Objective: Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood. Methods: Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham- operated group (n = 10). Results: Analysis of infarct size (planimetry) in a separate group of rots demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 ± 8 vs. RP: 35 ± 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 ± 3 vs. 167 ± 4 μm, p = 0.02), in the right ventricle (154 ± 4 vs. 167 ± 3 μm, p = 0.02) and in the septum (158 ± 4 vs. 169 ± 4 μm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 ± 1.7 X 103 vs. 44.1 ± 1.6 x 103 μm3, p = 0.06; right ventricle 36.7 ± 1.6 x 103 vs. 42.7 ± 2.0 x 103 μm3, p = 0.02; septum 41.0 ± 1.6 x 103 vs. 44.2 ± 1.8 x 103 μm3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti- remodeling effect remote from the area perfused by this artery.
Bibliographical noteFunding Information:
The authors acknowledge Dr. Jay N. Cohn for his critical review of the data and Susan Quirt for her expert assistance in the preparation of this manuscript. This work was supported in part by Program Project Grant PO-132427 from the National Heart, Lung and Blood Institute.
- Myocyte hypertrophy
- Rat myocardial infarction
- Ventricular remodeling