LEFT-VENTRICULAR STRUCTURE AND FUNCTION IN CHILDREN INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS - THE PROSPECTIVE P(2)C(2) HIV MULTICENTER STUDY

Citation
Se. Lipshultz et al., LEFT-VENTRICULAR STRUCTURE AND FUNCTION IN CHILDREN INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS - THE PROSPECTIVE P(2)C(2) HIV MULTICENTER STUDY, Circulation, 97(13), 1998, pp. 1246-1256
Citations number
36
Categorie Soggetti
Peripheal Vascular Diseas",Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097322
Volume
97
Issue
13
Year of publication
1998
Pages
1246 - 1256
Database
ISI
SICI code
0009-7322(1998)97:13<1246:LSAFIC>2.0.ZU;2-W
Abstract
Background-The frequency of, course of, and factors associated with ca rdiovascular abnormalities in pediatric HIV are incompletely understoo d. Methods and Results-A baseline echocardiogram (median age, 2.1 year s) and 2 years of follow-up every 4 months were obtained as part of a prospective study on 196 vertically HIV-infected children. Age-or body surface area-adjusted z scores were calculated by use of data from no rmal control subjects. Although 88% had symptomatic HIV infection, onl y 2 had CHF at enrollment, with a 2-year cumulative incidence of 4.7% (95% CI, 1.5% to 7.9%). All mean cardiac measurements were abnormal at baseline (decreased left ventricular fractional shortening [LV FS] an d contractility and increased heart rate and LV dimension, mass, and w all stresses). Most of the abnormal baseline cardiac measurements corr elated with depressed CD4 cell count z scores and the presence of HIV encephalopathy. Heart rate and LV mass showed significantly progressiv e abnormalities, whereas FS and contractility tended to decline. No as sociation was seen between longitudinal changes in FS and CD4 cell cou nt z score. Children who developed encephalopathy during follow-up had depressed initial FS, and FS continued to decline during follow-up. C onclusions-Subclinical cardiac abnormalities in HIV-infected children are common, persistent, and often progressive. Dilated cardiomyopathy (depressed contractility and dilatation) and inappropriate LV hypertro phy (elevated LV mass in the setting of decreased height and weight) w ere noted. Depressed LV function correlated with immune dysfunction at baseline but not longitudinally, suggesting that the CD4 cell count m ay not be a useful surrogate marker of HIV-associated LV dysfunction. However, the development of encephalopathy may signal a decline in FS.