title: Left ventricular mechanics in preeclampsia.
abstract: Increased systemic vascular resistance and contracted blood volume are characteristic findings in preeclampsia. These alterations in cardiovascular hemodynamics can adversely affect ejection phase indices of left ventricular performance making it difficult to separate abnormalities resulting from changes in load from those caused by depressed myocardial contractility. To address this issue the contractility-sensitive, load-independent relationship between left ventricular end-systolic wall stress and rate-corrected velocity of fiber shortening was assessed in 10 nulliparous patients with preeclampsia. Comparisons were made with data obtained from 10 age-matched normotensive women with uncomplicated pregnancies (control subjects). Studies were performed by means of two-dimensionally targeted M-mode echocardiography and calibrated carotid pulse tracings during early labor, 1 day after delivery, and 4 weeks after delivery. During early labor and 1 day after delivery, patients with preeclampsia had elevated blood pressure and increased total systemic resistance. These parameters returned to normal by 4 weeks after delivery. Before delivery and 24 hours after delivery, the patients with preeclampsia had lower overall left ventricular performance (as measured by cardiac output and rate-corrected velocity of fiber shortening) and higher left ventricular afterload (as measured by left ventricular end-systolic wall stress) when compared with control subjects. These differences were no longer present 4 weeks after delivery. Despite the time-related intergroup differences in hemodynamics, left ventricular contractility was similar between normotensive and preeclamptic subjects at all stages of the study. Thus when load is eliminated as a confounding variable, the decrements in overall left ventricular performance measured in patients with preeclampsia reflect a mechanically appropriate response to increased afterload rather than an abnormality in the ventricular contractile state.
authors.affiliation: Department of Medicine, University of Chicago Medical Center, IL 60637.
authors.forename: R M
authors.initials: RM
authors.lastname: Lang
authors.forename: G
authors.initials: G
authors.lastname: Pridjian
authors.forename: T
authors.initials: T
authors.lastname: Feldman
authors.forename: A
authors.initials: A
authors.lastname: Neumann
authors.forename: M
authors.initials: M
authors.lastname: Lindheimer
authors.forename: K M
authors.initials: KM
authors.lastname: Borow
mesh_terms: D000328:Adult; D002319:Cardiovascular System / Q000503:physiopathology; D036861:Delivery, Obstetric; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007743:Labor, Obstetric; D009200:Myocardial Contraction; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D012016:Reference Values; D016277:Ventricular Function, Left