Control mechanisms for physiological hypertrophy of pregnancy

Pregnancy represents an excellent model of acute physiological hypertrophy and atrophy secondary to a transient hemodynamic load. This investigation examined the effects of pregnancy on ventricular mechanics using load-independent indexes of contractility to test the hypothesis that the cardiac trophic response functions as a servomechanism with wall stress as the feedback variable.

Serial studies were performed in 33 women at six time periods during and shortly after normal gestation. Changes in ventricular dimension, wall thickness, and left ventricular mass were parallel to changes in body size. Fractional shortening and velocity of shortening progressively diminished during pregnancy, with a nadir at the first postpartum examination, despite a progressive fall in afterload. Cardiac index rose rapidly in early gestation and remained elevated throughout pregnancy. Peak wall stress was elevated in early gestation coincident with the rapid rise in cardiac index due to elevated volume before compensatory rise in mass. With compensatory hypertrophy, peak wall stress normalized by midgestation. The change in left ventricular mass was closely related to peak wall stress but correlated poorly with mean, total, and end-systolic wall stress.

Normal pregnancy is associated with a reversible fall in contractility. Systolic function is preserved throughout most of pregnancy by a fall in afterload but decreases near term and early postpartum because of decreased contractility and diminished preload. Left ventricular hypertrophy and atrophy are temporally related to changes in hemodynamic load. The response is consistent with a tightly coupled servomechanism transduced by peak wall stress with a 1- to 4-week compensatory response time.