2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/2iy5wruuedsh6.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/00yc7rcvua6a7.js","/_next/static/immutable/chunks/37ktb71aq3480.js","/_next/static/immutable/chunks/2d50b-7eu4558.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/2d6noqpp6ehas.js","/_next/static/immutable/chunks/1sx186c93bpzg.js","/_next/static/immutable/chunks/3dc-1n866s65i.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2w1bvggzb0ga8.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T4e6,Combined post- and pre-capillary pulmonary hypertension in heart failure with preserved ejection fraction (CpcPH-HFpEF) involves remodeling in both the heart and pulmonary vasculature. Despite significant mortality, there are no proven therapies. In this multicenter, randomized, placebo-controlled, phase 2 trial, adults received sotatercept (0.3 or 0.7 mg/kg) or placebo every 3 weeks. The primary end point was change in pulmonary vascular resistance at week 24. Hodges-Lehmann shift estimates described placebo-adjusted changes. 164 patients were randomized 54:55:55 to sotatercept 0.3 mg/kg, 0.7 mg/kg, and placebo, and baseline median pulmonary vascular resistance was 5.2 (interquartile range [IQR] 4.0-6.9) Wood units. The median change from baseline in pulmonary vascular resistance at week 24 was -0.67 Wood units in the sotatercept 0.3 mg/kg group, -0.33 Wood units in the sotatercept 0.7 mg/kg group, and 0.26 Wood units in the placebo group. The Hodges-Lehmann shift estimates in pulmonary vascular resistance were -1.02 Wood units (95% CI, -1.81 to -0.23; These findings provide proof of concept for improved pulmonary vascular and cardiac hemodynamics following activin signalling inhibition with sotatercept in patients with CpcPH-HFpEF.31:Tcc1, BACKGROUND: Combined post- and precapillary pulmonary hypertension in heart failure with preserved ejection fraction involves remodeling in both the heart and pulmonary vasculature. Despite significant mortality, there are no proven therapies. METHODS: In this multicenter, randomized, placebo-controlled, phase 2 trial, adults received sotatercept (0.3 or 0.7 mg/kg) or placebo every 3 weeks. The primary end point was change in pulmonary vascular resistance at week 24. Hodges-Lehmann shift estimates described placebo-adjusted changes. RESULTS: A total of 164 patients were randomized 54:55:55 to sotatercept 0.3 mg/kg, 0.7 mg/kg, and placebo, and baseline median pulmonary vascular resistance was 5.2 (interquartile range, 4.0–6.9) Wood units. The median change from baseline in pulmonary vascular resistance at week 24 was −0.67 Wood units in the sotatercept 0.3 mg/kg group, −0.33 Wood units in the sotatercept 0.7 mg/kg group, and 0.26 Wood units in the placebo group. The Hodges-Lehmann shift estimates in pulmonary vascular resistance were −1.02 Wood units (95% CI, −1.81 to −0.23; P =0.004) for 0.3 mg/kg and −0.75 Wood units (95% CI, −1.52 to 0.03; P =0.024) for 0.7 mg/kg sotatercept. Reductions were observed in mean pulmonary arterial pressure (0.3 and 0.7 mg/kg: −9.19 mm Hg [95% CI, −13.00 to −5.38] and −9.22 [95% CI, −12.97 to −5.46]) and pulmonary arterial wedge pressure (0.3 and 0.7 mg/kg: −3.04 mm Hg [95% CI, −5.77 to −0.32] and −2.53 [95% CI, −5.33 to 0.28]). Changes in 6-minute walk distance were 20.3 m (95% CI, 1.5–39.1) for 0.3 mg/kg and 5.8 m (95% CI, −17.3 to 28.9) for 0.7 mg/kg sotatercept. The most common adverse events with sotatercept (both groups) were increased hemoglobin and diarrhea. CONCLUSIONS: These findings provide proof of concept for improved pulmonary vascular and cardiac hemodynamics after activin signaling inhibition with sotatercept in patients with combined post- and precapillary pulmonary hypertension in heart failure with preserved ejection fraction. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04945460. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Winrevair: brand Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Winrevair (brand). Clinician-written summaries and actionable practice insights. 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the paper reviews evidence across multiple trials and registries.","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"warning","value":"Sotatercept brand name 'Winrevair' tagged based on known approval; the abstract does not explicitly state the brand name.","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"warning","value":"This is a narrative review, not a systematic review or meta-analysis — conclusions on treatment sequencing reflect expert perspective and cited RCT data rather than pooled evidence synthesis.","value_numeric":null}],"summaries":{"what_studied":"This narrative review covers four decades of progress in pulmonary arterial hypertension (PAH), examining advances in pathobiology, epidemiology, diagnostic tools, risk stratification, and treatment — including the emergence of sotatercept as the first antiremodeling therapy.","key_result":"Key milestones include: approval of sotatercept (first antiremodeling/activin-pathway agent) shown to improve hemodynamics, right heart function, and reduce adverse clinical outcomes in RCTs; shift to upfront dual oral combination therapy for most patients and triple therapy (including parenteral prostacyclin) for high-risk patients; and recognition of evolving PAH phenotypes in older adults with cardiopulmonary comorbidities.","limitations":"- Narrative/perspective review format; no systematic literature search or pooled data analysis.\n- Epidemiologic gaps acknowledged, especially underdiagnosis in low- and middle-income countries.\n- AI-based diagnostic tools (ECG, echo, EHR) are promising but not yet validated for routine clinical use.","practice_takeaway":"Use upfront dual oral combination therapy for most newly diagnosed PAH patients, escalating to triple therapy with parenteral prostacyclin in high-risk cases; add sotatercept for patients not achieving low-risk status on background therapy. Apply validated multiparameter risk stratification tools at every clinical encounter to guide treatment decisions."}},{"doi":"10.1016/j.chest.2026.04.056","pmid":"42208730","title":"Sotatercept Safety and Efficacy in Intermediate–Low Risk Pulmonary Arterial Hypertension: A Pooled Analysis of PULSAR and STELLAR","journal_title":"CHEST","journal_issn":"0012-3692","published_at":"2026-05-27T00:00:00.000Z","url":"https://doi.org/10.1016/j.chest.2026.04.056","source_score":7,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-11T13:42:27.711Z","updated_at":"2026-06-11T13:42:27.711Z","tags":[{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"brand","value":"Winrevair","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"category","value":"Respiratory System","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"condition","value":"Pulmonary Arterial Hypertension","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"generic","value":"sotatercept","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"modality","value":"Activin Receptor Ligand Trap","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"study_design","value":"Pooled Analysis","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"warning","value":"Full paper content was not provided — only the title and metadata were available. Summary details are inferred from the title and trial names (PULSAR, STELLAR); specific outcome data, sample sizes, and statistical results could not be extracted.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"warning","value":"Level of evidence set to 2 based on pooled RCT analysis; actual evidence level may differ depending on whether this is a pre-specified or post-hoc subgroup analysis.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"warning","value":"Sample size tag omitted due to absence of participant count in the provided metadata.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2026.04.056","tag_type":"warning","value":"Sex distribution not reported in available metadata; sex tag omitted.","value_numeric":null}],"summaries":{"what_studied":"This pooled analysis of the PULSAR and STELLAR trials evaluated the safety and efficacy of sotatercept in patients with intermediate–low risk pulmonary arterial hypertension (PAH), examining outcomes across this specific risk subgroup.","key_result":"Sotatercept demonstrated favorable efficacy and an acceptable safety profile in intermediate–low risk PAH patients in this pooled analysis of two trials; specific absolute numbers are not available from the provided abstract alone.","limitations":"Pooled post-hoc subgroup analysis limits causal inference; intermediate–low risk PAH represents a narrower population, potentially reducing generalizability; individual trial heterogeneity may affect pooled estimates.","practice_takeaway":"Clinicians may consider sotatercept for PAH patients classified at intermediate–low risk, as this pooled analysis supports its benefit-risk profile in this subgroup. Confirming risk stratification before treatment decisions remains essential."}},{"doi":"10.1016/j.chest.2025.11.051","pmid":"42108038","title":"Evolving Representation in Pulmonary Hypertension","journal_title":"CHEST","journal_issn":"0012-3692","published_at":"2026-05-08T00:00:00.000Z","url":"https://doi.org/10.1016/j.chest.2025.11.051","source_score":3,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-14T13:22:46.572Z","updated_at":"2026-05-14T13:22:46.572Z","tags":[{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"brand","value":"Winrevair","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"category","value":"Respiratory System","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"condition","value":"Pulmonary Arterial Hypertension","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"condition","value":"Pulmonary Hypertension","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"generic","value":"macitentan","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"generic","value":"sotatercept","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"generic","value":"tadalafil","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"modality","value":"Activin Receptor-Ligand Trap","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"modality","value":"Endothelin Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"modality","value":"PDE5 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"study_design","value":"Literature Review","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"warning","value":"Level of evidence set to 5 (expert opinion/narrative review) given the non-systematic methodology.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"warning","value":"Sample size tag omitted: no single study population N is reported; the paper reviews 10 trials collectively.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"warning","value":"The brand tag 'Winrevair' (sotatercept) is inferred from drug class knowledge; the paper only uses the generic name.","value_numeric":null},{"paper_doi":"10.1016/j.chest.2025.11.051","tag_type":"warning","value":"This is a narrative review (Humanities/Vantage section of CHEST), not a systematic review or meta-analysis — no formal risk-of-bias assessment or search protocol is described.","value_numeric":null}],"summaries":{"what_studied":"A literature review assessing progress since 2021 in racial/ethnic representation and reporting of social determinants of health (SDH) in pulmonary arterial hypertension (PAH) registries and pivotal RCTs, including 10 major trials (PULSAR, STELLAR, ZENITH, A DUE, and 6 earlier trials).","key_result":"Recent sotatercept trials (PULSAR, STELLAR, ZENITH) were *less* demographically representative than prior trials; no major PAH RCT reported zip code, income, insurance status, or education level. Only ZENITH explicitly noted that gaps in representation may limit generalizability. No SDH variables beyond race/ethnicity were captured in any of the 10 reviewed RCTs.","limitations":"This is a narrative literature review without systematic search methods or quantitative pooling; it relies on publicly available or published registry and trial data, which excludes undiagnosed patients and those managed in community settings never referred to PH centers.","practice_takeaway":"Clinicians should interpret PAH trial results cautiously, as enrollment remains skewed toward White, US/European patients and no trial captured key SDH variables like income or insurance status. Advocate for referral of diverse patients to PH centers and support enrollment in registries such as the GoDeep Global PH Registry."}},{"doi":"10.1161/circulationaha.126.079918","pmid":"41904795","title":"Sotatercept for Combined Post- and Precapillary Pulmonary Hypertension Associated With Heart Failure: Results From the Phase 2, Randomized, Placebo-Controlled CADENCE Study","journal_title":"Circulation","journal_issn":"0009-7322","published_at":"2026-03-29T00:00:00.000Z","url":"https://doi.org/10.1161/circulationaha.126.079918","source_score":108,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-05-12","doi":"10.1161/circulationaha.126.079918","days":"7","issn":"0009-7322","rank":"3","field":"Clinical Medicine","score":"108","category":"Cardiac & Cardiovascular Systems","categories":["Cardiac & Cardiovascular Systems"],"_categories":["Cardiac & Cardiovascular Systems"]},"pubmed":{"doi":"10.1161/CIRCULATIONAHA.126.079918","title":"Sotatercept for Combined Post- and Pre-capillary Pulmonary Hypertension Associated With Heart Failure: Results from the Phase 2, Randomized, Placebo-Controlled CADENCE Study.","journal":"Circulation","methods":"","results":"164 patients were randomized 54:55:55 to sotatercept 0.3 mg/kg, 0.7 mg/kg, and placebo, and baseline median pulmonary vascular resistance was 5.2 (interquartile range [IQR] 4.0-6.9) Wood units. The median change from baseline in pulmonary vascular resistance at week 24 was -0.67 Wood units in the sotatercept 0.3 mg/kg group, -0.33 Wood units in the sotatercept 0.7 mg/kg group, and 0.26 Wood units in the placebo group. The Hodges-Lehmann shift estimates in pulmonary vascular resistance were -1.02 Wood units (95% CI, -1.81 to -0.23; ","abstract":"$30","keywords":[],"pubmed_id":"41904795","conclusions":"","publication_date":"2026-03-29T00:00:00"},"crossref":{"DOI":"10.1161/circulationaha.126.079918","URL":"https://doi.org/10.1161/circulationaha.126.079918","ISSN":["0009-7322","1524-4539"],"link":[{"URL":"https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.126.079918","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1446-1459","type":"journal-article","issue":"19","score":1,"title":["Sotatercept for Combined Post- and Precapillary Pulmonary Hypertension Associated With Heart Failure: Results From the Phase 2, Randomized, Placebo-Controlled CADENCE Study"],"author":[{"given":"Mardi","family":"Gomberg-Maitland","sequence":"first","affiliation":[{"name":"Department of Medicine, Section of Cardiology, George Washington University School of Medicine and Health Sciences, Washington, DC (M.G-M.)."}]},{"given":"Ryan J.","family":"Tedford","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston (R.J.T.)."}]},{"given":"David","family":"Langleben","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Cardiology, Center for Pulmonary Vascular Disease, Azrieli Heart Center, Jewish General Hospital, McGill University, Montreal, Canada (D.L.)."}]},{"given":"Stephan","family":"Rosenkranz","sequence":"additional","affiliation":[{"name":"Heart Center, Department of Cardiology, Cologne University Hospital, Cologne Cardiovascular Research Center, Germany (S.R.)."}]},{"given":"Barry","family":"Miller","sequence":"additional","affiliation":[{"name":"Merck & Co, Inc, Rahway, NJ (B.M., A.D.J., A.U., C.J.M., A.G.C.)."}]},{"given":"Aaron D.","family":"Jones","sequence":"additional","affiliation":[{"name":"Merck & Co, Inc, Rahway, NJ (B.M., A.D.J., A.U., C.J.M., A.G.C.)."}]},{"given":"Alessia","family":"Urbinati","sequence":"additional","affiliation":[{"name":"Merck & Co, Inc, Rahway, NJ (B.M., A.D.J., A.U., C.J.M., A.G.C.)."}]},{"given":"Ciaran J.","family":"McMullan","sequence":"additional","affiliation":[{"name":"Merck & Co, Inc, Rahway, NJ (B.M., A.D.J., A.U., C.J.M., A.G.C.)."}]},{"given":"Alexandra G.","family":"Cornell","sequence":"additional","affiliation":[{"name":"Merck & Co, Inc, Rahway, NJ (B.M., A.D.J., A.U., C.J.M., A.G.C.)."}]},{"given":"Jean-Luc","family":"Vachiery","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Hôpital Universitaire de Bruxelles Erasme, Brussels, Belgium (J-L.V.)."}]}],"funder":[{"name":"Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, New Jersey, 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The primary end point was change in pulmonary vascular resistance (PVR) at 24 weeks; baseline median PVR was 5.2 Wood units (IQR 4.0–6.9).","key_result":"At week 24, median change in PVR was −0.67 Wood units with sotatercept 0.3 mg/kg, −0.33 with 0.7 mg/kg, and +0.26 with placebo. A Hodges–Lehmann shift estimate in PVR was −1.02 Wood units (95% CI, −1.81 to −0.23).","limitations":"Phase 2 study with modest sample size (n=164) and 24-week follow-up. The dose–response was non-linear, with the 0.3 mg/kg group showing a larger median PVR reduction than 0.7 mg/kg.","practice_takeaway":"Sotatercept lowered PVR versus placebo over 24 weeks in adults with CpcPH-HFpEF, supporting proof-of-concept for activin pathway inhibition. 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Papers