442. Bradycardia in Athletes: Prevalence, Mechanisms, and Risks.
作者: Paolo D'Ambrosio.;Jarne De Paepe.;Luke W Spencer.;Monique Ohanian.;Kristel Janssens.;Amy M Mitchell.;M Darragh Flannery.;Youri Bekhuis.;Rik Pauwels.;Boris Delpire.;Christophe Dausin.;Stephanie J Rowe.;Tim Van Puyvelde.;Paul E Young.;Magdalena J Soka.;Renee Johnson.;Chenglong Yu.;Gwilym M Morris.;Tomas Robyns.;Paul Lacaze.;Eleni Giannoulatou.;Peter M Kistler.;Jonathan M Kalman.;Hein Heidbuchel.;Rik Willems.;Guido Claessen.;Diane Fatkin.;André La Gerche.; .
来源: Circulation. 2026年153卷9期616-630页
Sinus bradycardia is a well-recognized physiological adaptation in endurance athletes, primarily attributed to sinus node remodeling or increased vagal modulation. Although genetic influences on resting heart rate (HR) have been observed, the genetic contribution to athletic bradycardia has not been elucidated.
443. Macrophage-Specific E3 Ubiquitin Ligase TRIM31 Reduces Atherosclerotic Plaque Formation by Targeting LOX-1.
作者: Jie Zhang.;Liwen Yu.;Wei Yang.;Lei Cao.;Xiaohong Wang.;Chunyu Kao.;Zijing Li.;Ruiqing Ren.;Wenqian Qi.;Lijuan Lyu.;Wenjing Xiong.;Wenhai Sui.;Xiao Wu.;Na Li.;Bingjie Liu.;Shasha Wang.;Peili Bu.;Yun Zhang.;Chengjiang Gao.;Cheng Zhang.;Meng Zhang.
来源: Circulation. 2026年153卷8期576-596页
Atherosclerosis is a chronic inflammatory disease marked by lipid accumulation and immune cell infiltration in arterial walls. Macrophages contribute by internalizing oxidized low-density lipoprotein, forming foam cells, and driving inflammation. The ubiquitin-proteasome system regulates immune and inflammatory responses in atherosclerosis. This study investigated the protective role of TRIM31 (tripartite motif-containing 31), an E3 ubiquitin ligase, in macrophage lipid metabolism and inflammation through selective regulation of LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1).
444. IMPROVE-DiCE, a 2-Part, Open-Label, Phase 2a Trial Evaluating the Safety and Effectiveness of Ninerafaxstat in Patients With Cardiometabolic Syndromes.
作者: Moritz J Hundertmark.;Sarah M Birkhoelzer.;Clara Portwood.;Adrienne G Siu.;Violet Matthews.;Andrew J Lewis.;James Grist.;Ferenc Mózes.;John A Henry.;Jai Patel.;Paul Chamberlin.;Rizwan Sarwar.;Arash Yavari.;Hakim-Moulay Dehbi.;Prashant Rao.;Xu Shi.;Shuning Zheng.;Jeremy M Robbins.;Robert E Gerszten.;Michael P Frenneaux.;Ladislav Valkovič.;Jack J J J Miller.;Stefan Neubauer.;Damian J Tyler.;Oliver J Rider.
来源: Circulation. 2026年153卷8期550-563页
We report IMPROVE-DiCE (Improve Diabetic Cardiac Energetics), a 2-part open-label, phase 2a trial evaluating the safety and effectiveness of ninerafaxstat, a novel therapeutic designed to enhance cardiac energetics. Between May and September 2021, part 1 enrolled patients with type 2 diabetes and obesity without heart failure with preserved ejection fraction (HFpEF). Between January 2023 and June 2024, part 2 enrolled patients with type 2 diabetes, obesity, and HFpEF.
445. Endothelial Transcription Factor EB Protects Against Doxorubicin-Induced Endothelial Toxicity and Cardiac Dysfunction.
作者: Wa Du.;Madison Ringer.;Darshini Desai.;Golam Iftakhar Khandakar.;Luis E Tron Esqueda.;Chenran Wang.;Jun-Lin Guan.;Richard C Becker.;Sakthivel Sadayappan.;Guo-Chang Fan.;Yigang Wang.;Yanbo Fan.
来源: Circulation. 2026年153卷9期653-672页
Doxorubicin (DOX), an effective chemotherapeutic drug for various cancers, has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell (EC) dysfunction is recognized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. TFEB (transcription factor EB), a master regulator of autophagy and lysosome biogenesis, regulates cardiovascular homeostasis. In the present study, we aimed to test whether endothelial TFEB protects against EC damage and alleviates cardiac dysfunction induced by DOX treatment.
447. Higher Life-Course Blood Pressure Associates With Reduced Myocardial Perfusion in Older Age: Insights From MyoFit46.
作者: Constantin-Cristian Topriceanu.;Matthew Webber.;Hunain Shiwani.;Fiona Chan.;Emma Martin.;Debbie Falconer.;Matthew A Stanley.;Jonathan Bennett.;Pablo Gonzalez-Martin.;Haytham Shah.;Swapnanil De.;Andrew Wong.;Iain Pierce.;Rhodri H Davies.;Pier D Lambiase.;Nishi Chaturvedi.;Peter Kellman.;Rebecca Hardy.;James C Moon.;Alun D Hughes.;Gabriella Captur.
来源: Circ Cardiovasc Imaging. 2026年19卷2期e019105页
Elevated blood pressure (BP) is a major contributor to coronary artery disease. We explored the impact of life-course BP on later-life normalized stress myocardial blood flow (sMBFN) and myocardial perfusion reserve by cardiovascular magnetic resonance (CMR).
448. Depression and Anxiety Associate With Adverse Cardiovascular Events via Neural, Autonomic, and Inflammatory Pathways.
作者: Shady Abohashem.;Iqra Qamar.;Simran S Grewal.;Giovanni Civieri.;Sabeeh Islam.;Wesam Aldosoky.;Sandeep Bollepalli.;Rachel P Rosovsky.;Antonia V Seligowski.;Lisa M Shin.;Antonis A Armoundas.;Michael T Osborne.;Ahmed Tawakol.
来源: Circ Cardiovasc Imaging. 2026年19卷1期e017706页
Depression is linked to major adverse cardiac events (MACE), yet the role of stress-related neural activity-previously implicated in stress and anxiety in mediating this association remains unclear. Because anxiety and depression frequently co-occur and share neurobiological pathways, we hypothesized that the relationship between depression, anxiety, and their co-occurrence with MACE is partially mediated by increased stress-related neural activity and related autonomic-immune mechanisms.
451. Periodontal Disease and Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association.
作者: Andrew H Tran.;Abbas H Zaidi.;Ann F Bolger.;Oscar H Del Brutto.;Rashmi Hegde.;Lauren L Patton.;Jamie Rausch.;Justin P Zachariah.; .
来源: Circulation. 2026年153卷6期e73-e88页
Since the publication of the 2012 American Heart Association scientific statement on the association between periodontal disease and atherosclerotic cardiovascular disease, the body of literature on this topic has grown substantially. Atherosclerotic cardiovascular disease is the leading cause of death globally, and understanding contributors and potential targets to decrease this risk is paramount. This updated scientific statement synthesizes new evidence concerning an association between periodontal disease and atherosclerotic cardiovascular disease, including findings from Mendelian randomization studies, interventions targeting periodontal disease, and studies exploring systemic markers, such as inflammatory cytokines and vascular measures. The scientific statement also highlights disparities in the prevalence of periodontal disease, particularly among underresourced populations; explores potential mechanisms linking periodontal disease with cardiovascular outcomes through direct pathways, such as bacteremia, and indirect pathways, such as chronic systemic inflammation; and identifies areas needing further clarification that would benefit from additional research.
459. Diffusion Tensor CMR Assessment of the Microstructural Response to Dobutamine Stress in Health and Comparison With Patients With Recovered Dilated Cardiomyopathy.
作者: Zohya Khalique.;Andrew D Scott.;Pedro F Ferreira.;Maria Molto.;Sonia Nielles-Vallespin.;Dudley J Pennell.
来源: Circ Cardiovasc Imaging. 2026年19卷2期e018226页
Contractile reserve assessment assesses myocardial performance and prognosis. The microstructural mechanisms that facilitate increased cardiac function have not been described, but can be studied using diffusion tensor cardiovascular magnetic resonance. Resting microstructural contractile function is characterized by reorientation of aggregated cardiomyocytes (sheetlets) from wall-parallel in diastole to a more wall-perpendicular configuration in systole, with the diffusion tensor cardiovascular magnetic resonance parameter E2A defining their orientation, and sheetlet mobility defining the angle through which they rotate. We used diffusion tensor cardiovascular magnetic resonance to identify the microstructural response to dobutamine stress in healthy volunteers and then compared with patients with recovered dilated cardiomyopathy (rDCM).
460. Cell-Specific Inducible Human APOL1 Risk Variant Expression in Mice Causes Hypertension and Renal Damage.
作者: Fang Li.;Bibek Poudel.;Magaiver Andrade-Silva.;Junnan Wu.;Archana Raman.;Elisa Cruz-Morales.;Joseph Wahba.;Allison Vassalotti.;Chenyu Li.;Amin Abedini.;Konstantin A Klötzer.;Xiaoqiang Ding.;Christopher A Hunter.;Jonathan J Miner.;Katalin Susztak.
来源: Circulation. 2026年153卷6期396-414页
Black people bear a disproportionate burden of hypertension and hypertension-attributed chronic kidney disease. A role of apolipoprotein L1 (APOL1) risk variants (RVs; G1 and G2) in these conditions has been proposed, but genetic and observational studies have shown inconsistent results.
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