title: Uremia aggravates left ventricular remodeling after myocardial infarction.
abstract: BACKGROUND
  Renal failure is a well-established cardiovascular risk factor. We hypothesized that uremia negatively affects post-myocardial infarction (MI) remodeling and left ventricular (LV) function and examined the pathohistological correlations.
  
  
  METHODS
  Subtotally nephrectomized rats (SNX) and controls with MI only (MIC) were examined 1, 4 and 8 weeks after MI. MI size, ejection fraction (EF), cardiac fibrosis, vascular density and cardiomyocyte density were studied.
  
  
  RESULTS
  The extension of MI was 0.08 +/- 0.02 in SNX versus 0.06 +/- 0.02 in MIC rats (p < 0.031). Prior to MI, EF was comparable in SNX and MIC (74 +/- 3 vs. 72 +/- 2%, n.s.). Despite a relatively small infarct size EF in SNX decreased to 58 +/- 4% 1 week after infarction and progressively worsened to 51 +/- 4% after 8 weeks. In MIC animals EF only slightly decreased 1 week after MI (70 +/- 3%) and remained unchanged at follow-up. In SNX animals LV end-diastolic diameter continuously increased following MI throughout the study period indicating accelerated remodeling. Furthermore, accelerated myocardial fibrosis was already notable 1 week after MI in SNX animals and the volume density of capillaries and cardiomyocytes was significantly lower in SNX rats.
  
  
  CONCLUSIONS
  MI in experimental uremia is associated with progressive impairment of LV function, LV dilatation and accelerated myocardial fibrosis.
authors.affiliation: Department of Nephrology, University of Heidelberg, Heidelberg, Germany.
authors.forename: Ralf
authors.initials: R
authors.lastname: Dikow
authors.forename: Ulrike
authors.initials: U
authors.lastname: Schmidt
authors.forename: Lars P
authors.initials: LP
authors.lastname: Kihm
authors.forename: Matthias
authors.initials: M
authors.lastname: Schaier
authors.forename: Vedat
authors.initials: V
authors.lastname: Schwenger
authors.forename: Marie-Luise
authors.initials: ML
authors.lastname: Gross
authors.forename: Hugo A
authors.initials: HA
authors.lastname: Katus
authors.forename: Martin
authors.initials: M
authors.lastname: Zeier
authors.forename: Stefan E
authors.initials: SE
authors.lastname: Hardt
mesh_terms: D000818:Animals; D001706:Biopsy; D001794:Blood Pressure; D001835:Body Weight; D024141:Collagen Type IV / Q000378:metabolism; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004452:Echocardiography; D005355:Fibrosis; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D008297:Male; D009017:Morbidity; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D014511:Uremia / Q000453:epidemiology / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D024141:Collagen Type IV