title: Left-Ventricular Plication Reduces Wall Stress and Cardiomyocyte Hypertrophy in a Rat Model of Ischemic Cardiomyopathy.
abstract: BACKGROUND
  The indications of left-ventricular plication (LVP) are controversial, although several studies have reported favorable outcomes in heart failure patients. The aim of this study was to assess left-ventricular (LV) wall stress and myocardial remodeling after LVP in a rat model of myocardial infarction (MI).
  
  
  METHODS
  Sixteen rats underwent LVP by excluding the LV anterior wall scar 4 weeks after ligation of the left anterior descending artery. After 4 weeks, LV wall stress was assessed using transthoracic echocardiography and an LV catheter. Gene expression of the wall stress markers, atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP), were evaluated via reverse transcription polymerase chain reaction. Cardiomyocyte area and myocardial fibrosis were also examined through histological examinations. These parameters were compared to those in 16 rats that underwent coronary artery ligation but not LVP.
  
  
  RESULTS
  We noted that the LV end-diastolic dimension was smaller (9.9 ± 0.3 vs. 11.2 ± 0.2 mm, p < 0.05) and fractional shortening was greater (25 ± 2 vs. 15 ± 1%, p < 0.05) in LVP rats than in sham rats. Moreover, systolic wall stress was lower in LVP rats (71 ± 7 vs. 111 ± 9 × 103 dyn/cm2, p < 0.05). Myocardial ANF and BNP expression levels were lower in LVP rats (2.6 ± 0.3 vs. 4.4 ± 0.5 and 1.0 ± 0.1 vs. 1.5 ± 0.2 arbitrary units, respectively; p < 0.05). Cardiomyocyte area was significantly decreased in LVP rats (556 ± 15 vs. 670 ± 28 μm2, p = 0.003) and was correlated with LV wall stress (r = 0.669, p = 0.002). The reduction in myocardial fibrosis after LVP was not significant.
  
  
  CONCLUSIONS
  LVP reduced LV wall stress and cardiomyocyte hypertrophy in a rat model of MI.
authors.affiliation: Department of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
authors.forename: Hidetsugu
authors.initials: H
authors.lastname: Asai
authors.forename: Yasushige
authors.initials: Y
authors.lastname: Shingu
authors.forename: Tomoji
authors.initials: T
authors.lastname: Yamakawa
authors.forename: Haruki
authors.initials: H
authors.lastname: Niwano
authors.forename: Satoru
authors.initials: S
authors.lastname: Wakasa
authors.forename: Tomonori
authors.initials: T
authors.lastname: Ooka
authors.forename: Hiroki
authors.initials: H
authors.lastname: Kato
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Tachibana
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Matsui
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D006328:Cardiac Catheterization; D006348:Cardiac Surgical Procedures / Q000379:methods*; D004195:Disease Models, Animal; D004452:Echocardiography; D006984:Hypertrophy; D008297:Male; D017202:Myocardial Ischemia / Q000473:pathology / Q000601:surgery*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000473:pathology; D009929:Organ Size; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers