Pulmonary Hypertension in HIV Infected Persons

9/24/01 (Shang)

RE: A 30 year old African American male with worsening cough.

Question: Is pulmonary hypertension a recognized phenomenon in HIV infection?

Link Directly to Fulltext Article at Publisher

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Unique Identifier: 21333387 / PubMed Identifier: 11440333

Authors: Seoane L. Shellito J. Welsh D. de Boisblanc BP.

Institution: Section of Pulmonary/Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, USA.

Abstract: Pulmonary hypertension occurs with increased frequency among patients with human immunodeficiency virus (HIV) infection. Although the pathogenesis of HIV-associated pulmonary hypertension remains unknown, it appears to occur independently of other risk factors associated with pulmonary vasculopathy, such as chronic hepatitis C infection and intravenous drug use. Signs and symptoms are typical of those immunocompetent patients with primary pulmonary hypertension, but because many HIV-infected patients are receiving intensive medical supervision, the diagnosis of pulmonary hypertension is often made at an earlier stage. Acute responses to epoprostenol are similar to those among non-HIV-infected individuals, but the benefits of long-term, intravenous treatment with epoprostenol in HIV-infected patients is unknown. Future investigations should define the true incidence of pulmonary hypertension and the long-term effects of epoprostenol on survival among HIV-infected individuals. Physicians should be alert to possible pulmonary hypertension in persons infected with HIV. [References: 49]

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Unique Identifier: 21073527 / PubMed Identifier: 11205929

Authors: Pellicelli AM. Barbaro G. Palmieri F. Girardi E. D'Ambrosio C. Rianda A. Barbarini G. Frigiotti D. Borgia MC. Petrosillo N.

Institution: Second Division of Infectious Diseases, IRCCS Lazzaro Spallanzani Hospital, Rome, Italy. adriapel@tin.it

Abstract: The relationship between grade of pulmonary hypertension and factors associated with human immunodeficiency virus among patients with HIV infection is poorly documented. This report documents the most extensive attempt made thus far to determine whether a relationship exists between degree of pulmonary hypertension and the following conditions: HIV risk factor, degree of immunosuppression, presence or absence of AIDS, and presence or absence of liver cirrhosis. A retrospective study involving a search of the published literature on primary pulmonary hypertension among HIV cases from 1987 to 1998, using the Medline and Aidsline databases was conducted. Patients for whom secondary causes of pulmonary hypertension could be excluded were selected, and the following information for each was recorded: age, gender, risk factors for HIV infection, HIV disease stage according to the Centers for Disease Control, previous opportunistic and neoplastic diseases, CD4+ cell count (cells/L), presence or absence of liver cirrhosis, pulmonary systolic artery pressure level, and lung pathology specimens. Information about the patient's survival time was also recorded. Seventy-six patients were judged to have primary pulmonary hypertension and were included in the study. While no correlation was found between pulmonary systolic artery pressure level and CD4+ cell counts, a statistically significant difference was found between HIV-positive patients with and without AIDS as determined by the Centers for Disease Control criteria with regard to the degree of pulmonary hypertension, expressed as pulmonary systolic artery pressure level (85.4 +/- 17 mm Hg vs 71.8 +/- 15 mm Hg, p < 0.013). Although a higher PAPS was present in HIV cirrhotic patients, a statistically significant difference was not found between degree of pulmonary hypertension and evidence of hepatic cirrhosis (85 +/- 21 mm Hg vs 73.1 +/- 15 mm Hg, p < 0.062). Patients with AIDS and primary pulmonary hypertension present a higher degree of pulmonary hypertension than non-AIDS patients. Pulmonary hypertension associated with HIV seems to be related to a cytokine-related stimulation and proliferation of endothelium. High levels of cytokines present in AIDS patients can favor pulmonary hypertension, but the role of a host response to HIV--determined by one or more HLA subtypes--is suspected to enhance high cytokine production levels. [References: 64]

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[Link Directly to Fulltext Article in OVID]

Unique Identifier: 20490288 / PubMed Identifier: 11035689

Authors: Mehta NJ. Khan IA. Mehta RN. Sepkowitz DA.

Institution: Department of Medicine, Long Island College Hospital, Brooklyn, NY, USA.

Abstract: OBJECTIVE: To report two new cases of HIV-related pulmonary hypertension and to review and analyze the existing reports on the subject. METHOD: Two new cases of HIV-related pulmonary hypertension are described, and the cases, case series, and related articles on the subject in all languages were identified through a comprehensive MEDLINE search. RESULTS: Among the 131 reviewed cases, 54% were male, and the age range was 2 to 56 years (mean, 33 years). The interval between the diagnosis of HIV disease and the diagnosis of pulmonary hypertension was 33 months. In 82% of cases, pulmonary hypertension was related solely to HIV infection. Presenting symptoms were progressive shortness of breath (85%), pedal edema (30%), nonproductive cough (19%), fatigue (13%), syncope or near-syncope (12%), and chest pain (7%). The mean (+/- SD) pulmonary arterial systolic BP was 67 +/- 18 mm Hg (n = 116), and diastolic BP was 40+/-11 mm Hg (n = 39). Pulmonary vascular resistance was 983+/-420 dyne. s. cm(-5) (n = 29). Chest radiographs demonstrated cardiomegaly (72%) and pulmonary artery prominence (71%). Right ventricular hypertrophy was the most common electrocardiographic finding (67%). Dilatation of the right heart chambers was the most common echocardiographic finding (98%). Plexogenic pulmonary arteriopathy was the most common histopathology (78%). Pulmonary function tests demonstrated mild restrictive patterns with variably reduced diffusing capacities. The responses to vasodilator agents and antiretroviral therapy was variable. Sixty-six patients died during a median follow-up period of 8 months. The median length of time from diagnosis to death was 6 months. CONCLUSION: HIV infection is an independent risk factor for the development of pulmonary hypertension. The appearance of unexplained cardiopulmonary symptoms in HIV-infected individuals should suggest pulmonary hypertension. [References: 55]