Alterations in cardiac and pulmonary function in pediatric rapid human immunodeficiency virus type 1 disease progressors

Objective. Infants with human immunodeficiency virus type 1 (HIV- 1) can be divided into rapid progressors (RPs) and non-rapid progressors (non-RPs) b ased on symptoms and immunologic status, but detailed information about car diac and pulmonary function in RP and non-RP children needs to be adequatel y described. Methodology. Cardiac, pulmonary, and immunologic data and HIV- 1 RNA burden were periodically measured in 3 groups: group I, 205 vertically infected c hildren enrolled from 1990 to 1994 and followed through 1996; group II, a p rospectively studied cohort enrolled at birth that included 93 infected (gr oup 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 s ignifance at 1 month, 12 months, 24 months, 30 months, and 48 months of fol low-up. Non-RP and group IIb (HIV-uninfected children) had similar mean res piratory 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 res piratory 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 ra tes in group IIa RP, non-RP, and group IIb differed at every age. Rapid pro gressors had higher mean heart rates than non-RP at all ages through 24 mon ths. 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 g roup 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 ye ars, 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 fraction al 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 t o the 2 HIV-infected groups (RP and non-RP). Mean fractional shortening inc reased 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 t he 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. Be cause 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 r ise in mean fractional shortening seen in the group II infants. In group IIa, RP had more clinical (eg, oxygen saturation <96%) and chest r adiographic abnormalities (eg, cardiomegaly) at 18 months of life. RP also had significantly higher 5-year cumulative mortality than non-RP, higher HI V-1 viral burdens than non-RP, and lower CD8(+) T-cell counts. Conclusions. Rapid disease progression in HIV-1-infected infants is associa ted with significant alterations in heart and lung function: increased resp iratory rate, increased heart rate, and decreased fractional shortening. Th e same children exhibited the anticipated significantly increased 5-year cu mulative mortality, increased serum HIV-1 RNA load, and decreased CD8(+) (c ytotoxic) T-cell counts. Measurements of cardiopulmonary function in HIV-1- infected children seem to be useful in the total assessment of HIV-1 diseas e progression.