Publication

Cardiac Dysfunction and Mortality in HIV-Infected Children : The Prospective P2C2 HIV Multicenter Study

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Last modified
  • 02/25/2025
Type of Material
Authors
    Steven E. Lipshultz, University of RochesterKirk Easley, Emory UniversityE. John Orav, Boston UniversitySamuel Kaplan, University of California, Los AngelesThomas J Starc, Columbia UniversityJ. Timothy Bricker, Baylor CollegeWyman W. Lai, Mt Sinai School of MedicineDouglas S. Moodie, Cleveland Clinic FoundationGeorge Sopko, Baylor CollegeSteven D. Colan, Harvard University
Language
  • English
Date
  • 2000-09-26
Publisher
  • American Heart Association
Publication Version
Copyright Statement
  • © 2000 American Heart Association, Inc.
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 0009-7322
Volume
  • 102
Issue
  • 13
Start Page
  • 1542
End Page
  • 1548
Grant/Funding Information
  • This study was supported by the National Heart, Lung, and Blood Institute (NO1-HR-96037, NO1-HR-96038, NO1-HR-96039, NO1-HR-96040, NO1-HR-96041, NO1-HR-96042, and NO1-HR-96043) and in part by the National Institutes of Health (RR-00865, RR-00188, RR-02172, RR-00533, RR-00071, RR-00645, RR-00685, and RR-00043).
Abstract
  • Background—Left 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 Results—Baseline 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. Conclusions—Depressed 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.
Author Notes
  • Guest Editor for this article was David A. Sahn, MD, Oregon Health Sciences University, Portland.
Keywords
Research Categories
  • Health Sciences, Immunology
  • Health Sciences, General

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