Heart最新文献

{"title":"When absence of evidence equates to evidence of absence: the case of routine use of cerebral embolic protection devices in transcatheter aortic valve implantation.","authors":"Samuel Heuts, Michal J Kawczynski, Bart Maesen, Pieter A Vriesendorp","doi":"10.1136/heartjnl-2025-326208","DOIUrl":"https://doi.org/10.1136/heartjnl-2025-326208","url":null,"abstract":"<p><strong>Objectives: </strong>This updated hierarchical Bayesian meta-analysis aims to integrate the latest randomised controlled trials (RCTs) on the use of cerebral embolic protection (CEP) in transcatheter aortic valve implantation (TAVI) into previously available data, providing a definite answer to the clinical effectiveness of CEP in TAVI patients.</p><p><strong>Methods: </strong>A systematic search was updated on 31 March 2025. RCTs were included when comparing transfemoral TAVI with use of CEP versus transfemoral TAVI without CEP. The primary outcome was all stroke, while the secondary outcome was disabling stroke. A hierarchical Bayesian meta-analysis was performed on the (log) relative risk (RR) scale and transformed to absolute risk differences (ARDs) and numbers needed to treat (NNTs). The threshold for clinical relevance was based on published expert consensus and established on 1.1% ARD (NNT 91).</p><p><strong>Results: </strong>The study was updated with one new RCT, totalling a number of eight RCTs (n=11 590, CEP n=5921 patients, control n=5669 patients). The prevalence of all stroke and disabling stroke was 2.9% and 1.4% in the control group. The median RR for all stroke was 0.94 (95% credible interval (CrI) 0.72-1.25), translating to a mean of -0.17% ARD (NNT 588), and a posterior probability of a clinically relevant CEP effect of <1%. The median RR for disabling stroke was 0.76 (95% CrI 0.44-1.23), translating to a mean of -0.36% ARD (NNT 278), and a posterior probability of a clinically relevant CEP effect of <1%.</p><p><strong>Conclusion: </strong>Current-generation CEP devices are ineffective in reducing periprocedural TAVI-stroke risk to a clinically relevant degree, rendering future trials with these devices futile.</p><p><strong>Prospero registration number: </strong>CRD42023407006.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274651","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":"Can PCI match CABG for multivessel disease? Here is how.","authors":"Alexander Levy, Gregg W Stone","doi":"10.1136/heartjnl-2025-326361","DOIUrl":"https://doi.org/10.1136/heartjnl-2025-326361","url":null,"abstract":"","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215680","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":"Monitoring patients with transthyretin amyloid cardiomyopathy.","authors":"Wouter E Kok","doi":"10.1136/heartjnl-2025-325736","DOIUrl":"https://doi.org/10.1136/heartjnl-2025-325736","url":null,"abstract":"","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215681","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":"Identifying clinical phenotype clusters in patients with coronary artery disease.","authors":"Joris Holtrop, Carl-Emil Lim, Alicia Uijl, Peter Ueda, Tomas Jernberg, Manon G van der Meer, Pim van der Harst, Adriaan O Kraaijeveld, Jan-Willem Balder, Steven H J Hageman, Frank L J Visseren, Jannick A N Dorresteijn","doi":"10.1136/heartjnl-2025-325740","DOIUrl":"10.1136/heartjnl-2025-325740","url":null,"abstract":"<p><strong>Background: </strong>Guideline recommendations for the prevention of cardiovascular (CV) events in patients with coronary artery disease (CAD) are predominantly one-size-fits-all. Clinically identifiable phenotypes needing specific considerations might exist. The purpose of this study is to identify such clinical phenotypic clusters in patients with CAD and assess their relationship with the risk of recurrent CV events.</p><p><strong>Methods: </strong>Unsupervised machine learning through latent class analysis was performed in patients with CAD from the Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART) registry (n=88 894) and Utrecht Cardiovascular Cohort-Second Manifestations of Arterial Disease (UCC-SMART) cohort (n=5506). Characteristics for clustering were based on availability, missingness and clinical relevance. Clustering was performed in SWEDEHEART and validated in UCC-SMART. Association between clusters and the composite of myocardial infarction, stroke or CV death was assessed using Cox proportional hazard models.</p><p><strong>Results: </strong>Four phenotypes could be distinguished: cluster 1 (38%, n=33 777) of predominantly younger males with increased body mass index, blood pressure and C-reactive protein, cluster 2 (21%, n=18 775) of smokers with few traditional risk factors, cluster 3 (30%, n=26 501) of older patients with few comorbidities and cluster 4 (11%, n=9841) of patients with multimorbidity. Compared with cluster 1, cluster 4 was at the highest risk (HR 4.38 95% CI (4.01 to 4.78)), followed by cluster 3 (HR 1.78 (1.70 to 1.85)), and cluster 2 (HR 0.97 (0.88 to 1.07)). Validation in UCC-SMART yielded similar results.</p><p><strong>Conclusion: </strong>Four distinct and reproducible phenotypes, with differences in the risk of recurrent CV events, were identified among patients with CAD. These may be relevant in practice and warrant research into specific pathophysiology and differences in treatment effects.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198947","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":"Where are the women? Fixing the broken pipeline in cardiovascular research.","authors":"Gurleen Kaur, Martha Gulati","doi":"10.1136/heartjnl-2025-325979","DOIUrl":"https://doi.org/10.1136/heartjnl-2025-325979","url":null,"abstract":"","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198949","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":"Contemporary diagnosis and management of spontaneous coronary artery dissection.","authors":"Cathevine Yang, Jocelyn Chai, Jacqueline Saw","doi":"10.1136/heartjnl-2024-324732","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-324732","url":null,"abstract":"<p><p>Spontaneous coronary artery dissection (SCAD) has emerged over the last decade as an increasingly recognised cause of myocardial infarction, especially among younger women. The advances in our understanding of SCAD and the evolution of coronary angiography and intracoronary imaging have led to improved diagnoses and outcomes; however, there are still knowledge gaps and challenges in the management of this condition. In this review, we summarise the pathogenesis, genetics, diagnosis and acute and chronic management of patients with SCAD. We also provide focused updates on the following: genetics of SCAD, the role of cardiac CT angiography and cardiac MRI, the use of intracoronary imaging, revascularisation techniques and the overlap between SCAD and Takotsubo syndrome.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198946","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":"Strategies to enhance recruitment of female participants to cardiovascular research: a joint British Cardiovascular Societies' consensus document in collaboration with the British Heart Foundation Clinical Research Collaborative.","authors":"Vijay Kunadian, Graziella Pompei, Indranil Dasgupta, Pauline Swift, Dawn Adamson, Anita Banerjee, Tomasz J Guzik, David Hildick-Smith, Madalina Garbi, Nabila Laskar, Lisa Anderson, Rosita Zakeri, Fozia Ahmed, Stuart D Rosen, Clare Bannister, Eleri Roberts, Michael A Quail, Louise Coats, Stephen P Page, Eleanor Wicks, Narain Moorjani, Mahmoud Loubani, Heather Probert, Aynsley Cowie, Raj Thakkar, Jim Moore, Aparna Deshpande, Daniel X Augustine, Maria F Paton, Gaby Captur, Anvesha Singh, Holly Morgan, Oliver Brown, Fang Feng Ting, Sharlene Hogan, Katie Sanders, Joanne Rachel Ashton, Roland Malkin, Sarah Brown, Allyson Arnold, Mariana Rodas, Vasilena Zhecheva, G Andre Ng","doi":"10.1136/heartjnl-2024-325545","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325545","url":null,"abstract":"<p><p>Despite significant progress in cardiovascular pharmacotherapy and interventional strategies, cardiovascular disease (CVD) remains the leading cause of morbidity and mortality among females in the UK and worldwide. This might be due to lack of robust evidence in the best care of females with CVD related to under-representation of females in clinical trials (females accounting for <30% of trial participants). Recently, the British Cardiovascular Society (BCS), together with the affiliated societies, put together a consensus document specifically describing the current status on the sex differences in each of the major disease areas and proposed strategies/actionable points to overcome the barriers in access to diagnosis and treatment of CVD among females.In order to address the disparities, several research organisations, including the UK National Institute for Health and Care Research (NIHR), have produced guidance to diversify research participation and representation. The UK government has developed a Women's Health Strategy for England. In the present consensus, we evaluate the barriers to research participation of female participants across the CVD spectrum and describe specific strategies/actionable points to enhance female involvement in clinical cardiovascular research. It is hoped that this document will stimulate a multifaceted approach to address disparities, including raising awareness and undertaking sex/gender-based research. We aim to improve the current status of management in various disease areas among females by collaboration across different affiliations within the BCS, the British Heart Foundation Clinical Research Collaborative and the NIHR to collectively work towards improving the health and well-being of females with CVD.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198948","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":"Effect of low-dose colchicine on pericoronary inflammation and coronary plaque composition in chronic coronary disease: a subanalysis of the LoDoCo2 trial.","authors":"Aernoud T L Fiolet, Andrew Lin, Jacek Kwiecinski, Julie Tutein Nolthenius, Priscilla McElhinney, Kajetan Grodecki, Bas Kietselaer, Tjerk S Opstal, Jan Hein Cornel, Remco Jj Knol, Jeroen Schaap, Ruud A H M Aarts, Annemieke M F A Tutein Nolthenius, Stefan M Nidorf, Birgitta K Velthuis, Damini Dey, Arend Mosterd","doi":"10.1136/heartjnl-2024-325527","DOIUrl":"10.1136/heartjnl-2024-325527","url":null,"abstract":"<p><strong>Background: </strong>Low-dose colchicine (0.5 mg once daily) reduces the risk of major cardiovascular events in coronary disease, but its mechanism of action is not yet fully understood. We investigated whether low-dose colchicine is associated with changes in pericoronary inflammation and plaque composition in patients with chronic coronary disease.</p><p><strong>Methods: </strong>We performed a cross-sectional, nationwide, subanalysis of the Low-Dose Colchicine 2 Trial (LoDoCo2, n=5522). CT angiography studies were performed in 151 participants randomised to colchicine or placebo after a median treatment duration of 28.2 months. Pericoronary adipose tissue (PCAT) attenuation measurements around proximal coronary artery segments and quantitative plaque analysis for the entire coronary tree were performed using artificial intelligence-enabled plaque analysis software.</p><p><strong>Results: </strong>Median PCAT attenuation was not significantly different between the two groups (-79.5 Hounsfield units (HU) for colchicine versus -78.7 HU for placebo, p=0.236). Participants assigned to colchicine had a higher volume (169.6 mm³ vs 113.1 mm³, p=0.041) and burden (9.6% vs 7.0%, p=0.035) of calcified plaque, and higher volume of dense calcified plaque (192.8 mm³ vs 144.3 mm³, p=0.048) compared with placebo, independent of statin therapy. Colchicine treatment was associated with a lower burden of low-attenuation plaque in participants on a low-intensity statin, but not in those on a high-intensity statin (p_interaction=0.037).</p><p><strong>Conclusions: </strong>Pericoronary inflammation did not differ among participants who received low-dose colchicine compared with placebo. Low-dose colchicine was associated with a higher volume of calcified plaque, particularly dense calcified plaque, which is considered a feature of plaque stability.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110530","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":"Insomnia symptom trajectories and incident cardiovascular disease in older adults: a longitudinal cohort study.","authors":"Qing-Mei Huang, Hao-Yu Yan, Huan Chen, Jia-Hao Xie, Jian Gao, Zhi-Hao Li, Chen Mao","doi":"10.1136/heartjnl-2024-325362","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325362","url":null,"abstract":"<p><strong>Background: </strong>Insomnia symptoms are prevalent in older adults and linked to cardiovascular disease (CVD), but the role of long-term symptom trajectories remains unclear. We investigated associations between insomnia symptoms, their trajectories over time and incident CVD in a population-based cohort.</p><p><strong>Methods: </strong>This longitudinal study included 12 102 participants aged ≥50 years without baseline CVD from the US Health and Retirement Study (2002-2018). Insomnia symptoms (non-restorative sleep, difficulty initiating/maintaining sleep, early awakening) were assessed at baseline; trajectories were modelled over 4 years (2002-2006) using latent class analysis. Cox models estimated HRs for incident CVD (heart disease or stroke), adjusted for sociodemographics, lifestyle and comorbidities.</p><p><strong>Results: </strong>During a median of 10.2-year follow-up, 3962 incident CVD events occurred. Compared with no symptoms, participants with one, two, or three to four symptoms had higher CVD risk (HR 1.16, 95% CI 1.05 to 1.27; HR 1.16, 95% CI 1.05 to 1.28; HR 1.26, 95% CI 1.15 to 1.38, respectively). Four trajectories were identified: persistent low (56.3%), decreasing (27.1%), increasing (7.2%) and persistent high (9.5%). Compared with persistent low, increasing (HR 1.28, 95% CI 1.10 to 1.50) and persistent high (HR 1.32, 95% CI 1.15 to 1.50) trajectories were associated with elevated CVD risk.</p><p><strong>Conclusions: </strong>Greater burden of insomnia symptoms at baseline and trajectories over time were associated with higher CVD incidence in older adults.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158156","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":"Current and emerging treatment options for transthyretin amyloid cardiomyopathy.","authors":"Giuseppe Vergaro, Yu Fu Ferrari Chen, Adam Ioannou, Giorgia Panichella, Vincenzo Castiglione, Alberto Aimo, Michele Emdin, Marianna Fontana","doi":"10.1136/heartjnl-2024-325184","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325184","url":null,"abstract":"<p><p>Transthyretin amyloidosis (ATTR) is a condition caused by TTR protein misfolding and amyloid deposition, particularly in the heart and nervous system, leading to organ dysfunction. Advances in therapeutic strategies have revolutionised the management of ATTR amyloidosis. Treatments available in clinical practice include TTR stabilisers (tafamidis and acoramidis), which prevent the dissociation of TTR tetramer into monomers and oligomers that subsequently form amyloid fibrils, and gene-silencing therapies (patisiran, inotersen and vutrisiran), which suppress the hepatic synthesis of TTR, which is the amyloid precursor protein. Novel treatment strategies that are at various stages of development include Clustered Regularly Interspaced Short Palindromic Repeats-Cas9 gene-editing technology (nexiguran ziclumeran), which, if successful, offers the prospect of a single-dose treatment, and monoclonal (cormitug and ALXN220) and pan-amyloid antibodies (AT-02) that seek to target and remove amyloid fibrils that have deposited in the myocardium. Amyloid removal remains a significant unmet clinical need, and hence, the ability to promote amyloid degradation and clearance through the use of antiamyloid therapies would represent a groundbreaking advancement in the treatment of ATTR amyloidosis. The success of ATTR-specific disease-modifying therapies has already altered the treatment landscape and changed the perception of ATTR amyloidosis from a progressive and fatal disease to one that is treatable through the availability of highly effective disease-modifying therapies. However, important questions remain, including the long-term safety of these drugs, whether combining therapies with different mechanisms of action has an additive prognostic benefit and how best to monitor the treatment response.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158067","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}