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J Am Coll Cardiol, 2003; 41:753-760, doi:10.1016/S0735-1097(02)02959-5
© 2003 by the American College of Cardiology Foundation
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CLINICAL STUDY: HEART FAILURE

Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure

Antonio Abbate, MD*,*, Giuseppe G. L. Biondi-Zoccai, MD*, Rossana Bussani, MD{dagger}, Aldo Dobrina, MD{ddagger}, Debora Camilot, MD{dagger}, Florinda Feroce, MD§, Raffaele Rossiello, MD§, Feliciano Baldi, MD§, Furio Silvestri, MD{dagger}, Luigi M. Biasucci, MD, FACC* and Alfonso Baldi, MD§

* Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy
{dagger} Department of Pathologic Anatomy, University of Trieste, Trieste, Italy
{ddagger} Department of Physiology and Pathology, University of Trieste, Trieste, Italy
§ Department of Biochemistry and Biophysics "F. Cedrangolo", Section of Pathologic Anatomy, Second University of Naples, Naples, Italy

Manuscript received July 2, 2002; revised manuscript received November 1, 2002, accepted November 19, 2002.

* Reprint requests and correspondence: Dr. Antonio Abbate, Catholic University of Rome, Institute of Cardiology, Largo A. Gemelli, 8, Rome, RM 00168, Italy.
abbatea{at}yahoo.com

OBJECTIVES: The purpose of this study was to evaluate a potential correlation between apoptotic rate (AR), post-infarction left ventricular (LV) remodeling, and clinical characteristics in subjects who died late (≥10 days) after an acute myocardial infarction (AMI) with evidence of persistent occlusion of the infarct-related artery at autopsy.

BACKGROUND: Apoptosis contributes to myocardiocyte loss in cardiac disease and may have a pathophysiologic role in post-infarction LV remodeling.

METHODS: The AR was calculated at the site of infarction and in remote unaffected LV regions, using co-localization of in situ end labeling for deoxyribonucleic acid fragmentation and immunohistochemistry for caspase-3, in 14 subjects who died within two months after AMI. Correlation between AR and clinical characteristics such as age, site of AMI, transmural extension, multivessel coronary disease, and signs and/or symptoms of heart failure (HF), at the time of initial hospitalization for AMI or subsequently before death, was assessed using non-parametric statistical tests. Parameters of LV remodeling including diameters, free wall thickness, diameter-to-wall-thickness ratio, and mass were measured at gross examination at autopsy. Values are expressed as median (interquartile range).

RESULTS: Among clinical variables, early symptomatic post-infarction HF (9 cases, 64%) was associated with nearly fourfold increased AR at the site of infarction (26.2% [24.5% to 28.8%] vs. 6.4% [1.9% to 13.3%], p = 0.001). Moreover, AR both at the site of infarction and in unaffected regions was significantly correlated with parameters of progressive LV remodeling (p < 0.05).

CONCLUSIONS: Our data show that in patients dying ≥10 days after AMI, myocardial apoptosis is strongly associated with and may be a major determinant of unfavorable LV remodeling and early symptomatic post-infarction HF.

Abbreviations and Acronyms
  AEC
  3-amino-9-ethylcarbazide
  AMI
  acute myocardial infarction
  AR
  apoptotic rate
  DNA
  deoxyribonucleic acid
  HF
  heart failure
  IRA
  infarct-related artery
  LV
  left ventricle/ventricular
  PCNA
  proliferating cell nuclear antigen
  TUNEL
  terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling




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