Mitrani R D, Klein L S, Miles W M, Hackett F K, Burt R W, Wellman H N, Zipes D P
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202-4800.
J Am Coll Cardiol. 1993 Nov 1;22(5):1344-53. doi: 10.1016/0735-1097(93)90541-8.
The aim of this study was to determine whether patients with ventricular arrhythmias in the absence of coronary artery disease also have abnormalities in sympathetic innervation.
We have previously shown by cardiac sympathetic scintigraphy using iodine-123-metaiodobenzylguanidine (I-123-MIBG) that patients with ventricular tachycardia after myocardial infarction have regional cardiac sympathetic denervation. It is not known whether patients with ventricular tachycardia in the absence of coronary artery disease also have regional cardiac sympathetic denervation.
We performed cardiac I-123-MIBG and thallium-201 single-photon emission computed tomographic (SPECT) scans at rest in 18 patients (mean age 47 +/- 18 years) with cardiomyopathy (n = 6), left ventricular hypertrophy (n = 1), valvular disease (n = 2) or a structurally normal heart (n = 9) who presented with monomorphic (n = 15) or polymorphic (n = 3) ventricular tachycardia. These scans were compared with scans in 12 control patients without ventricular tachycardia (mean age 30 +/- 17 years) who had cardiomyopathy (n = 3) or a structurally normal heart (n = 9). Cardiac sympathetic denervation was defined as myocardial areas having thallium uptake with reduced or absent I-123-MIBG uptake.
Twelve (67%) of 18 patients with ventricular tachycardia had regional cardiac sympathetic denervation compared with 1 (8%) of 12 patients who did not have ventricular tachycardia (p = 0.002). In the nine patients with a structurally normal heart and ventricular tachycardia, five (55%) patients had regional cardiac sympathetic denervation compared with zero of nine control patients with a structurally normal heart (p = 0.029). Five patients underwent right ventricular radiofrequency ablation for ventricular tachycardia, and sympathetic denervation was adjacent to the ablation site in one of these patients.
Patients with ventricular tachycardia in the absence of coronary artery disease have abnormal cardiac sympathetic innervation detectable by cardiac sympathetic scintigraphy. The role of regional cardiac sympathetic denervation in arrhythmogenesis remains to be determined.
本研究旨在确定无冠状动脉疾病的室性心律失常患者是否也存在交感神经支配异常。
我们之前通过使用碘-123-间碘苄胍（I-123-MIBG）的心脏交感神经闪烁显像显示，心肌梗死后室性心动过速患者存在局部心脏交感神经去神经支配。尚不清楚无冠状动脉疾病的室性心动过速患者是否也存在局部心脏交感神经去神经支配。
我们对18例（平均年龄47±18岁）患有心肌病（n = 6）、左心室肥厚（n = 1）、瓣膜病（n = 2）或心脏结构正常（n = 9）且出现单形性（n = 15）或多形性（n = 3）室性心动过速的患者进行了静息状态下的心脏I-123-MIBG和铊-201单光子发射计算机断层扫描（SPECT）。将这些扫描结果与12例无室性心动过速的对照患者（平均年龄30±17岁）的扫描结果进行比较，这些对照患者患有心肌病（n = 3）或心脏结构正常（n = 9）。心脏交感神经去神经支配定义为铊摄取而I-123-MIBG摄取减少或缺失的心肌区域。
18例室性心动过速患者中有12例（67%）存在局部心脏交感神经去神经支配，而12例无室性心动过速的患者中有1例（8%）存在（p = 0.002）。在9例心脏结构正常且有室性心动过速的患者中，5例（55%）存在局部心脏交感神经去神经支配，而9例心脏结构正常的对照患者中无一例存在（p = 0.029）。5例患者因室性心动过速接受了右心室射频消融，其中1例患者的交感神经去神经支配与消融部位相邻。
无冠状动脉疾病的室性心动过速患者存在可通过心脏交感神经闪烁显像检测到的心脏交感神经支配异常。局部心脏交感神经去神经支配在心律失常发生中的作用仍有待确定。
