title: Subendocardial fibrosis in remote myocardium results from reduction of coronary driving pressure during acute infarction in rats.
abstract: OBJECTIVE
  To investigate the role of hemodynamic changes occurring during acute MI in subsequent fibrosis deposition within non-MI.
  
  
  METHODS
  By using the rat model of MI, 3 groups of 7 rats each [sham, SMI (MI <30%), and LMI (MI >30%)] were compared. Systemic and left ventricular (LV) hemodynamics were recorded 10 minutes before and after coronary artery ligature. Collagen volume fraction (CVF) was calculated in picrosirius red-stained heart tissue sections 4 weeks later.
  
  
  RESULTS
  Before surgery, all hemodynamic variables were comparable among groups. After surgery, LV end-diastolic pressure increased and coronary driving pressure decreased significantly in the LMI compared with the sham group. LV dP/dt max and dP/dt min of both the SMI and LMI groups were statistically different from those of the sham group. CVF within non-MI interventricular septum and right ventricle did not differ between each MI group and the sham group. Otherwise, subendocardial (SE) CVF was statistically greater in the LMI group. SE CVF correlated negatively with post-MI systemic blood pressure and coronary driving pressure, and positively with post-MI LV dP/dt min. Stepwise regression analysis identified post-MI coronary driving pressure as an independent predictor of SE CVF.
  
  
  CONCLUSIONS
  LV remodeling in rats with MI is characterized by predominant SE collagen deposition in non-MI and results from a reduction in myocardial perfusion pressure occurring early on in the setting of MI.
authors.affiliation: Medical School, University of São Paulo, São Paulo, Brazil. frimm@emercli.fm.usp.br
authors.forename: Clovis
authors.initials: C
authors.lastname: de Carvalho Frimm
authors.forename: Marcia Kiyomi
authors.initials: MK
authors.lastname: Koike
authors.forename: Mariana
authors.initials: M
authors.lastname: Cúri
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004699:Endocardium / Q000473:pathology*; D005355:Fibrosis / Q000473:pathology; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D020257:Ventricular Remodeling