title: Regional remodeling strain and its association with myocardial apoptosis after myocardial infarction in an ovine model.
abstract: OBJECTIVE
  Progressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling.
  
  
  METHODS
  Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins.
  
  
  RESULTS
  At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 +/- 0.1 mm Hg, a decrease in ejection fraction from 54.19% +/- 5.68% to 30.55% +/- 2.72%, and an end-diastolic volume increase of 46.08 +/- 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.27, P < .05), caspase-3 (r(2) = 0.31, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.28, P < .05), caspase-3 (r(2) = 0.43, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.37, P < .05).
  
  
  CONCLUSIONS
  Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.
authors.affiliation: Department of Surgery, University of Maryland, Baltimore, MD 21201, USA.
authors.forename: Godfred K
authors.initials: GK
authors.lastname: Yankey
authors.forename: Tieluo
authors.initials: T
authors.lastname: Li
authors.forename: Ahmet
authors.initials: A
authors.lastname: Kilic
authors.forename: Guangming
authors.initials: G
authors.lastname: Cheng
authors.forename: Aditee
authors.initials: A
authors.lastname: Satpute
authors.forename: Kinjal
authors.initials: K
authors.lastname: Savai
authors.forename: Shuying
authors.initials: S
authors.lastname: Li
authors.forename: Sina L
authors.initials: SL
authors.lastname: Moainie
authors.forename: Deyanira
authors.initials: D
authors.lastname: Prastein
authors.forename: Christopher
authors.initials: C
authors.lastname: DeFillipi
authors.forename: Zhongjun J
authors.initials: ZJ
authors.lastname: Wu
authors.forename: Bartley P
authors.initials: BP
authors.lastname: Griffith
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D007150:Immunohistochemistry; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D012756:Sheep; D020257:Ventricular Remodeling / Q000502:physiology*