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Am J Physiol Heart Circ Physiol 283: H1627-H1633, 2002. First published May 23, 2002; doi:10.1152/ajpheart.00966.2001
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Vol. 283, Issue 4, H1627-H1633, October 2002

Structural and functional changes in left ventricle during normotensive and preeclamptic pregnancy

Lisa A. Simmons1,2, Adrian G. Gillin1,3, and Richmond W. Jeremy1,2

1 Department of Medicine, University of Sydney, Sydney, New South Wales 2006; and Departments of 2 Cardiology and 3 Renal Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales 2050, Australia

Increased cardiac output in pregnancy is associated with cardiac remodeling and possible reduction in contractility, which may worsen in preeclampsia. Left ventricular (LV) geometry and function were compared between nonpregnant controls (n = 12) and normotensive (n = 44) and preeclamptic (n = 15) pregnant women using echocardiography. Load-independent comparisons of LV systolic function compared end-systolic stress (ESS) and rate-corrected velocity of circumferential fiber shortening (VCFC). Mean arterial pressures were 101 ± 14 mmHg in preeclampsia, 76 ± 6 mmHg in normotensive pregnancy, and 78 ± 6 mmHg in controls (P < 0.005 vs. preeclampsia). LV mass increased during normotensive pregnancy (66 ± 13 to 76 ± 16 g/m2; P < 0.05; controls, 65 ± 10 g/m2; P < 0.05) and was greater in preeclampsia (90 ± 18 g/m2; P < 0.05). In normotensive pregnancy, ESS decreased (59 ± 9 to 52 ± 11 g/cm2; P < 0.05; controls, 66 ± 14 g/cm2; P < 0.005). ESS was greater in preeclampsia (60 ± 14 g/cm2; P < 0.05). In controls, there was an inverse relationship between ESS and VCFC (r = -0.78). The ESS-VCFC relationships in normotensive and preeclamptic pregnancy were unchanged from controls. We conclude that LV hypertrophy in normotensive and preeclamptic pregnancy matches changes in cardiac work, and LV contractility is preserved.

preeclampsia; echocardiography; ventricular function; myocardial contractility; hypertension


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