doi: 10.1161/CIRCULATIONAHA.104.499202
(Circulation. 2005;112:1274-1283.)
© 2005 American Heart Association, Inc.
Cardiovascular Surgery |
Cardiac Support Device Modifies Left Ventricular Geometry and Myocardial Structure After Myocardial Infarction
From the Departments of Surgery (A.S.B., J.A., R.C.G., J.H.G., M.A.A.) and Radiology (J.J.P.), University of Pennsylvania Medical Center, Philadelphia; Division of Cardiothoracic Surgery (R.M., A.S.L., W.M.Y., J.T.M., J.W.H., R.E.S., J.E.M., F.G.S.), Medical University of South Carolina, Charleston; and Ralph H. Johnson Department of Veterans Affairs (F.G.S.), Charleston, SC.
Correspondence to Michael A. Acker, MD, Professor of Surgery and Chief, Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, 6th Floor Silverstein Pavilion, Philadelphia, PA 19104. E-mail macker{at}mail.med.upenn.edu
Received August 10, 2004; revision received March 25, 2005; accepted April 7, 2005.
Background— Whether mechanical restraint of the left ventricle (LV) can influence remodeling after myocardial infarction (MI) remains poorly understood. This study surgically placed a cardiac support device (CSD) over the entire LV and examined LV and myocyte geometry and function after MI.
Methods and Results— Post-MI sheep (35 to 45 kg; MI size, 23±2%) were randomized to placement of the CorCap CSD (Acorn Cardiovascular, Inc) (MI+CSD; n=6) or remained untreated (MI only; n=5). Uninstrumented sheep (n=10) served as controls. At 3 months after MI, LV end-diastolic volume (by MRI) was increased in the MI only group compared with controls (98±8 versus 43±4 mL; P<0.05). In the MI+CSD group, LV end-diastolic volume was lower than MI only values (56±7 mL; P<0.05) but remained higher than controls (P<0.05). Isolated LV myocyte shortening velocity was reduced by 35% from control values (P<0.05) in both MI groups. LV myocyte ß-adrenergic response was reduced with MI but normalized in the MI+CSD group. LV myocyte length increased in the MI group and was reduced in the MI+CSD group. Relative collagen content was increased and matrix metalloproteinase-9 was decreased within the MI border region of the CSD group.
Conclusions— A CSD beneficially modified LV and myocyte remodeling after MI through both cellular and extracellular mechanisms. These findings provide evidence that nonpharmacological strategies can interrupt adverse LV remodeling after MI.
Key Words: collagen • contractility • myocardial infarction • matrix metalloproteinases • heart-assist device
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Circulation 2005 112: 1245-1247.
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