Sroubek Jakub, Probst Vincent, Mazzanti Andrea, Delise Pietro, Hevia Jesus Castro, Ohkubo Kimie, Zorzi Alessandro, Champagne Jean, Kostopoulou Anna, Yin Xiaoyan, Napolitano Carlo, Milan David J, Wilde Arthur, Sacher Frederic, Borggrefe Martin, Ellinor Patrick T, Theodorakis George, Nault Isabelle, Corrado Domenico, Watanabe Ichiro, Antzelevitch Charles, Allocca Giuseppe, Priori Silvia G, Lubitz Steven A
From Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, MA (J.S.); Service de Cardiologue du CHU de Nantes, CHU de Nantes, Hôpital Nord, Nantes, France (V.P.); Molecular Cardiology, IRCCS Fondazione Salvatore Maugeri, Pavia, Italy (A.M., C.N., S.G.P.); Dipartimento di Medicina, Molecolare Università di Pavia, Pavia, Italy (S.G.P.); Division of Cardiology, Casa di Cura Pederzoli, Peschiera del Garda, Verona, Italy (P.D.); Arrhythmia Unit, Cardiovascular Surgery and Cardiology Institute, Havana, Cuba (J.C.H.); Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan (K.O., I.W.); Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padova, Italy (A.Z., D.C.); Institut Universitaire de Cardiologie et Pneumologie de Québec, Quebec City, QC, Canada (J.C., I.N.); Department of Electrophysiology and Pacing, Onassis Cardiac Surgery Center, Athens, Greece (A.K., G.T.); Boston University and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA (X.Y.); Cardiovascular Research Center and Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston (D.J.M., P.T.E., S.A.L.); Heart Centre AMC, Department of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands (A.W.); Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, Kingdom of Saudi Arabia (A.W.); Bordeaux University Hospital, LIRYC Institute/INSERM 1045, Bordeaux, France (F.S.); First Department of Medicine-Cardiology, University Medical Centre Mannheim, Mannheim, Germany (M.B.); DZHK (German Centre for Cardiovascular Research), partner site Heidelberg/Mannheim, Mannheim, Germany (M.B.); Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA (P.T.E., S.A.L.); Department of Cardiology, General Hospital of Conegliano, Conegliano, Treviso, Italy (G.A.); and Lankenau I
Circulation. 2016 Feb 16;133(7):622-30. doi: 10.1161/CIRCULATIONAHA.115.017885. Epub 2016 Jan 21.
The role of programmed ventricular stimulation in identifying patients with Brugada syndrome at the highest risk for sudden death is uncertain.
We performed a systematic review and pooled analysis of prospective, observational studies of patients with Brugada syndrome without a history of sudden cardiac arrest who underwent programmed ventricular stimulation. We estimated incidence rates and relative hazards of cardiac arrest or implantable cardioverter-defibrillator shock. We analyzed individual-level data from 8 studies comprising 1312 patients who experienced 65 cardiac events (median follow-up, 38.3 months). A total of 527 patients were induced into arrhythmias with up to triple extrastimuli. Induction was associated with cardiac events during follow-up (hazard ratio, 2.66; 95% confidence interval [CI], 1.44-4.92, P<0.001), with the greatest risk observed among those induced with single or double extrastimuli. Annual event rates varied substantially by syncope history, presence of spontaneous type 1 ECG pattern, and arrhythmia induction. The lowest risk occurred in individuals without syncope and with drug-induced type 1 patterns (0.23%, 95% CI, 0.05-0.68 for no induced arrhythmia with up to double extrastimuli; 0.45%, 95% CI, 0.01-2.49 for induced arrhythmia), and the highest risk occurred in individuals with syncope and spontaneous type 1 patterns (2.55%, 95% CI, 1.58-3.89 for no induced arrhythmia; 5.60%, 95% CI, 2.98-9.58 for induced arrhythmia).
In patients with Brugada syndrome, arrhythmias induced with programmed ventricular stimulation are associated with future ventricular arrhythmia risk. Induction with fewer extrastimuli is associated with higher risk. However, clinical risk factors are important determinants of arrhythmia risk, and lack of induction does not necessarily portend low ventricular arrhythmia risk, particularly in patients with high-risk clinical features.
程控心室刺激在识别 Brugada 综合征猝死风险最高的患者中的作用尚不确定。
我们对无心脏骤停病史且接受程控心室刺激的 Brugada 综合征患者的前瞻性观察性研究进行了系统评价和汇总分析。我们估计了心脏骤停或植入式心律转复除颤器电击的发生率和相对风险。我们分析了 8 项研究的个体水平数据,这些研究包括 1312 名经历了 65 次心脏事件的患者(中位随访时间为 38.3 个月)。共有 527 名患者被诱发出心律失常,刺激次数最多达三联律。诱发与随访期间的心脏事件相关(风险比为 2.66;95%置信区间[CI]为 1.44 - 4.92,P<0.001),在单次或双次额外刺激诱发的患者中观察到的风险最高。年度事件发生率因晕厥病史、自发性 1 型心电图模式的存在以及心律失常的诱发情况而有很大差异。风险最低的是没有晕厥且有药物诱发 1 型模式的个体(对于双次额外刺激以内未诱发心律失常的情况,95%CI 为 0.23%,0.05 - 0.68;对于诱发心律失常的情况,95%CI 为 0.45%,0.01 - 2.49),风险最高的是有晕厥且有自发性 1 型模式的个体(对于未诱发心律失常的情况,95%CI 为 2.55%,1.58 - 3.89;对于诱发心律失常的情况,95%CI 为 5.60%,2.98 - 9.58)。
在 Brugada 综合征患者中,程控心室刺激诱发的心律失常与未来室性心律失常风险相关。较少额外刺激诱发与较高风险相关。然而,临床风险因素是心律失常风险的重要决定因素,未诱发并不一定预示室性心律失常风险低,特别是在具有高危临床特征的患者中。