Coronary occlusion and reperfusion in dogs caused significantly larger cross-sectional cell areas in the infarcted posterior wall compared to controls (e.g., 317 vs 233 µm² in subendocardium; p<0.05).
Does myocardial infarction followed by reperfusion induce myocardial cell hypertrophy in the ischemic zone in a canine model?
In a canine model, myocardial infarction followed by reperfusion leads to significant cellular hypertrophy in both infarcted and noninfarcted zones, which may contribute to late recovery of regional function.
valor p: p=<0.05
BACKGROUND: The potential role of myocardial cell hypertrophy in the ischemic zone in the mechanism of late recovery of regional contractile function after myocardial infarction followed by reperfusion has not been examined. METHODS AND RESULTS: Eight chronically instrumented, conscious dogs were subjected to 90-120 minutes of circumflex coronary artery occlusion followed by reperfusion. The thickness and function of the anterior (AT) and posterior (PT) walls was measured by ultrasonic gauges at control, during occlusion, and after reperfusion. After 3 weeks, cross-sectional areas of surviving cells were determined from subepicardial (epi), midwall (mid), and subendocardial (endo) regions in six dogs and compared with those from six animals without infarction, including three sham-operated control dogs. PT systolic wall thickening showed dyskinesia during occlusion but recovered after reperfusion to 48% of control at 1 week and 67% at 3 weeks. End-diastolic thickness of the PT wall increased markedly after reperfusion, but AT and PT walls were only slightly thicker (p = NS) than in control dogs at 3 weeks. Cross-sectional areas of reperfused dogs in the infarct region averaged 279 (PTepi), 291 (PTmid), and 317 microns 2 (PTendo) and were significantly larger than in control animals (237 PTepi, 241 PTmid, and 233 microns 2 PTendo). PT cell areas were significantly larger than AT cells, ENDO cell areas were larger than EPI cells (both p < 0.05), and ENDO cells of the AT wall were larger than those of noninfarcted dogs (p < 0.05). CONCLUSIONS: In dogs with myocardial infarction followed by reperfusion, the cross-sectional areas of cells in the infarcted PT wall were larger than those in the noninfarcted AT wall, and within both the infarcted and noninfarcted zones, cell areas were larger in the endocardial than the epicardial region. In all regions of the infarcted wall and in the ENDO region of the noninfarcted wall, cell areas were generally larger than those of control dogs without infarction, and the control dogs showed no transmural differences in cell areas. The mechanisms responsible for this significant remodeling of the reperfused infarcted zone, which involves myocardial cellular hypertrophy, are unknown, but it is possible that hypertrophy of surviving regions of the infarcted wall played a role in the late recovery of regional function that accompanied this hypertrophic response.
Kambayashi et al. (Tue,) conducted a other in Myocardial infarction with reperfusion (n=14). Coronary artery occlusion followed by reperfusion vs. Control dogs without infarction was evaluated on Cross-sectional areas of surviving cells (p=<0.05). Coronary occlusion and reperfusion in dogs caused significantly larger cross-sectional cell areas in the infarcted posterior wall compared to controls (e.g., 317 vs 233 µm² in subendocardium; p<0.05).