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Eur J Cardiothorac Surg 2007;31:55-64. doi:10.1016/j.ejcts.2006.09.024
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Effect of passive cardiac containment on ventricular synchrony and cardiac function in awake dogs

^a Department of Surgery, Division of Cardiothoracic Surgery, Columbia University, College of Physicians and Surgeons, New York, NY, United States
^b Department of Medicine, Division of Cardiology, Columbia University, College of Physicians and Surgeons, New York, NY, United States
^c Department of Cardiac-Nephrology, Chinese PLA General Hospital, Beijing, PR China
^d Department of Biomedical Engineering, Columbia University, New York, NY, United States
^e The Jack Skirball Center for Cardiovascular Research, Orangeburg, NY, United States
^f Institute of Molecular and Experimental Therapeutics, East China Normal University, Shanghai, PR China

Received 16 May 2006; received in revised form 18 September 2006; accepted 20 September 2006.

^_* Correspondence to: Kun-Lun He, Chinese PLA General Hospital, Beijing, PR China. Tel.: +86 10 6815270; fax: +86 10 68181689 or Jie Wang, Institute of Molecular and Experimental Therapeutics, East China Normal University, Shanghai, PR China. Tel.: +86 201 888 0809; fax: +86 201 541 7088. (Email: hekunlun2002{at}yahoo.com; drjiewang{at}gmail.com).

Objective: Passive restraint of the left ventricle (LV) has been shown to have beneficial effects on acute hemodynamics and reverse remodeling in both animal and human models. The goals of this study were to test whether a left ventricular support device (LVSD) improves LV synchrony and/or affects cardiac performance. Methods: Ten dogs were chronically instrumented to measure hemodynamics and LV volume (sonomicrometry). Congestive heart failure (CHF) was induced by repeated intracoronary microembolization via a chronically implanted coronary catheter. The LVSD was implanted after establishment of CHF in five animals, and five animals were observed as controls. All animals were then observed for 8 weeks. A mathematical model to measure LV synchrony was used to evaluate LV motion over time. Results: Mean arterial pressure and LV pressures was significantly increased after LVSD therapy, and LV pressure–volume relationships were shifted leftwards, although no change was seen in ejection fraction, end-systolic elastance, or LV dP/dt versus control. There was no significant change in diastolic function in LVSD animals compared with control animals. End-diastolic volumes were reduced by 15% after 8 weeks with LVSD treatment, versus an increase of 8% in control animals (p < 0.05). Synchrony was significantly improved with LVSD therapy compared with control (9% vs 76% of baseline) in 1 of 11 ventricular dimension axes (Anterior–Apex). Conclusions: LVSD therapy provided only minimal improvement in ventricular synchrony and partially improved hemodynamics. Further study into mechanisms of benefit are warranted.

Key Words: Heart failure surgery • Myocardial remodeling • Cardiac function