title: Cardiac support device modifies left ventricular geometry and myocardial structure after myocardial infarction.
abstract: 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.
  
  
  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 beta-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.
authors.affiliation: Department of Surgery, University of Pennsylvania Medical Center, Philadelphia, PA, USA.
authors.forename: Aaron S
authors.initials: AS
authors.lastname: Blom
authors.forename: Rupak
authors.initials: R
authors.lastname: Mukherjee
authors.forename: James J
authors.initials: JJ
authors.lastname: Pilla
authors.forename: Abigail S
authors.initials: AS
authors.lastname: Lowry
authors.forename: William M
authors.initials: WM
authors.lastname: Yarbrough
authors.forename: Joseph T
authors.initials: JT
authors.lastname: Mingoia
authors.forename: Jennifer W
authors.initials: JW
authors.lastname: Hendrick
authors.forename: Robert E
authors.initials: RE
authors.lastname: Stroud
authors.forename: Julie E
authors.initials: JE
authors.lastname: McLean
authors.forename: John
authors.initials: J
authors.lastname: Affuso
authors.forename: Robert C
authors.initials: RC
authors.lastname: Gorman
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Gorman
authors.forename: Michael A
authors.initials: MA
authors.lastname: Acker
authors.forename: Francis G
authors.initials: FG
authors.lastname: Spinale
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D003094:Collagen / Q000032:analysis; D005109:Extracellular Matrix / Q000502:physiology; D006353:Heart-Assist Devices; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000032:analysis; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology; D012756:Sheep; D019714:Tissue Inhibitor of Metalloproteinases / Q000032:analysis; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D000199:Actins; D019714:Tissue Inhibitor of Metalloproteinases; D003094:Collagen; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9