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Reduced post-infarction myocardial apoptosis in women: a clue to their different clinical course?
  1. G G L Biondi-Zoccai1,
  2. A Abate1,
  3. R Bussani2,
  4. D Camilot2,
  5. F D Giorgio3,
  6. M-P D Marino4,
  7. F Silvestri2,
  8. F Baldi4,
  9. L M Biasucci1,
  10. A Baldi4
  1. 1Institute of Cardiology, Catholic University, Rome, Italy
  2. 2Department of Pathologic Anatomy, University of Trieste, Italy
  3. 3Institute of Legal Medicine, Catholic University, Rome, Italy
  4. 4Department of Biochemistry and Biophysics, F Cedrangolo, Section of Pathologic Anatomy, Second University of Naples, Italy
  1. Correspondence to:
    Dr Alfonso Baldi
    Via G.Orsi, 25, 80128, Naples, Italy;

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Heart failure (HF) is less prevalent and has a better prognosis in women than in men. Also, the outlook after acute myocardial infarction (AMI) is more favourable in elderly women.1 Such sex related differences are probably related to sex specific cardiac remodelling processes.2 However, despite several hypothetical pathogenetic mechanisms, there are no established explanations.

Myocardial apoptosis is a pivotal determinant of left ventricular (LV) dysfunction and cardiac failure in experimental and clinical studies, including after AMI. Sex may indeed influence apoptosis, as shown in normal aging and in end stage HF.3 However, little is known about the role of sex in post-infarction apoptosis. We thus evaluated the influence of sex on expression of pro-apoptotic mediators and myocardiocyte apoptotic index (AI) in subjects dying after AMI.


Using established methods,4 we selected six females who had died after AMI with permanent infarct related artery occlusion at necropsy (< 30 hours after death); 15 males with similar characteristics were selected during the same period. Three men and one woman dying from non-cardiac causes were included as controls.

Re-infarction was excluded on clinicopathologic grounds in all cases. Infarct size was quantified at gross pathology on a four grade scale (small, moderate, moderate to extensive, and extensive).

Tissue specimens were obtained at peri-infarct and remote sites. In situ end labelling of DNA fragmentation by transferase-mediated biotinylated UTP nick end labelling (TUNEL) was performed (Apoptag, Oncor) and sections were stained with antibodies against muscle actin (DAKO-Carpintera; dilution 1:50), and activated caspase-3 (Cell …

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