Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy

Abstract

To determine whether left ventricular failure after acute myocardial infarction is associated with a growth response of the myocytes that tends to compensate for the loss of muscle mass and function, the left coronary artery in rats was ligated near its origin, and the animals were killed 3 days later. Elevated left ventricular end-diastolic pressure and decreased first derivative of left ventricular pressure and systolic arterial pressure indicated significant impairment of ventricular function. Absolute infarct size, determined morphometrically by measurement of the fraction of myocyte nuclei lost, averaged 57%. Hypertrophy of surviving left ventricular myocytes was 28%, involving a 14% increase in cell length and a 6% increase in diameter. Right ventricular myocyte volume per nucleus increased 21% by a 10% enlargement of cellular diameter with no change in length. These results show on a cellular basis that myocardial hypertrophy in the left ventricle is accomplished by cellular shape changes characteristic of a combination of pressure and volume overload hypertrophy, whereas cellular growth in the right ventricle is consistent with pressure overload hypertrophy.

Repercussões cardíacas após infarto do miocárdio em ratas submetidas previamente a exercício físico

“…The animals undergoing sham surgery went through the same surgical procedures, but without coronary ligation. The rats returned to their plastic boxes and were kept under observation for six weeks, a period that covers complete healing of MI in rats 25 . Diagnostic confirmation of MI was performed by echocardiography, six weeks after MI was induced by surgery.…”

Infarto do miocárdio experimental em ratos: análise do modelo

“…One of the main characteristic of myocardial infarction is associated to the fact that the loss of contractile tissue triggers an adaptive cell growth process in the non-infarcted tissue [32][33][34][35][36][37] . In the rat model, the left ventricular hypertrophy is characterized for having an eccentric pattern, being an early event and being detectable on the third day after the coronary occlusion.…”

Left Ventricular End-Systolic Wall Stress is a Potent Prognostic Variable in Patients With Dilated Cardiomyopathy

“…However, this cellular hypertrophy is usually inadequate to fully compensate for the degree of myocyte loss. 22 Thus, in treating patients with left ventricular dysfunction, it is very important to attenuate the wall stress. In fact, it is well recognized that left ventricular wall stress is one of the most important determinants relating to the change of left ventricular remodeling after myocardial infarction.…”