Paganelli F, Barnay P, Imbert-Joscht I, Gelisse R, Saadjian A, Mundler O, Lévy S
Division of Cardiology, Hospital Nord, University of Marseilles, School of Medicine, France.
Eur Heart J. 2001 Oct;22(20):1931-7. doi: 10.1053/euhj.2001.2628.
The purpose of this study was to assess the possible effect of residual myocardial ischaemia on induced ventricular arrhythmia during programmed ventricular stimulation in survivors of a first acute myocardial infarction.
Most deaths after hospital discharge for acute myocardial infarction are sudden and presumably arrhythmic. Sudden cardiac death results from a dynamic interaction of structural abnormalities and transient triggering factors. The role of myocardial ischaemia as a trigger for ventricular arrhythmias remains unclear. We hypothesized that residual myocardial ischaemia after a first acute myocardial infarction is a potent trigger for sustained ventricular tachyarrhythmias, particularly in the presence of an abnormal myocardium.
In this prospective study, programmed electrical stimulation, coronary angiography and dipyridamole-thallium-201 scintigraphy single-photon emission computed tomography were performed in 90 consecutive survivors of a first acute myocardial infarction. Patients, divided in two groups - group 1 with induced ventricular tachyarrhythmia (n=24) and group 2 without induced ventricular tachyarrhythmia (n=66) - were compared regarding residual myocardial ischaemia. The two groups were comparable in terms of mean left ventricular ejection fraction, infarct size and location, gender ratio, peak creatine kinase value, and extent of coronary disease. Residual myocardial ischaemia was detected in 32 patients: 15 (42.5%) belonged to group 1 and 17 (25.7%) to group 2. There was a statistically significant difference between the two groups regarding the presence and the extent of residual myocardial ischaemia (P<0.05).
Residual myocardial ischaemia, revealed by dipyridamole-thallium-201 scintigraphy following a first acute myocardial infarction, might contribute to electrical instability evaluated by programmed ventricular stimulation.
本研究旨在评估首次急性心肌梗死幸存者在程序性心室刺激期间残余心肌缺血对诱发室性心律失常的可能影响。
急性心肌梗死后出院的大多数死亡是突然发生的，推测为心律失常性死亡。心脏性猝死是由结构异常和短暂触发因素的动态相互作用导致的。心肌缺血作为室性心律失常触发因素的作用仍不清楚。我们假设首次急性心肌梗死后的残余心肌缺血是持续性室性快速心律失常的有力触发因素，尤其是在存在异常心肌的情况下。
在这项前瞻性研究中，对90例连续的首次急性心肌梗死幸存者进行了程序性电刺激、冠状动脉造影和双嘧达莫 - 铊 - 201心肌灌注单光子发射计算机断层扫描。将患者分为两组——诱发室性快速心律失常的第1组（n = 24）和未诱发室性快速心律失常的第2组（n = 66）——比较两组的残余心肌缺血情况。两组在平均左心室射血分数、梗死面积和部位、性别比例、肌酸激酶峰值以及冠状动脉疾病程度方面具有可比性。32例患者检测到残余心肌缺血：第1组有15例（42.5%），第2组有17例（25.7%）。两组在残余心肌缺血的存在和程度方面存在统计学显著差异（P<0.05）。
首次急性心肌梗死后双嘧达莫 - 铊 - 201心肌灌注单光子发射计算机断层扫描显示的残余心肌缺血可能导致程序性心室刺激评估的电不稳定性。
