Age at time of infarction differentially affects the remodeling responses in viable cardiac tissue in young versus old rats

Ventricular remodeling after myocardial infarction elicits structural and functional changes that can compromise global cardiac function. To determine whether age influences this process, we characterized remodeling after myocardial infarction in Fischer 344 rats that undergo natural age-related changes in heart structure and function that parallel those observed in human hearts. Young (3 month, n=7) and old (18 month, n=7) rats underwent myocardial infarction by coronary occlusion. Sham-infarct procedures were performed in both groups as controls. Twelve weeks after infarction, hearts were excised, fixed, and sliced into 2 mm thick cross-sections. Ultrasonic RF signals were acquired with a 50 MHz transducer and integrated backscatter was calculated from 30 to 50 MHz. Heart slices were then stained and their images digitized to permit histology with computer assisted planimetry. Infarct sizes were similar in young and old rats (12.1/spl plusmn/2.4% and 11.6/spl plusmn/5.4%; p=NS). Integrated backscatter from the infarct scar tissue in both the young and old rats were similar, (-41.4/spl plusmn/1.2 dB vs. -42.7/spl plusmn/1.1 dB, p=NS). Integrated backscatter from the remodeled but non-infarcted viable tissue was -48.4/spl plusmn/0.8 dB and -45.4/spl plusmn/1.0 dB in young and old rats, respectively, both statistically different from integrated backscatter from scar tissue (p<0.05). Significantly, the integrated backscatter from the remodeled but viable non-infarcted regions of the old infarct rats was increased by 100% over that from the young rats (p<0.05). These data suggest that alterations in microscopic structure and material properties associated with remodeling of viable myocardial tissue differ depending on age, as delineated by quantitative acoustic microscopy.