Sarabanda Alvaro Valentim Lima, Sosa Eduardo, Simões Marcus Vinícius, Figueiredo Geraldo Luís, Pintya Antônio Osvaldo, Marin-Neto José Antônio
Division of Cardiology, Department of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, Hospital das Clínicas-Av. Bandeirantes, 3900, CEP: 14048-900, Ribeirão Preto, SP, Brazil.
Int J Cardiol. 2005 Jun 22;102(1):9-19. doi: 10.1016/j.ijcard.2004.03.087.
Ventricular tachycardia (VT) is common among patients with Chagas' heart disease but the ultimate mechanisms responsible for its sustained and nonsustained forms are not understood. This study aimed at determining which factors differentiate between patients with sustained (S-VT) and nonsustained VT (NS-VT). Fifty-six consecutive chagasic patients with VT were prospectively selected: 28 patients with spontaneous S-VT and 28 patients with NS-VT. The patients underwent clinical, angiographic, electrophysiologic and myocardial perfusion examination. Syncope episodes (S-VT: 43% versus NS-VT: 11%, p = 0.007) and induction of S-VT by programmed ventricular stimulation (S-VT: 89% versus NS-VT: 7%, p = 0.001) were significantly more frequent in S-VT patients. Evidence of a scar-related reentry was observed in all 24 S-VT patients who underwent endocardial mapping for attempted radiofrequency ablation of 33 VTs. Overall, 29 VTs arose from the LV (88%) and 4 VTs arose from the RV (12%). Among these, 27 VTs (82%) were related to LV inferolateral scar, 2 VTs (6%) were related to LV apical scar, and 4 VTs (12%) were related to RV scars. A significantly higher prevalence of wall motion abnormalities (S-VT: 82% versus NS-VT: 46%, p = 0.005) and myocardial perfusion defects (basal segments, S-VT: 95.5% versus NS-VT: 44%, p = 0.001) was documented within the LV inferior and/or posterolateral regions in S-VT patients compared to NS-VT.
(a) VT may arise from various regions in both ventricles, but LV inferolateral scar is the main source of S-VT reentrant circuits; (b) there is good topographic correlation between myocardial perfusion, wall motion abnormalities and areas that originate S-VT; (c) although to a lesser extent, wall motion and perfusion defects also occur in a relevant proportion of chagasics with NS-VT.
室性心动过速（VT）在恰加斯心脏病患者中很常见，但导致其持续性和非持续性形式的最终机制尚不清楚。本研究旨在确定哪些因素可区分持续性室性心动过速（S-VT）患者和非持续性室性心动过速（NS-VT）患者。前瞻性选取了56例连续的患有室性心动过速的恰加斯病患者：28例自发性持续性室性心动过速患者和28例非持续性室性心动过速患者。患者接受了临床、血管造影、电生理和心肌灌注检查。晕厥发作（持续性室性心动过速组：43% 对比非持续性室性心动过速组：11%，p = 0.007）以及程序性心室刺激诱发持续性室性心动过速（持续性室性心动过速组：89% 对比非持续性室性心动过速组：7%，p = 0.001）在持续性室性心动过速患者中显著更常见。在所有24例接受心内膜标测以尝试对33次室性心动过速进行射频消融的持续性室性心动过速患者中均观察到与瘢痕相关的折返证据。总体而言，29次室性心动过速起源于左心室（88%），4次室性心动过速起源于右心室（12%）。其中，27次室性心动过速（82%）与左心室下外侧瘢痕有关，2次室性心动过速（6%）与左心室心尖瘢痕有关，4次室性心动过速（12%）与右心室瘢痕有关。与非持续性室性心动过速患者相比，持续性室性心动过速患者左心室下和/或后外侧区域的壁运动异常（持续性室性心动过速组：82% 对比非持续性室性心动过速组：46%，p = 0.005）和心肌灌注缺损（基底节段，持续性室性心动过速组：95.5% 对比非持续性室性心动过速组：44%，p = 0.001）的患病率显著更高。
（a）室性心动过速可能起源于两个心室的不同区域，但左心室下外侧瘢痕是持续性室性心动过速折返环路的主要来源；（b）心肌灌注、壁运动异常与起源持续性室性心动过速的区域之间存在良好的地形相关性；（c）尽管程度较轻，但壁运动和灌注缺损在相当比例的非持续性室性心动过速恰加斯病患者中也会出现。
