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J Thorac Cardiovasc Surg 2003;126:1467-1475
© 2003 The American Association for Thoracic Surgery


Cardiopulmonary support and physiology

Passive ventricular constraint to improve left ventricular function and mechanics in an ovine model of heart failure secondary to acute myocardial infarction

James J. Pilla, PhDa, Aaron S. Blom, BAa, Daniel J. Brockman, BVSca, Victor A. Ferrari, MDa, Qing Yuan, PhDa, Michael A. Acker, MD*,a

a Departments of Surgery, Radiology, and Medicine, University of Pennsylvania Medical Center, Philadelphia, Pa, USA

Received for publication June 6, 2002; revisions received August 5, 2002; accepted for publication January 22, 2003.

* Address for reprints: Michael A. Acker, MD, Associate Professor of Surgery, Hospital of the University of Pennsylvania, 6th Floor Silverstein Pavilion, Philadelphia, PA, USA 19104.

OBJECTIVE: This study investigated the effects on global cardiac function and myocardial energetics of limiting progressive dilatation after infarction by means of a woven polyester jacket cardiac support device. We hypothesized that placement of the cardiac support device results in a decrease in myocardial wall stress and improvement in cardiac function and myocardial energetics.

METHODS: To investigate the effect of passive constraint on left ventricular function and mechanics, a total of 10 sheep were studied with pressure-volume analysis and magnetic resonance imaging. A baseline study was followed by the creation of an anterior infarct. After 1 week, the animals underwent a second study. The cardiac support device was then placed over the epicardium in 5 sheep; the remaining animals served as controls. A terminal study was performed at 2 months after the infarct.

RESULTS: The cardiac support device group at the terminal study exhibited a decrease in end-diastolic volume (control 110.3 ± 19.8 mL vs cardiac support device 67.6 ± 4.7 mL, P = .006) and an improved ejection fraction (control 15.5% ± 5.7% vs cardiac support device 29.46% ± 4.42%, P = .008) relative to the control group. Myocardial energetics were also enhanced in the cardiac support device group, as evidenced by the significant improvements in potential energy (control 2015 ± 503 mL · mm Hg/beat vs cardiac support device 885 ± 220 mL · mm Hg/beat, P = .006), efficiency (control 39.4% ± 13.6% vs cardiac support device 59.8% ± 8.5%, P = .044), and oxygen consumption (control 0.072 ± 0.013 mL O2/beat vs cardiac support device 0.052 ± 0.007 mL O2/beat, P = .034).

CONCLUSION: Passive constraint with the cardiac support device after infarct prevents further remodeling and may stimulate reverse remodeling in heart failure secondary to acute myocardial infarction. These results suggest that in human beings placement of the cardiac support device after a large anterior myocardial infarction may be effective in halting the remodeling process that often leads to end-stage heart failure. If proved effective, placement of a cardiac support device after large heart attacks has the potential to decrease the incidence of heart failure that results after large myocardial infarctions.





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