743
HIV is Associated with Pulmonary Hypertension Independent of Known Risk Factors
Priscilla Hsue*1,2, D Waters1,2, H Farah1,2, A Bolger1,2, S Palav1, L Huang1,2, S Deeks1,2, A Ellman2, S Dollard3, and J Martin1,2
1San Francisco Gen Hosp Med Ctr, CA, US; 2Univ of California, San Francisco, US; and 3CDC, Atlanta, GA, US
Background: Previous data have suggested a
high prevalence of elevated pulmonary artery pressures (PAP) in HIV-infected patients,
but this work has been limited by the lack of a well-characterized
HIV-uninfected comparison group. In
patients without HIV, human herpesvirus 8 (HHV-8) infection has been recently linked to pulmonary
hypertension. Because HIV-infected patients have a high prevalence of HHV-8
infection, we hypothesized that, when compared to carefully characterized
HIV-uninfected individuals, HIV-infected persons would have a higher prevalence
of elevated PAP and that this would be related to HHV-8 infection.
Methods:
Among a clinic-based cohort of HIV-infected adults (the SCOPE cohort in San Francisco) and
community-based HIV-uninfected volunteers, we calculated PAP echocardiographically by measuring the velocity of
tricuspid regurgitation to obtain right ventricular (RV) systolic pressure.
Mean right atrial (RA) pressure was estimated by
assessing inferior vena cava size and collapse. PAP was the sum of estimated RV
and RA pressures. HHV-8 antibodies were detected using two enzyme-linked
immunoassays and one immunofluorescence assay.
Results: We examined 186 HIV-infected and 36 HIV-uninfected adults.
HIV-infected subjects had a median PAP of 26mm Hg (interquartile
range (IQR): 19 to 31) compared to 21mm Hg (IQR: 17 to 26) among HIV-uninfected
subjects (p=0.001). PAP > 30mm Hg was found in 30% of HIV patients compared
to 6% of controls (p=0.003). After adjustment for age, gender, smoking, and intravenous
drug use, HIV-infected subjects had 5.5 fold greater odds of having a PAP >
30mm Hg (p=0.02). PAP > 40mm Hg was found in 6% of HIV patients compared to
0% of controls (p=0.28). Of HIV-infected subjects, 56% were HHV-8 antibody
positive, but we found no evidence of an association between HHV-8 seropositivity and PAP > 30mm Hg (OR =1.4, p=0.38), even
after adjustment for confounding factors.
Conclusions: HIV-infected patients have higher PA systolic pressures
independent of age, gender, smoking, and injection drug use history. In
contrast, we found no evidence to support an association between HHV-8
infection and elevated PAP. The mechanisms for the higher
prevalence of elevated PAP in HIV-infected subjects as well as the natural
history of elevated PAP in this group merit further study.
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