Apoptosis and Post-infarction Left Ventricular Remodeling

doi:10.1006/jmcc.2001.1498

Journal of Molecular and Cellular Cardiology

Volume 34, Issue 2, February 2002, Pages 165-174

https://doi.org/10.1006/jmcc.2001.1498 Get rights and content

Abstract

Apoptosis is a common pathological feature in acute myocardial infarction (AMI), however, its role in the later phases (>10 days) of AMI and in post-infarction left ventricular remodeling has not been characterized. The aim of the study was to identify signs of ongoing cell apoptosis late post AMI. Sixteen hearts were collected at autopsy from subjects 12 to 62 days after the onset of AMI. In situ end-labeling of DNA fragmentation (TUNEL) and co-staining with caspase-3 were performed. Double-positive cells were defined as apoptotic and the apoptotic rate was calculated. Values are expressed as median and interquartile range. Co-stainings with muscle-actin, splicing factor (SC35), PCNA, bax and bcl-2 were also performed. Apoptotic rates at site of infarction [25.4% (17.0–28.4%)] were significantly higherv those at remote regions [0.7% (0.5–0.8%) P<0.001] and significantly correlated to left ventricular longitudinal and transverse diameters [ r=+0.70 (P=0.016) andr =+0.63 (P=0.004) respectively]. Moreover, in subjects with persistently occluded infarct-related artery (14 cases) there was a significantly higher apoptotic rate at the site of infarction compared to those (2 cases) with patent artery [26.0% (21.9–28.5%) v 4.5% (0.6% and 8,4%);P=0.033]. A significantly greater bax immuno-reactivity close to the infarction v remote areas was found (P<0.001). High grade apoptosis is present at sites of infarction in the later phases post AMI. This is more evident if the infarct-related artery is persistently occluded and signs of ventricular remodeling are present. These data may provide an explanation of progressive late left ventricular dysfunction.

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^f1: The first two authors contributed equally to the realization of this manuscript.

^f2: Please address all correspondence to: Dr Alfonso Baldi, Via G. Orsi, 25, 80128 Naples, Italy. Fax: +39-081-5569693.E-mail: [email protected]

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Regular ArticlesApoptosis and Post-infarction Left Ventricular Remodeling

Abstract

Hum Pathol

J Mol Cell Cardiol

J Am Coll Cardiol

J Mol Cell Cardiol

J Biol Chem

Trends Cardiovas Med

Lancet

Necrosis and apoptosis: distinct modes of cell death with fundamentally different significance

Pathol Annu

Developmental remodeling and shortening of the cardiac outflow tract involves myocyte programmed cell death

Development

Stretch-induced programmed myocyte cell death

J Clin Invest

Apoptosis. Basic mechanisms and implications for cardiovascular disease

Circ Res

Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats

Lab Invest

Apoptosis in myocytes in end-stage heart failure

N Engl J Med

Apoptosis in the failing human heart

N Engl J Med

Cardiomyocyte apoptosis and progression of heart failure to transplantation

Eur J Clin Invest

Homage to James B Herrick: a contemporary look at myocardial infarction and sickle-cell heart disease, the 32nd Annual Herrick lecture of the council of Clinical Cardiology of the American heart Association

Circulation

Morphologic criteria and detection of apoptosis

Herz

Regular Articles
Apoptosis and Post-infarction Left Ventricular Remodeling