Clinical and therapeutical follow-up of HIV-associated pulmonary hypertension

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Abstract
Objective: To determine the clinical course and prognosis of pulmonary hypertension (PH) in HIV-infected patients in comparison with a group of PH patients without HIV infection. The secondary objective was to ascertain whether more powerful antiretroviral treatments (highly active antiretroviral therapy) could modify the course of PH in HIV-infected patients. Design: Patients with PH and HIV (HIV-PH, group 1) and patients without HIV (PPH, group 2) were prospectively followed. Setting: A tertiary care institution. Patients: Group 1 included 10 patients, and group 2 included 25 patients. Interventions: In group 1, HIV infection was staged according to Centers for Disease Control and Prevention (CDC) classification when patients entered the study, and was re-staged every fourth month. In both groups, PH functional classes and right heart catheterization (RHC) were determined at baseline. Results: In group 1, one of 10 patients was assigned to New York Heart Association (NYHA) class II, seven patients to NYHA class III, and two patients to NYHA class IV. CDC stages ranged from A1 (three patients) to C3 (one patient). No patient showed progression of HIV disease during follow-up. By May 2001, six patients had died. The median survival by the time of RHC was 15.1 months. Causes of death were heart failure in three cases, sepsis in two, and suicide in one case. In seven patients, epoprostenol was started; three patients survived and four died. The cause of death was heart failure in one patient, suicide in one, non-catheter-related sepsis in one patient and catheter-related sepsis in the last patient. In group 2, 11 patients out of 25 were assigned to NYHA class II, 11 patients to NYHA class III, and three patients to NYHA class IV. RHC was not statistically different in the two groups. By May 2001, nine of 25 patients died and one underwent a double-lung transplant. The median survival from the time of RHC was 6.86 months. Cumulative survival rates by RHC were not statistically different (hazard ratio close to 1). Conclusions: In HIV-infected patients, the onset of PH adversely affects the prognosis at any stage of infection. Clinically adverse progression of PH is not correlated with HIV initial stage and evolution. Moreover, prognosis in patients with sporadic or familial PPH and in patients with HIV-PH with similar RHC is so similar as to strengthen the concept that pulmonary vascular disease overshadows the overall clinical problem in HIV-infected patients.