Risk of Echocardiographic Pulmonary Hypertension in Individuals with Human Immunodeficiency Virus–Hepatitis C Virus Coinfection

Human immunodeficiency virus (HIV) infection is a risk factor for pulmonary hypertension (PH). Chronic hepatitis C virus (HCV) infection may have unique or synergistic effects on the pulmonary vasculature, but the prevalence and risk factors for PH in HIV-HCV coinfected persons are not known.To define the prevalence of echocardiographic PH in a cohort of patients with HIV-HCV coinfection, to compare this estimate with the reported prevalence of PH among those with HIV infection alone, and to identify potential risk factors for PH in coinfected individuals.We performed a retrospective study of HIV-HCV coinfected patients followed at our institution from 2003 to 2012 with evidence of HCV infection (positive HCV antibody, measurable HCV ribonucleic acid viral load, and/or genotype) within 6 months of transthoracic echocardiogram. PH was defined by an estimated pulmonary artery systolic pressure (PASP) of greater than or equal to 40 mm Hg or more than moderate right ventricular dysfunction. We excluded those diagnosed with cirrhosis, left ventricular ejection fraction less than 50%, or more than moderate aortic or mitral valve disease.Sixty-eight patients were included, and 43 had adequate estimates of PASP. The median (interquartile range) age was 52 (48-57) years, and 45 (67%) were men. Eight (19%) had PH, and three (7%) had more than moderate right ventricular dysfunction. After age and sex adjustment, interferon (IFN)-based HCV treatment was associated with higher PASP (β, 6.00 mm Hg; 95% confidence interval, 0.09-11.90; P = 0.047) and with the risk of PH (odds ratio, 5.65; 95% confidence interval, 1.07-29.93; P = 0.042). These associations persisted after adjustment for comorbidities but were attenuated by adjustment for duration of HCV diagnosis.The prevalence of echocardiographic PH may be higher in HIV-HCV coinfected individuals than in those with HIV monoinfection. IFN-based HCV treatment and time since HCV diagnosis were associated with the development of PH as assessed by echocardiography. Further studies are needed to examine HIV-HCV coinfection, HCV treatment, and duration of infection as possible causes of pulmonary vascular disease.