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Longitudinal Evaluation of Pulmonary Artery Pressures in HIV Infection
Jennifer Ho*, H Farah, A Bolger, C Kalapus, A Schnell, S Deeks, J Martin, and P Hsue
Univ of California, San Francisco, US
Background: The
natural history of pulmonary hypertension in HIV infection is unclear.
Previously, we established a high prevalence of elevated pulmonary artery
systolic pressure (PASP) among asymptomatic HIV-infected adults. Whether
elevated PASP has long-term clinical implications is not known.
Methods: We
determined PASP using echocardiography in a clinic-based cohort of asymptomatic
HIV-infected adults at study entry and followed clinical outcomes over 1 year. PASP
was assessed according to American Society of Echocardiography standards.
Results: We
initially studied 196 HIV-infected adults; 139 returned for follow-up studies
(7 died, 51 declined further study or were lost to follow-up). Among patients
with follow-up studies, the median age was 47 years (IQR 41 to 51), 88% were
male, 32% were cigarette smokers, and 3% were current intravenous drug users.
The median duration of HIV infection was 15 years (IQR 10 to 18), and 86% were
on ART. At baseline, the median PASP was 27 mmHg (IQR 22 to 32); 40% had a PASP
above the normal range (≥30 mmHg). At 1-year follow-up, the median PASP
was 25 mmHg (IQR 17 to 32), and PASP ≥30 mmHg was found in 35%. The
median change in PASP was –1 mmHg (IQR –5 to +2, p = 0.017 compared to
no change). Among 56 subjects with elevated PASP at study entry, 63% maintained
PASP ≥30 mmHg at 1 year. Clinical parameters of HIV infection and
cardiovascular risk factors did not appear to predict PASP progression over 1
year. Vital status at 1-year follow-up was ascertained for 195 of 196 patients
seen at baseline. Of the 7 patients who died, 6 had a baseline PASP ≥30
mmHg. In univariate analyses, significant predictors of mortality were PASP
≥30 mmHg (p = 0.04), lower CD4+ count (p = 0.004),
and higher viral load (p = 0.001). After adjustment for CD4 count and
viral load, PASP ≥30 mmHg remained significantly associated with
all-cause mortality (p = 0.02).
Conclusions:
Among a contemporary cohort of asymptomatic HIV-infected individuals, more than
one-third had mildly elevated PASP at baseline. Although PASP declined slightly
over 1 year, the prevalence of elevated PASP remained high. Over 1 year of
follow-up, baseline PASP ≥30 mmHg was associated with all-cause
mortality. Although limited to few events, these data suggest that asymptomatic
elevations in PASP may have important clinical consequences. Long-term studies
are needed to determine the clinical significance, pathogenesis, and treatment
of HIV-associated pulmonary hypertension.
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