Stambler Bruce S, Akosah Kwame O, Mohanty Pramod K, Wood Mark A, Ellenbogen Kenneth A
Department of Medicine/Cardiology, McGuire Veterans Affairs Medical Center and Medical College of Virginia, Richmond, Virginia, USA.
J Cardiovasc Electrophysiol. 2004 Aug;15(8):901-7. doi: 10.1046/j.1540-8167.2004.04057.x.
This study examined the relationship between dobutamine facilitation of ventricular tachyarrhythmia (VT) inducibility with programmed electrical stimulation (PES) and dobutamine stress-induced myocardial ischemia.
Twenty patients with prior myocardial infarction and cardiac arrest or sustained VT but no sustained VT induced at baseline electrophysiologic testing underwent repeat PES during dobutamine infusion. Ischemia (new or worsened wall-motion abnormality) was documented by echocardiography performed in conjunction with PES. Eight patients were receiving Class I or III antiarrhythmic drugs and seven beta-blockers. Dobutamine facilitated induction of sustained VT in 16 patients (80%) and provoked ischemia in 13 patients (65%). Induction of VT was associated with ischemia in 9 patients (56%). VTs associated with ischemia were induced at higher dobutamine doses (26 +/- 11 vs 11 +/- 10 microg/kg per min, P = 0.02) than were VTs without ischemia (n = 7). Among 13 patients with provoked ischemia, 9 (69%) had VTs induced and 4 remained noninducible. The onset of ischemia occurred at the same dose as induction of VT in 5 patients and at a lower dose in 4 patients. Monomorphic VT (318 +/- 59 ms) was induced in 13 patients, of whom 8 (62%) had ischemia. The ECG morphology of VT suggested an origin in a myocardial segment that demonstrated initial viability at low doses then ischemic dysfunction at higher doses preceding VT induction in 7 (88%) of 8 patients.
Dobutamine enhances inducibility of sustained VTs during PES. The temporal and anatomic association of dobutamine-induced ischemia and VT suggests that at high dobutamine doses, ischemia may contribute to ventricular arrhythmia inducibility in some patients.
本研究探讨了多巴酚丁胺通过程序电刺激(PES)促进室性心律失常(VT)诱发与多巴酚丁胺应激诱导的心肌缺血之间的关系。
20例既往有心肌梗死且发生过心脏骤停或持续性VT但在基线电生理检查时未诱发持续性VT的患者,在多巴酚丁胺输注期间接受重复PES。通过与PES同步进行的超声心动图记录缺血情况(新出现或加重的壁运动异常)。8例患者正在接受I类或III类抗心律失常药物治疗,7例正在接受β受体阻滞剂治疗。多巴酚丁胺使16例患者(80%)诱发持续性VT,使13例患者(65%)出现缺血。9例患者(56%)诱发VT与缺血有关。与无缺血的VT相比,与缺血相关的VT在更高的多巴酚丁胺剂量下诱发(26±11 vs 11±10μg/kg每分钟,P=0.02)(无缺血的VT有7例)。在13例出现缺血的患者中,9例(69%)诱发了VT,4例仍未诱发出VT。5例患者缺血发作与VT诱发的剂量相同,4例患者缺血发作的剂量更低。13例患者诱发了单形性VT(318±59毫秒),其中8例(62%)有缺血。VT的心电图形态提示起源于一个心肌节段,在8例患者中的7例(88%)中,该节段在低剂量时显示初始存活,然后在VT诱发前更高剂量时出现缺血性功能障碍。
多巴酚丁胺可增强PES期间持续性VT的诱发率。多巴酚丁胺诱导的缺血与VT在时间和解剖学上的关联表明,在高多巴酚丁胺剂量下,缺血可能在一些患者中导致室性心律失常的诱发。