Pulmonary hypertension in <scp>HIV</scp> infection: a prospective echocardiographic study

Schwarze-Zander, C; Pabst, Stefan; Hammerstingl, Christoph; Ohlig, J; Wasmuth, JC; Boesecke, Christoph; Stoffel‐Wagner, Birgit; Carstensen, A; Nickenig, Georg; Strassburg, CP; Rockstroh, JK; Skowasch, Dirk; Schueler, Robert

doi:10.1111/hiv.12261

Cited by 28 publications

(47 citation statements)

References 15 publications

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“…HIV‐associated PAH is a devastating and life‐threatening condition with recent cohort studies reporting prevalence ranging from 2.6% to 15.5% . Furthermore, a higher percentage of HIV‐infected individuals among intravenous drug users correlate with higher prevalence of HIV‐PAH in HIV‐infected patients . Our previous published findings also extensively highlight the exacerbated pulmonary vascular remodeling in the presence of both HIV‐viral proteins and drugs of abuse such as cocaine and morphine, therefore supporting the multiple‐hit hypothesis of PAH …”

Section: Introductionsupporting

confidence: 79%

Network of MicroRNAs Mediate Translational Repression of Bone Morphogenetic Protein Receptor‐2: Involvement in HIV‐Associated Pulmonary Vascular Remodeling

Chinnappan

Mohan

Agarwal

et al. 2018

JAHA

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BackgroundEarlier, we reported that the simultaneous exposure of pulmonary arterial smooth muscle cells to HIV proteins and cocaine results in the attenuation of antiproliferative bone morphogenetic protein receptor‐2 (BMPR2) protein expression without any decrease in its mRNA levels. Therefore, in this study, we aimed to investigate the micro RNA‐mediated posttranscriptional regulation of BMPR2 expression.Methods and ResultsWe identified a network of BMPR2 targeting micro RNAs including miR‐216a to be upregulated in response to cocaine and Tat‐mediated augmentation of oxidative stress and transforming growth factor‐β signaling in human pulmonary arterial smooth muscle cells. By using a loss or gain of function studies, we observed that these upregulated micro RNAs are involved in the Tat‐ and cocaine‐mediated smooth muscle hyperplasia via regulation of BMPR2 protein expression. These in vitro findings were further corroborated using rat pulmonary arterial smooth muscle cells isolated from HIV transgenic rats exposed to cocaine. More importantly, luciferase reporter and in vitro translation assays demonstrated that direct binding of novel miR‐216a and miR‐301a to 3′UTR of BMPR2 results in the translational repression of BMPR2 without any degradation of its mRNA.ConclusionsWe identified for the first time miR‐216a as a negative modulator of BMPR2 translation and observed it to be involved in HIV protein(s) and cocaine‐mediated enhanced proliferation of pulmonary smooth muscle cells.

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Section: Introductionsupporting

confidence: 79%

Network of MicroRNAs Mediate Translational Repression of Bone Morphogenetic Protein Receptor‐2: Involvement in HIV‐Associated Pulmonary Vascular Remodeling

Chinnappan

Mohan

Agarwal

et al. 2018

JAHA

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“…In the large prevalence study by Sitbon et al, PAH prevalence in HIV‐infected patients was found to be 0.46%. However, in many studies performed years after this study, the prevalence was detected to be 2.6%–6.1% . These findings indicated that HIV‐infected patients in the general population should be assessed for PAH development more carefully, and a screening strategy is necessary.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have demonstrated that HIV‐associated PAH prevalence is comparable with the prevalence in pre‐HAART era (0.46%) . Recent studies have shown that prevalence has increased to 2.6%–6.1% . Current pulmonary hypertension (PH) classification consists of five main groups .…”

Section: Introductionmentioning

confidence: 99%

Echocardiographic assessment of pulmonary arterial stiffness in human immunodeficiency virus‐infected patients

et al. 2019

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Background Pulmonary hypertension (PH) is one of the complications of human immunodeficiency virus (HIV) infection. Despite the emergence of effective therapies, pulmonary arterial hypertension is commonly seen, especially at advanced stages. At the time of diagnosis, a majority of patients are at New York Heart Association‐Functional Class III or IV. Many of the current screening modalities are dependent on detecting a rise in pulmonary arterial pressure (PAP). However, high capacitance of the pulmonary circulation implies that early microcirculation loss is not accompanied by a change in resting PAP. Therefore, we aimed to demonstrate early changes in pulmonary vascular disease in HIV‐infected patients with a new echocardiographic parameter, called as pulmonary arterial stiffness (PAS). Methods and Results Thirty‐six HIV‐infected patients and 36 age‐ and sex‐matched healthy control subjects were enrolled in this study. PAS was calculated echocardiographically by using maximal frequency shift and acceleration time of the pulmonary artery flow trace. There was no significant difference in diastolic functions, right ventricular diameters, systolic PAP, inferior vena cava widths, right atrial area, and tricuspid annular plane systolic excursion values between the two groups. However, PAS was calculated as 24.3 ± 6.4 Hz/msn in HIV‐infected patients and 19.3 ± 3.1 Hz/msn in healthy control group (P < 0.001). Increase in PAS was correlated with duration of HIV infection (P < 0.05). Conclusion Our results suggest that HIV infection affects pulmonary vascular bed starting early onset of disease and this can be demonstrated by an easy‐to‐measure echocardiographic parameter.

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“…Prevalence is lower than COPD and symptoms of fatigue, dyspnea and cough may initially be absent (64). Echo-based screening may both over and under-diagnose PAH depending on sPAP cut-offs used (110, 111). These observations lead some to conclude screening asymptomatic HIV-seropositive patients for PAH should not be performed (69).…”

Section: Screening For Lung Disease In Hivmentioning

confidence: 99%

“…These observations lead some to conclude screening asymptomatic HIV-seropositive patients for PAH should not be performed (69). The invasiveness and availability of RHC limit its use as a screening tool; however, growth differentiation factor (GDF)-15 and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in serum are strongly associated with increased sPAP (63, 111), so could have potential as biomarkers in a screening protocol.…”

Section: Screening For Lung Disease In Hivmentioning

confidence: 99%

Maintaining lung health with longstanding HIV

Collini

Morris

2016

Current Opinion in Infectious Diseases

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Purpose of review Human immunodeficiency virus (HIV) is now managed as a chronic disease. Non-infectious pulmonary conditions have replaced infection as the biggest threat to lung health, particularly as HIV cohorts age, but there is no consensus on how best to maintain long-term lung health. We review the epidemiology and pathogenesis of chronic obstructive pulmonary disease (COPD), pulmonary arterial hypertension (PAH) and lung cancer in HIV-seropositive individuals. Recent Findings Diagnoses of COPD are now up to 50% more prevalent in HIV-seropositive individuals than HIV-uninfected controls, and prospective pulmonary function studies find significant impairment in 7%–>50% of HIV-seropositive individuals. The prevalence of HIV-PAH is 0.2%–0.5%, and lung cancer is 2–3 times more prevalent in HIV-seropositive individuals. Although host factors such as age and smoking have a role, HIV is an independent contributor to the pathogenesis of COPD, PAH and lung cancer. Chronic inflammation, immune senescence, oxidative stress and direct effects of viral proteins are all potential pathogenetic mechanisms. Despite their prevalence, non-infectious lung diseases remain under-recognized and evidence for effective screening strategies in HIV-seropositive individuals is limited. Summary COPD, PAH and lung cancer are a growing threat to lung health in the HAART era necessitating early recognition.

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Pulmonary hypertension in HIV infection: a prospective echocardiographic study

Cited by 28 publications

References 15 publications

Network of MicroRNAs Mediate Translational Repression of Bone Morphogenetic Protein Receptor‐2: Involvement in HIV‐Associated Pulmonary Vascular Remodeling

Network of MicroRNAs Mediate Translational Repression of Bone Morphogenetic Protein Receptor‐2: Involvement in HIV‐Associated Pulmonary Vascular Remodeling

Echocardiographic assessment of pulmonary arterial stiffness in human immunodeficiency virus‐infected patients

Maintaining lung health with longstanding HIV

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