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Apoptosis and post-infarction left ventricular remodeling.

Alfonso Baldi1, Antonio Abbate, Rossana Bussani

  • 1Department of Biochemistry and Biophysics, F. Cedrangolo, Section of Anatomy, Second University of Naples, Italy. alfonsobaldi@tiscalinet.it

Journal of Molecular and Cellular Cardiology
|February 20, 2002
PubMed
Summary

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Ongoing cell apoptosis occurs late after acute myocardial infarction (AMI), especially with artery occlusion. This late apoptosis correlates with left ventricular remodeling and dysfunction.

Area of Science:

  • Cardiovascular Pathology
  • Cellular Biology

Background:

  • Apoptosis is a known feature of acute myocardial infarction (AMI).
  • The role of apoptosis in later stages (>10 days) post-AMI and its impact on left ventricular remodeling remain unclear.

Purpose of the Study:

  • To investigate the presence and extent of ongoing apoptosis in the late phases following acute myocardial infarction.
  • To correlate late apoptotic rates with left ventricular remodeling and infarct-related artery status.

Main Methods:

  • Autopsy hearts from 16 subjects 12-62 days post-AMI were analyzed.
  • In situ end-labeling (TUNEL) and co-staining with caspase-3 identified apoptotic cells.
  • Immunohistochemistry for muscle-actin, SC35, PCNA, bax, and bcl-2 was performed.

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Main Results:

  • Significantly higher apoptotic rates were observed at infarct sites (25.4%) compared to remote regions (0.7%) (P<0.001).
  • Apoptotic rates correlated with left ventricular dimensions (longitudinal r=+0.70, transverse r=+0.63).
  • Higher apoptosis rates were found in persistently occluded infarct-related arteries (26.0%) versus patent arteries (4.5%) (P=0.033).

Conclusions:

  • High-grade apoptosis persists late post-AMI, particularly at infarct sites.
  • Persistent artery occlusion and ventricular remodeling are associated with increased late apoptosis.
  • These findings may explain progressive left ventricular dysfunction after AMI.