首页 > 最新文献

JACC: Basic to Translational Science最新文献

英文 中文
Pulsatile Ventricular Assist Platform 搏动性心室辅助平台
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.02.009
Marcelo B. Bastos MD, MHSc , Oren Malchin MBA , Sara Knigge PhD , Günes Dogan MD , Ezin Deniz MD , Jan D. Schmitto MD, PhD
{"title":"Pulsatile Ventricular Assist Platform","authors":"Marcelo B. Bastos MD, MHSc , Oren Malchin MBA , Sara Knigge PhD , Günes Dogan MD , Ezin Deniz MD , Jan D. Schmitto MD, PhD","doi":"10.1016/j.jacbts.2024.02.009","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.02.009","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000871/pdfft?md5=f0ccd68a0e32c7dd1e0138a39c575aef&pid=1-s2.0-S2452302X24000871-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Transcatheter Pulmonary Artery Banding for HFrEF 经导管肺动脉束带治疗高频低氧血症
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.02.008
Elchanan Bruckheimer MBBS , Gediminas Rackauskas MD , Stefan Verheye MD , Edgard Prihadi MD , Nir Flint MD , Petr Neužil MD, PhD , Offer Amir MD , Horst Sievert MD , Sean Pinney MD , Vivek Y. Reddy MD
{"title":"Transcatheter Pulmonary Artery Banding for HFrEF","authors":"Elchanan Bruckheimer MBBS , Gediminas Rackauskas MD , Stefan Verheye MD , Edgard Prihadi MD , Nir Flint MD , Petr Neužil MD, PhD , Offer Amir MD , Horst Sievert MD , Sean Pinney MD , Vivek Y. Reddy MD","doi":"10.1016/j.jacbts.2024.02.008","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.02.008","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X2400055X/pdfft?md5=ddb13a1772bceb1116f7be05b607ce5f&pid=1-s2.0-S2452302X2400055X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Full Issue PDF 全期 PDF
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/S2452-302X(24)00124-4
{"title":"Full Issue PDF","authors":"","doi":"10.1016/S2452-302X(24)00124-4","DOIUrl":"https://doi.org/10.1016/S2452-302X(24)00124-4","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24001244/pdfft?md5=591efb5a5849a27a2ea89be949b092c5&pid=1-s2.0-S2452302X24001244-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Atrial Metabolic Stress 心房代谢压力
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.01.002
Thomas H. Schindler MD, PhD
{"title":"Atrial Metabolic Stress","authors":"Thomas H. Schindler MD, PhD","doi":"10.1016/j.jacbts.2024.01.002","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.01.002","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000068/pdfft?md5=ff61757ddadcd257bb586d67591ebdc4&pid=1-s2.0-S2452302X24000068-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise 运动对心脏有益的内在和外在因素
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2023.07.011
Margaret H. Hastings PhD , Claire Castro PhD , Rebecca Freeman BA , Azrul Abdul Kadir PhD , Carolin Lerchenmüller MD , Haobo Li PhD , James Rhee MD, PhD , Jason D. Roh MD, MHS , Kangsan Roh PhD , Anand P. Singh PhD , Chao Wu MD, PhD , Peng Xia PhD , Qiulian Zhou PhD , Junjie Xiao MD, PhD , Anthony Rosenzweig MD

Among its many cardiovascular benefits, exercise training improves heart function and protects the heart against age-related decline, pathological stress, and injury. Here, we focus on cardiac benefits with an emphasis on more recent updates to our understanding. While the cardiomyocyte continues to play a central role as both a target and effector of exercise’s benefits, there is a growing recognition of the important roles of other, noncardiomyocyte lineages and pathways, including some that lie outside the heart itself. We review what is known about mediators of exercise’s benefits—both those intrinsic to the heart (at the level of cardiomyocytes, fibroblasts, or vascular cells) and those that are systemic (including metabolism, inflammation, the microbiome, and aging)—highlighting what is known about the molecular mechanisms responsible.

运动训练对心血管有诸多益处,其中包括改善心脏功能,保护心脏免受衰老、病理压力和损伤的影响。在此,我们将重点讨论对心脏的益处,并着重介绍我们最近的最新认识。虽然心肌细胞作为运动益处的目标和效应器继续发挥着核心作用,但人们越来越认识到其他非心肌细胞系和通路的重要作用,包括一些位于心脏本身之外的细胞系和通路。我们回顾了目前已知的运动益处介导因素--包括心脏固有介导因素(心肌细胞、成纤维细胞或血管细胞水平)和系统介导因素(包括新陈代谢、炎症、微生物组和衰老)--重点介绍了目前已知的分子机制。
{"title":"Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise","authors":"Margaret H. Hastings PhD ,&nbsp;Claire Castro PhD ,&nbsp;Rebecca Freeman BA ,&nbsp;Azrul Abdul Kadir PhD ,&nbsp;Carolin Lerchenmüller MD ,&nbsp;Haobo Li PhD ,&nbsp;James Rhee MD, PhD ,&nbsp;Jason D. Roh MD, MHS ,&nbsp;Kangsan Roh PhD ,&nbsp;Anand P. Singh PhD ,&nbsp;Chao Wu MD, PhD ,&nbsp;Peng Xia PhD ,&nbsp;Qiulian Zhou PhD ,&nbsp;Junjie Xiao MD, PhD ,&nbsp;Anthony Rosenzweig MD","doi":"10.1016/j.jacbts.2023.07.011","DOIUrl":"10.1016/j.jacbts.2023.07.011","url":null,"abstract":"<div><p>Among its many cardiovascular benefits, exercise training improves heart function and protects the heart against age-related decline, pathological stress, and injury. Here, we focus on cardiac benefits with an emphasis on more recent updates to our understanding. While the cardiomyocyte continues to play a central role as both a target and effector of exercise’s benefits, there is a growing recognition of the important roles of other, noncardiomyocyte lineages and pathways, including some that lie outside the heart itself. We review what is known about mediators of exercise’s benefits—both those intrinsic to the heart (at the level of cardiomyocytes, fibroblasts, or vascular cells) and those that are systemic (including metabolism, inflammation, the microbiome, and aging)—highlighting what is known about the molecular mechanisms responsible.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X23002942/pdfft?md5=48d166bf1f1061b3bc98170a1187c0e0&pid=1-s2.0-S2452302X23002942-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135848999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Carotid Baroreceptor Stimulation Improves Pulmonary Arterial Remodeling and Right Ventricular Dysfunction in Pulmonary Arterial Hypertension 刺激颈动脉感受器可改善肺动脉高压的肺动脉重塑和右心室功能障碍
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.01.012
Jing Wang MM , Jie Chen MM , Ling Shu MM , Ruoliu Zhang MB , Mingyan Dai MD , Xuesheng Fang MB , Zhiling Hu MB , Lingling Xiao MB , Zhaoqing Xi MB , Junxia Zhang MD , Mingwei Bao MD

Autonomic nervous system imbalance is intricately associated with the severity and prognosis of pulmonary arterial hypertension (PAH). Carotid baroreceptor stimulation (CBS) is a nonpharmaceutical intervention for autonomic neuromodulation. The effects of CBS on monocrotaline-induced PAH were investigated in this study, and its underlying mechanisms were elucidated. The results indicated that CBS improved pulmonary hemodynamic status and alleviated right ventricular dysfunction, improving pulmonary arterial remodeling and right ventricular remodeling, thus enhancing the survival rate of monocrotaline-induced PAH rats. The beneficial effects of CBS treatment on PAH might be mediated through the inhibition of sympathetic overactivation and inflammatory immune signaling pathways.

自主神经系统失衡与肺动脉高压(PAH)的严重程度和预后密切相关。颈动脉气压感受器刺激(CBS)是一种非药物的自律神经调节干预方法。本研究探讨了 CBS 对单克罗林诱导的 PAH 的影响,并阐明了其潜在机制。结果表明,CBS能改善肺血流动力学状态,缓解右心室功能障碍,改善肺动脉重塑和右心室重塑,从而提高单克隆肾上腺素诱导的PAH大鼠的存活率。CBS治疗对PAH的有益作用可能是通过抑制交感神经过度激活和炎症免疫信号通路介导的。
{"title":"Carotid Baroreceptor Stimulation Improves Pulmonary Arterial Remodeling and Right Ventricular Dysfunction in Pulmonary Arterial Hypertension","authors":"Jing Wang MM ,&nbsp;Jie Chen MM ,&nbsp;Ling Shu MM ,&nbsp;Ruoliu Zhang MB ,&nbsp;Mingyan Dai MD ,&nbsp;Xuesheng Fang MB ,&nbsp;Zhiling Hu MB ,&nbsp;Lingling Xiao MB ,&nbsp;Zhaoqing Xi MB ,&nbsp;Junxia Zhang MD ,&nbsp;Mingwei Bao MD","doi":"10.1016/j.jacbts.2024.01.012","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.01.012","url":null,"abstract":"<div><p>Autonomic nervous system imbalance is intricately associated with the severity and prognosis of pulmonary arterial hypertension (PAH). Carotid baroreceptor stimulation (CBS) is a nonpharmaceutical intervention for autonomic neuromodulation. The effects of CBS on monocrotaline-induced PAH were investigated in this study, and its underlying mechanisms were elucidated. The results indicated that CBS improved pulmonary hemodynamic status and alleviated right ventricular dysfunction, improving pulmonary arterial remodeling and right ventricular remodeling, thus enhancing the survival rate of monocrotaline-induced PAH rats. The beneficial effects of CBS treatment on PAH might be mediated through the inhibition of sympathetic overactivation and inflammatory immune signaling pathways.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X2400041X/pdfft?md5=998f48ef8365f3b6ee9c3a2cdfdc1acb&pid=1-s2.0-S2452302X2400041X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial Ca2+ Uniporter–Dependent Energetic Dysfunction Drives Hypertrophy in Heart Failure 线粒体 Ca2+ 单通道依赖性能量功能障碍导致心力衰竭患者肥大
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.01.007
Hugo Alves-Figueiredo PhD , Christian Silva-Platas PhD , Manuel Estrada PhD , Yuriana Oropeza-Almazán PhD , Martin Ramos-González MD, PhD , Judith Bernal-Ramírez PhD , Eduardo Vázquez-Garza MD, PhD , Armando Tellez PhD , Felipe Salazar-Ramírez MD, MSc , Abraham Méndez-Fernández MSc , José Luis Galaz MD , Pedro Lobos PhD , Keith Youker PhD , Omar Lozano PhD , Guillermo Torre-Amione MD, PhD , Gerardo García-Rivas PhD

The role of the mitochondrial calcium uniporter (MCU) in energy dysfunction and hypertrophy in heart failure (HF) remains unknown. In angiotensin II (ANGII)–induced hypertrophic cardiac cells we have shown that hypertrophic cells overexpress MCU and present bioenergetic dysfunction. However, by silencing MCU, cell hypertrophy and mitochondrial dysfunction are prevented by blocking mitochondrial calcium overload, increase mitochondrial reactive oxygen species, and activation of nuclear factor kappa B–dependent hypertrophic and proinflammatory signaling. Moreover, we identified a calcium/calmodulin–independent protein kinase II/cyclic adenosine monophosphate response element–binding protein signaling modulating MCU upregulation by ANGII. Additionally, we found upregulation of MCU in ANGII-induced left ventricular HF in mice, and in the LV of HF patients, which was correlated with pathological remodeling. Following left ventricular assist device implantation, MCU expression decreased, suggesting tissue plasticity to modulate MCU expression.

线粒体钙离子通道(MCU)在心力衰竭(HF)的能量功能障碍和肥大中的作用仍不清楚。在血管紧张素 II(ANGII)诱导的肥大心脏细胞中,我们发现肥大细胞过度表达 MCU 并出现生物能量功能障碍。然而,通过沉默 MCU,细胞肥大和线粒体功能障碍可通过阻断线粒体钙超载、线粒体活性氧增加以及核因子卡巴 B 依赖性肥大和促炎信号的激活而得到预防。此外,我们还发现钙/钙调蛋白依赖性蛋白激酶 II/环磷酸腺苷反应元件结合蛋白信号调节 ANGII 对 MCU 的上调。此外,我们还发现在 ANGII 诱导的左心室高频小鼠和高频患者的左心室中,MCU 的上调与病理重塑相关。植入左心室辅助装置后,MCU的表达量减少,这表明组织具有调节MCU表达的可塑性。
{"title":"Mitochondrial Ca2+ Uniporter–Dependent Energetic Dysfunction Drives Hypertrophy in Heart Failure","authors":"Hugo Alves-Figueiredo PhD ,&nbsp;Christian Silva-Platas PhD ,&nbsp;Manuel Estrada PhD ,&nbsp;Yuriana Oropeza-Almazán PhD ,&nbsp;Martin Ramos-González MD, PhD ,&nbsp;Judith Bernal-Ramírez PhD ,&nbsp;Eduardo Vázquez-Garza MD, PhD ,&nbsp;Armando Tellez PhD ,&nbsp;Felipe Salazar-Ramírez MD, MSc ,&nbsp;Abraham Méndez-Fernández MSc ,&nbsp;José Luis Galaz MD ,&nbsp;Pedro Lobos PhD ,&nbsp;Keith Youker PhD ,&nbsp;Omar Lozano PhD ,&nbsp;Guillermo Torre-Amione MD, PhD ,&nbsp;Gerardo García-Rivas PhD","doi":"10.1016/j.jacbts.2024.01.007","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.01.007","url":null,"abstract":"<div><p>The role of the mitochondrial calcium uniporter (MCU) in energy dysfunction and hypertrophy in heart failure (HF) remains unknown. In angiotensin II (ANGII)–induced hypertrophic cardiac cells we have shown that hypertrophic cells overexpress MCU and present bioenergetic dysfunction. However, by silencing MCU, cell hypertrophy and mitochondrial dysfunction are prevented by blocking mitochondrial calcium overload, increase mitochondrial reactive oxygen species, and activation of nuclear factor kappa B–dependent hypertrophic and proinflammatory signaling. Moreover, we identified a calcium/calmodulin–independent protein kinase II/cyclic adenosine monophosphate response element–binding protein signaling modulating MCU upregulation by ANGII. Additionally, we found upregulation of MCU in ANGII-induced left ventricular HF in mice, and in the LV of HF patients, which was correlated with pathological remodeling. Following left ventricular assist device implantation, MCU expression decreased, suggesting tissue plasticity to modulate MCU expression.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000111/pdfft?md5=33f5014a0200ad9d38463fc1925dcf56&pid=1-s2.0-S2452302X24000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Left Atrial Glucose Metabolism Evaluation by 18F-FDG-PET in Persistent Atrial Fibrillation and in Sinus Rhythm 通过 18F-FDG-PET 评估持续性心房颤动和窦性心律的左心房葡萄糖代谢情况
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2023.11.001
Sébastien Marchandise MD , Véronique Roelants MD, PhD , Tristan Raoult MD , Quentin Garnir MD , Christophe Scavée MD , Varnavas Varnavas MD PhD , Aurélien Wauters MD, PhD , Damien Gruson MD, PhD , Eric Nellessen MD , Michel Hesse PhD , Christophe Beauloye MD, PhD , Bernhard L. Gerber MD, PhD

The role of atrial metabolism alterations for initiation and atrial fibrillation (AF) persistence remains poorly understood. Therefore, we evaluated left atrial glucose metabolism by nicotinic acid derivative stimulated 18-fluorodeoxyglucose positron emission tomography in 36 patients with persistent AF undergoing catheter ablation before and 3 months after return to sinus rhythm and compared values against healthy controls. Under identical hemodynamics and metabolic conditions, and although left ventricular FDG uptake remained unchanged, patients in persistent AF presented significantly higher total left atrial and left atrial appendage uptake, which decreased significantly after return to sinus rhythm, despite improvement of passive and active atrial contractile function. These findings support a role of altered glucose metabolism and metabolic wasting underlying the pathophysiology of persistent AF.

人们对心房代谢改变在心房颤动(房颤)起始和持续中的作用仍知之甚少。因此,我们通过烟酸衍生物刺激 18 氟脱氧葡萄糖正电子发射断层扫描评估了 36 名接受导管消融术的持续性房颤患者在恢复窦性心律前和恢复窦性心律后 3 个月的左心房葡萄糖代谢情况,并将其值与健康对照组进行了比较。在相同的血液动力学和新陈代谢条件下,虽然左心室 FDG 摄取量保持不变,但持续性房颤患者的左心房和左心房附壁总摄取量明显较高,尽管被动和主动心房收缩功能有所改善,但恢复窦性心律后摄取量明显下降。这些研究结果支持葡萄糖代谢改变和代谢消耗在持续性房颤病理生理学中的作用。
{"title":"Left Atrial Glucose Metabolism Evaluation by 18F-FDG-PET in Persistent Atrial Fibrillation and in Sinus Rhythm","authors":"Sébastien Marchandise MD ,&nbsp;Véronique Roelants MD, PhD ,&nbsp;Tristan Raoult MD ,&nbsp;Quentin Garnir MD ,&nbsp;Christophe Scavée MD ,&nbsp;Varnavas Varnavas MD PhD ,&nbsp;Aurélien Wauters MD, PhD ,&nbsp;Damien Gruson MD, PhD ,&nbsp;Eric Nellessen MD ,&nbsp;Michel Hesse PhD ,&nbsp;Christophe Beauloye MD, PhD ,&nbsp;Bernhard L. Gerber MD, PhD","doi":"10.1016/j.jacbts.2023.11.001","DOIUrl":"10.1016/j.jacbts.2023.11.001","url":null,"abstract":"<div><p>The role of atrial metabolism alterations for initiation and atrial fibrillation (AF) persistence remains poorly understood. Therefore, we evaluated left atrial glucose metabolism by nicotinic acid derivative stimulated 18-fluorodeoxyglucose positron emission tomography in 36 patients with persistent AF undergoing catheter ablation before and 3 months after return to sinus rhythm and compared values against healthy controls. Under identical hemodynamics and metabolic conditions, and although left ventricular FDG uptake remained unchanged, patients in persistent AF presented significantly higher total left atrial and left atrial appendage uptake, which decreased significantly after return to sinus rhythm, despite improvement of passive and active atrial contractile function. These findings support a role of altered glucose metabolism and metabolic wasting underlying the pathophysiology of persistent AF.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X23005132/pdfft?md5=ba19dd4a2189016bb341b4eccfdb8337&pid=1-s2.0-S2452302X23005132-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139509842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial Calcium Flux—Friend or Foe in Chronic Heart Failure?∗ 线粒体钙通量--慢性心力衰竭中的 "敌 "还是 "友"?
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.02.018
Natalie M. Niemi PhD
{"title":"Mitochondrial Calcium Flux—Friend or Foe in Chronic Heart Failure?∗","authors":"Natalie M. Niemi PhD","doi":"10.1016/j.jacbts.2024.02.018","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.02.018","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000974/pdfft?md5=46390f1d2a093731402ea4392fcde236&pid=1-s2.0-S2452302X24000974-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Recognizing Early Career Translational Investigators 表彰早期职业转化研究人员
IF 9.7 1区 医学 Q1 Medicine Pub Date : 2024-04-01 DOI: 10.1016/j.jacbts.2024.04.004
Douglas L. Mann MD (Editor-in-Chief: JACC: Basic to Translational Science)
{"title":"Recognizing Early Career Translational Investigators","authors":"Douglas L. Mann MD (Editor-in-Chief: JACC: Basic to Translational Science)","doi":"10.1016/j.jacbts.2024.04.004","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.04.004","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":9.7,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24001426/pdfft?md5=544c4db770b66b262e00fa69e7f11f20&pid=1-s2.0-S2452302X24001426-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140880237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
JACC: Basic to Translational Science
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1