CELLULAR BASIS OF VENTRICULAR REMODELING AFTER MYOCARDIAL-INFARCTION IN RATS

The remodeling of the spared non-ischemic left ventricular myocardium after different time intervals from the occlusion of the left coronary artery was examined in rats. In the presence of large infarcts, ventr icular failure developed two to three days after surgery, because of c hamber dilation and thinning of the wall, resulting in an average 7.5- fold increase in diastolic stress on the surviving myocardium. Mural t hinning of the ventricular wall remote from and bordering the infarcti on occurred through side-to-side slippage of myocytes and capillaries within the wall. Although an average hypertrophic growth of 22% of the spared myocytes has been found, this amount of hypertrophy was insuff icient to restore normal myocardial function. Long-term cardiac restru cturing after infarction was characterized by the persistence of chamb er dilatation and thinning of the ventricular wall. In addition to the side-to-side slippage, lengthening of the myocytes was an important c ause of ventricular changes. As the reactive hypertrophy of the unaffe cted ventricle was insufficient to re-establish the ratio of ventricul ar mass to chamber volume, the diastolic stress remained elevated and decompensated eccentric ventricular hypertrophy developed. The anatomi cal remodeling of the spared left ventricular myocardium is an importa nt conditioning factor in the short- and long-term outcome of ischemic cardiomyopathy.