Background One third of patients with chronic heart failurehave electrocardiographic evidence of a major intraventricularconduction delay, which may worsen left ventricular systolicdysfunction through asynchronous ventricular contraction. Uncontrolledstudies suggest that multisite biventricular pacing improveshemodynamics and well-being by reducing ventricular asynchrony.We assessed the clinical efficacy and safety of this new therapy.
Methods Sixty-seven patients with severe heart failure (NewYork Heart Association class III) due to chronic left ventricularsystolic dysfunction, with normal sinus rhythm and a durationof the QRS interval of more than 150 msec, received transvenousatriobiventricular pacemakers (with leads in one atrium andeach ventricle). This single-blind, randomized, controlled crossoverstudy compared the responses of the patients during two periods:a three-month period of inactive pacing (ventricular inhibitedpacing at a basic rate of 40 bpm) and a three-month period ofactive (atriobiventricular) pacing. The primary end point wasthe distance walked in six minutes; the secondary end pointswere the quality of life as measured by questionnaire, peakoxygen consumption, hospitalizations related to heart failure,the patients' treatment preference (active vs. inactive pacing),and the mortality rate.
Results Nine patients were withdrawn from the study before randomization,and 10 failed to complete both study periods. Thus, 48 patientscompleted both phases of the study. The mean (±SD) distancewalked in six minutes was 23 percent greater with active pacing(399±100 m vs. 326±134 m, P<0.001), the quality-of-lifescore improved by 32 percent (P<0.001), peak oxygen uptakeincreased by 8 percent (P<0.03), hospitalizations were decreasedby two thirds (P<0.05), and active pacing was preferred by85 percent of the patients (P<0.001).
Conclusions Although it is technically complex, atriobiventricularpacing significantly improves exercise tolerance and qualityof life in patients with chronic heart failure and intraventricularconduction delay.
Source Information
From InParys, Saint-Cloud, France (S.C.); the Centre Cardio-Pneumologique, Centre Hospitalier Universitaire, Rennes, France (C. Leclercq, J.-C.D.), Hôpital Broussais, Paris (T.L.); Harefield Hospital, Harefield, United Kingdom (S.W.); St. George's Hospital, London (C.V.); Karolinska Hospital, Stockholm, Sweden (C. Linde); Hôpital Cardiologique du Haut Levêque, Bordeaux, France (S.G.); Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland (L.K.); Derriford Hospital, Plymouth, United Kingdom (G.A.H.); Ospedale San Filippo Neri, Rome (M.S.); and ELA Recherche, Le Plessis Robinson, France (C.B.). Other authors were Philippe Mabo, M.D. (Centre Cardio-Pneumologique); Arnaud Lazarus, M.D. (InParys); Philippe Ritter, M.D. (Hôpital Broussais); Terry Levy, M.D. (Harefield Hospital); and William McKenna, M.D. (St. George's Hospital).
Address reprint requests to Dr. Daubert at the Département de Cardiologie et Maladies Vasculaires, Centre Cardio-Pneumologique, Hôpital Pontchaillou–Centre Hospitalier Universitaire, 35033 Rennes CEDEX, France, or at jean-claude.daubert{at}CHU-rennes.fr.
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