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This study examines how cardiomyocyte apoptosis contributes to changes in the left ventricle after myocardial infarction in rats.

Cardiomyocyte apoptosis and ventricular remodeling after myocardial infarction in rats

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This study examines how cardiomyocyte apoptosis contributes to changes in the left ventricle after myocardial infarction in rats.
Investigated infarct size and cardiomyocyte apoptosis from 24 hours to 12 weeks post-myocardial infarction in rats.
Utilized planimetry, TUNEL methodology, and echocardiography to measure left ventricular changes.
Compared cardiomyocyte apoptosis rates and heart function between infarcted and sham-operated groups.
Cardiomyocyte apoptosis was high in infarct areas (1.4%) and border zones (4.9%) within the first 24 hours.
Diastolic diameter increase correlated with apoptosis levels in non-infarcted myocardium (r = 0.60, P < 0.01) over 4 weeks.
Sham-operated rats showed stable diastolic diameter and ejection fraction throughout the study.

Population

Rats with experimentally induced myocardial infarction and sham-operated controls

Intervention

Myocardial infarction (experimental model)

Comparator

Sham operation

Outcome

Cardiomyocyte apoptosis (TUNEL positivity) and ventricular remodeling (left ventricular diastolic diameter and ejection fraction)surrogate

Cardiomyocyte apoptosis in the noninfarcted myocardium correlates with left ventricular dilation after myocardial infarction in rats.

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Apoptosis in noninfarcted myocardium may drive post-MI LV dilation in rats; leaves open its role in human remodeling.

Palojoki et al. (2001) studied this question.

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