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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 |
* Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy
Department of Pathologic Anatomy, University of Trieste, Trieste, Italy
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.
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