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

• Published in: The American journal of physiology Vol. 248; no. 6 Pt 2; p. H876
• Main Authors: Anversa, P, Loud, A V, Levicky, V, Guideri, G
• Format: Journal Article
• Language: English
• Published: United States 01.06.1985
• Subjects: Animals; Body Weight; Cardiomegaly - etiology; Cardiomegaly - physiopathology; Cell Division; Heart - physiopathology; Hypertrophy; Male; Mathematics; Myocardial Infarction - complications; Myocardial Infarction - physiopathology; Myocardium - pathology; Organ Size; Rats; Rats, Inbred Strains
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1985.248.6.h876

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.