title: A new paradigm for physiologic ventricular pacing.
abstract: Clinical trials in patients with pacemakers for sinus node dysfunction or atrioventricular block (AVB) and implantable cardioverter-defibrillators provide increasing evidence showing that desynchronization of ventricular electrical activation and contraction, induced by conventional right ventricular apex (RVA) pacing, is a serious threat for long-term cardiac morbidity and mortality. The risk of heart failure is increased even in hearts with initially normal pump function and in case of part-time ventricular pacing. These epidemiologic data fit with knowledge from decades of pathophysiological research, indicating that right ventricular (RV) pacing creates abnormal contraction, reduced pump function, hypertrophy, and ultrastructural abnormalities. This paper presents a new paradigm that aims to tailor ventricular pacing to the individual patient to achieve a way of pacing that is as physiologic as possible. In patients without AVB and no intraventricular conduction abnormalities, ventricular pacing should be avoided as much as possible, using atrial-based pacing. In patients with AVB, alternate single-site RV or left ventricular pacing or biventricular pacing may be superior to RVA pacing. Efforts to optimize the pacing mode or site should be greater in patients with a longer expected duration of pacing, poorer cardiac function, and larger mechanical asynchrony. Awareness of the problem of desynchronization should also lead to more regular monitoring of cardiac pump function and mechanical asynchrony in any patient with ventricular pacing.
authors.affiliation: Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. mosweeney@partners.org
authors.forename: Michael O
authors.initials: MO
authors.lastname: Sweeney
authors.forename: Frits W
authors.initials: FW
authors.lastname: Prinzen
mesh_terms: D000818:Animals; D002036:Bundle of His / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D013599:Systole / Q000502:physiology; D018754:Ventricular Dysfunction / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology