title: Alterations in cardiac and pulmonary function in pediatric rapid human immunodeficiency virus type 1 disease progressors. Pediatric Pulmonary and Cardiovascular Complications of Vertically Transmitted Human Immunodeficiency Virus Study Group.
abstract: OBJECTIVE
  Infants with human immunodeficiency virus type 1 (HIV-1) can be divided into rapid progressors (RPs) and non-rapid progressors (non-RPs) based on symptoms and immunologic status, but detailed information about cardiac and pulmonary function in RP and non-RP children needs to be adequately described.
  
  
  METHODS
  Cardiac, pulmonary, and immunologic data and HIV-1 RNA burden were periodically measured in 3 groups: group I, 205 vertically infected children enrolled from 1990 to 1994 and followed through 1996; group II, a prospectively studied cohort enrolled at birth that included 93 infected (group IIa); and 463 noninfected infants (group IIb).
  
  
  RESULTS
  Mean respiratory rates were generally higher in group IIa RP than non-RP children throughout the period of follow-up, achieving statistical signifance at 1 month, 12 months, 24 months, 30 months, and 48 months of follow-up. Non-RP and group IIb (HIV-uninfected children) had similar mean respiratory rates from birth to 5 years of age. Significant differences in mean respiratory rates were found between group I RP and non-RP at 7 age intervals over the first 6 years of life. Mean respiratory rates were higher in RP than in non-RP at <1 year, 2.0 years, 2.5 years, 3.0 years, 3. 5 years, 4.0 years, and 6.0 years of age. Mean heart rates in group IIa RP, non-RP, and group IIb differed at every age. Rapid progressors had higher mean heart rates than non-RP at all ages through 24 months. Mean heart rates at 30 months through 60 months of age were similar for RP and non-RP children. Non-RP children had higher mean heart rates than did group IIb at 8 months, 24 months, 36 months, 42 months, 48 months, 54 months, and 60 months of age. In group I, RP had higher mean heart rates than non-RP at 2.0 years, 2.5 years, 3.0 years, and 4.0 years of age. After 4 years of age, the non-RP and RP had similar mean heart rates. Mean fractional shortening differed between the 3 group II subsets (RP, non-RP, and IIb) at 4, 8, 12, 16, and 20 months of age. Although mean fractional shortening was lower in RP than in non-RP in group II at all time points between 1 and 20 months, the mean fractional shortening was significantly lower in RP only at 8 months when restricting the statistical comparisons to the 2 HIV-infected groups (RP and non-RP). Mean fractional shortening increased in the first 8 months of life followed by a gradual decline through 5 years of age among group IIb children. No significant differences among the 3 groups in mean fractional shortening were detected after 20 months of age. In group I, differences between RP and non-RP in mean fractional shortening were detected at 1.5, 2.0, 2.5, and 3.0 years of age. After 3 years of age, group means for fractional shortening in RP and non-RP did not differ. Because of the limited data from the first months of the group I patients, it could not be determined whether this group experienced the gradual early rise in mean fractional shortening seen in the group II infants. In group IIa, RP had more clinical (eg, oxygen saturation <96%) and chest radiographic abnormalities (eg, cardiomegaly) at 18 months of life. RP also had significantly higher 5-year cumulative mortality than non-RP, higher HIV-1 viral burdens than non-RP, and lower CD8(+) T-cell counts.
  
  
  CONCLUSIONS
  Rapid disease progression in HIV-1- infected infants is associated with significant alterations in heart and lung function: increased respiratory rate, increased heart rate, and decreased fractional shortening. The same children exhibited the anticipated significantly increased 5-year cumulative mortality, increased serum HIV-1 RNA load, and decreased CD8(+) (cytotoxic) T-cell counts. Measurements of cardiopulmonary function in HIV-1-infected children seem to be useful in the total assessment of HIV-1 disease progression.
authors.affiliation: Baylor College of Medicine, Houston, Texas, USA. wshearer@bcm.tmc.edu
authors.forename: W T
authors.initials: WT
authors.lastname: Shearer
authors.forename: S E
authors.initials: SE
authors.lastname: Lipshultz
authors.forename: K A
authors.initials: KA
authors.lastname: Easley
authors.forename: K
authors.initials: K
authors.lastname: McIntosh
authors.forename: J
authors.initials: J
authors.lastname: Pitt
authors.forename: T C
authors.initials: TC
authors.lastname: Quinn
authors.forename: M
authors.initials: M
authors.lastname: Kattan
authors.forename: J
authors.initials: J
authors.lastname: Goldfarb
authors.forename: E
authors.initials: E
authors.lastname: Cooper
authors.forename: Y
authors.initials: Y
authors.lastname: Bryson
authors.forename: A
authors.initials: A
authors.lastname: Kovacs
authors.forename: J T
authors.initials: JT
authors.lastname: Bricker
authors.forename: H
authors.initials: H
authors.lastname: Peavy
authors.forename: R B
authors.initials: RB
authors.lastname: Mellins
authors.forename: N
authors.initials: N
authors.lastname: Heart
authors.forename: L B
authors.initials: LB
authors.lastname: Institute
mesh_terms: D018414:CD8-Positive T-Lymphocytes; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000401:mortality / Q000503:physiopathology*; D015497:HIV-1 / Q000302:isolation & purification; D006339:Heart Rate; D006801:Humans; D007223:Infant; D018655:Lymphocyte Count; D008297:Male; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D013902:Radiography, Thoracic; D012119:Respiration
chemical_list: D012367:RNA, Viral