From the Department of Cardiology (S.E.L., S.D.C.) and Division of
Infectious Diseases (K.M.), Children's Hospital, and Department of
Pediatrics, Harvard Medical School (S.E.L., S.D.C., K.M.); Department of
Pediatrics, Boston City Hospital and Boston University School of Medicine,
Boston, Mass (S.E.L.); Departments of Biostatistics and Epidemiology (K.A.E.,
M.D.S.) and Pediatrics, Division of Pediatric Cardiology (D.S.M.), Cleveland
Clinic Foundation, Cleveland, Ohio; Department of Medicine, Brigham and
Woman's Hospital, Boston, Mass (E.J.O.); Department of Pediatrics,
Division of Pediatric Cardiology, University of California, Los Angeles,
Medical Center and School of Medicine (S.K.); Department of Pediatrics,
Division of Pediatric Cardiology, Mt Sinai School of Medicine, New York, NY
(W.W.L.); Department of Pediatrics, Division of Pediatric Cardiology,
Presbyterian Hospital/Columbia University School of Medicine, New York, NY
(T.J.S.); and Department of Pediatrics, Division of Pediatric Cardiology,
Baylor College of Medicine, Houston, Tex (J.T.B.).
Correspondence to Steven E. Lipshultz, MD, Division of Pediatric Cardiology, University of Rochester Medical Center, 601 Elmwood Ave, Box 631, Rochester, NY 14642. E-mail slipshultz{at}cc.urmc.rochester.edu
Background—The frequency of, course
of, and factors associated with cardiovascular
abnormalities in pediatric HIV are incompletely understood.
Methods and Results—A baseline echocardiogram (median age, 2.1
years) 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 normal control subjects. Although 88% had
symptomatic HIV infection, only 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] and
contractility and increased heart rate and LV
dimension, mass, and wall stresses). Most of the abnormal baseline
cardiac measurements correlated with depressed CD4 cell count
z scores and the presence of HIV encephalopathy. Heart
rate and LV mass showed significantly progressive abnormalities,
whereas FS and contractility tended to decline. No
association was seen between longitudinal changes in FS and CD4 cell
count z score. Children who developed encephalopathy
during follow-up had depressed initial FS, and FS continued to decline
during follow-up.
Conclusions—Subclinical cardiac abnormalities in HIV-infected
children are common, persistent, and often progressive. Dilated
cardiomyopathy (depressed
contractility and dilatation) and inappropriate LV
hypertrophy (elevated LV mass in the setting of decreased
height and weight) were noted. Depressed LV function correlated with
immune dysfunction at baseline but not longitudinally, suggesting that
the CD4 cell count may not be a useful surrogate marker of
HIV-associated LV dysfunction. However, the development of
encephalopathy may signal a decline in FS.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Left Ventricular Structure and Function in Children Infected With Human Immunodeficiency Virus
The Prospective P2C2 HIV Multicenter Study
Key Words: HIV • AIDS • pediatrics • heart failure • cardiomyopathy
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