Myocyte diameters were measured in two models of healed myocardial infarction to test the hypothesis that myocyte hypertrophy is a function of proximity to the infarct. Left ventricular transmural and non-transmural myocardial infarctions were produced in cats by multiple ligatures of the distal tributaries of the left coronary artery system. Thirteen to twenty months after surgery the left ventricular free wall was cut longitudinally, embedded in plastic and stained for reticulum with modified silver stain. Myocardial cell diameters were measured from apex to base through the infarct. No regional differences were found in non-operated control hearts. In the transmural infarct hearts, all cell diameters were significantly increased in comparison to controls (P ≤ 0.05). In the hearts with non-transmural infarcts, cell diameters were significantly increased in tissues adjacent to the infarct, but as distance from the infarct increased the cell diameters were not different from controls. Cells from the transmural infarctions had a greater percent increase in diameter, compared to controls, than did cells from the non-transmural infarctions. There is a gradient increase in myocyte diameters in transmural and non-transmural healed myocardial infarctions; this increase is greatest in the tissues adjacent to the infarct. We conclude that cells close to a healed myocardial infarction hypertropy because they are contracting against a non-compliant scar.
- Healed myocardial infarction
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine