CALCIUM TRANSIENTS IN FELINE LEFT-VENTRICULAR MYOCYTES WITH HYPERTROPHY INDUCED BY SLOW PROGRESSIVE PRESSURE OVERLOAD

A model of chronic, progressive pressure overload of the left ventricle was characterized in the cat. The aortas of young cats (10 weeks) were partially constricted with a 2.8 mm ID band, and the cats were allowed to grow to adulthood (8-13 months). This procedure resulted in severe cardiac hypertrophy as indicated by heart wt/body wt (g/kg) of 3.3 ± 0.2 in controls (C) vs. 8.2 ± 0.6 in left ventricular hypertrophy (LVH). The degree of aortic constriction (measured as the peak gradient across the root of the aorta) was significantly elevated in LVH 76 ± 14 vs. -3.2 ± 6 mmHg (C). Left ventricular systolic pressure was significantly elevated in LVH (162 ± 18 vs. 96 ± 7 mmHg in C). Cardiac index was significantly reduced in LVH 100 ± 17 vs. 149 ± 17 ml/min/kg in C, suggesting that the animals may have been progressing from a state of compensated hypertrophy to a decompensated state. The mechanical and contractile properties of isolated myocytes were also studied. LVH myocytes had significantly reduced magnitudes of shortening (6.2 ± 0.4 vs. 7.8 ± 0.12 %DCL), rates of shortening (0.28 ± 0.03 vs. 0.45 ± 0.05 %DCL/s), rates of relengthening (0.24 ± 0.03 vs. 0.40 ± 0.05 %DCL/s) and prolonged duration of twitch (0.67 ± 0.04 vs. 0.55 ± 0.03 s) compared to controls. Ca2+ transients were measured using indo-1. LVH myocytes had significantly depressed peak Ca2+ ( I410 I480 2.31 ± 0.07 vs. 2.53 ± 0.08 in C) and significantly prolonged transient durations (0.74 ± 0.03 vs. 0.59 ± 0.02 s). These results suggest that this model of chronic progressive LV pressure overload may provide better insights into the possible cellular mechanisms underlying the development of congestive heart failure. © 1992.