HIV-ASSOCIATED PRIMARY PULMONARY-HYPERTENSION - A CASE-CONTROL STUDY

To assess the clinical and echocardiographic time course, prognosis, a nd possible etiology of HIV-associated primary pulmonary hypertension (PPH), we prospectively followed all 19 patients in whom PPH was diagn osed in our centers. Women (12 cases) and injecting drug use (16 cases ) predominated; the median CD4 lymphocytes count was 83/mu l (range, 1 to 740). Matched control subjects without PPH were identified within the Swiss HIV Cohort Study. Frozen serum samples of both groups were t hen reanalyzed for autoimmune parameters, neopterin, beta-2-microglobu lin, and thyroid-stimulating hormone. The median follow up of the pati ents was 1.3 yr. Follow-up Doppler echocardiography was available in 1 3 patients. The RVSP-RAP pressure gradient decreased by 3.2 mm Hg for those six patients who received antiretroviral treatment but increased by 19.0 mm Hg for untreated patients (p = 0.026). PPH was the cause o f eight of 17 deaths. The probability of surviving was significantly d ecreased in patients with PPH in comparison with the control subjects; the median survival was 1.3 versus 2.6 yr (p < 0.05). Patients with P PH had significantly higher anticardiolipin IgM, anti SS-B, and neopte rin, but all other laboratory values did not differ between cases and control subjects. In conclusion, HIV-associated PPH contributed signif icantly to mortality. Antiretroviral treatment may exert a beneficial effect on the pressure gradient. A possible role of an autoimmune phen omenon in the pathogenesis could not be substantiated.