Increased apoptosis in remote non-infarcted myocardium in multivessel coronary disease
| Autor: | BIONDI ZOCCAI, Giuseppe, Antonio, Abbate, Fortunata, Vasaturo, Scarpa, Susanna, Daniele, Santini, Antonio Maria Leone, Parisi, O., Fabio De Giorgio, Rossana, Bussani, Furio, Silvestri, Feliciano, Baldi, Biasucci, Luigi M., Alfonso, Baldi, Santini, Daniele |
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| Přispěvatelé: | BIONDI ZOCCAI, Gg, Abbate, A, Vasaturo, F, Scarpa, S, Santini, D, Leone, Am, Parisi, Q, DE GIORGIO, F, Bussani, Rossana, Silvestri, Furio, Baldi, F, Biasucci, Lm, Baldi, A., Bussani, R, Silvestri, F, Baldi, Alfonso |
| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_specialty Myocardial ischemia Myocardial Infarction Ischemia non-infarcted myocardium Infarction Autopsy apoptosis coronary artery disease multivessel myocardial infarction myocardial ischemia remodeling coronary disease Coronary artery disease Internal medicine medicine Humans cardiovascular diseases Myocardial infarction Artery occlusion Multivessel Ventricular Remodeling business.industry Vascular disease Apoptosi Settore MED/43 - MEDICINA LEGALE medicine.disease Coronary Vessels Immunohistochemistry Remodeling medicine.anatomical_structure cardiovascular system Cardiology Cardiology and Cardiovascular Medicine business Artery |
| Zdroj: | International Journal of Cardiology. 94:105-110 |
| ISSN: | 0167-5273 |
| Popis: | Background: Multivessel coronary disease after myocardial infarction is a major risk factor for unfavorable cardiac remodeling and death due to pump failure, but underlying pathophysiologic mechanisms are still uncompletely established. Post-infarction myocardial apoptosis has been recently implicated as a cause of ongoing cell loss leading to cardiac failure. Our aim was to assess the role of post-infarction myocardial apoptosis and pro-apoptotic factor expression in the non-infarcted remote myocardium of subjects with multivessel coronary disease. Methods: Twenty-one males dying after recent myocardial infarction with permanent occlusion of the infarct-related artery were selected at autopsy. Apoptosis was assessed at viable myocardial regions remote from infarction by co-staining for in situ end-labeling of DNA fragmentation and cleaved caspase-3. Expression of pro-apoptotic factor bax and hypoxia-induced factor-1alpha was evaluated by immunohistochemistry. Results: Subjects with multivessel disease (N = 11) showed a significantly two-fold higher myocardial apoptosis in comparison to subjects with single vessel disease (N = 10) (0.9% vs. 0.5%, p = 0.013). Similarly, myocardial bax expression was increased in patients with multivessel disease (3.0% vs. 1.4%, p = 0.029). Stratification for the number of diseased coronary vessels confirmed the association between extent of coronary disease and apoptotic rates (p = 0.022). Even in subjects dying over 30 days after infarction multivessel disease remained predictive of enhanced myocardiocyte apoptosis at remote regions (p = 0.033). Conclusions: Post-infarction myocardial apoptosis and bax expression in remote left ventricular regions are significantly increased in male patients with multivessel coronary disease in comparison to those with isolated infarct-related artery occlusion. These findings suggest that apoptotic cell loss in the viable non-infarcted myocardium, possibly due ongoing ischemia, may play a relevant role in the unfavorable clinical course typical of multivessel disease after myocardial infarction. © 2004 Published by Elsevier Ireland Ltd. |
| Databáze: | OpenAIRE |
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