Nature cardiovascular research最新文献

{"title":"Deep learning-enabled assessment of right ventricular size and function is associated with cardiovascular outcomes.","authors":"Mostafa A Al-Alusi, Kavya Kopparapu, Pulkit Singh, Paolo di Achille, Christopher Reeder, Emily S Lau, Tal Shnitzer, Carl T Andrews, Shinwan Kany, Joel T Rämö, Julian S Haimovich, Shaan Khurshid, Michael H Picard, Jennifer E Ho, Puneet Batra, Mahnaz Maddah, Steven A Lubitz, Patrick T Ellinor","doi":"10.1038/s44161-026-00886-4","DOIUrl":"10.1038/s44161-026-00886-4","url":null,"abstract":"<p><p>Right ventricular (RV) size and function inform prognosis in many cardiovascular diseases, but assessment by two-dimensional transthoracic echocardiography is challenging. Here we show that a deep learning model, Dimensional Reconstruction of Imaging Data-Right Ventricle (DROID-RV), can estimate RV end-diastolic diameter and identify RV systolic dysfunction from transthoracic echocardiography videos. We trained DROID-RV in 17,141 ambulatory cardiology patients (51,188 studies and 383,881 video clips) and validated model predictions in 9,112 primary care patients and 831 patients with RV ejection fraction assessed by three-dimensional transthoracic echocardiography. Across multiple test samples, DROID-RV accurately estimates RV end-diastolic diameter and identifies RV dysfunction, although model prediction error increases at extremes of RV size and function. We additionally show that RV size and function predictions are associated with incident mortality, atrial fibrillation and heart failure. Our work demonstrates how deep learning can automate RV assessment and risk stratification at scale using two-dimensional echocardiography.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multiview video-text model detects obstructive coronary stenosis and predicts 1-year cardiovascular events from angiography.","authors":"Sarra Harrabi, Yichen Wu, Omar Majwal, Gabriel Asslo, George Azar, Geoffrey H Tison, Minhaj Ansari, Milos Vukadinovic, David Ouyang, Joshua P Barrios, Jacques Delfrate, Robert Avram","doi":"10.1038/s44161-026-00890-8","DOIUrl":"https://doi.org/10.1038/s44161-026-00890-8","url":null,"abstract":"<p><p>Invasive coronary angiography is the reference standard for diagnosing coronary artery disease, yet assessment is subjective, and existing artificial-intelligence tools typically assess stenosis in individual frames or videos and do not integrate the full multiview angiographic study. Here we show that DeepCORO-CLIP, trained on 203,808 angiographic videos and reports from 28,117 patients, interprets whole multiple-video angiograms at once. It detects obstructive stenoses (≥70%), with an area under the receiver operating characteristic curve (AUROC) of 0.89 internally and externally, and identifies chronic total occlusion (AUROC = 0.90 to 0.95), intra-coronary thrombus and calcification (AUROC = 0.90 to 0.91). It also predicts 1-year cardiovascular events (AUROC = 0.79, 95% CI of 0.74 to 0.84, versus 0.65 for a model derived using clinical variables) and left ventricular ejection fraction (mean absolute error 7.3% versus 8.8% for a previous model), both achieved using coronary angiography alone. In a blinded review of 365 evaluations across 288 angiograms, its reports were clinically usable in 76% of evaluations versus 88% for cardiologists, with comparable false positives (17% versus 14%, P = 0.38); residual missed stenoses reflected an adjustable threshold rather than an absent signal.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human adult and pediatric multimodal transcriptomic atlas of progression from pressure-loaded to failing right ventricle.","authors":"Ivan A Kuznetsov, Kristina Li, Yasmine Guedira, Bridget Simonson, Mark Chaffin, Yonathan T Aberra, Kenneth C Bedi, Trace Thome, Yijun Yang, Kirsten Branch, Wencao Zhao, Wenkai Zhu, Wei Zhou, Farid F Kadyrov, Junedh M Amrute, Ling Lai, Joanna Griffin, Li Li, Jian Li, Shelley D Miyamoto, Patrick Ellinor, Kenneth B Margulies, Kory J Lavine, Zoltan Arany, Jonathan J Edwards","doi":"10.1038/s44161-026-00885-5","DOIUrl":"10.1038/s44161-026-00885-5","url":null,"abstract":"<p><p>Right ventricular failure (RVF) independently predicts mortality in heart failure, yet its pathophysiology is poorly understood. Here we present a multi-modal atlas of human right ventricular pressure loading and failure, including bulk (n = 142), single-nucleus (n = 11) and Xenium spatial (n = 9) transcriptomics in adults, plus pediatric (n = 14) and mouse pulmonary artery banding cohorts. Subclustering resolved 34 cell subtypes across 12 lineages along a two-phase trajectory. Phase 1 (non-failing to pressure-loaded) accounts for most of the transcriptional change detectable by bulk and single-nucleus RNA sequencing and is marked by loss of resident macrophage identity, fibroblast activation, endothelial expansion and erosion of tissue-protective programs. Phase 2 (pressure-loaded to RVF) produces little change in bulk RNA sequencing but is resolved by spatial transcriptomics, engaging multi-lineage fibrotic, endothelial-activation and cardiomyocyte-reactivation programs, with a gain of extracellular matrix (collagen, laminin, thrombospondin) signaling over a stable cell contact adhesion baseline. Mitochondrial respirometry revealed respiratory dysfunction in adult and mouse RVF but not pediatric RVF. Multi-lineage remodeling of the cardiac microenvironment emerges as the central molecular program of RVF, meriting further study as possible disease-modifying targets.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All-fiber wireless auscultation garment for cardiopulmonary diagnostics.","authors":"Qianyi Li, Ziang Li, Xiaoyu Zhang, Hakan Akgun, Swetika Chaturvedi, Hooi Khee Teo, Kamalesh Anbalakan, David Sim, Kenneth Michael Chew Yun Chi, Kee Thai Yeo, Derek John Hausenloy, Tural Khudiyev","doi":"10.1038/s44161-026-00882-8","DOIUrl":"https://doi.org/10.1038/s44161-026-00882-8","url":null,"abstract":"<p><p>Daily apparel could enable continuous, noninvasive monitoring of cardiopulmonary health for the early detection and treatment of cardiopulmonary diseases, the leading causes of death and disability worldwide. Here we develop an all-fiber wireless auscultation system seamlessly integrated into garments. An ~150-μm-diameter fiber contact microphone is sewn, knitted or woven into clothing to capture deep-body acoustic signals while overcoming acoustic impedance mismatch and electromagnetic noise. An ~500-μm knitted fiber computer enables real-time signal processing and Bluetooth transmission to a mobile device. A clinical study in 10 patients with heart failure and 20 neonates demonstrated cardiopulmonary sound capture, including qualitative examples of pathological acoustic features such as cardiac murmurs, S3 gallops and crackles. Comparative validation against a digital stethoscope confirms the garment's ability to suppress environmental noise for high-fidelity cardiopulmonary sound capture. In addition, the fiber integrated within the garment array enables spatial sound mapping of cardiac and pulmonary abnormalities for localized diagnostics.</p>","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Refining stress echocardiography reduces the need for invasive testing in heart failure with preserved ejection fraction","authors":"Andrea Tavosanis","doi":"10.1038/s44161-026-00893-5","DOIUrl":"10.1038/s44161-026-00893-5","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"907-907"},"PeriodicalIF":12.6,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic upregulation of gene expression in inherited cardiomyopathies from current approaches to future directions","authors":"Rosemary B. Kirk,&nbsp;Celine F. Santiago,&nbsp;Hugh Watkins,&nbsp;Christopher N. Toepfer","doi":"10.1038/s44161-026-00884-6","DOIUrl":"10.1038/s44161-026-00884-6","url":null,"abstract":"A substantial proportion of inherited cardiomyopathy cases are driven by mechanisms of haploinsufficiency, where a loss-of-function variant in one allele leads to insufficient protein expression, resulting in loss of normal cardiac function. Current therapies treat symptoms or mitigate risk of complications and do not prevent disease onset or progression. Recently, substantial advances have been made in gene therapies for cardiomyopathies in both preclinical and clinical settings, particularly using viral delivery of whole genes and gene-editing approaches. Alongside these is an emerging area of therapies that aim to upregulate endogenous gene expression. This encompasses a broad array of strategies that may act by removing gene repression or directly enhancing expression, can enhance transcription or translation and may use a variety of modalities such as gene editing or oligonucleotides. Here, we review the mechanisms and current uses of gene upregulation strategies and critically evaluate their advantages and limitations as therapies for inherited cardiomyopathies. Inherited cardiomyopathies caused by haploinsufficiency are promising targets for therapies that restore endogenous gene expression. In this Review, Kirk et al. discuss emerging gene upregulation strategies, evaluate their mechanisms, therapeutic potential and challenges for preventing disease progression.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"941-960"},"PeriodicalIF":12.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A metabolic–epigenetic switch governs multicellular cardiac repair following succinate dehydrogenase inhibition","authors":"Yi Fan,&nbsp;Dakota J. Nuttall,&nbsp;Yi Zhao,&nbsp;Dina Abbasian,&nbsp;Clarissa Shoffler,&nbsp;Christopher Petucci,&nbsp;Wyatt G. Paltzer,&nbsp;Yu-Ling Chang,&nbsp;James Marchant,&nbsp;Diana Presas-Ramos,&nbsp;Kai P. Atlass,&nbsp;Stephen A. Nemr,&nbsp;Jiyoung Bae,&nbsp;Sanjeev S. Ranade,&nbsp;Alexandre R. Colas,&nbsp;Xiao Li,&nbsp;James F. Martin,&nbsp;Ahmed I. Mahmoud","doi":"10.1038/s44161-026-00881-9","DOIUrl":"10.1038/s44161-026-00881-9","url":null,"abstract":"Cardiac regeneration is limited in the adult mammalian heart because of restricted cardiomyocyte proliferation and persistent fibrosis. We previously demonstrated that transient pharmacological inhibition of succinate dehydrogenase (SDH) with malonate promotes regeneration after myocardial infarction. Here, we integrate single-nucleus RNA sequencing and ATAC-seq to reveal multicellular transcriptional and epigenetic reprogramming underlying this response. Cell-specific Sdhb deletion dissected contributions of SDH inhibition; cardiomyocyte-specific Sdhb deletion transiently increased cardiomyocyte proliferation but did not improve post-myocardial infarction function, whereas myofibroblast-specific Sdhb deletion suppressed myofibroblast activation and fibrosis and improved cardiac function. SDH inhibition promoted reductive mitochondrial metabolism and remodeled H3K4me3-marked and H3K27me3-marked chromatin states in cardiomyocytes and fibroblasts. Integration of CUT&amp;RUN, chromatin accessibility and transcriptional profiling identified regulatory targets linking metabolic and epigenetic remodeling to regenerative responses. Together, these findings establish SDH as a multicellular regulator of cardiac regeneration and define distinct cell-specific mechanisms contributing to the regenerative effects of transient pharmacological SDH inhibition. Using integrated multiomics and cell-specific genetic models, Fan et al. reveal how succinate dehydrogenase inhibition promotes multicellular cardiac repair after myocardial infarction through coordinated metabolic and epigenetic reprogramming, while defining distinct contributions of cardiomyocytes and myofibroblasts to this response.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"1034-1054"},"PeriodicalIF":12.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00881-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A failing heart is a failing heart — until proteomics looks beyond etiology","authors":"Alicia Lundby","doi":"10.1038/s44161-026-00875-7","DOIUrl":"10.1038/s44161-026-00875-7","url":null,"abstract":"Proteomic profiling of 149 explanted human hearts shows that, in end-stage heart failure, protein profiles converge across etiologies. Proteome profiles indicate that molecular subtyping, rather than clinical phenotyping, may better capture patient heterogeneity.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"908-910"},"PeriodicalIF":12.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149066559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac proteomic and phosphoproteomic profiling defines clinically relevant molecular subgroups in human heart failure","authors":"Omar Hamed,&nbsp;Cristine J. Reitz,&nbsp;Uros Kuzmanov,&nbsp;Shreya Gramolini,&nbsp;Mostin Hu,&nbsp;Jillian Halpern,&nbsp;Filio Billia,&nbsp;Anthony O. Gramolini","doi":"10.1038/s44161-026-00880-w","DOIUrl":"10.1038/s44161-026-00880-w","url":null,"abstract":"Molecular heterogeneity in heart failure (HF) is increasingly recognized as a major barrier to effective therapy development. Here we performed proteomic profiling of left ventricular tissues from 149 patients with advanced HF spanning nine clinical etiologies. Despite clinical diversity, etiology-stratified analyses revealed convergence toward a shared end-stage proteomic landscape. By contrast, unbiased proteome-based clustering stratified patients into two molecular subgroups characterized by divergent remodeling phenotypes, including differences in fibrosis and immune cell infiltration. Phosphoproteomic profiling was consistent with this stratification, and the analyses further uncovered selective activation of druggable signaling networks in a molecularly defined subgroup of patients. Moreover, our remodeling-associated subgrouping proteins also stratified patients and predicted survival trajectories in an independent plasma-based HF cohort from the UK Biobank, extending our findings to earlier disease stages. Together, our study provides a rich resource for molecular classification of patients with HF, supporting the development of precision-guided therapeutic strategies. Hamed et. al generate a comprehensive analysis of large-scale proteomic and phosphoproteomic profiling to characterize molecular heterogeneity in advanced heart failure, identifying two molecularly distinct patient subgroups associated with divergent remodeling phenotypes, signaling pathways and clinical outcomes.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"1016-1033"},"PeriodicalIF":12.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149066609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiome shifts in chronic systolic heart failure are associated with disease severity and clinical improvement","authors":"Petra Mamic,&nbsp;Handuo Shi,&nbsp;Wenyu Zhou,&nbsp;Nasim Bararpour,&nbsp;Kevin Contrepois,&nbsp;Heyjun Park,&nbsp;Monika Avina,&nbsp;Sophia Miryam Schüssler-Fiorenza Rose,&nbsp;Andrew W. Brooks,&nbsp;Masakazu Kotaka,&nbsp;Paul A. Heidenreich,&nbsp;Kiran Kaur Khush,&nbsp;Michael B. Fowler,&nbsp;W. H. Wilson Tang,&nbsp;Karim Sallam,&nbsp;Justin L. Sonnenburg,&nbsp;Kerwyn Casey Huang,&nbsp;Michael P. Snyder","doi":"10.1038/s44161-026-00854-y","DOIUrl":"10.1038/s44161-026-00854-y","url":null,"abstract":"The contribution of the gut microbiome to chronic heart failure (HF) remains poorly defined. We performed integrated microbiome and host multi-omic profiling of adults with chronic systolic HF due to nonischemic cardiomyopathy (n = 59) and healthy participants (n = 50), including longitudinal sampling in some cases. Here we show that patients with HF have depletion of anti-inflammatory Bifidobacterium and reduced short-chain fatty acid biosynthetic potential, alongside altered microbiome–immune system interactions. Longitudinal analysis revealed that higher Bifidobacterium abundance was associated with clinical improvement. Multi-omic integration prioritized indole-3-propionic acid (IPA), a gut metabolite with cardioprotective properties, as a candidate mechanistic link. We confirmed that Bifidobacterium species can produce IPA in vitro and circulating IPA levels were associated with milder HF severity. Together, these findings define gut microbiome alterations in chronic systolic HF, identify candidate microbiome biomarkers of disease severity and trajectory, and suggest microbiome-derived metabolites as potential therapeutic targets. Through multi-omic cohort profiling with longitudinal follow-up in a subset of cases, Mamic et al. identify gut microbiome signatures in nonischemic cardiomyopathy-related systolic heart failure, which are associated with disease severity and clinical improvement.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"5 10","pages":"1055-1070"},"PeriodicalIF":12.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-026-00854-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}