title: Down-regulation of apoptosis after left ventricular aneurysm repair.
abstract: BACKGROUND
  Apoptosis is a common feature of the cardiomyopathic process contributing to progressive decline in ventricular function after transmural myocardial infarction. We hypothesized that left ventricular aneurysm repair (LVAR) down-regulates apoptotic potential of cardiomyocytes in the surviving myocardium.
  
  
  METHODS
  In the rat infarct model, LV aneurysms were repaired by pursestring suture 2 weeks after coronary artery ligation. Cardiac function and myocardial infarction size were assessed by echocardiography and transverse heart sections, respectively, before sacrifice 12 weeks later. Cardiomyocytes and TdT-mediated dUTP terminal nick-end labeling (TUNEL) assays of apoptotic nuclei were analyzed adjacent to and remote from the aneurysm (8 in infarction group, 7 in aneurysm group, and 11 in repair group). Biochemical samples for immunoblot were also obtained from surviving myocardium.
  
  
  RESULTS
  A statistically significant increase in apoptotic rate was seen in both adjacent and remote areas (p < 0.01) after aneurysm formation. After LVAR, heart function was improved, and TUNEL assays also show significant decrease when compared with aneurysm group. But significant decreases were noted only in activated caspase-9 and increases in Bcl-2 in immunoblot analysis when comparing repair group with aneurysm group.
  
  
  CONCLUSIONS
  Down-regulation of apoptosis accounts for the change in the long-term benefit after LVAR. To prevent heart failure, LVAR is indicated when it is large enough, and the infarction area should be excluded as much as possible.
authors: Division of Cardiovascular Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan.
authors: Chiao-Po
authors: CP
authors: Hsu
authors: Chun-Yao
authors: CY
authors: Huang
authors: Jih-Shiuan
authors: JS
authors: Wang
authors: Hsin-I
authors: HI
authors: Chiang
authors: Chun-Che
authors: CC
authors: Shih
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004195:Disease Models, Animal; D015536:Down-Regulation; D005260:Female; D006322:Heart Aneurysm / Q000209:etiology / Q000473:pathology / Q000601:surgery*; D006333:Heart Failure / Q000517:prevention & control; D006352:Heart Ventricles / Q000473:pathology / Q000601:surgery; D015151:Immunoblotting; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D009203:Myocardial Infarction / Q000150:complications; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values