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Acute Hemodynamic Effects of Atrial Pacing with Cardiac Resynchronization Therapy


  • This study was supported by Boston Scientific Corporation CRM, St. Paul, Minnesota, USA.

  • Dr. Gold has received research grants, honoraria, and serves as a consultant to Boston Scientific. Dr. Niazi and Dr. Leman received research grants from Boston Scientific. Dr. Giudici received research grants from Boston Scientific and Ablation Frontiers. Dr. Kim received a research grant from Boston Scientific and serves on the advisory board of Medtronic. Mr. Waggoner has received honoraria and serves as a consultant for Boston Scientific Inc. Dr. Sturdivant participated in clinical trials sponsored by St. Jude Medical, Boston Scientific, sanofi-aventis, Medtronic, Cameron Health, Boehringer Ingelheim Pharnaceuticals, ProRhythm, Guidant, Aryx Therapeutics, Vicor Technologies, Biotronik Inc., and Bristol Myers Squibb. Dr. Ding, Ms. Arcot-Krishnamurthy, Dr. Daum, and Ms. Yu are employees of Boston Scientific Inc.

Address for correspondence: Michael R. Gold, M.D., Ph.D., Division of Cardiology, Medical University of South Carolina, 25 Courtenay Drive, Room 7031 ART, MSC 592, Charleston, SC 29425, USA. Fax: 843-876-4809; E-mail:


Background: Chronotropic incompetence is common among patients with advanced heart failure (HF), thus atrial pacing (AP) is frequently utilized in this population. The hemodynamic effects of AP during cardiac resynchronization therapy (CRT) have not been well studied.

Objective: The purpose of this study was to compare the acute hemodynamic response during CRT of AP with that during atrial sensing (AS).

Methods: This study included 26 patients undergoing CRT. At implant, invasive left ventricular (LV) dP/dt was measured by a micromanometer catheter during biventricular pacing in AS and AP modes at 5 different atrioventricluar delays (AVD), tested in randomized order. Postimplant, echocardiography was performed to obtain aortic and mitral flow velocity integrals at baseline (no CRT) and during CRT.

Results: Compared with intrinsic rhythm, CRT increased LV dP/dt by 11 ± 11% during AS (heart rate: 74 ± 13 bpm) and by 17 ± 11% during AP (heart rate: 86 ± 12 bpm, P < 0.001). The AVD associated with maximal hemodynamic response (AVDmax) during AP was 72 ± 40 ms longer than during AS. However, aortic and mitral flow velocity integrals decreased by 15–20% during AP. The aortic and mitral flow velocities at AVDmax for LV dP/dtmax were highly correlated with their maximum values (r > 0.98).

Conclusion: AP increases LV dP/dt during CRT, but requires a substantially longer AV delay. However, AP results in modest reductions of LV filling and stoke volume. Further studies are needed to assess the long-term impact of AP on HF functional status and LV remodeling.

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