title: Patient-specific finite element-based analysis of ventricular myofiber stress after Coapsys: importance of residual stress.
abstract: BACKGROUND
  We sought to determine regional myofiber stress after Coapsys device (Myocor, Inc, Maple Grove, MN) implantation using a finite element model of the left ventricle (LV). Chronic ischemic mitral regurgitation is caused by LV remodeling after posterolateral myocardial infarction. The Coapsys device consists of a single trans-LV chord placed below the mitral valve such that when tensioned it alters LV shape and decreases chronic ischemic mitral regurgitation.
  
  
  METHODS
  Finite element models of the LV were based on magnetic resonance images obtained before (preoperatively) and after (postoperatively) coronary artery bypass grafting with Coapsys implantation in a single patient. To determine the effect of Coapsys and LV before stress, virtual Coapsys was performed on the preoperative model. Diastolic and systolic material variables in the preoperative, postoperative, and virtual Coapsys models were adjusted so that model LV volume agreed with magnetic resonance imaging data. Chronic ischemic mitral regurgitation was abolished in the postoperative models. In each case, myofiber stress and pump function were calculated.
  
  
  RESULTS
  Both postoperative and virtual Coapsys models shifted end-systolic and end-diastolic pressure-volume relationships to the left. As a consequence and because chronic ischemic mitral regurgitation was reduced after Coapsys, pump function was unchanged. Coapsys decreased myofiber stress at end-diastole and end-systole in both the remote and infarct regions of the myocardium. However, knowledge of Coapsys and LV prestress was necessary for accurate calculation of LV myofiber stress, especially in the remote zone.
  
  
  CONCLUSIONS
  Coapsys decreases myofiber stress at end-diastole and end-systole. The improvement in myofiber stress may contribute to the long-term effect of Coapsys on LV remodeling.
authors.affiliation: College of Medicine of the University of Vermont, Burlington, Vermont, USA.
authors.forename: Richard
authors.initials: R
authors.lastname: Carrick
authors.forename: Liang
authors.initials: L
authors.lastname: Ge
authors.forename: Lik Chuan
authors.initials: LC
authors.lastname: Lee
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Zhang
authors.forename: Rakesh
authors.initials: R
authors.lastname: Mishra
authors.forename: Leon
authors.initials: L
authors.lastname: Axel
authors.forename: Julius M
authors.initials: JM
authors.lastname: Guccione
authors.forename: Eugene A
authors.initials: EA
authors.lastname: Grossi
authors.forename: Mark B
authors.initials: MB
authors.lastname: Ratcliffe
mesh_terms: D001794:Blood Pressure / Q000502:physiology*; D002306:Cardiac Volume / Q000502:physiology; D003198:Computer Simulation; D003287:Contrast Media; D001026:Coronary Artery Bypass; D003971:Diastole / Q000502:physiology; D004867:Equipment Design; D020342:Finite Element Analysis; D019786:Gadolinium DTPA; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods; D008297:Male; D008875:Middle Aged; D058386:Mitral Valve Annuloplasty / Q000295:instrumentation*; D008944:Mitral Valve Insufficiency / Q000503:physiopathology* / Q000601:surgery*; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000601:surgery*; D009210:Myofibrils / Q000502:physiology*; D011183:Postoperative Complications / Q000503:physiopathology*; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology* / Q000601:surgery*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D003287:Contrast Media; D019786:Gadolinium DTPA