title: High dose aspirin and left ventricular remodeling after myocardial infarction: aspirin and myocardial infarction.
abstract: BACKGROUND
  Proinflammatory proteins like inflammatory cytokines are implicated in myocardial depression and left ventricular remodeling after myocardial infarction. High-dose aspirin inhibits cytokine activation. Therefore, we tested the influence of high-dose aspirin treatment on left ventricular remodeling in mice after myocardial infarction.
  
  
  RESULTS
  Mice were treated for 4 weeks with placebo or aspirin (120 mg/kg per day) by Alzet mini-osmotic pumps after ligation of the left anterior descending coronary artery. Serial transthoracic echocardiography was performed at days 1, 7, and 28. Over the 4 weeks, mortality was not different between the groups (placebo 30.8%, aspirin 30.8%). On echocardiography, animals after myocardial infarction exhibited left ventricular dilatation (week 4, end-systolic area, placebo sham 8.9 +/- 1.7 vs. placebo MI 15.9 +/- 2.5 mm(2)), which was not changed by aspirin treatment (week 4, end-systolic area, aspirin MI 14.5 +/- 1.3 mm(2), p= ns vs. placebo MI). The expression of the proinflammatory cytokines TNF and IL-1beta were markedly upregulated in mice with myocardial infarction on placebo. Cytokine expression was significantly reduced by aspirin treatment while collagen deposition was not influenced.
  
  
  CONCLUSIONS
  Continuous aspirin treatment (120 mg/kg/d) reduces the expression of proinflammatory cytokines after myocardial infarction, but does not affect post-infarct cardiac remodeling and cardiac function.
authors.affiliation: Medizinische Klinik und Poliklinik I der Universität Würzburg, Josef Schneider-Strasse 2, 97080 Würzburg, Germany.
authors.forename: Anna
authors.initials: A
authors.lastname: Adamek
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Barbara
authors.initials: B
authors.lastname: Bayer
authors.forename: Helga
authors.initials: H
authors.lastname: Wagner
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Johann
authors.initials: J
authors.lastname: Bauersachs
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D003094:Collagen / Q000378:metabolism; D003331:Coronary Vessels / Q000601:surgery; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D015918:Infusion Pumps, Implantable; D053583:Interleukin-1beta / Q000378:metabolism; D008026:Ligation; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016277:Ventricular Function, Left / Q000187:drug effects*; D017725:Ventricular Pressure / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D003094:Collagen; D001241:Aspirin