title: Myocardial infarction scar plication in the rat: cardiac mechanics in an animal model for surgical procedures.
abstract: BACKGROUND
  The immediate effects of surgical reduction of left ventricle cavity on cardiac mechanics have not been well defined.
  
  
  METHODS
  Cardiac mechanics were analyzed before and after myocardial infarction scar plication in 11 isolated infarcted rat hearts.
  
  
  RESULTS
  Despite a decrease in myocardial stiffness, an increase in chamber stiffness was noted after myocardial infarction scar plication. Systolic function was favored in more than one way. For the same diastolic pressures, maximal developed pressures were higher after myocardial infarction scar plication, and the slope of the systolic pressure-volume relationship was steeper afterwards as compared with before; this means that Frank-Starling recruitment is accentuated in smaller cavities. In addition, the developed net forces needed to generate these pressures were clearly lower afterward than before, indicating reduced ventricular afterload.
  
  
  CONCLUSIONS
  The study results show that diastolic function is harmed and systolic function is favored by myocardial infarction scar plication. We suggest that preoperative evaluation of the degree of diastolic dysfunction and impairment of the Frank-Starling mechanism may help to identify patients who may have a poor postoperative outcome due to diastolic or systolic dysfunction.
authors.affiliation: Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Rosemeire M
authors.initials: RM
authors.lastname: Kanashiro
authors.forename: Emilia
authors.initials: E
authors.lastname: Nozawa
authors.forename: Neif
authors.initials: N
authors.lastname: Murad
authors.forename: Luis R
authors.initials: LR
authors.lastname: Gerola
authors.forename: Valdir A
authors.initials: VA
authors.lastname: Moisés
authors.forename: Paulo J F
authors.initials: PJ
authors.lastname: Tucci
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology / Q000601:surgery*; D002921:Cicatrix / Q000503:physiopathology / Q000601:surgery*; D004195:Disease Models, Animal; D006333:Heart Failure / Q000503:physiopathology / Q000601:surgery*; D006439:Hemodynamics / Q000502:physiology*; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology / Q000601:surgery*; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000601:surgery*; D016277:Ventricular Function, Left / Q000502:physiology