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
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.