(Circulation. 2000;102:1542.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Division of Pediatric Cardiology (S.E.L.), University of Rochester Medical Center and Childrens Hospital at Strong and Department of Pediatrics (S.E.L.), University of Rochester School of Medicine and Dentistry, Rochester, NY; Department of Cardiology (S.E.L., S.D.C.), Childrens Hospital, Department of Pediatrics, Harvard Medical School (S.E.L., S.D.C.), Department of Pediatrics, Boston Medical Center and Boston University School of Medicine (S.E.L.), and Department of Medicine, Brigham and Womans Hospital (E.J.O.), Boston, Mass; Department of Biostatistics and Epidemiology (K.A.E.) and Department of Pediatrics, Division of Pediatric Cardiology (D.S.M.), Cleveland Clinic Foundation, Cleveland, Ohio; Department of Pediatrics, Division of Pediatric Cardiology, University of California, Los Angeles Medical Center and School of Medicine, Los Angeles (S.K.); Department of Pediatrics, Division of Pediatric Cardiology, Mt Sinai School of Medicine (W.W.L.), and Department of Pediatrics, Division of Pediatric Cardiology, Presbyterian Hospital/Columbia University College of Physicians and Surgeons (T.J.S.), New York, NY; Department of Pediatrics, Division of Pediatric Cardiology, Baylor College of Medicine, Houston, Tex (J.T.B.); and the National Heart, Lung, and Blood Institute, Bethesda, Md (G.S.).
Correspondence to Dr Steven E. Lipshultz, Division of Pediatric Cardiology, University of Rochester Medical Center, 601 Elmwood Ave, Box 631, Rochester, NY 14642. E-mail steve_lipshultz{at}urmc.rochester.edu
BackgroundLeft ventricular (LV) dysfunction is common in children infected with the human immunodeficiency virus (HIV), but its clinical importance is unclear. Our objective was to determine whether abnormalities of LV structure and function independently predict all-cause mortality in HIV-infected children.
Methods and ResultsBaseline echocardiograms were obtained on 193
children with vertically transmitted HIV infection (median age, 2.1
years). Children were followed up for a median of 5 years. Cox
regression was used to identify measures of LV structure and function
predictive of mortality after adjustment for other important
demographic and baseline clinical risk factors. The time course of
cardiac variables before mortality was also examined. The 5-year
cumulative survival was 64%. Mortality was higher in children who, at
baseline, had depressed LV fractional shortening (FS) or
contractility; increased LV dimension, thickness, mass,
or wall stress; or increased heart rate or blood pressure
(P
0.02 for each). Decreased LV FS
(P<0.001) and increased wall thickness
(P=0.004) were also predictive of increased mortality
after adjustment for CD4 count (P<0.001), clinical
center (P<0.001), and encephalopathy
(P<0.001). FS showed abnormalities for up to 3 years
before death, whereas wall thickness identified a population at risk
only 18 to 24 months before death.
ConclusionsDepressed LV FS and increased wall thickness are risk factors for mortality in HIV-infected children independent of depressed CD4 cell count and neurological disease. FS may be useful as a long-term predictor and wall thickness as a short-term predictor of mortality.
Key Words: viruses mortality pediatrics AIDS
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