1 Alpert Medical School of Brown University.
Ann Am Thorac Soc. 2014 Dec;11(10):1553-9. doi: 10.1513/AnnalsATS.201405-225OC.
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.
人类免疫缺陷病毒（HIV）感染是肺动脉高压（PH）的一个危险因素。慢性丙型肝炎病毒（HCV）感染可能对肺血管有独特或协同作用，但 HIV-HCV 合并感染患者 PH 的患病率和危险因素尚不清楚。
在 HIV-HCV 合并感染患者的队列中确定超声心动图 PH 的患病率，将这一估计与单独感染 HIV 患者的 PH 报告患病率进行比较，并确定合并感染个体 PH 的潜在危险因素。
我们对 2003 年至 2012 年在我们机构接受治疗的 HIV-HCV 合并感染患者进行了回顾性研究，这些患者在接受经胸超声心动图检查的 6 个月内有 HCV 感染的证据（阳性 HCV 抗体、可测量的 HCV 核糖核酸病毒载量和/或基因型）。PH 通过估计肺动脉收缩压（PASP）大于或等于 40mmHg 或中重度右心室功能障碍来定义。我们排除了那些诊断为肝硬化、左心室射血分数小于 50%或中重度主动脉或二尖瓣疾病的患者。
共纳入 68 例患者，其中 43 例有足够的 PASP 估计值。中位（四分位间距）年龄为 52（48-57）岁，45 例（67%）为男性。8 例（19%）患有 PH，3 例（7%）患有中重度右心室功能障碍。在年龄和性别调整后，基于干扰素（IFN）的 HCV 治疗与较高的 PASP（β，6.00mmHg；95%置信区间，0.09-11.90；P=0.047）和 PH 风险（比值比，5.65；95%置信区间，1.07-29.93；P=0.042）相关。这些关联在调整合并症后仍然存在，但在调整 HCV 诊断时间后有所减弱。
与单独感染 HIV 的患者相比，HIV-HCV 合并感染患者的超声心动图 PH 患病率可能更高。基于 IFN 的 HCV 治疗和 HCV 诊断后时间与超声心动图评估的 PH 发展相关。需要进一步研究 HIV-HCV 合并感染、HCV 治疗和感染持续时间作为肺血管疾病的可能病因。
