can be considered as having angina with normal coronary arteries. Although studies of myocardial lactate metabolism and other signs of myocardial ischemia distinguish clearly between these two groups of patients, the coronary hemodynamics were similar. Resting coronary flow, its increase for the same myocardial oxygen demands and coronary resistances were comparable in both groups, and not significantly different from the values obtained in a control group of patients without coronary artery disease or chest pain. These results confirm that about 30 per cent of patients investigated for chest pain suggestive of angina pectoris who have angiographically normal coronary arteries, develop signs of myocardial ischemia during atrial pacing. The physiopathological explanation remains unclear as coronary hemodynamics have been found to be normal.
60例无器质性心脏病但有提示心绞痛的胸痛症状且冠状动脉造影正常的患者接受了临床、血流动力学和代谢研究。通过心房起搏（168±14次/分钟）期间对心肌乳酸代谢的研究，可将患者分为两组：——40例乳酸摄取系数正常（K≥9%）；——20例乳酸摄取系数病理性降低（K＜9%），提示心肌缺血。第一组中，胸痛常不典型（75%的病例）。血流动力学研究显示48%的病例左心室有轻微异常。这些患者被排除心绞痛诊断。第二组中，大多数患者在最大心率时出现胸痛（85%的病例），伴有明显的ST段压低（80%的病例）。50%的病例胸痛为典型心绞痛。几乎所有病例中左心室的血流动力学和血管造影检查完全正常。只有这些有心肌缺血临床、心电图和代谢体征的患者可被视为冠状动脉正常的心绞痛患者。尽管心肌乳酸代谢研究和其他心肌缺血体征能清楚区分这两组患者，但冠状动脉血流动力学相似。静息冠状动脉血流量、相同心肌需氧量时的增加量以及冠状动脉阻力在两组中相当，且与无冠状动脉疾病或胸痛的对照组患者所测得的值无显著差异。这些结果证实，约30%因提示心绞痛的胸痛症状而接受检查且冠状动脉造影正常的患者，在心房起搏期间出现心肌缺血体征。由于冠状动脉血流动力学正常，其生理病理机制仍不清楚。
