In a rat model, pressure-induced cardiac hypertrophy alters myocardial mechanics, and anomalous excitation-contraction coupling may persist even after hypertrophy regression.
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Persistent contraction changes after rat hypertrophy regression suggest incomplete recovery; leaves open translation to human remodeling reversal.
Moderate cardiac hypertrophy (CH) was produced in rats by abdominal aorta constriction for 5, 8, 15, 21, and 28 days. Aortic constriction release after 5, 8, and 15 days led to CH regression, which was complete within 15 days. A study of left ventricular papillary muscle mechanics during CH development demonstrated an early but transitory decrease in both maximum isometric force (Po) and maximum muscle shortening velocity (max V); in addition, the time-to-peak tension increased, and there was a decrease in isometric relaxation rate and in force-frequency relationship (negative staircase.) After CH regression, isometric relaxation and negative staircase were similar to controls, whereas the prolonged duration of contraction persisted. After release of the aortic constriction at 8 and 15 days, Po and max V were normal; however, after the earlier release (5 days), Po was higher than control, when muscle thickness was taken into consideration. These findings suggest 1) that an alteration in muscle mechanics may be related to the hypertrophy itself; 2) that anomalous excitation-contraction coupling might persist after CH regression.
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Jouannot et al. (1975) studied this question.
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