Heart Failure Reviews最新文献

{"title":"Beyond clinical congestion in acute heart failure: integrating lung ultrasound, venous doppler, and echocardiographic hemodynamics for imaging-guided decongestion.","authors":"Muzamil Yousuf Lone, Sivadasanpillai Harikrishnan","doi":"10.1007/s10741-026-10658-8","DOIUrl":"10.1007/s10741-026-10658-8","url":null,"abstract":"<p><p>Acute heart failure (AHF) is a major cause of hospitalisation worldwide and remains associated with substantial early rehospitalisation and short-term mortality. Accurate assessment of congestion remains challenging because symptoms, physical signs, body weight, and conventional biomarkers may not fully capture the severity, distribution, or persistence of haemodynamic congestion. This limitation contributes to incomplete decongestion and may partly explain recurrent decompensation after discharge. In this review, we examine the complementary roles of three point-of-care ultrasound modalities in residual congestion assessment: lung ultrasound for pulmonary congestion, venous Doppler/VExUS for systemic venous and end-organ congestion, and focused transthoracic echocardiography for cardiac and haemodynamic profiling. We propose the ICON (Integrated Congestion-Oriented Navigation) framework as a pragmatic bedside model that translates these modalities into a three-phase acute heart failure workflow: initial assessment, inpatient monitoring, and predischarge reassessment. Within this workflow, ICON supports phenotype-based interpretation of residual congestion, including pulmonary-dominant, systemic venous/RV-dominant, mixed, cold-wet/low-output, and near-decongested profiles. Current evidence supports the prognostic value of residual congestion and suggests that ultrasound-guided strategies may improve congestion assessment, but the evidence remains heterogeneous. The ICON framework should therefore be viewed as a proposed physiology-based model requiring prospective validation before adoption as a standard-of-care pathway.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-viral myocarditis.","authors":"Mateusz Sokolski, Wiktoria Zychla, Michal Wilk, Bartosz Balcer, Patryk Jakubasz, Justyna Sokolska, Federica Guidetti, Julia Krupa-Zabiegała, William Chick, Daniel Bromage","doi":"10.1007/s10741-026-10654-y","DOIUrl":"10.1007/s10741-026-10654-y","url":null,"abstract":"<p><p>Myocarditis is an inflammatory disease of the myocardium characterized by complex histological, immunological and molecular changes occur that may ultimately lead to post-viral cardiomyopathy, a specific phenotype of dilated cardiomyopathy and heart failure (HF) after a viral infection. Viral infections remain a major cause, with pathogens like parvovirus B19, human herpesvirus 6, and enteroviruses frequently associated with both acute myocarditis and its progression to chronic myocardial dysfunction. This review aims to provide an overview of the mechanisms linking viral myocarditis to the development of dilated cardiomyopathy and HF, with emphasis on factors contributing to disease persistence, progression, and current diagnostic approaches. Progression of myocarditis reflects overlapping phases of viral entry, immune activation, and remodeling. While direct cytotoxic effects contribute to early myocardial injury, ongoing damage is primarily driven by persistent immune activation, often despite limited viral replication. Viral persistence, dysregulated interferon signaling, inflammasome activation, and autoimmune responses sustain myocardial inflammation, promoting fibrosis and ventricular dysfunction. These processes are further reinforced by neurohormonal and metabolic changes, leading to adverse remodeling. Clinically, myocarditis presents with a broad spectrum ranging from mild symptoms to fulminant HF and malignant arrhythmias. Diagnosis relies on biomarkers, cardiac magnetic resonance, and endomyocardial biopsy to assess myocardial injury and detect viral presence. Management remains mainly supportive, with limited and inconsistent evidence for targeted immunomodulatory or antiviral therapies. In conclusion, improved understanding of the interplay between viral persistence and immune-mediated injury is essential for identifying patients at risk of progression and for developing mechanism-based therapeutic strategies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13356092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiomyopathy in glycogen storage diseases: diagnosis, prognosis, and advanced management.","authors":"Umang Patel, Eren Gunes, Apaara Chawla, Kiara Ashman, Adam Taub, Tigran Arakelyan, Ariyan Madani, Krishay Patel, Quan Bui, Eric Adler","doi":"10.1007/s10741-026-10648-w","DOIUrl":"10.1007/s10741-026-10648-w","url":null,"abstract":"<p><p>Glycogen storage diseases (GSDs) are a heterogeneous group of rare and often under-recognized causes of inherited cardiomyopathy characterized by pathological glycogen or autophagic vacuole accumulation of debris within various tissues, including the heart. These diseases often present as phenocopies of sarcomeric hypertrophic cardiomyopathy, though they may also manifest with dilated or mixed phenotypes. Key GSDs with cardiomyopathy include Pompe disease (GSD IIa), Danon disease (IIb), Cori/Forbes disease (GSD III), Andersen disease (GSD IV), Tarui disease (GSD VII), phosphorylase kinase deficiency (GSD IX), glycogenin-1 deficiency (GSD XV), and PRKAG2 syndrome, each presenting unique clinical trajectories. Accurate diagnosis requires integration of clinical red flags, multimodality cardiac imaging, and electrocardiography, alongside definitive diagnostic tools like enzyme screening, genetic testing, and endomyocardial biopsy. There is a dearth of evidence regarding specific treatment of each unique GSD cardiomyopathy, but emerging therapeutics across the spectrum of GSDs aim to address this need. This review covers current knowledge on the spectrum of GSD-related cardiomyopathies, discussing pathophysiology, diagnosis, and evolving treatment strategies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13354686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart failure with mildly reduced ejection fraction (HFmrEF): where are we now?","authors":"Muhammad Memon, Yusuf Qadeer, Hafeez Ul Hassan Virk, Affan Rizwan, Paritosh Perry Coomar, Mahboob Alam, Muzamil Khawaja, Mario Rodriguez Rivera, W H Wilson Tang, Chayakrit Krittanawong","doi":"10.1007/s10741-026-10646-y","DOIUrl":"10.1007/s10741-026-10646-y","url":null,"abstract":"<p><p>Heart failure (HF) with mildly reduced ejection fraction (HFmrEF), recently also termed HF with mid-range EF, describes a patient with a left ventricular ejection fraction of 40-49% (5). This classification was initially introduced to bridge the gap between traditional HF with reduced ejection fraction (HFrEF, EF < 40%) and HF with preserved ejection fraction (HFpEF, EF ≥ 50%), as many trial populations and guidelines had previously classified patients by EF (2). HFmrEF patients often display intermediate characteristics: they share etiologies and risk factors with HFrEF (i.e., ischemic heart disease), while their comorbidity profile and overall prognosis more closely resemble HFpEF (1). HFmrEF displays considerable overlap in pathophysiology with HFpEF and HFrEF. Since EF values in this range can fluctuate over time, this introduces even more complexity to its classification. Many individuals with HFmrEF have either improved from a lower EF or deteriorated from a higher EF, and up to one-third will transition to HFrEF or HFpEF during follow-up (58). In terms of outcomes, patients with HFmrEF have mortality and quality-of-life metrics generally between those of HFrEF and HFpEF (often closer to the latter) (9). Importantly, management of HFmrEF is similar to that of HFrEF. Evidence from subgroup analyses and recent trials suggests that standard neurohormonal therapies are beneficial in this EF range. Agents, including β-blockers, renin-angiotensin system inhibitors, angiotensin receptor-neprilysin inhibitors (ARNIs), and mineralocorticoid receptor antagonists (MRAs), all demonstrate reduced hospitalizations and/or mortality in HFmrEF patients, which highlights the similarity in treatment profiles with HFrEF (33). Additional therapies have solidified the treatment approach: sodium-glucose cotransporter 2 inhibitors (SGLT2 inhibitors) significantly lowered HF hospitalization risk in patients with EF > 40% (HFmrEF/HFpEF) (42), and the FINEARTS-HF trial showed finerenone (a non-steroidal MRA) meaningfully improved outcomes in this group (53). As a result, guidelines now give Class I recommendations for SGLT2 inhibitors in HFmrEF, and finerenone is emerging as an important add-on therapy (43). Device therapy (ICD/CRT) remains generally reserved for those who have either had EF ≤ 35% or other indications. This review synthesizes current evidence on HFmrEF, reframing it as a clinical spectrum rather than a distinct phenotype, with emphasis on management implications, biological overlap, and directions for future research.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tachycardia-induced cardiomyopathy: evolution of the concept and contemporary insights.","authors":"Naoki Sato","doi":"10.1007/s10741-026-10650-2","DOIUrl":"10.1007/s10741-026-10650-2","url":null,"abstract":"<p><p>Tachycardia-induced cardiomyopathy (TIC) is a reversible form of myocardial dysfunction caused by sustained or recurrent tachyarrhythmias. Despite increasing recognition, its diagnosis and management remain challenging in clinical practice. This review summarizes the historical evolution, epidemiology, pathophysiology, diagnosis, and management of TIC, and highlights current gaps in knowledge. Experimental and clinical studies have established that not only persistent tachycardia but also high arrhythmic burden and ventricular dyssynchrony contribute to myocardial dysfunction, leading to the broader concept of arrhythmia-induced cardiomyopathy (AiCM). Mechanistically, TIC involves neurohormonal activation, impaired calcium handling, energetic remodeling, oxidative stress, and microvascular dysfunction. Advances in understanding myocardial metabolism and reversibility have provided new insights into disease progression and recovery. However, in humans, the mechanisms underlying TIC/AiCM, as well as responsible for incomplete recovery of cardiac function, have not yet been fully elucidated. TIC is an underrecognized yet potentially reversible cause of heart failure. Early identification and appropriate control of the underlying arrhythmia are essential to improve outcomes. However, the lack of specific diagnostic markers and limited evidence for optimal management strategies remain significant challenges. Further research is needed to refine diagnostic approaches and develop targeted therapies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Left ventricular excessive trabeculation: pathophysiology, diagnostic challenges, and prognostic significance.","authors":"Matteo Beltrami, Viviana Maestrini, Anna Baritussio, Lucrezia Netti, Nicola Colalillo, Sonia Di Franco, Alberto Palazzuoli","doi":"10.1007/s10741-026-10649-9","DOIUrl":"10.1007/s10741-026-10649-9","url":null,"abstract":"<p><p>Excessive trabeculation has been considered the morphological hallmark of left ventricular non-compaction (LVNC), traditionally viewed as a primary cardiomyopathy resulting from an arrest in myocardial compaction during embryonic development. However, more recent evidence suggests that excessive trabeculation of the left ventricle (LVET) may represent a phenotypic trait with heterogeneous etiologies, which can be observed in both physiological and pathological conditions. LVET phenotype may represent the result of a complex interaction between genetic factors, embryonic developmental processes, and acquired hemodynamic adaptations. Additionally, it could represent a secondary morphological remodeling in response to increased preload or afterload Finally, it could be a morphological expression of shared genotype-phenotype continuum encompassing dilated, hypertrophic, and arrhythmogenic cardiomyopathies. Due to its heterogeneity, the clinical significance and the practical management remain unclear, including a significant potential for overdiagnosis, and unnecessary follow-up. The bulk of current evidence suggests that the phenotypic feature of excessive trabeculation has no independent prognostic relevance in otherwise healthy individuals in absence of specific cardiac and extracardiac conditions or symptoms. Moreover, the relationship between excessive LVET and arrhythmic risk remains controversial and appears highly dependent on the underlying cardiomyopathic substrate rather than trabecular morphology per se. However genetic studies have substantially reshaped the conceptual framework of excessive trabeculation; several genes and multiple signaling pathways have been described to clarify the peculiar morpho-tissue organization that characterizes this myocardial phenotype. This review summarizes current evidence on the prevalence, imaging characterization, genetic background, and clinical impact of excessive trabeculation in physiological phenotypes and in cardiomyopathies, and discusses whether this feature represents a remodelling response, or a phenotypic modifier influencing outcomes.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mavacamten in adolescent obstructive hypertrophic cardiomyopathy: SCOUTing a way forward.","authors":"Joshua D Bennetts, Doan T M Ngo, Baljash Cheema, Kaveh Hosseini, Nicolas Verheyen, Viktoria Santner, Daniela Tomasoni, Aaron L Sverdlov","doi":"10.1007/s10741-026-10655-x","DOIUrl":"10.1007/s10741-026-10655-x","url":null,"abstract":"<p><p>Paediatric obstructive hypertrophic cardiomyopathy (oHCM) is a rare inherited cardiac disease that may present from childhood through adolescence and is associated with substantial long-term morbidity and mortality. Its management is based largely on observational studies and clinical experience and currently focusses on symptom improvement through medical therapy and, when indicated, septal reduction therapy to alleviate left ventricular outflow tract (LVOT) obstruction. In adult oHCM, mavacamten has established cardiac myosin inhibition as an effective strategy to reduce LVOT obstruction, but paediatric trial evidence has been lacking. The SCOUT-HCM trial is the first randomised placebo-controlled trial in adolescents to investigate the efficacy and safety of mavacamten for symptomatic oHCM. Among 44 adolescents (mean age 14.7 ± 1.7 years) mavacamten significantly reduced Valsalva-provoked LVOT gradients at 28 weeks, confirming short-term physiological efficacy. Secondary and exploratory findings, including NYHA functional class, cardiac structure and biomarkers, showed a trend to improvement, without a signal of left ventricular systolic dysfunction. The positive results of SCOUT-HCM, align with larger and longer adult oHCM trials and are likely to influence clinical practice, supporting a cautious integration of mavacamten in adolescent oHCM management. Longer follow-up and broader paediatric studies should determine durability of benefit, validated patient-reported outcomes, exercise capacity, arrhythmia burden, long-term safety and the need for septal reduction therapy in paediatric oHCM.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overcoming barriers to early diagnosis and treatment of p.Val142Ile amyloid transthyretin (ATTR) cardiomyopathy.","authors":"Keith C Ferdinand, Senthil Selvaraj, Kevin M Alexander, Saurabh Malhotra","doi":"10.1007/s10741-026-10651-1","DOIUrl":"10.1007/s10741-026-10651-1","url":null,"abstract":"<p><p>The most common hereditary transthyretin (ATTRv) amyloidosis variant in the United States, Val122Ile (p.Val142Ile), is predominantly detected in populations of African ancestry. In this narrative review, we highlight the current challenges and discuss priority focus areas to improve the timely diagnosis and treatment of p.Val142Ile ATTRv amyloidosis across populations. Studies suggest geographic, economic, and socio-economic discordance in timely diagnosis, treatment access, and outcomes in regions with a high proportion of at‑risk individuals. Many ATTR amyloidosis symptoms overlap with other diseases due to their nonspecific and heterogenous nature. Consequently, optimized screening tools for biomarker identification and specialty care services/networks are required to determine at-risk individuals and improve clinical outcomes. However, access to genetic screening can be limited and diagnosis is complicated by variable p.Val142Ile ATTRv amyloidosis penetrance coupled with phenotypic evolution. To enhance existing treatment guidelines, regular monitoring of \"at-risk\" patients, multidisciplinary management, and purposeful clinical trial recruitment of minority populations are recommended.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148368211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond vasodilation: sotatercept and the remodeling hypothesis in hfpef-associated pulmonary hypertension.","authors":"Brett W Sperry, Irene Carlino, Alberto Palazzuoli","doi":"10.1007/s10741-026-10652-0","DOIUrl":"10.1007/s10741-026-10652-0","url":null,"abstract":"<p><p>Pulmonary hypertension complicating heart failure with preserved ejection fraction (HFpEF), particularly the combined post- and pre-capillary form (CpcPH), has lacked any mechanism-specific therapy, as repeated trials of pulmonary vasodilators have failed or caused harm. This mini-review highlights findings from the Phase 2 CADENCE study evaluating sotatercept, an activin signaling inhibitor that targets vascular remodeling rather than vascular tone. Sotatercept met its primary endpoint by reducing pulmonary vascular resistance at 24 weeks and produced concordant improvements in mean pulmonary artery pressure, wedge pressure, 6-minute walk distance, NYHA class, and NT-proBNP, without the compensatory rise in left-sided filling pressure that characterizes vasodilator therapy. Notably, the lower 0.3 mg/kg dose appeared to outperform the 0.7 mg/kg dose across several hemodynamic and functional endpoints while offering a more favorable safety profile. These findings position sotatercept as the first non-vasodilatory, potentially disease-modifying option for advanced HFpEF-associated pulmonary hypertension, and a confirmatory Phase 3 trial is warranted to determine whether this hemodynamic benefit translates into durable clinical outcomes.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the right ventricle: left heart involvement in pulmonary arterial hypertension.","authors":"María José Cabada-García, Jahir Rodríguez-Rivera, Jathniel Panneflek, Salma Andrade-Leal, Ana Lucía Martínez-Rodríguez, Enrique Paredes-Gutiérrez, Humberto De Leon-Gutierrez, Andres Gerardo Peña-Bladé, Raul Monjaras-Alvarado, Jesús Antonio Morón-Mosso, Alejandra Torres, Daniel Aguirre, María José Serrano, Carlos Jerjes Sanchez-Ramirez, Pedro Gutiérrez-Fajardo, Alicia Ramirez-Rivera, Carlos Jerjes-Sanchez","doi":"10.1007/s10741-026-10643-1","DOIUrl":"10.1007/s10741-026-10643-1","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is characterized by progressive remodeling of the pulmonary vasculature, leading to increased pulmonary vascular resistance and chronic right ventricular (RV) pressure overload. As RV dysfunction develops, ventricular interdependence alters the structural and functional relationship between the right and left ventricles. Although normal left-sided filling pressures define PAH, growing evidence indicates that left ventricular (LV) mechanics may be substantially affected. Leftward septal displacement, pericardial constraint, and reduced pulmonary venous return contribute to chronic underfilling of the left atrium and LV, impairing ventricular geometry and contractile dynamics despite preserved intrinsic myocardial function. However, secondary myocardial remodeling in advanced disease remains debated. These alterations may lead to subclinical or overt LV dysfunction and represent an underrecognized component of PAH pathobiology. Imaging markers such as LV global longitudinal strain, LV outflow tract velocity-time integral, and left atrial strain have emerged as potential indicators of left-sided involvement and may provide additional prognostic information. In this narrative review, we summarize current evidence on the pathobiological mechanisms linking RV dysfunction to left-sided cardiac alterations and discuss the role of ventricular interdependence in the coupling of the pulmonary circulation. Understanding this interaction may help redefine PAH as a progressive biventricular syndrome and may improve risk stratification and clinical assessment.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13282292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}