2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T4ea,Right ventricular failure drives both morbidity and mortality in pulmonary arterial hypertension (PAH), but the mechanism of transition from compensated right ventricle (cRV) to decompensated RV (dRV) is unknown, and some PAH patients develop dRV faster than others. We explored the role of RV cardiac myofibroblasts (cMFBs) on this transition utilizing 2 rat models: monocrotaline (MCT) versus the less inflammatory pulmonary artery banding (PAB); and 3 patient cohorts (n=81) of PAH versus group 2 pulmonary hypertension (PHT-2). We hypothesized that loss of UCP2 (uncoupling protein 2), critical for mitochondrial calcium (mCa We separated rat cRV from dRV based on catheterization and echocardiographic criteria and found a significant increase in cMFBs from MCT but not PAB RV (which decompensated much later than MCT RV). In isolated hearts, MCT RV contractility was lower in dRV but not in isolated cardiomyocytes (CMs), pointing to a non-CM cause. Mitochondrial respiration was lower in MCT dRV cMFBs than in control and cRV cFBs but increased in MCT-RV CMs. mCa Our data suggest that a change of cell identity (cFBs to cMFBs) in the RV is a driver of RV decompensation. TNF-α or rs659366 is a potential biomarker for early RV decompensation in PAH.31:Tb3b, BACKGROUND: Right ventricular failure drives both morbidity and mortality in pulmonary arterial hypertension (PAH), but the mechanism of transition from compensated right ventricle (cRV) to decompensated RV (dRV) is unknown, and some PAH patients develop dRV faster than others. METHODS: We explored the role of RV cardiac myofibroblasts (cMFBs) on this transition utilizing 2 rat models: monocrotaline (MCT) versus the less inflammatory pulmonary artery banding (PAB); and 3 patient cohorts (n=81) of PAH versus group 2 pulmonary hypertension (PHT-2). We hypothesized that loss of UCP2 (uncoupling protein 2), critical for mitochondrial calcium (mCa ++ ) regulation and cardiac fibroblasts (cFBs) differentiation to cMFBs, is associated with dRV; and that a loss-of-function UCP2 single nucleotide polymorphism (SNP; rs659366) may predict dRV in human PAH. RESULTS: We separated rat cRV from dRV based on catheterization and echocardiographic criteria and found a significant increase in cMFBs from MCT but not PAB RV (which decompensated much later than MCT RV). In isolated hearts, MCT RV contractility was lower in dRV but not in isolated cardiomyocytes (CMs), pointing to a non-CM cause. Mitochondrial respiration was lower in MCT dRV cMFBs than in control and cRV cFBs but increased in MCT–RV CMs. mCa ++ was progressively decreased from normal to MCT–cRV to dRV cMFBs, and the same was true for c(M)FBs (but not CMs) UCP2. Tumor necrosis factor alpha (TNF-α) decreased UCP2 mRNA/protein levels in RV cFBs but not RV CMs. In human PAH, but not PHT-2, dRVs had more cMFBs and less UCP2 than control and cRVs. Decreased UCP2 levels and rs659366 were associated with worse RV performance (tricuspid annular plane systolic excursion and cardiac index), even among patients with similar mean pulmonary arterial pressure. CONCLUSIONS: Our data suggest that a change of cell identity (cFBs to cMFBs) in the RV is a driver of RV decompensation. TNF-α or rs659366 is a potential biomarker for early RV decompensation in PAH. 32:T596,Right ventricular failure (RVF) is a complex clinical syndrome resulting from anatomical and physiological dysfunction of the right ventricle, marked by insufficient cardiac output state, elevated filling pressures, and elevated central venous pressures. Historically, acute RVF in the medical intensive care unit (MICU) has posed significant diagnostic and therapeutic challenges, often leading to poor patient outcomes and increased healthcare utilization. RVF is a pervasive and critically underdiagnosed condition in MICUs, often masked by nonspecific symptoms and overlooked in favor of left-sided pathology, despite its profound impact on patient outcomes and mortality. This difficulty stems from a limited understanding of its underlying mechanisms and a lack of high-quality evidence to guide management in critical care settings. Effective care for RVF demands early recognition, precise identification of the underlying etiology, and prompt, targeted interventions. Intensivists must possess comprehensive knowledge and a diverse skill set to navigate these complexities and address unforeseen complications. Over the past two decades, advancements in diagnostic and therapeutic technologies have transformed the approach to RVF, driving significant progress in the field. This review explores the historical evolution, pathophysiology, clinical presentation, and contemporary management strategies for RVF in the MICU.33:T5db,Abstract Right ventricular failure (RVF) is a complex clinical syndrome resulting from anatomical and physiological dysfunction of the right ventricle, marked by insufficient cardiac output state, elevated filling pressures, and elevated central venous pressures. Historically, acute RVF in the medical intensive care unit (MICU) has posed significant diagnostic and therapeutic challenges, often leading to poor patient outcomes and increased healthcare utilization. RVF is a pervasive and critically underdiagnosed condition in MICUs, often masked by nonspecific symptoms and overlooked in favor of left-sided pathology, despite its profound impact on patient outcomes and mortality. This difficulty stems from a limited understanding of its underlying mechanisms and a lack of high-quality evidence to guide management in critical care settings. Effective care for RVF demands early recognition, precise identification of the underlying etiology, and prompt, targeted interventions. Intensivists must possess comprehensive knowledge and a diverse skill set to navigate these complexities and address unforeseen complications. Over the past two decades, advancements in diagnostic and therapeutic technologies have transformed the approach to RVF, driving significant progress in the field. This review explores the historical evolution, pathophysiology, clinical presentation, and contemporary management strategies for RVF in the MICU.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Right Ventricular Failure: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Right Ventricular Failure (condition). Clinician-written summaries and actionable practice insights. 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the 'mixed' sex tag is inferred from typical HFpEF cohort composition.","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.126.014620","tag_type":"warning","value":"Study design is mixed (mostly retrospective with a prospective subset), which introduces selection bias risk.","value_numeric":null},{"paper_doi":"10.1161/circheartfailure.126.014620","tag_type":"warning","value":"The biopsy/transcriptomics subgroup is very small (n=10); gene-level findings should be considered hypothesis-generating only.","value_numeric":null}],"summaries":{"what_studied":"A multimodal framework was used to evaluate mechanisms of RV failure in PH-HFpEF (n=48), stratifying patients by cardiac MRI-derived RV ejection fraction (<45% = RV dysfunction, n=19; normal RV, n=29), with subsets undergoing pulmonary vascular mechanics, 4D flow MRI, and endomyocardial biopsy with long-read RNA sequencing over a 1-year follow-up.","key_result":"RV dysfunction was associated with an 8.2-fold higher risk of mortality or first HF hospitalization at 1 year (HR 8.2, 95% CI 2.5–25.4), increased proximal pulmonary arterial stiffness, higher RV energy expenditure, disturbed 4D flow patterns, and RV myocardial pathway shifts (upregulated RNA metabolism, downregulated mitochondrial pathways).","limitations":"- Very small subgroup sample sizes (mechanics n=17, 4D flow n=15, biopsy n=10) severely limit statistical power for individual gene-level findings.\n- Predominantly retrospective cohort design with a prospective subset only.\n- Findings may not generalize beyond the specific PH-HFpEF phenotype studied.","practice_takeaway":"Cardiac MRI-derived RV ejection fraction <45% identifies PH-HFpEF patients at markedly higher risk of death or HF hospitalization within 1 year (HR 8.2), supporting its use as a prognostic stratifier. Segmental pulmonary vascular remodeling and mitochondrial pathway downregulation may represent future therapeutic targets, though validation in larger cohorts is needed before clinical translation."}},{"doi":"10.1016/j.athoracsur.2026.07.010","pmid":"42508675","title":"The Society of Thoracic Surgeons / World Society for Pediatric and Congenital Heart Surgery / European Congenital Heart Surgeons Association 2026 Expert Consensus Document on Timing, Indications, and Options for Pulmonary Valve Replacement in Children with Repaired Tetralogy of Fallot","journal_title":"The Annals of Thoracic Surgery","journal_issn":"0003-4975","published_at":"2026-07-27T00:00:00.000Z","url":"https://doi.org/10.1016/j.athoracsur.2026.07.010","source_score":2,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-31T13:36:55.242Z","updated_at":"2026-07-31T13:36:55.242Z","tags":[{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"age_group","value":"pediatric","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"category","value":"Respiratory System","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"condition","value":"Pulmonary Regurgitation","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"condition","value":"Right Ventricular Failure","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"condition","value":"Tetralogy of Fallot","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"modality","value":"Surgical Pulmonary Valve Replacement","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"modality","value":"Transcatheter Pulmonary Valve Replacement","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"study_design","value":"Expert Consensus Document (Modified Delphi)","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"warning","value":"Full text is behind a paywall; the specific content of all 13 recommendations, evidence grades, and supporting data were not accessible for detailed extraction.","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"warning","value":"No sample size is applicable — this is a consensus/guideline document, not an original research study with enrolled patients.","value_numeric":null},{"paper_doi":"10.1016/j.athoracsur.2026.07.010","tag_type":"warning","value":"The impact_flag 'practice_changing' is applied because this is the first pediatric-specific guideline in this area, filling a recognized gap; however, the strength of individual recommendations cannot be verified without full-text access.","value_numeric":null}],"summaries":{"what_studied":"A multidisciplinary expert panel (congenital surgeons and cardiologists) used a Modified Delphi process to develop consensus recommendations on timing, indications, and surgical vs. transcatheter options for pulmonary valve replacement (PVR) in children with repaired Tetralogy of Fallot and chronic pulmonary regurgitation.","key_result":"Consensus was reached on 13 recommendations covering two key topics: (1) pediatric-specific considerations for PVR timing/indications, and (2) surgical vs. transcatheter PVR technique selection.","limitations":"Full text is paywalled; specific recommendation content and supporting evidence grades are not available for review. The document is consensus-based (Modified Delphi), not derived from a formal systematic review or RCT, limiting the strength of individual recommendations.","practice_takeaway":"Congenital heart teams should apply these 13 consensus-based recommendations to guide PVR timing and technique selection in children with repaired TOF and chronic pulmonary regurgitation, filling a gap left by adult-focused guidelines. Engage a multidisciplinary team of congenital surgeons and cardiologists, as decision-making involves both surgical and transcatheter options."}},{"doi":"10.1161/circulationaha.126.079274","pmid":"42441757","title":"Transforming Pulmonary Arterial Hypertension: Key Milestones and Future Perspectives","journal_title":"Circulation","journal_issn":"0009-7322","published_at":"2026-07-13T00:00:00.000Z","url":"https://doi.org/10.1161/circulationaha.126.079274","source_score":29,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-22T13:37:53.878Z","updated_at":"2026-07-22T13:37:53.878Z","tags":[{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"brand","value":"Winrevair","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"condition","value":"Pulmonary Arterial Hypertension","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"condition","value":"Right Ventricular Failure","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"generic","value":"sotatercept","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"modality","value":"Activin Receptor Ligand Trap","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"modality","value":"Endothelin Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"modality","value":"Lung Transplantation","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"modality","value":"Phosphodiesterase-5 Inhibitor","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"modality","value":"Prostacyclin Analog","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1161/circulationaha.126.079274","tag_type":"warning","value":"Sample size tag omitted: no single study population is reported; 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":"10.1152/ajplung.00104.2026","pmid":"42030209","title":"The right time, the right cell: the potential for precision senotherapy in pulmonary arterial hypertension","journal_title":"American Journal of Physiology-Lung Cellular and Molecular Physiology","journal_issn":"1040-0605","published_at":"2026-04-24T00:00:00.000Z","url":"https://doi.org/10.1152/ajplung.00104.2026","source_score":2,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-03T13:44:37.417Z","updated_at":"2026-06-03T13:44:37.417Z","tags":[{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"category","value":"Respiratory System","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"condition","value":"Pulmonary Arterial Hypertension","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"condition","value":"Right Ventricular Failure","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"modality","value":"Senolytic","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"warning","value":"No clinical trial evidence in PAH patients exists yet to support the proposed precision senotherapy framework.","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"warning","value":"No original patient data or meta-analysis; this is a perspective/narrative review and conclusions reflect author interpretation of a conflicting preclinical literature.","value_numeric":null},{"paper_doi":"10.1152/ajplung.00104.2026","tag_type":"warning","value":"Study design classified as Narrative Review; the paper uses the framing of a 'review' but also presents a novel conceptual framework, which may place it closer to a perspective article.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the role of cellular senescence in pulmonary arterial hypertension (PAH) pathophysiology and examines preclinical and human evidence for senolytic therapies, proposing a 'precision senotherapy' framework that accounts for senescent cell type, senolytic mechanism, and disease stage at time of intervention.","key_result":"Human data show senescent cells accumulate in remodeled pulmonary vascular lesions and may drive proliferation and apoptosis resistance in neighboring cells; however, preclinical senolytic studies have produced conflicting results, suggesting that cell-type heterogeneity, off-target drug effects, and disease-stage timing all contribute to divergent outcomes.","limitations":"This is a narrative review without original data or meta-analysis, so conclusions are shaped by the authors' interpretation of an inconsistent preclinical literature. No clinical trial data in PAH patients are available to validate the proposed precision framework.","practice_takeaway":"Senolytics are not yet ready for routine PAH practice, but clinicians and researchers should note that intermittent, short-course regimens and combination approaches tailored to cell type and disease stage may improve safety and efficacy in future trials."}},{"doi":"10.1161/circulationaha.125.078674","pmid":"41797703","title":"Critical Contribution of Cardiac Myofibroblasts in Right Ventricular Failure and the Role of UCP2 SNPs in the Predisposition to RV Decompensation in Pulmonary Arterial Hypertension","journal_title":"Circulation","journal_issn":"0009-7322","published_at":"2026-03-09T00:00:00.000Z","url":"https://doi.org/10.1161/circulationaha.125.078674","source_score":38,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-12","doi":"10.1161/circulationaha.125.078674","days":"7","issn":"0009-7322","rank":"8","field":"Clinical Medicine","score":"38","category":"Cardiac & Cardiovascular Systems","categories":["Cardiac & Cardiovascular Systems"],"_categories":["Cardiac & Cardiovascular Systems"]},"pubmed":{"doi":"10.1161/CIRCULATIONAHA.125.078674","title":"Critical Contribution of Cardiac Myofibroblasts in Right Ventricular Failure and the Role of UCP2 SNPs in the Predisposition to RV Decompensation in Pulmonary Arterial Hypertension.","journal":"Circulation","methods":"","results":"We separated rat cRV from dRV based on catheterization and echocardiographic criteria and found a significant increase in cMFBs from MCT but not PAB RV (which decompensated much later than MCT RV). In isolated hearts, MCT RV contractility was lower in dRV but not in isolated cardiomyocytes (CMs), pointing to a non-CM cause. Mitochondrial respiration was lower in MCT dRV cMFBs than in control and cRV cFBs but increased in MCT-RV CMs. mCa","abstract":"$30","keywords":["calcium","heart failure","hypertension, pulmonary","hypertrophy, right ventricular","myofibroblasts","tumor necrosis factor-alpha","uncoupling protein 2"],"pubmed_id":"41797703","conclusions":"","publication_date":"2026-03-09T00:00:00"},"crossref":{"DOI":"10.1161/circulationaha.125.078674","URL":"https://doi.org/10.1161/circulationaha.125.078674","ISSN":["0009-7322","1524-4539"],"link":[{"URL":"https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.125.078674","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1494-1515","type":"journal-article","issue":"19","score":1,"title":["Critical Contribution of Cardiac Myofibroblasts in Right Ventricular Failure and the Role of UCP2 SNPs in the Predisposition to RV Decompensation in Pulmonary Arterial 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