title: Left ventricular structure and function in children infected with human immunodeficiency virus: the prospective P2C2 HIV Multicenter Study. Pediatric Pulmonary and Cardiac Complications of Vertically Transmitted HIV Infection (P2C2 HIV) Study Group.
abstract: BACKGROUND
  The frequency of, course of, and factors associated with cardiovascular abnormalities in pediatric HIV are incompletely understood.
  
  
  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.
authors.affiliation: Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, Mass, USA. slipshultz@cc.urmc.rochester.edu
authors.forename: S E
authors.initials: SE
authors.lastname: Lipshultz
authors.forename: K A
authors.initials: KA
authors.lastname: Easley
authors.forename: E J
authors.initials: EJ
authors.lastname: Orav
authors.forename: S
authors.initials: S
authors.lastname: Kaplan
authors.forename: T J
authors.initials: TJ
authors.lastname: Starc
authors.forename: J T
authors.initials: JT
authors.lastname: Bricker
authors.forename: W W
authors.initials: WW
authors.lastname: Lai
authors.forename: D S
authors.initials: DS
authors.lastname: Moodie
authors.forename: K
authors.initials: K
authors.lastname: McIntosh
authors.forename: M D
authors.initials: MD
authors.lastname: Schluchter
authors.forename: S D
authors.initials: SD
authors.lastname: Colan
mesh_terms: D015526:AIDS Dementia Complex / Q000473:pathology / Q000503:physiopathology; D000293:Adolescent; D018791:CD4 Lymphocyte Count; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D015658:HIV Infections / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011446:Prospective Studies; D012307:Risk Factors; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000503:physiopathology