MYOCARDIAL FUNCTION DURING ATRIAL-PACING IN PATIENTS WITH ANGINA-PECTORIS AND NORMAL CORONARY ARTERIOGRAMS - COMPARISON WITH PATIENTS HAVING SIGNIFICANT CORONARY-ARTERY DISEASE
MYOCARDIAL FUNCTION DURING ATRIAL-PACING IN PATIENTS WITH ANGINA-PECTORIS AND NORMAL CORONARY ARTERIOGRAMS - COMPARISON WITH PATIENTS HAVING SIGNIFICANT CORONARY-ARTERY DISEASE
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DOI：
10.1016/s0002-9149(73)80130-4
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发表时间：
1973-01-01
影响因子：
2.8
通讯作者：
BOURASSA, MG
中科院分区：
文献类型：
--
作者：
ARBOGAST, R;BOURASSA, MG
10例冠状动脉造影正常且胸痛通常为典型心绞痛的患者（X组）右心房起搏140次/分，持续8分钟，诱发心电图“缺血型”。将结果与11例明显冠状动脉狭窄患者进行比较，这些患者在起搏期间具有相同的心电图“缺血模式”（C组）。X组6例，C组8例在起搏过程中出现心绞痛。此外，5例X组患者和7例c组患者在起搏过程中出现低水平的心肌提取（小于10%）或乳酸生成。X组患者心脏指数（P<0.05）和左心室分功指数（P<0.01）显著升高，左心室舒张末期压显著降低（P<0.01），全身血管阻力不变。C组患者心脏指数明显降低（P<0.01），左室分功指数和左室舒张末期压不变，全身血管阻力升高（P<0.001）。通过绘制左心室卒中工作指数与左心室舒张压的关系得出的“起搏心室功能曲线”显示出两组患者之间的显著差异。尽管两组的临床、心电图和代谢表现相似，但这些异常的机制可能不同。的确，如果心绞痛综合征和正常冠状动脉的患者发生心肌缺血，他们应该像冠状动脉疾病的患者一样，在起搏压力下表现为左心室功能下降或不变，而不是增强。
Right atrial pacing at 140 beats/min for 8 minutes induced an electrocardiographic “ischemic pattern” in 10 patients with normal coronary arteriograms and chest pain usually typical of angina pectoris (group X). The findings were compared with those in 11 patients with demonstrable coronary arterial stenosis who had the same electrocardiographic “ischemic pattern” during pacing (group C). Six patients of group X and eight patients of group C experienced angina during pacing. In addition, a low level of myocardial extraction (less than 10 percent) or production of lactate was observed during pacing in five patients of group X and in seven of group C. Patients of group X showed a significant rise in cardiac index (P<0.05) and left ventricular minute work index (P<0.01), a significant reduction in left ventricular end-diastolic pressure (P<0.01) and unchanged systemic vascular resistance. In contrast, patients of group C showed a significant lowering of cardiac index (P<0.01), unchanged left ventricular minute work index and left ventricular end-diastolic pressure and increased systemic vascular resistance (P<0.001). “Pacing ventricular function curves,” obtained by plotting left ventricular stroke work index against left ventricular enddiastolic pressure, showed marked differences between the two groups. Although the clinical, electrocardiographic and metabolic manifestations were similar in both groups, the mechanism underlying these abnormalities is probably different. Indeed, if patients with the anginal syndrome and normal coronary arteries had myocardial ischemia, they should, like patients with coronary artery disease, exhibit a depressed or unchanged rather than enhanced left ventricular function during pacing stress.