[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"_public_publisher_byId_2d08410c-37bf-439a-8075-56eba5f93e17":3,"_public_publication_all{\"sortAscending\":false,\"sortField\":\"updateTime\",\"page\":0,\"size\":10,\"facet\":true,\"searchKey\":\"publisherId:2d08410c-37bf-439a-8075-56eba5f93e17,\"}":174},{"code":4,"data":5,"meta":22},"SUCCESS",{"id":6,"createTime":7,"updateTime":8,"relativeEntities":9,"slug":10,"properties":11,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":24,"manageAffiliations":31,"indexDatabases":46,"url":22,"thumbnailPath":22,"statistic":81,"gsStatistic":22,"type":173,"analyzePriority":22},"2d08410c-37bf-439a-8075-56eba5f93e17","2024-04-07T02:53:15.693+00:00","2025-11-21T10:05:04.839+00:00",[],"Current-Cardiology-Reports",{"eissn":12,"issn":14,"title":16,"url":18},{"VOID":13},"15233782",{"VOID":15},"15343170",{"EN":17},"Current Cardiology Reports",{"VOID":19},"https:\u002F\u002Flink.springer.com\u002Fjournal\u002F11886","PUBLISHER","PENDING",null,0,[25],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":27,"label":28,"description":30,"parentId":22,"standard":22,"scholarHubFieldId":22},"2e748c70-3f53-41a9-99c9-1e3e45a3dc6d",[],{"EN":29},"Cardiology and Cardiovascular Medicine",{},[32,39],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":34,"slug":22,"properties":35,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":38,"statistic":22},"26a19206-5cad-4456-bb2f-49abd254fbc6",[],{"title":36},{"EN":37},"SPRINGER",[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":41,"slug":22,"properties":42,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":45,"statistic":22},"aeebfe70-bb47-4404-91bd-6d44079a5c1d",[],{"title":43},{"EN":44},"Current Medicine Group",[],[47,64],{"id":48,"indexDatabase":49,"url":61,"indexYears":22,"academicFieldIds":62,"indexDatabaseRanking":22},"bda1b1ed-548f-4aaa-895c-29624a94156b",{"id":50,"createTime":22,"updateTime":22,"relativeEntities":51,"label":52,"description":54,"key":57,"publicationTags":58,"standard":22},"a4921856-b128-4d9f-8f1f-e80813d3bbd4",[],{"EN":53,"VI":53},"ISI\u002FSCIE - Science Citation Index Expanded",{"EN":55,"VI":56},"SCIE database","Cơ sở dữ liệu SCIE","scie",[59,60],"SCIE","ISI","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=1523-3782",[63],"22fd6c38-3ec0-41e0-8ae8-a4290171207e",{"id":65,"indexDatabase":66,"url":76,"indexYears":77,"academicFieldIds":78,"indexDatabaseRanking":80},"ba82b00f-69f9-421c-ae10-5d22c467d7bb",{"id":67,"createTime":22,"updateTime":22,"relativeEntities":68,"label":69,"description":71,"key":73,"publicationTags":74,"standard":22},"3c7051d4-eb7d-4c57-a56b-36fc74c5d1e9",[],{"EN":70,"VI":70},"Scopus - Elsevier",{"EN":70,"VI":72},"Cơ sở dữ liệu Scopus thuộc Elsevier","scopus",[75],"SCOPUS","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F23118","1999-2025",[79],"d44e3b1d-4abe-47f2-b4aa-783c24a9f903","SCOPUS__Q2",{"impactFactor":23,"impactFactorByYear":82,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":98,"totalCitation":120,"totalCitationByYear":121,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":147,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},0.23,0.6,0.61,0.43,0.56,0.59,0.48,0.51,0.92,1.11,0.85,0.7,150,43,1932,{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},41,69,60,63,57,52,50,55,48,56,72,78,80,86,90,95,115,120,125,147,22,5625,{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},91,216,198,166,153,64,34,26,20,101,134,66,369,315,397,558,557,334,455,441,471,276,102,28,2.91,{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},2.22,3.13,3.3,2.63,2.55,1.12,0.65,0.52,0.36,1.94,2.79,1.18,0.89,6.47,4.38,5.09,6.97,6.48,3.71,4.79,3.83,3.92,2.21,0.69,38,"JOURNAL",{"meta":175,"data":177},{"total":176},"1936",[178,271,357,469,580,700,789,926,1028,1130],{"id":179,"createTime":180,"updateTime":181,"relativeEntities":182,"slug":183,"properties":184,"entityType":194,"verifyStatus":195,"verifyTime":196,"verifyNote":197,"languages":22,"translateLanguages":198,"viewCount":23,"primaryUrl":200,"fullTextUrl":22,"authors":201,"publicationType":218,"publisherRelationship":219,"citationCount":22,"citationInfo":22,"publishDate":267,"publishYear":268,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":269,"openAccess":22,"references":22,"isForceReanalyzing":270},"202958b4-71f2-4b8f-899f-a2db2ea5b6b6","2024-02-14T04:45:15.194+00:00","2026-09-07T08:14:50.279+00:00",[],"The-role-of-warfarin-and-aspirin-in-secondary-prevention-of-stroke",{"abstract":185,"title":187,"references":190,"doi":192},{"EN":186},"Antithrombotic therapy plays a central role in secondary prevention after ischemic stroke and transient ischemic attack. The choice among warfarin, aspirin, and other antiplatelet agents, however, depends on the cause of stroke and other individual patient characteristics. The use of warfarin anticoagulation in patients with atrial fibrillation and ischemic stroke has demonstrated robust reductions in risk of recurrent events, comparable with those achieved in primary prevention. Warfarin may also be recommended for patients with other high-risk cardioembolic sources of stroke. The role of warfarin in noncardioembolic ischemic stroke is more controversial. The Warfarin Aspirin Recurrent Stroke Study found no evidence of superiority of warfarin over aspirin in stroke patients overall, nor in any major stroke subtype, including those patients with patent foramen ovale. In post-hoc analyses, there was some evidence of benefit with warfarin in patients with cryptogenic stroke without hypertension. Risks of major bleeding did not differ significantly between warfarin and aspirin groups. For most patients with noncardioembolic strokes, therefore, antiplatelet therapy is the preferred option, although clinician experience still dictates practice in individual situations. Newer antiplatelet agents, and the combination of novel agents with aspirin, are also finding a role in stroke prevention as clinical trial data become available.",{"EN":188,"VI":189},"The role of warfarin and aspirin in secondary prevention of stroke","Vai trò của warfarin và aspirin trong phòng ngừa thứ phát đột quỵ",{"VOID":191},"Wolf PA, Abbott RD, Kannel WB: Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991, 22:983–988.\nPetersen P, Boysen G, Gotfredsen J, et al.: Placebo-controlled, randomised trial of warfarin and aspirin for prevention of thromboembolic complications in chronic atrial fibrillation: the Copenhagen AFASAK Study. Lancet 1989, 1:175–179.\nBoston Area Anticoagulation Trial in Atrial Fibrillation Investigators: The effect of low dose warfarin on the risk of stroke in patients with non-rheumatic atrial fibrillation. N Engl J Med 1990, 323:1505–1511.\nStroke Prevention in Atrial Fibrillation Investigators: Warfarin versus aspirin for the prevention of thromboembolism in atrial fibrillation: Stroke Prevention in Atrial Fibrillation II Study. Lancet 1994, 343:687–691.\nEuropean Atrial Fibrillation Trial Study Group: Secondary prevention in nonrheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet 1993, 342:1255–1262.\nStroke Prevention in Atrial Fibrillation Investigators: Stroke prevention in atrial fibrillation study, final results. Circulation 1991, 84:527–539.\nStroke Prevention in Atrial Fibrillation Investigators: Adjusteddose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial. Lancet 1996, 348:633–638.\nBaudet EM, Oca CC, Roques XF, et al.: A 5 1\u002F2 year experience with the St. Jude Medical cardiac valve prosthesis. Early and late results of 737 valve replacements in 671 patients. J Thorac Cardiovasc Surg 1985, 90:137–144.\nLoh E, Sutton MSJ, Wun CC, et al.: Ventricular dysfunction and the risk of stroke after myocardial infarction. N Engl J Med 1997, 336:251–257.\nWolf PA, Clagett GP, Easton JD, et al.: Preventing ischemic stroke in patients with prior stroke and transient ischemic attack. A statement for healthcare professionals from the Stroke Council of the American Heart Association. Stroke 1999, 30:1991–1994.\nAlbers GW, Amarenco P, Easton JD, et al.: Antithrombotic and thrombolytic therapy for ischemic stroke. Chest 2001, 119:300S-320S. This excellent review provides a comprehensive analysis of the use of antithrombotic therapies in acute stroke and stroke prevention.\nMohr JP, Thompson JLP, Lazar RM, et al., for the Warfarin-Aspirin Recurrent Stroke Study Group: A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med 2001, 345:1444–1451. This paper provides the final results of the landmark WARSS study regarding the relative benefits and risks of warfarin versus aspirin in secondary prevention of stroke.\nHomma S, Sacco RL, Di Tullio MR, et al.: Effect of medical treatment in stroke patients with patent foramen ovale: Patent Foramen Ovale in Cryptogenic Stroke Study. Circulation 2002, 105:2625–2631. This paper provides the final results of the PICSS substudy of WARSS, which addressed the role of warfarin versus aspirin in patients with a history of ischemic stroke and PFO. The paper provides evidence that PFO may be associated with cryptogenic stroke, but did not demonstrate an effect of PFO on stroke recurrence risk, nor a role for warfarin over aspirin in this setting.\nThe Stroke Prevention in Reversible Ischemia Trial (SPIRIT) Study Group: A randomized trial of anticoagulants versus aspirin after cerebral ischemia of presumed arterial origin. Ann Neurol 1997, 42:857–865.\nLechat P, Mas JL, Lascault G, et al.: Prevalence of patent foramen ovale in patients with stroke. N Engl J Med 1988, 318:1148–1152.\nDi Tullio M, Sacco RL, Gopal A, et al.: Patent foramen ovale as a risk factor for cryptogenic stroke. Ann Intern Med 1992, 117:461–465.\nMas JL, Arquizan C, Lamy C, et al.: Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001, 345:1740–1746.\nChimowitz MI, Kokkinos J, Strong J, et al.: The Warfarin-Aspirin Symptomatic Intracranial Disease study. Neurology. 1995, 45:1488–1493.\nESPRIT Study Group: Oral anticoagulation in patients after cerebral ischemia of arterial origin and risk of intracranial hemorrhage. Stroke 2003, 34:e46-e47.\nThe Canadian Cooperative Study Group: A randomized trial of aspirin and sulfinpyrazone in threatened stroke. N Engl J Med 1978, 299:53–59.\nThe SALT Collaborative Group: Swedish Aspirin Low-dose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischemic events. Lancet 1991, 338:1345–1349.\nDiener HC, Cunha L, Forbes C, et al.: European Stroke Prevention Study 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke. J Neurolog Sci 1996, 143:1–13.\nThe Dutch TIA Trial Study Group: A comparison of two doses of aspirin (30 mg vs. 283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke. N Engl J Med 1991, 325:1261–1266.\nFarrell B, Godwin J, Richards S, Warlow C: The United Kingdom transient ischaemic attack (UK-TIA) aspirin trial: final results. J Neurol Neurosurg Psychiatry 1991, 54:1044–1054.\nGent M, Blakely JA, Easton JD, et al.: The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke. Lancet 1989, i:1215–1220.\nHass WK, Easton JD, Adams HP Jr., et al.: A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. N Engl J Med 1989, 321:501–507.\nGorelick PB, Richardson D, Kelly M, et al.: African American Antiplatelet Stroke Prevention study investigators. Aspirin and ticlopidine for prevention of recurrent stroke in black patients: a randomized trial. JAMA 2003, 289:2947–2957.\nThe CAPRIE Steering Committee: A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996, 348:1329–1339.\nBennett CL, Connors JM, Carwile JM, et al.: Thrombotic thrombocytopenic purpura associated with clopidogrel. N Engl J Med 2000, 342:1773–1777.\nThe Clopidogrel in Unstable Angina to Prevent Recurrent Events trial investigators: Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001, 345:494–502.",{"VOID":193},"10.1007\u002Fs11886-004-0012-0","PUBLICATION","VERIFIED","2024-12-16T09:33:18.064+00:00","Auto Verify",[199],"VI","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-004-0012-0",[202],{"id":203,"sortIndex":23,"researcher":22,"roles":204,"affiliations":206,"properties":215,"displayName":217,"givenName":22,"familyName":22},"2b4545f3-5925-401d-9a2c-ec35608796db",[205],"AUTHOR",[207],{"id":208,"sortIndex":23,"affiliation":209,"properties":22},"98e1cca6-4007-4b9d-960f-f379fe0aa60f",{"id":208,"createTime":22,"updateTime":22,"relativeEntities":210,"slug":22,"properties":211,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":214,"statistic":22},[],{"title":212},{"VI":213},"Department of Neurology, Columbia University College of Physicians and Surgeons, New York, USA",[],{"title":216},{"VI":217},"Mitchell S. V. Elkind","ARTICLE",{"url":200,"publisher":220,"properties":262},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":221,"slug":10,"properties":222,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":226,"manageAffiliations":231,"indexDatabases":242,"url":22,"thumbnailPath":22,"statistic":257,"gsStatistic":22,"type":173,"analyzePriority":22},[],{"issn":223,"title":224,"eissn":225},{"VOID":15},{"EN":17},{"VOID":13},[227],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":228,"label":229,"description":230,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},[232,237],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":233,"slug":22,"properties":234,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":236,"statistic":22},[],{"title":235},{"EN":37},[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":238,"slug":22,"properties":239,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":241,"statistic":22},[],{"title":240},{"EN":44},[],[243,250],{"id":48,"indexDatabase":244,"url":61,"indexYears":22,"academicFieldIds":249,"indexDatabaseRanking":22},{"id":50,"createTime":22,"updateTime":22,"relativeEntities":245,"label":246,"description":247,"key":57,"publicationTags":248,"standard":22},[],{"EN":53,"VI":53},{"EN":55,"VI":56},[59,60],[63],{"id":65,"indexDatabase":251,"url":76,"indexYears":77,"academicFieldIds":256,"indexDatabaseRanking":80},{"id":67,"createTime":22,"updateTime":22,"relativeEntities":252,"label":253,"description":254,"key":73,"publicationTags":255,"standard":22},[],{"EN":70,"VI":70},{"EN":70,"VI":72},[75],[79],{"impactFactor":23,"impactFactorByYear":258,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":259,"totalCitation":120,"totalCitationByYear":260,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":261,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},{"pages":263,"volume":265},{"VOID":264},"135-142",{"VOID":266},"6","2004-03-01",2004,[80,59],false,{"id":272,"createTime":273,"updateTime":274,"relativeEntities":275,"slug":276,"properties":277,"entityType":194,"verifyStatus":195,"verifyTime":287,"verifyNote":197,"languages":22,"translateLanguages":288,"viewCount":23,"primaryUrl":289,"fullTextUrl":22,"authors":290,"publicationType":218,"publisherRelationship":306,"citationCount":22,"citationInfo":22,"publishDate":354,"publishYear":355,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":356,"openAccess":22,"references":22,"isForceReanalyzing":270},"70021cbe-4071-4c5a-b1f3-ca55564bdfe5","2024-02-09T16:26:36.036+00:00","2026-09-07T05:13:41.295+00:00",[],"Antiplatelet-resistance-with-aspirin-and-clopidogrel-Is-it-real-and-does-it-matter-",{"abstract":278,"title":280,"references":283,"doi":285},{"EN":279},"Platelets play a pivotal role in the pathophysiology of ischemic complications of atherosclerotic cardiovascular disease. Aspirin and clopidogrel are oral antiplatelet drugs that have been shown to reduce adverse clinical events across the wide spectrum of patients with atherothrombotic disease. However, recurrent ischemic events still occur in a significant proportion of patients despite treatment with these antiplatelet drugs. The concept of antiplatelet resistance therefore emerges. Although uniform definitions and standardized assays are not yet available, numerous studies have documented the interindividual variability in platelet responsiveness to oral antiplatelet drugs. Evidence is also accumulating to demonstrate that hyporesponsiveness to antiplatelet drugs in the laboratory (ie, resistance) is associated with adverse clinical events in different patient populations. Clinical application of antiplatelet resistance will require proof from prospective randomized trials that modifications of antiplatelet therapy based on tests of antiplatelet responsiveness will improve the outcomes of patients with antiplatelet resistance.",{"EN":281,"VI":282},"Antiplatelet resistance with aspirin and clopidogrel: Is it real and does it matter?","Kháng thuốc kháng kết tập tiểu cầu với aspirin và clopidogrel: Có thực sự tồn tại và có quan trọng không?",{"VOID":284},"Antithrombotic Trialists#x2019; Collaboration: Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002, 324:71–86.\nBarnathan ES, Schwartz JS, Taylor L, et al.: Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty. Circulation 1987, 76:125–134.\nSchwartz L, Bourassa MG, Lesperance J, et al.: Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engl J Med 1988, 318:1714–1719.\nLembo NJ, Black AJR, Roubin GS, et al.: Effect of pre-treatment with aspirin versus aspirin plus dipyridamole on frequency and type of acute complications of percutaneous transluminal coronary angioplasty. Am J Cardiol 1990, 65:422–426.\nPatrono C, Bachmann F, Baigent C, et al.: Expert consensus document on the use of antiplatelet agents. The task force on the use of antiplatelet agents in patients with atherosclerotic cardiovascular disease of the European society of cardiology. Eur Heart J 2004, 25:166–181.\nCAPRIE Steering Committee: A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996, 348:1329–1339.\nYusuf S, Zhao F, Mehta SR, et al.: Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001, 345:494–502.\nSteinhubl SR, Berger PB, Mann JT 3rd, et al.: Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA 2002, 288:2411–2420.\nSabatine MS, Cannon CP, Gibson CM, et al.: Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med 2005, 352:1179–1189.\nChen ZM, Pan HC, Chen YP, et al.: Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet 2005, 366:1607–1621.\nMehta J, Mehta P, Burger C, Pepine CJ: Platelet aggregation studies in coronary artery disease. Part 4. Effect of aspirin. Atherosclerosis 1978, 31:169–175.\nGrotemeyer KH: Effects of acetylsalicylic acid in stroke patients. Evidence of nonresponders in a subpopulation of treated patients. Thromb Res 1991, 63:587–593.\nPappas JM, Westengard JC, Bull BS: Population variability in the effect of aspirin on platelet function. Implications for clinical trials and therapy. Arch Pathol Lab Med 1994, 118:801–804.\nBuchanan MR, Brister SJ: Individual variation in the effects of ASA on platelet function: implications for the use of ASA clinically. Can J Cardiol 1995, 11:221–227.\nMueller MR, Salat A, Stangl P, et al.: Variable platelet response to low-dose aspirin and the risk of limb deterioration in patients submitted to peripheral arterial angioplasty. Thromb Haemost 1997, 78:1003–1007.\nHurlen M, Seljeflot I, Arnesen H: The effect of different antithrombotic regimens on platelet aggregation after myocardial infarction. Scand Cardiovasc J 1998, 32:233–237.\nGum PA, Kottke-Marchant K, Poggio ED, et al.: Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am J Cardiol 2001, 88:230–235.\nAndersen K, Hurlen M, Arnesen H, Seljeflot I: Aspirin nonresponsiveness as measured by PFA-100 in patients with coronary artery disease. Thromb Res 2002, 108:37–42.\nMacchi L, Christiaens L, Brabant S, et al.: Resistance to aspirin in vitro is associated with increased platelet sensitivity to adenosine diphosphate. Thromb Res 2002, 107:45–49.\nGrundmann K, Jaschonek K, Kleine B, et al.: Aspirin non-responder status in patients with recurrent cerebral ischemic attacks. J Neurol 2003, 250:63–66.\nWang JC, Aucoin-Barry D, Manuelian D, et al.: Incidence of aspirin nonresponsiveness using the Ultegra Rapid Platelet Function Assay-ASA. Am J Cardiol 2003, 92:1492–1494.\nLee PY, Chen WH, Ng W, et al.: Low-dose aspirin increases aspirin resistance in patients with coronary artery disease. Am J Med 2005, 118:723–727.\n• McKee SA, Sane DC, Deliargyris EN: Aspirin resistance in cardiovascular disease: a review of prevalence, mechanisms, and clinical significance. Thromb Haemost 2002, 88:711–715.Informative review on the mechanisms of aspirin resistance\nBhatt DL: Aspirin resistance: more than just a laboratory curiosity. J Am Coll Cardiol 2004, 43:1127–1129.\nGrotemeyer KH, Scharafinski HW, Husstedt IW: Twoyear follow-up of aspirin responder and aspirin non-responder. A pilot study including 180 post-stroke patients. Thromb Res 1993, 71:397–403.\n•• Eikelboom JW, Hirsh J, Weitz JI, et al.: Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002, 105:1650–1655.Influential paper describing the clinical risk associated with aspirin resistance that aroused widespread interest in this field\n•• Gum PA, Kottke-Marchant K, Welsh PA, et al.: A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. J Am Coll Cardiol 2003, 41:961–965.First prospective study documenting adverse outcomes of aspirinresistant patients using gold standard platelet function test\n• Chen WH, Lee PY, Ng W, et al.: Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment. J Am Coll Cardiol 2004, 43:1122–1126.Simple study revealing the importance of hyporesponsiveness to aspirin#x2019;s platelet antiaggregatory effect on myocardial necrosis after PCI\nChen WH, Lee PY, Ng W, et al.: Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary intervention. Am J Cardiol 2005, 96:760–763.\nJaremo P, Lindahl TL, Fransson SG, Richter A: Individual variations of platelet inhibition after loading doses of clopidogrel. J Intern Med 2002, 252:233–238.\nGurbel PA, Bliden KP: Durability of platelet inhibition by clopidogrel. Am J Cardiol 2003, 91:1123–1125.\nMuller I, Besta F, Schulz C, et al.: Prevalence of clopidogrel non-responders among patients with stable angina pectoris scheduled for elective coronary stent placement. Thromb Haemost 2003, 89:783–787.\nSoffer D, Moussa I, Harjai KJ, et al.: Impact of angina class on inhibition of platelet aggregation following clopidogrel loading in patients undergoing coronary intervention: do we need more aggressive dosing regimens in unstable angina? Catheter Cardiovasc Interv 2003, 59:21–25.\nGurbel PA, Bliden KP, Hiatt BL, O#x2019;Connor CM: Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity. Circulation 2003, 107:2908–2913.\nMobley JE, Bresee SJ, Wortham DC, et al.: Frequency of nonresponse antiplatelet activity of clopidogrel during pretreatment for cardiac catheterization. Am J Cardiol 2004, 93:456–458.\nSerebruany VL, Steinhubl SR, Berger PB, et al.: Variability in platelet responsiveness to clopidogrel among 544 individuals. J Am Coll Cardiol 2005, 45:246–251.\nWiviott SD, Antman EM: Clopidogrel resistance: a new chapter in a fast-moving story. Circulation 2004, 109:3064–3067.\n• Nguyen TA, Diodati JG, Pharand C: Resistance to clopidogrel: a review of the evidence. J Am Coll Cardiol 2005, 45:1157–1164.Comprehensive review on clopidogrel pharmacology and mechanisms of clopidogrel resistance\nBarragan P, Bouvier JL, Roquebert PO, et al.: Resistance to thienopyridines: clinical detection of coronary stent thrombosis by monitoring of vasodilator-stimulated phosphoprotein phosphorylation. Catheter Cardiovasc Interv 2003, 59:295–302.\n•• Matetzky S, Shenkman B, Guetta V, et al.: Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction. Circulation 2004, 109:3171–3175.Key prospective study illustrating clinical significance of clopidogrel resistance in a high-risk population\nLev EI, Patel RT, Maresh KJ, et al.: Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance. J Am Coll Cardiol 2006, 47:27–33.\nBhatt DL, Topol EJ: Clopidogrel added to aspirin versus aspirin alone in secondary prevention and high-risk primary prevention: rationale and design of the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA) trial. Am Heart J 2004, 148:263–268.\nPettersen AA, Seljeflot I, Abdelnoor M, Arnesen H: Unstable angina, stroke, myocardial infarction and death in aspirin non-responders. A prospective, randomized trial. The ASCET (ASpirin non-responsiveness and Clopidogrel Endpoint Trial) design. Scand Cardiovasc J 2004, 38:353–356.",{"VOID":286},"10.1007\u002Fs11886-006-0063-5","2025-02-21T11:52:02.380+00:00",[199],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-006-0063-5",[291],{"id":292,"sortIndex":23,"researcher":22,"roles":293,"affiliations":294,"properties":303,"displayName":305,"givenName":22,"familyName":22},"1863d1a7-9e61-4aa3-92e7-ae5d7ae54c2c",[205],[295],{"id":296,"sortIndex":23,"affiliation":297,"properties":22},"3d1e9a3a-c7a0-4df3-b3f8-eade6c459544",{"id":296,"createTime":22,"updateTime":22,"relativeEntities":298,"slug":22,"properties":299,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":302,"statistic":22},[],{"title":300},{"VI":301},"Division of Cardiology, Department of Medicine, The University of Hong Kong Room 1929C, Block K, Queen Mary Hospital, Hong Kong, China",[],{"title":304},{"VI":305},"Wai-Hong Chen",{"url":289,"publisher":307,"properties":349},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":308,"slug":10,"properties":309,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":313,"manageAffiliations":318,"indexDatabases":329,"url":22,"thumbnailPath":22,"statistic":344,"gsStatistic":22,"type":173,"analyzePriority":22},[],{"issn":310,"title":311,"eissn":312},{"VOID":15},{"EN":17},{"VOID":13},[314],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":315,"label":316,"description":317,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},[319,324],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":320,"slug":22,"properties":321,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":323,"statistic":22},[],{"title":322},{"EN":37},[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":325,"slug":22,"properties":326,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":328,"statistic":22},[],{"title":327},{"EN":44},[],[330,337],{"id":48,"indexDatabase":331,"url":61,"indexYears":22,"academicFieldIds":336,"indexDatabaseRanking":22},{"id":50,"createTime":22,"updateTime":22,"relativeEntities":332,"label":333,"description":334,"key":57,"publicationTags":335,"standard":22},[],{"EN":53,"VI":53},{"EN":55,"VI":56},[59,60],[63],{"id":65,"indexDatabase":338,"url":76,"indexYears":77,"academicFieldIds":343,"indexDatabaseRanking":80},{"id":67,"createTime":22,"updateTime":22,"relativeEntities":339,"label":340,"description":341,"key":73,"publicationTags":342,"standard":22},[],{"EN":70,"VI":70},{"EN":70,"VI":72},[75],[79],{"impactFactor":23,"impactFactorByYear":345,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":346,"totalCitation":120,"totalCitationByYear":347,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":348,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},{"pages":350,"volume":352},{"VOID":351},"301-306",{"VOID":353},"8","2006-07-01",2006,[80,59],{"id":358,"createTime":359,"updateTime":360,"relativeEntities":361,"slug":362,"properties":363,"entityType":194,"verifyStatus":195,"verifyTime":374,"verifyNote":197,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":375,"fullTextUrl":22,"authors":376,"publicationType":218,"publisherRelationship":416,"citationCount":22,"citationInfo":22,"publishDate":464,"publishYear":465,"citationAnalyzeStatus":466,"lastCitationAnalyze":467,"indexDatabases":468,"openAccess":22,"references":22,"isForceReanalyzing":270},"26dfa930-92eb-4660-8143-8b4bbf662723","2024-01-20T22:23:03.129+00:00","2026-08-24T14:47:45.779+00:00",[],"Exploring-the-Inner-Workings-of-Direct-Cardiac-Reprogramming",{"abstract":364,"title":366,"gsPaper":368,"references":370,"doi":372},{"EN":365},"Following cardiac injury, the heart has limited ability to regenerate leading to decreased efficiency and function. Cardiac reprogramming offers a promising treatment to ameliorate the damage caused by ischemia through conversion of cardiac fibroblasts to induced cardiomyocytes (iCMs). Here, we aim to highlight the recent advancements of the last 5 years by discussing the various aspects of cardiac reprogramming including characterization of the cardiac fibroblast, the endogenous environment of the heart, the molecular mechanisms during reprogramming, the epigenetic landscape, and the mechanics of delivering reprogramming factors. Due to generally low efficiency of direct cardiac reprogramming, many researchers have continued to improve the efficiency of iCM induction and continued exploration of the basic science behind the technique. The field is continuing to optimize individual aspects of reprogramming that can be leveraged together to improve overall effectiveness. Over the last several years, knowledge regarding the process of direct cardiac reprogramming and the many factors that affect its efficiency has increased significantly. Individual aspects have continued to be optimized, and it will be essential going forward to synthesize this information. Cardiac reprogramming continues to advance towards clinical translatability.",{"EN":367},"Exploring the Inner Workings of Direct Cardiac Reprogramming",{"VOID":369},"[\"10704562415878654647\"]",{"VOID":371},"Tsao CW, Aday AW, Almarzooq ZI, Alonso A, Beaton AZ, Bittencourt MS, et al. Heart disease and stroke statistics-2022 update: a report from the American Heart Association. Circulation. 2022;145:e153-639.\nSutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation. 2000;101:2981–8.\nKikuchi K, Poss KD. Cardiac regenerative capacity and mechanisms. Annu Rev Cell Dev Biol. 2012;28:719–41.\nTakahashi K, Yamanaka S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell. 2006;126:663–76.\nZhang J, Wilson GF, Soerens AG, Koonce CH, Yu J, Palecek SP, et al. Functional cardiomyocytes derived from human induced pluripotent stem cells. Circ Res. 2009;104:e30-41.\nIeda M, Fu J-D, Delgado-Olguin P, Vedantham V, Hayashi Y, Bruneau BG, et al. Direct reprogramming of fibroblasts into functional cardiomyocytes by defined factors. Cell. 2010;142:375–86.\nQian L, Huang Y, Spencer CI, Foley A, Vedantham V, Liu L, et al. In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes. Nature. 2012;485:593–8.\nSong K, Nam Y-J, Luo X, Qi X, Tan W, Huang GN, et al. Heart repair by reprogramming non-myocytes with cardiac transcription factors. Nature. 2012;485:599–604.\nJayawardena TM, Egemnazarov B, Finch EA, Zhang L, Payne JA, Pandya K, et al. MicroRNA-mediated in vitro and in vivo direct reprogramming of cardiac fibroblasts to cardiomyocytes. Circ Res. 2012;110:1465–73.\nJayawardena TM, Finch EA, Zhang L, Zhang H, Hodgkinson CP, Pratt RE, et al. MicroRNA induced cardiac reprogramming in vivo: evidence for mature cardiac myocytes and improved cardiac function. Circ Res. 2015;116:418–24.\nZhou H, Dickson ME, Kim MS, Bassel-Duby R, Olson EN. Akt1\u002Fprotein kinase B enhances transcriptional reprogramming of fibroblasts to functional cardiomyocytes. Proc Natl Acad Sci USA. 2015;112:11864–9.\nProtze S, Khattak S, Poulet C, Lindemann D, Tanaka EM, Ravens U. A new approach to transcription factor screening for reprogramming of fibroblasts to cardiomyocyte-like cells. J Mol Cell Cardiol. 2012;53:323–32.\nHirai H, Katoku-Kikyo N, Keirstead SA, Kikyo N. Accelerated direct reprogramming of fibroblasts into cardiomyocyte-like cells with the MyoD transactivation domain. Cardiovasc Res. 2013;100:105–13.\nChristoforou N, Chellappan M, Adler AF, Kirkton RD, Wu T, Addis RC, et al. Transcription factors MYOCD, SRF, Mesp1 and SMARCD3 enhance the cardio-inducing effect of GATA4, TBX5, and MEF2C during direct cellular reprogramming. PLoS ONE. 2013;8: e63577.\nAddis RC, Ifkovits JL, Pinto F, Kellam LD, Esteso P, Rentschler S, et al. Optimization of direct fibroblast reprogramming to cardiomyocytes using calcium activity as a functional measure of success. J Mol Cell Cardiol. 2013;60:97–106.\nMuraoka N, Yamakawa H, Miyamoto K, Sadahiro T, Umei T, Isomi M, et al. MiR-133 promotes cardiac reprogramming by directly repressing Snai1 and silencing fibroblast signatures. EMBO J. 2014;33:1565–81.\nNam Y-J, Song K, Luo X, Daniel E, Lambeth K, West K, et al. Reprogramming of human fibroblasts toward a cardiac fate. Proc Natl Acad Sci USA. 2013;110:5588–93.\nLitviňuková M, Talavera-López C, Maatz H, Reichart D, Worth CL, Lindberg EL, et al. Cells of the adult human heart. Nature. 2020;588:466–72.\nPetrov VV, Fagard RH, Lijnen PJ. Stimulation of collagen production by transforming growth factor-beta1 during differentiation of cardiac fibroblasts to myofibroblasts. Hypertension. 2002;39:258–63.\nDaseke MJ, Tenkorang MAA, Chalise U, Konfrst SR, Lindsey ML. Cardiac fibroblast activation during myocardial infarction wound healing: Fibroblast polarization after MI. Matrix Biol. 2020;91–92:109–16.\nZhang Z, Zhang W, Blakes R, Sundby LJ, Shi Z, Rockey DC, et al. Fibroblast fate determination during cardiac reprogramming by remodeling of actin filaments. Stem Cell Reports. 2022;17:1604–19.\n• Wang L, Yang Y, Ma H, Xie Y, Xu J, Near D, et al. Single-cell dual-omics reveals the transcriptomic and epigenomic diversity of cardiac non-myocytes. Cardiovasc Res. 2022;118:1548–63. This study emphasizes the heterogeneity of heart tissues and defines the complexity of various cell types within the heart.\nKurotsu S, Sadahiro T, Fujita R, Tani H, Yamakawa H, Tamura F, et al. Soft matrix promotes cardiac reprogramming via inhibition of YAP\u002FTAZ and suppression of fibroblast signatures. Stem Cell Reports. 2020;15:612–28.\nLi Y, Dal-Pra S, Mirotsou M, Jayawardena TM, Hodgkinson CP, Bursac N, et al. Tissue-engineered 3-dimensional (3D) microenvironment enhances the direct reprogramming of fibroblasts into cardiomyocytes by microRNAs. Sci Rep. 2016;6:38815.\nYamakawa H, Muraoka N, Miyamoto K, Sadahiro T, Isomi M, Haginiwa S, et al. Fibroblast growth factors and vascular endothelial growth factor promote cardiac reprogramming under defined conditions. Stem Cell Reports. 2015;5:1128–42.\n• Paoletti C, Marcello E, Melis ML, Divieto C, Nurzynska D, Chiono V, et al. Cardiac tissue-like 3D microenvironment enhances route towards human fibroblast direct reprogramming into induced cardiomyocytes by microRNAs. Cells. 2022;11. This study emphasizes the importance of the heart environment to cell fate and integrates information from many of the previous structural studies to improve cardiac reprogramming.\nIfkovits JL, Addis RC, Epstein JA, Gearhart JD. Inhibition of TGFβ signaling increases direct conversion of fibroblasts to induced cardiomyocytes. PLoS ONE. 2014;9: e89678.\nLalit PA, Salick MR, Nelson DO, Squirrell JM, Shafer CM, Patel NG, et al. Lineage reprogramming of fibroblasts into proliferative induced cardiac progenitor cells by defined factors. Cell Stem Cell. 2016;18:354–67.\nJang J, Ku SY, Kim JE, Choi K, Kim YY, Kim HS, et al. Notch inhibition promotes human embryonic stem cell-derived cardiac mesoderm differentiation. Stem Cells. 2008;26:2782–90.\nChen VC, Stull R, Joo D, Cheng X, Keller G. Notch signaling respecifies the hemangioblast to a cardiac fate. Nat Biotechnol. 2008;26:1169–78.\nLi H, Yu B, Zhang Y, Pan Z, Xu W, Li H. Jagged1 protein enhances the differentiation of mesenchymal stem cells into cardiomyocytes. Biochem Biophys Res Commun. 2006;341:320–5.\nKoyanagi M, Bushoven P, Iwasaki M, Urbich C, Zeiher AM, Dimmeler S. Notch signaling contributes to the expression of cardiac markers in human circulating progenitor cells. Circ Res. 2007;101:1139–45.\nAbad M, Hashimoto H, Zhou H, Morales MG, Chen B, Bassel-Duby R, et al. Notch inhibition enhances cardiac reprogramming by increasing MEF2C transcriptional activity. Stem Cell Reports. 2017;8:548–60.\nHodgkinson CP, Pratt RE, Kirste I, Dal-Pra S, Cooke JP, Dzau VJ. Cardiomyocyte maturation requires TLR3 activated nuclear factor kappa B. Stem Cells. 2018;36:1198–209.\nHu J, Hodgkinson CP, Pratt RE, Lee J, Sullenger BA, Dzau VJ. Enhancing cardiac reprogramming via synthetic RNA oligonucleotides. Mol Ther Nucleic Acids. 2021;23:55–62.\nZhao H, Zhang Y, Xu X, Sun Q, Yang C, Wang H, et al. Sall4 and myocd empower direct cardiac reprogramming from adult cardiac fibroblasts after injury. Front Cell Dev Biol. 2021;9: 608367.\nWang L, Ma H, Huang P, Xie Y, Near D, Wang H, et al. Down-regulation of Beclin1 promotes direct cardiac reprogramming. Sci Transl Med. 2020;12.\nZhou Y, Wang L, Liu Z, Alimohamadi S, Yin C, Liu J, et al. Comparative gene expression analyses reveal distinct molecular signatures between differentially reprogrammed cardiomyocytes. Cell Rep. 2017;20:3014–24.\nLiu Z, Chen O, Zheng M, Wang L, Zhou Y, Yin C, et al. Re-patterning of H3K27me3, H3K4me3 and DNA methylation during fibroblast conversion into induced cardiomyocytes. Stem Cell Res. 2016;16:507–18.\nZhou Y, Wang L, Vaseghi HR, Liu Z, Lu R, Alimohamadi S, et al. Bmi1 is a key epigenetic barrier to direct cardiac reprogramming. Cell Stem Cell. 2016;18:382–95.\nZhou Y, Alimohamadi S, Wang L, Liu Z, Wall JB, Yin C, et al. A loss of function screen of epigenetic modifiers and splicing factors during early stage of cardiac reprogramming. Stem Cells Int. 2018;2018:3814747.\nDal-Pra S, Hodgkinson CP, Mirotsou M, Kirste I, Dzau VJ. Demethylation of H3K27 is essential for the induction of direct cardiac reprogramming by mir combo. Circ Res. 2017;120:1403–13.\nStone NR, Gifford CA, Thomas R, Pratt KJB, Samse-Knapp K, Mohamed TMA, et al. Context-specific transcription factor functions regulate epigenomic and transcriptional dynamics during cardiac reprogramming. Cell Stem Cell. 2019;25:87-102.e9.\nGarry GA, Bezprozvannaya S, Chen K, Zhou H, Hashimoto H, Morales MG, et al. The histone reader PHF7 cooperates with the SWI\u002FSNF complex at cardiac super enhancers to promote direct reprogramming. Nat Cell Biol. 2021;23:467–75.\n•• Wang H, Keepers B, Qian Y, Xie Y, Colon M, Liu J, et al. Cross-lineage potential of Ascl1 uncovered by comparing diverse reprogramming regulatomes. Cell Stem Cell. 2022;29:1491-1504.e9. This paper was the first to study the epigenetic regulatomes across three types of lineage reprogramming, with the unexpected discovery of Ascl1’s cross lineage potential.\nSadahiro T, Yamanaka S, Ieda M. Direct cardiac reprogramming: progress and challenges in basic biology and clinical applications. Circ Res. 2015;116:1378–91.\nMiyamoto K, Akiyama M, Tamura F, Isomi M, Yamakawa H, Sadahiro T, et al. Direct in vivo reprogramming with sendai virus vectors improves cardiac function after myocardial infarction. Cell Stem Cell. 2018;22:91-103.e5.\nKaur K, Hadas Y, Kurian AA, Żak MM, Yoo J, Mahmood A, et al. Direct reprogramming induces vascular regeneration post muscle ischemic injury. Mol Ther. 2021;29:3042–58.\nNicoletti L, Paoletti C, Tarricone G, Andreana I, Stella B, Arpicco S, et al. Lipoplexes for effective in vitro delivery of microRNAs to adult human cardiac fibroblasts for perspective direct cardiac cell reprogramming. Nanomedicine. 2022;45: 102589.\nKim H, Song B-W, Park S-J, Choi SW, Moon H, Hwang K-C, et al. Ultraefficient extracellular vesicle-guided direct reprogramming of fibroblasts into functional cardiomyocytes. Sci Adv. 2022;8:eabj6621.\n•• Wang Q, Song Y, Chen J, Li Q, Gao J, Tan H, et al. Direct in vivo reprogramming with non-viral sequential targeting nanoparticles promotes cardiac regeneration. Biomaterials. 2021;276:121028. This study was the first to identify a direct reprogramming technique that would allow for systemic administration instead of an intramyocardial injection.",{"VOID":373},"10.1007\u002Fs11886-023-01868-9","2024-06-26T18:00:37.249+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-023-01868-9",[377,403],{"id":378,"sortIndex":23,"researcher":22,"roles":379,"affiliations":380,"properties":398,"displayName":400,"givenName":22,"familyName":22},"220b8d7e-77ed-47bf-8680-72c023b230da",[205],[381,389],{"id":382,"sortIndex":23,"affiliation":383,"properties":22},"b2fb5c69-1734-44f6-973a-9752633276f9",{"id":382,"createTime":22,"updateTime":22,"relativeEntities":384,"slug":22,"properties":385,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":388,"statistic":22},[],{"title":386},{"VI":387},"Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, USA, ",[],{"id":390,"sortIndex":391,"affiliation":392,"properties":22},"983e592c-b95f-4ddf-8b8f-2076c7d0fbae",1,{"id":390,"createTime":22,"updateTime":22,"relativeEntities":393,"slug":22,"properties":394,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":397,"statistic":22},[],{"title":395},{"VI":396},"McAllister Heart Institute, University of North Carolina, Chapel Hill, USA",[],{"title":399,"gsAuthor":401},{"VI":400},"Paige 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prevalence of atrial fibrillation increases significantly with age, affecting nearly 10 % of adults greater than 80 years of age. Complications from atrial fibrillation, including stroke, also increase with age. Medical therapy includes anticoagulation, ventricular rate control, and if symptoms persist, maintenance of sinus rhythm with antiarrhythmic drugs. However, anticoagulation and antiarrhythmic therapy is often challenging in the elderly due to side effects, comorbidities, and heightened sensitivity to medications. Catheter based ablation of atrial fibrillation is an effective treatment for paroxysmal atrial fibrillation. However, the major randomized controlled trials, such as Thermocool AF and STOP-AF studies, have excluded the elderly patients. Current guidelines suggest caution when considering ablation for elderly patients due to a lack of available data. We will review recent studies that have observed the outcomes of atrial fibrillation ablation in the elderly, specifically those studies that included octogenarians.",{"EN":479},"Atrial Fibrillation Ablation in Octogenarians: Where Do We Stand?",{"VOID":481},"[\"8857361517912111585\"]",{"VOID":483},"10.1007\u002Fs11886-013-0406-y","2024-05-06T06:04:48.124+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-013-0406-y","https:\u002F\u002Flink.springer.com\u002Fcontent\u002Fpdf\u002F10.1007\u002Fs11886-013-0406-y.pdf",[488,506],{"id":489,"sortIndex":23,"researcher":22,"roles":490,"affiliations":491,"properties":503,"displayName":505,"givenName":22,"familyName":22},"44c97f68-ae05-4cd1-81d6-9be91e48d3ba",[205],[492],{"id":493,"sortIndex":23,"affiliation":494,"properties":500},"df0771ba-3eba-4215-843f-aa031f3038b0",{"id":493,"createTime":22,"updateTime":22,"relativeEntities":495,"slug":22,"properties":496,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":499,"statistic":22},[],{"title":497},{"EN":498},"University of California, San Francisco, San Francisco, United States",[],{"title":501},{"VI":502},"University of California San Francisco, San Francisco, USA",{"title":504},{"VI":505},"Stepanyan, Gevorg",{"id":507,"sortIndex":391,"researcher":22,"roles":508,"affiliations":509,"properties":518,"displayName":520,"givenName":22,"familyName":22},"5e3d7b77-5738-4d8d-95bc-e86b62054ef2",[205],[510],{"id":493,"sortIndex":23,"affiliation":511,"properties":516},{"id":493,"createTime":22,"updateTime":22,"relativeEntities":512,"slug":22,"properties":513,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":515,"statistic":22},[],{"title":514},{"EN":498},[],{"title":517},{"VI":502},{"title":519},{"VI":520},"Gerstenfeld, Edward 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several decades of research and clinical experience, the basic mechanisms of the failing heart remain largely a secret. While pharmacological therapy can induce limited reverse remodeling, left ventricular assist device (LVAD) therapy offers the opportunity to induce significant improvements to the structure and function of the heart, with major clinical implications. LVAD therapy also provides significant insight into which changes have an impact on function and which do not, and could therefore reveal some of the secrets of the failing heart. In addition, LVAD-induced mechanical unloading may unlock further myocardial properties hitherto unknown such as the proliferation of the stem cell compartment. It may also serve as an important platform for emerging therapies such as gene and cell therapies. In this review, we highlight the most recent novel discoveries related to LVAD therapy and bridge to recovery (BTR). Discovering the integrated network of events that underlies BTR could unravel the secrets of the failing heart.",{"EN":590},"Can Bridge to Recovery Help to Reveal the Secrets of the Failing Heart?",{"VOID":592},"[\"4513005953665766848\"]",{"VOID":594},"Peterson S, Rayner M, Wolstenholme J. Heart failure supplement. British Heart Foundation Statistics. 2002 May 23;1–36.\nStewart S, MacIntyre K, Hole DJ, Capewell S, McMurray JJ. More “malignant” than cancer? Five-year survival following a first admission for heart failure. Eur J Heart Fail. 2001;3(3):315–22.\nKoitabashi N, Kass DA. Reverse remodeling in heart failure-mechanisms and therapeutic opportunities. Nat Rev Cardiol. 2011;9(3):147–57.\nKlotz S, Burkhoff D, Garrelds IM, Boomsma F, Danser AHJ. The impact of left ventricular assist device-induced left ventricular unloading on the myocardial renin-angiotensin-aldosterone system: therapeutic consequences? Eur Heart J. 2009;30(7):805–12.\nThompson LO, Skrabal CA, Loebe M, Lafuente JA, Roberts RR, Akgul A, Jones V, Bruckner BA, Thohan V, Noon GP, Youker KA. Plasma neurohormone levels correlate with left ventricular functional and morphological improvement in LVAD patients. J Surg Res. 2005;123(1):25–32.\nNag AC, Zak R. Dissociation of adult mammalian heart into single cell suspension: an ultrastructural study. J Anat. 1979;129(Pt 3):541–59.\nIbrahim M, Terracciano CM, Yacoub MH. Bridge to recovery: what remains to be discovered? Cardiol Clin. 2011;29(4):531–47.\nTerracciano CMN, Hardy J, Birks EJ, Khaghani A, Banner NR, Yacoub MH. Clinical recovery from end-stage heart failure using left-ventricular assist device and pharmacological therapy correlates with increased sarcoplasmic reticulum calcium content but not with regression of cellular hypertrophy. Circulation. 2004;109(19):2263–5.\nWei S, Guo A, Chen B, Kutschke W, Xie Y-P, Zimmerman K, Weiss RM, Anderson ME, Cheng H, Song L-S. T-tubule remodeling during transition from hypertrophy to heart failure. Circ Res. 2010;107(4):520–31.\nIbrahim M, Gorelik J, Yacoub MH, Terracciano CM. The structure and function of cardiac t-tubules in health and disease. Proc Biol Sci. 2011;278(1719):2714–23.\nNikolaev VO, Moshkov A, Lyon AR, Miragoli M, Novak P, Paur H, Lohse MJ, Korchev YE, Harding SE, Gorelik J. Beta2-adrenergic receptor redistribution in heart failure changes cAMP compartmentation. Science. 2010;327(5973):1653–7.\nIbrahim M, Navaratnarajah M, Siedlecka U, Rao C, Dias P, Moshkov A, Gorelik J, Yacoub M, Terracciano C. Mechanical unloading reverses T-tubule remodelling and normalises local Ca2+− induced Ca2+−release in a rodent model of heart failure. Eur J Heart Fail. 2012 Feb. 28;In Press.\nOgletree-Hughes ML, Stull LB, Sweet WE, Smedira NG, McCarthy PM, Moravec CS. Mechanical unloading restores beta-adrenergic responsiveness and reverses receptor downregulation in the failing human heart. Circulation. 2001;104(8):881–6.\nBick RJ, Grigore AM, Poindexter BJ, Schnee PM, Nussmeier NA, Gregoric ID, Shah NA, Myers TJ, Buja LM, Frazier OH. Left ventricular unloading with an assist device results in receptor relocalization as well as increased beta-adrenergic receptor numbers: are these changes indications for outcome? J Card Surg. 2005;20(4):332–6.\nDipla K, Mattiello JA, Jeevanandam V, Houser SR, Margulies KB. Myocyte recovery after mechanical circulatory support in humans with end-stage heart failure. Circulation. 1998;97(23):2316–22.\nLyon AR, Nikolaev VO, Miragoli M, Sikkel MB, Paur H, Benard L, Hulot J-S, Kohlbrenner E, Hajjar RJ, Peters NS, Korchev YE, MacLeod KT, Harding SE, Gorelik J. Plasticity of surface structures and β2-adrenergic receptor localization in failing ventricular cardiomyocytes during recovery from heart failure. Circulation: Heart Failure. 2012 Mar. 28.\nBirks E, Hall J, Barton P, Grindle S, Latif N. Gene profiling changes in cytoskeletal proteins during clinical recovery after left ventricular–assist device support. Circulation. 2005.\nMargulies KB, Matiwala S, Cornejo C, Olsen H, Craven WA, Bednarik D. Mixed messages: transcription patterns in failing and recovering human myocardium. Circ Res. 2005;96(5):592–9.\nVatta M, Stetson SJ, Perez-Verdia A, Entman ML, Noon GP, Torre-Amione G, Bowles NE, Towbin JA. Molecular remodelling of dystrophin in patients with end-stage cardiomyopathies and reversal in patients on assistance-device therapy. Lancet. 2002;359(9310):936–41.\nLatif N, Yacoub MH, George R, Barton PJR, Birks EJ. Changes in sarcomeric and non-sarcomeric cytoskeletal proteins and focal adhesion molecules during clinical myocardial recovery after left ventricular assist device support. J Heart Lung Transplant. 2007;26(3):230–5.\nHall JL, Birks EJ, Grindle S, Cullen ME, Barton PJ, Rider JE, Lee S, Harwalker S, Mariash A, Adhikari N, Charles NJ, Felkin LE, Polster S, George RS, Miller LW, Yacoub MH. Molecular signature of recovery following combination left ventricular assist device (LVAD) support and pharmacologic therapy. Eur Heart J. 2007;28(5):613–27.\nde Jonge N, van Wichen DF, Schipper MEI, Lahpor JR, Gmelig-Meyling FHJ, Robles de Medina EO, de Weger RA. Left ventricular assist device in end-stage heart failure: persistence of structural myocyte damage after unloading. An immunohistochemical analysis of the contractile myofilaments. JACC. 2002;39(6):963–9.\nBartling B, Milting H, Schumann H, Darmer D, Arusoglu L, Koerner MM, El-Banayosy A, Koerfer R, Holtz J, Zerkowski H-R. Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation. 1999;100(90002):216–23.\nBaba HA, Grabellus F, August C, Plenz G, Takeda A, Tjan TD, SCHMID C, Deng MC. Reversal of metallothionein expression is different throughout the human myocardium after prolonged left-ventricular mechanical support. HEALUN. 2000;19(7):668–74.\nBergmann O, Bhardwaj RD, Bernard S, Zdunek S, Barnabe-Heider F, Walsh S, Zupicich J, Alkass K, Buchholz BA, Druid H, Jovinge S, Frisen J. Evidence for cardiomyocyte renewal in humans. Science. 2009;324(5923):98–102.\nWohlschlaeger J, Levkau B, Brockhoff G, Schmitz KJ, von Winterfeld M, Takeda A, Takeda N, Stypmann J, Vahlhaus C, Schmid C, Pomjanski N, Böcking A, Baba HA. Hemodynamic support by left ventricular assist devices reduces cardiomyocyte DNA content in the failing human heart. Circulation. 2010;121(8):989–96.\nSuzuki R, Li T-S, Mikamo A, Takahashi M, Ohshima M, Kubo M, Ito H, Hamano K. The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment. J Thorac Cardiovasc Surg. 2007;133(4):1051–8.\nPorrello ER, Mahmoud AI, Simpson E, Hill JA, Richardson JA, Olson EN, Sadek HA. Transient regenerative potential of the neonatal mouse heart. Science. 2011;331(6020):1078–80.\nJopling C, Sleep E, Raya M, Martí M, Raya A, Izpisúa Belmonte JC. Zebrafish heart regeneration occurs by cardiomyocyte dedifferentiation and proliferation. Nature. 2010;464(7288):606–9.\nKlotz S, Foronjy RF, Dickstein ML, Gu A, Garrelds IM, Danser AHJ, Oz MC, D'Armiento J, Burkhoff D. Mechanical unloading during left ventricular assist device support increases left ventricular collagen cross-linking and myocardial stiffness. Circulation. 2005;112(3):364–74.\nBruckner BA, Razeghi P, Stetson S, Thompson L, Lafuente J, Entman M, Loebe M, Noon G, Taegtmeyer H, Frazier OH, Youker K. Degree of cardiac fibrosis and hypertrophy at time of implantation predicts myocardial improvement during left ventricular assist device support. HEALUN. 2004;23(1):36–42.\nKlotz S, Jan Danser AH, Burkhoff D. Impact of left ventricular assist device (LVAD) support on the cardiac reverse remodeling process. Prog Biophys Mol Biol. 2008;97(2–3):479–96.\nBruggink AH, Van Oosterhout MFM, de Jonge N, Ivangh B, van Kuik J, Voorbij RHAM, Cleutjens JPM, Gmelig-Meyling FHJ, de Weger RA. Reverse remodeling of the myocardial extracellular matrix after prolonged left ventricular assist device support follows a biphasic pattern. J Heart Lung Transplant. 2006;25(9):1091–8.\nDrakos SG, Kfoury AG, Hammond EH, Reid BB, Revelo MP, Rasmusson BY, Whitehead KJ, Salama ME, Selzman CH, Stehlik J, Clayson SE, Bristow MR, Renlund DG, Li DY. Impact of mechanical unloading on microvasculature and associated central remodeling features of the failing human heart. J Am Coll Cardiol. 2010;56(5):382–91.\nSmith RS, Smith TJ, Blieden TM, Phipps RP. Fibroblasts as sentinel cells. Synthesis of chemokines and regulation of inflammation. Am J Pathol. 1997;151(2):317–22.\nAccornero F, van Berlo JH, Benard MJ, Lorenz JN, Carmeliet P, Molkentin JD. Placental growth factor regulates cardiac adaptation and hypertrophy through a paracrine mechanism. Circ Res. 2011;109(3):272–80.\nTakeda N, Manabe I, Uchino Y, Eguchi K, Matsumoto S, Nishimura S, Shindo T, Sano M, Otsu K, Snider P, Conway SJ, Nagai R. Cardiac fibroblasts are essential for the adaptive response of the murine heart to pressure overload. J Clin Invest. 2010;120(1):254–65.\nRuffell D, Mourkioti F, Gambardella A, Kirstetter P, Lopez RG, Rosenthal N, Nerlov C. A CREB-C\u002FEBPbeta cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair. Proc Natl Acad Sci U S A. 2009;106(41):17475–80.",{"VOID":596},"10.1007\u002Fs11886-012-0282-x","2024-06-23T00:31:01.894+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-012-0282-x",[600,617,632],{"id":601,"sortIndex":23,"researcher":22,"roles":602,"affiliations":603,"properties":612,"displayName":614,"givenName":22,"familyName":22},"26a6752a-713f-449c-b8b8-c09fb08158c2",[205],[604],{"id":605,"sortIndex":23,"affiliation":606,"properties":22},"98b35376-2aea-48a2-b95c-a54a8e627039",{"id":605,"createTime":22,"updateTime":22,"relativeEntities":607,"slug":22,"properties":608,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":611,"statistic":22},[],{"title":609},{"VI":610},"Harefield Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital, London, UK",[],{"title":613,"gsAuthor":615},{"VI":614},"Michael Ibrahim",{"VOID":616},"[\"T1e_59IAAAAJ\"]",{"id":618,"sortIndex":391,"researcher":22,"roles":619,"affiliations":620,"properties":627,"displayName":629,"givenName":22,"familyName":22},"e827c5fa-fe30-4cff-b59f-235ca24d08e2",[205],[621],{"id":605,"sortIndex":23,"affiliation":622,"properties":22},{"id":605,"createTime":22,"updateTime":22,"relativeEntities":623,"slug":22,"properties":624,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":626,"statistic":22},[],{"title":625},{"VI":610},[],{"title":628,"gsAuthor":630},{"VI":629},"Cesare Terracciano",{"VOID":631},"[\"sCVVMlMAAAAJ\"]",{"id":633,"sortIndex":634,"researcher":22,"roles":635,"affiliations":636,"properties":643,"displayName":645,"givenName":22,"familyName":22},"9669b810-6607-4103-a8f0-351dd28a9bf7",2,[205],[637],{"id":605,"sortIndex":23,"affiliation":638,"properties":22},{"id":605,"createTime":22,"updateTime":22,"relativeEntities":639,"slug":22,"properties":640,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":642,"statistic":22},[],{"title":641},{"VI":610},[],{"title":644},{"VI":645},"Magdi H. 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Real-time three-dimensional echocardiography expands the diagnostic capabilities of cardiac ultrasound in assessing the location, composition, size, and relationship to other structures of cardiac masses. The improved characterization of the anatomy of the mass, in conjunction with the accurate calculation of the left ventricular ejection fraction, makes this new technology the imaging modality of choice in assessing cardiac masses.",{"EN":710},"Added value of real-time three-dimensional echocardiography in assessing cardiac masses",{"VOID":712},"[\"16470953050872795749\"]",{"VOID":714},"Mor-Avi V, Sugeng L, Lang RM: Real-time 3-dimensional echocardiography: an integral component of the routine echocardiographic examination in adult patients? Circulation 2009, 119:314–329.\nEspinola-Zavaleta N, Morales GH, Vargas-Barron J, et al.: Three-dimensional transesophageal echocardiography in tumors of the heart. J Am Soc Echocardiogr 2002, 15:972–979.\nHung J, Lang R, Flachskampf F, et al.: 3D echocardiography: a review of the current status and future directions. J Am Soc Echocardiogr 2007, 20:213–233.\nPothineni KR, Nanda NC, Burri MV, et al.: Live\u002Freal time three-dimensional transthoracic echocardiographic description of chordoma metastatic to the heart. Echocardiography 2008, 25:440–442.\nSuwanjutah T, Singh H, Plaisance BR, et al.: Live\u002Freal time three-dimensional transthoracic echocardiographic findings in primary left atrial leiomyosarcoma. Echocardiography 2008, 25:337–339.\nSugeng L, Shernan SK, Salgo IS, et al.: Live 3-dimensional transesophageal echocardiography initial experience using the fully-sampled matrix array probe. J Am Coll Cardiol 2008, 52:446–449.\nPothineni KR, Nanda NC, Burri MV, et al.: Live\u002Freal time three-dimensional transthoracic echocardiographic visualization of Chiari network. Echocardiography 2007, 24:995–997.\nMcKay T, Thomas L: Prominent crista terminalis and Eustachian ridge in the right atrium: two dimensional (2D) and three dimensional (3D) imaging. Eur J Echocardiogr 2007, 8:288–291.\nRoldan FJ, Vargas-Barron J, Vazquez-Antona C, et al.: Three-dimensional transesophageal echocardiography of the atrial septal defects. Cardiovasc Ultrasound 2008, 6:38.\nAsch FM, Bieganski SP, Panza JA, Weissman NJ: Real-time 3-dimensional echocardiography evaluation of intracardiac masses. Echocardiography 2006, 23:218–224.\nNanda NC, Abd-El Rahman SM, Khatri G, et al.: Incremental value of three-dimensional echocardiography over transesophageal multiplane two-dimensional echocardiography in qualitative and quantitative assessment of cardiac masses and defects. Echocardiography 1995, 12:619–628.\nJacobs LD, Salgo IS, Goonewardena S, et al.: Rapid online quantification of left ventricular volume from real-time three-dimensional echocardiographic data. Eur Heart J 2006, 27:460–468.\nQin JX, Jones M, Shiota T, et al.: Validation of real-time three-dimensional echocardiography for quantifying left ventricular volumes in the presence of a left ventricular aneurysm: in vitro and in vivo studies. J Am Coll Cardiol 2000, 36:900–907.\nArai K, Hozumi T, Matsumura Y, et al.: Accuracy of measurement of left ventricular volume and ejection fraction by new real-time three-dimensional echocardiography in patients with wall motion abnormalities secondary to myocardial infarction. Am J Cardiol 2004, 94:552–558.\nJenkins C, Bricknell K, Hanekom L, Marwick TH: Reproducibility and accuracy of echocardiographic measurements of left ventricular parameters using real-time three-dimensional echocardiography. J Am Coll Cardiol 2004, 44:878–886.\nNikitin NP, Constantin C, Loh PH, et al.: New generation 3-dimensional echocardiography for left ventricular volumetric and functional measurements: comparison with cardiac magnetic resonance. Eur J Echocardiogr 2006, 7:365–372.\nTighe DA, Rosetti M, Vinch CS, et al.: Influence of image quality on the accuracy of real time three-dimensional echocardiography to measure left ventricular volumes in unselected patients: a comparison with gated-SPECT imaging. Echocardiography 2007, 24:1073–1080.\nCorsi C, Coon P, Goonewardena S, et al.: Quantification of regional left ventricular wall motion from real-time 3-dimensional echocardiography in patients with poor acoustic windows: effects of contrast enhancement tested against cardiac magnetic resonance. J Am Soc Echocardiogr 2006, 19:886–893.\nStewart JA, Silimperi D, Harris P, et al.: Echocardiographic documentation of vegetative lesions in infective endocarditis: clinical implications. Circulation 1980, 61:374–380.\nZamorano J, Cordeiro P, Sugeng L, et al.: Real-time threedimensional echocardiography for rheumatic mitral valve stenosis evaluation: an accurate and novel approach. J Am Coll Cardiol 2004, 43:2091–2096.\nZamorano J, Perez de Isla L, Sugeng L, et al.: Non-invasive assessment of mitral valve area during percutaneous balloon mitral valvuloplasty: role of real-time 3D echocardiography. Eur Heart J 2004, 25:2086–2091.\nMonaghan MJ: Role of real time 3D echocardiography in evaluating the left ventricle. Heart 2006, 92:131–136.\nMuller S, Feuchtner G, Bonatti J, et al.: Value of transesophageal 3D echocardiography as an adjunct to conventional 2D imaging in preoperative evaluation of cardiac masses. Echocardiography 2008, 25:624–631.\nHandke M, Schochlin A, Schafer DM, et al.: Myxoma of the mitral valve: diagnosis by 2-dimensional and 3-dimensional echocardiography. J Am Soc Echocardiogr 1999, 12:773–776.\nLe Tourneau T, Pouwels S, Gal B, et al.: Assessment of papillary fibroelastomas with live three-dimensional transthoracic echocardiography. Echocardiography 2008, 25:489–495.\nSingh A, Miller AP, Nanda NC, et al.: Papillary fibroelastoma of the pulmonary valve: assessment by live\u002Freal time three-dimensional transthoracic echocardiography. Echocardiography 2006, 23:880–883.",{"VOID":716},"10.1007\u002Fs11886-009-0029-5","2024-08-30T16:25:30.693+00:00","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11886-009-0029-5",[720],{"id":721,"sortIndex":23,"researcher":22,"roles":722,"affiliations":723,"properties":732,"displayName":734,"givenName":22,"familyName":22},"698b7611-b38e-47fa-b9c3-b3d9dfefbdb6",[205],[724],{"id":725,"sortIndex":23,"affiliation":726,"properties":22},"e1c48a05-0464-4974-b20a-18c14fd64320",{"id":725,"createTime":22,"updateTime":22,"relativeEntities":727,"slug":22,"properties":728,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":731,"statistic":22},[],{"title":729},{"VI":730},"Department of Cardiology, The University of Texas M.D. Anderson Cancer Center, Houston, USA",[],{"title":733},{"VI":734},"Juan Carlos Plana",{"url":718,"publisher":736,"properties":778},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":737,"slug":10,"properties":738,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":742,"manageAffiliations":747,"indexDatabases":758,"url":22,"thumbnailPath":22,"statistic":773,"gsStatistic":22,"type":173,"analyzePriority":22},[],{"issn":739,"title":740,"eissn":741},{"VOID":15},{"EN":17},{"VOID":13},[743],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":744,"label":745,"description":746,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},[748,753],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":749,"slug":22,"properties":750,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":752,"statistic":22},[],{"title":751},{"EN":37},[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":754,"slug":22,"properties":755,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":757,"statistic":22},[],{"title":756},{"EN":44},[],[759,766],{"id":48,"indexDatabase":760,"url":61,"indexYears":22,"academicFieldIds":765,"indexDatabaseRanking":22},{"id":50,"createTime":22,"updateTime":22,"relativeEntities":761,"label":762,"description":763,"key":57,"publicationTags":764,"standard":22},[],{"EN":53,"VI":53},{"EN":55,"VI":56},[59,60],[63],{"id":65,"indexDatabase":767,"url":76,"indexYears":77,"academicFieldIds":772,"indexDatabaseRanking":80},{"id":67,"createTime":22,"updateTime":22,"relativeEntities":768,"label":769,"description":770,"key":73,"publicationTags":771,"standard":22},[],{"EN":70,"VI":70},{"EN":70,"VI":72},[75],[79],{"impactFactor":23,"impactFactorByYear":774,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":775,"totalCitation":120,"totalCitationByYear":776,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":777,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},{"pages":779,"volume":781},{"VOID":780},"205-209",{"VOID":782},"11",{"total":23,"publishYear":784,"statisticByYear":785},2009,{},"2009-05-06","DONE_ANALYZE_CITATION",[80,59],{"id":790,"createTime":791,"updateTime":792,"relativeEntities":793,"slug":794,"properties":795,"entityType":194,"verifyStatus":195,"verifyTime":806,"verifyNote":197,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":807,"fullTextUrl":22,"authors":808,"publicationType":218,"publisherRelationship":872,"citationCount":920,"citationInfo":921,"publishDate":924,"publishYear":922,"citationAnalyzeStatus":21,"lastCitationAnalyze":792,"indexDatabases":925,"openAccess":22,"references":22,"isForceReanalyzing":270},"6997af49-cc5c-496b-80c1-a3de79ca9758","2024-02-07T05:20:23.472+00:00","2026-07-22T05:40:50.442+00:00",[],"Treatment-of-Bicuspid-Aortic-Valve-Stenosis-with-TAVR-Filling-Knowledge-Gaps-Towards-Reducing-Complications",{"abstract":796,"title":798,"gsPaper":800,"references":802,"doi":804},{"EN":797},"Bicuspid aortic valve (BAV) disease is the most common congenital heart defect worldwide. When severe, symptomatic aortic stenosis ensues, the treatment has increasingly become transcatheter aortic valve replacement (TAVR). The purpose of this review is to identify BAV classification and imaging methods, outline TAVR outcomes in BAV anatomy, and discuss how computational modeling can enhance TAVR treatment in BAV patients. TAVR use in BAV patients, when compared to use in tricuspid aortic valves, showed lower device success rate, and there remains no long-term randomized trial data. It has been reported that BAV patients with severe calcification increase the rate of complications. Additionally, the asymmetrical morphology of BAVs often results in asymmetric stent geometries which have implications for increased thrombosis risk and decreased durability. These adverse outcomes are currently very difficult to predict from routine pre-procedural imaging alone. Recently developed patient specific experimental and computational techniques have the potential to assist in filling knowledge gaps in the mechanisms of these complications and provide more information during preclinical planning for better TAVR selection in low surgical risk BAV patients. Efficacy of TAVR for irregular BAV anatomies remains concerning due to the lack of a long-term randomized trial data, their increased rate of short-term complications, and signs that long-term durability could be an issue. More knowledge on identifying which BAV anatomies are at greater risk for these adverse outcomes can potentially improve patient selection for TAVR versus SAVR in low surgical risk BAV patients.",{"EN":799},"Treatment of Bicuspid Aortic Valve Stenosis with TAVR: Filling Knowledge Gaps Towards Reducing Complications",{"VOID":801},"[\"157378840747146295\"]",{"VOID":803},"Siu SC, Silversides CK. Bicuspid aortic valve disease. J Am Coll Cardiol. 2010;55:2789–800.\nYutzey KE, Demer LL, Body SC, et al. Calcific aortic valve disease: a consensus summary from the Alliance of Investigators on Calcific Aortic Valve Disease. Arterioscler Thromb Vasc Biol. 2014;34:2387–93.\nVerma S, Siu SC. Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med. 2014;370:1920–9.\nDaubert MA, Weissman NJ, Hahn RT, et al. Long-term valve performance of TAVR and SAVR: a report from the PARTNER I trial. JACC Cardiovasc Imaging. 2017;10:15–25.\nAldalati O, Kaura A, Khan H, et al. Bioprosthetic structural valve deterioration: How do TAVR and SAVR prostheses compare? Int J Cardiol. 2018;268:170–5.\nSummers MR, Leon MB, Smith CR, et al. Prosthetic valve endocarditis after TAVR and SAVR: insights from the PARTNER trials. Circulation. 2019;140:1984–94.\nMack MJ, Leon MB, Thourani VH, et al. Transcatheter aortic-valve replacement with a balloon-expandable valve in low-risk patients. N Engl J Med. 2019;380:1695–705.\nPopma JJ, Deeb GM, Yakubov SJ, et al. Transcatheter aortic-valve replacement with a self-expanding valve in low-risk patients. N Engl J Med. 2019;380:1706–15.\nLeon MB, Mack MJ, Hahn RT, et al. Outcomes 2 years after transcatheter aortic valve replacement in patients at low surgical risk. J Am Coll Cardiol. 2021;77:1149–61.\nEDWARDS LIFESCIENCES, LLC. Approval for modifying the labeling to remove the precaution regarding patients with a congenital bicuspid aortic valve. 2020. https:\u002F\u002Fwww.accessdata.fda.gov\u002Fscripts\u002Fcdrh\u002Fcfdocs\u002Fcfpma\u002Fpma.cfm?id=P140031S107.\nMedtronic, Inc. Medtronic CoreValve Evolut R System, And Medtronic Evolut PRO+ System. Approval for modifying a precaution in the labeling regarding patients with a congenital bicuspid aortic valve. 2020. https:\u002F\u002Fwww.accessdata.fda.gov\u002Fscripts\u002Fcdrh\u002Fcfdocs\u002Fcfpma\u002Fpma.cfm?id=P130021S076.\nKim W-K, Liebetrau C, Fischer-Rasokat U, et al. Challenges of recognizing bicuspid aortic valve in elderly patients undergoing TAVR. Int J Cardiovasc Imaging. 2020;36:251–6.\nUeshima D, Fovino LN, Brener SJ, et al. Transcatheter aortic valve replacement for bicuspid aortic valve stenosis with first-and new-generation bioprostheses: a systematic review and meta-analysis. Int J Cardiol. 2020;298:76–82.\nSievers H-H, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg. 2007;133:1226–33.\nJilaihawi H, Chen M, Webb J, et al. A bicuspid aortic valve imaging classification for the TAVR era. JACC Cardiovasc Imaging. 2016;9:1145–1158 %@ 1936–878X.\nYang L-T, Boler A, Medina-Inojosa JR, et al. Aortic stenosis progression, cardiac damage, and survival: comparison between bicuspid and tricuspid aortic valves. JACC Cardiovasc Imaging %@ 1936–878X. 2021.\nOtto CM, Nishimura RA, Bonow RO, et al. 2020 ACC\u002FAHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology\u002FAmerican Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021;77:e25-e197 %@ 1558–3597.\nWijesinghe N, Ye J, Rodés-Cabau J, et al. Transcatheter aortic valve implantation in patients with bicuspid aortic valve stenosis. JACC Cardiovasc Interv. 2010;3:1122–5.\nPerlman GY, Blanke P, Dvir D, et al. Bicuspid aortic valve stenosis: favorable early outcomes with a next-generation transcatheter heart valve in a multicenter study. JACC Cardiovasc Interv. 2016;9:817–24.\nMylotte D, Lefevre T, Søndergaard L, et al. Transcatheter aortic valve replacement in bicuspid aortic valve disease. J Am Coll Cardiol. 2014;64:2330–9.\nYoon S-H, Bleiziffer S, De Backer O, et al. Outcomes in transcatheter aortic valve replacement for bicuspid versus tricuspid aortic valve stenosis. J Am Coll Cardiol. 2017;69:2579–89.\n•• Yoon S-H, Kim W-K, Dhoble A, et al. Bicuspid aortic valve morphology and outcomes after transcatheter aortic valve replacement. J Am Coll Cardiol. 2020;76:1018–1030 %@ 1558–3597. This study shows calcium amount and location effects TAVR outcomes in bicuspid aortic valve patients.\nTchetche D, de Biase C, van Gils L, et al. Bicuspid aortic valve anatomy and relationship with devices: the Bavard multicenter Registry: a European picture of contemporary multidetector computed tomography sizing for bicuspid valves. Circ Cardiovasc Interv. 2019;12:e007107 %@ 1941–7632.\nMangione FM, Jatene T, Gonçalves A, et al. Leaflet thrombosis in surgically explanted or post-mortem TAVR valves. JACC Cardiovasc Imaging. 2017;10:82–5.\nDe Backer O, Dangas GD, Jilaihawi H, et al. Reduced leaflet motion after transcatheter aortic-valve replacement. N Engl J Med. 2020;382:130–139 %@ 0028–4793.\nMakkar RR, Yoon S-H, Leon MB, et al. Association between transcatheter aortic valve replacement for bicuspid vs tricuspid aortic stenosis and mortality or stroke. JAMA. 2019;321:2193–2202 %@ 0098–7484.\nMakkar S-HY RR, Chakravarty T, Kapadia SR, Krishnaswamy A, Shah PB, Kaneko T, et al. Outcomes of transcatheter aortic valve replacement for bicuspid aortic valve stenosis in the low-surgical risk population. EuroPCR. 2021.\n• Vincent TJF, Denimal T, Shen M, Redfors B, Delhaye C, Simonato M, et al. Transcatheter Aortic Valve Replacement in Bicuspid Aortic Valve Stenosis. Circulation. 2021;143:1043–1061. This review of TAVR in BAV patients considers the need for a long term clinical trial and possible methods to better TAVR for BAV patient selection.\nHansson NC, Nørgaard BL, Barbanti M, et al. The impact of calcium volume and distribution in aortic root injury related to balloon-expandable transcatheter aortic valve replacement. J Cardiovasc Comput Tomogr. 2015;9:382–92.\nPasic M, Unbehaun A, Buz S, et al. Annular rupture during transcatheter aortic valve replacement: classification, pathophysiology, diagnostics, treatment approaches, and prevention. JACC Cardiovasc Interv. 2015;8:1–9.\nSivakumar SK, Hatoum H, O'Neil S, et al. Effect of pre-deployment valve positioning on annular stress during transcatheter aortic valve implantation. Conference presentation BMES 2019. 2019.\nAzadani AN, Chitsaz S, Matthews PB, et al. Comparison of mechanical properties of human ascending aorta and aortic sinuses. Ann Thorac Surg. 2012;93:87–94.\nKodali S, Pibarot P, Douglas PS, et al. Paravalvular regurgitation after transcatheter aortic valve replacement with the Edwards sapien valve in the PARTNER trial: characterizing patients and impact on outcomes. Eur Heart J. 2015;36:449–56.\nYeats B, Sivakumar SK, Polsani V, et al. Improving transcatheter aortic valve replacement outcomes in bicuspid aortic valves through a preoperative computational modeling. American College of Cardiology Conference. 2021.\nGénéreux P, Head SJ, Hahn R, et al. Paravalvular leak after transcatheter aortic valve replacement: the new Achilles’ heel? A comprehensive review of the literature. J Am Coll Cardiol. 2013;61:1125–36.\nMauri V, Deuschl F, Frohn T, et al. Predictors of paravalvular regurgitation and permanent pacemaker implantation after TAVR with a next-generation self-expanding device. Clin Res Cardiol. 2018;107:688–697 %@ 1861–0692.\nKhalique OK, Hahn RT, Gada H, et al. Quantity and location of aortic valve complex calcification predicts severity and location of paravalvular regurgitation and frequency of post-dilation after balloon-expandable transcatheter aortic valve replacement. JACC Cardiovasc Interv. 2014;7:885–894 %@ 1936–8798.\nDaneault B, Koss E, Hahn RT, et al. Efficacy and safety of postdilatation to reduce paravalvular regurgitation during balloon-expandable transcatheter aortic valve replacement. Circ Cardiovasc Interv. 2013;6:85–91 %@ 1941–7640.\nFonseca P, Figueiredo B, Almeida C, et al. Aortic valve calcium volume predicts paravalvular regurgitation and the need for balloon post-dilatation after transcatheter aortic valve implantation. J Interv Cardiol. 2016;29:117–123 %@ 0896–4327.\nWang Q, Kodali S, Primiano C, et al. Simulations of transcatheter aortic valve implantation: implications for aortic root rupture. Biomech Model Mechanobiol. 2015;14:29–38.\nBianchi M, Marom G, Ghosh RP, et al. Patient-specific simulation of transcatheter aortic valve replacement: impact of deployment options on paravalvular leakage. Biomech Model Mechanobiol. 2019;18:435–51.\nMao W, Wang Q, Kodali S, et al. Numerical parametric study of paravalvular leak following a transcatheter aortic valve deployment into a patient-specific aortic root. J Biomech Eng. 2018;140.\nLavon K, Marom G, Bianchi M, et al. Biomechanical modeling of transcatheter aortic valve replacement in a stenotic bicuspid aortic valve: deployments and paravalvular leakage. Med Biol Eng Comput. 2019;57:2129–43.\nDowling C, Bavo AM, El Faquir N, et al. Patient-specific computer simulation of transcatheter aortic valve replacement in bicuspid aortic valve morphology. Circ Cardiovasc Imaging. 2019;12:e009178.\nYanagisawa R, Hayashida K, Yamada Y, et al. Incidence, predictors, and mid-term outcomes of possible leaflet thrombosis after TAVR. JACC Cardiovasc Imaging. 2017;10:1–11.\nDe Marchena E, Mesa J, Pomenti S, et al. Thrombus formation following transcatheter aortic valve replacement. JACC Cardiovasc Interv. 2015;8:728–739 %@ 1936–8798.\nMakkar RR, Fontana G, Jilaihawi H, et al. Possible subclinical leaflet thrombosis in bioprosthetic aortic valves. N Engl J Med. 2015;373:2015–2024 %@ 0028–4793.\nMidha PA, Raghav V, Sharma R, et al. The fluid mechanics of transcatheter heart valve leaflet thrombosis in the neosinus. Circulation. 2017;136:1598–1609 %@ 0009–7322.\nVahidkhah K, Barakat M, Abbasi M, et al. Valve thrombosis following transcatheter aortic valve replacement: significance of blood stasis on the leaflets. Eur J Cardiothorac Surg. 2017;51:927–935 %@ 1010–7940.\nTrusty PM, Sadri V, Madukauwa-David ID, et al. Neosinus flow stasis correlates with thrombus volume post-TAVR: a patient-specific in vitro study. JACC Cardiovasc Interv. 2019;12:1288–1290 %@ 1936–8798.\nGunning PS, Vaughan TJ, McNamara LM. Simulation of self expanding transcatheter aortic valve in a realistic aortic root: implications of deployment geometry on leaflet deformation. Ann Biomed Eng. 2014;42:1989–2001 %@ 0090–6964.\nAbbasi M, Azadani AN. Leaflet stress and strain distributions following incomplete transcatheter aortic valve expansion. J Biomech. 2015;48:3663–3671 %@ 0021–9290.\nXuan Y, Dvir D, Wang Z, et al. Stent and leaflet stresses across generations of balloon-expandable transcatheter aortic valves. Interact Cardiovasc Thorac Surg. 2020;30:879–886 %@ 1569–9293.\nXuan Y, Dvir D, Wang Z, et al. Stent and leaflet stresses in 26-mm, third-generation, balloon-expandable transcatheter aortic valve. J Thorac Cardiovasc Surg. 2019;157:528–536 %@ 0022–5223.\nAlhafez BA, Ocazionez D, Sohrabi S, et al. Aortic arch tortuosity, a novel biomarker for thoracic aortic disease, is increased in adults with bicuspid aortic valve. Int J Cardiol. 2019;284:84–89 %@ 0167–5273.\nHachinohe D, Shitan H, Kaneko U, et al. Transfemoral transcatheter aortic valve implantation for bicuspid aortic stenosis with tortuous aorta after total arch replacement. Cardiovasc Interv Ther. 2020;1–2 %@ 1868–4297.\nHatoum JDH, Lilly SM, Crestanello JA, Dasi LP. Sinus hemodynamics variation with tilted transcatheter aortic valve deployments. Ann Biomed Eng. 2019;47:75–84.\nGunning PS, Saikrishnan N, McNamara LM, et al. An in vitro evaluation of the impact of eccentric deployment on transcatheter aortic valve hemodynamics. Ann Biomed Eng. 2014;42:1195–1206 %@ 0090–6964.\nKhodaee F, Barakat M, Abbasi M, et al. Incomplete expansion of transcatheter aortic valves is associated with propensity for valve thrombosis. Interact Cardiovasc Thorac Surg. 2020;30:39–46 %@ 1569–9285.\nMangels DR, Siki M, Menon R, et al. Hemodynamic effects of valve asymmetry in SAPIEN 3 transcatheter aortic valves. J Invasive Cardiol. 2018;30:138–43.\nFlemister DC, Hatoum H, Guhan V, et al. Effect of left and right coronary flow waveforms on aortic sinus hemodynamics and leaflet shear stress: correlation with calcification locations. Ann Biomed Eng. 2020;1–13.\nHeinrich RS, Fontaine AA, Grimes RY, et al. Experimental analysis of fluid mechanical energy losses in aortic valve stenosis: importance of pressure recovery. Ann Biomed Eng. 1996;24:685–694 %@ 1573–9686.\nYoon S-H, Kim W-K, Dhoble A, et al. Bicuspid aortic valve morphology and outcomes after transcatheter aortic valve replacement. J Am Coll Cardiol. 2020;76:1018–30.\nHatoum H, Lilly S, Maureira P, et al. The hemodynamics of transcatheter aortic valves in transcatheter aortic valves. J Thorac Cardiovasc Surg. 2019.\nQian Z, Wang K, Liu S, et al. Quantitative prediction of paravalvular leak in transcatheter aortic valve replacement based on tissue-mimicking 3D printing. JACC Cardiovasc Imaging. 2017;10:719–31.\nKohli K, Wei ZA, Yoganathan AP, et al. Transcatheter mitral valve planning and the neo-LVOT: utilization of virtual simulation models and 3D printing. Curr Treat Options Cardiovasc Med. 2018;20:1–14 %@ 1534–3189.\nReiff C, Zhingre Sanchez JD, Mattison LM, et al. 3-Dimensional printing to predict paravalvular regurgitation after transcatheter aortic valve replacement. Catheter Cardiovasc Interv. 2020.",{"VOID":805},"10.1007\u002Fs11886-021-01617-w","2024-05-12T17:31:49.431+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-021-01617-w",[809,826,841,856],{"id":810,"sortIndex":23,"researcher":22,"roles":811,"affiliations":812,"properties":821,"displayName":823,"givenName":22,"familyName":22},"620a5869-5ed2-4bde-aee2-11cb827416aa",[205],[813],{"id":814,"sortIndex":23,"affiliation":815,"properties":22},"df01664e-2e52-44f2-9a8c-c0224e114df5",{"id":814,"createTime":22,"updateTime":22,"relativeEntities":816,"slug":22,"properties":817,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":820,"statistic":22},[],{"title":818},{"VI":819},"Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, USA",[],{"title":822,"gsAuthor":824},{"VI":823},"Breandan B. Yeats",{"VOID":825},"[\"RxBwWFUAAAAJ\"]",{"id":827,"sortIndex":391,"researcher":22,"roles":828,"affiliations":829,"properties":838,"displayName":840,"givenName":22,"familyName":22},"bc88f808-98b4-4002-b32b-8da91c4ba5ee",[205],[830],{"id":831,"sortIndex":23,"affiliation":832,"properties":22},"c2f4e0ec-11d0-46f5-b835-ac90db9c2ea7",{"id":831,"createTime":22,"updateTime":22,"relativeEntities":833,"slug":22,"properties":834,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":837,"statistic":22},[],{"title":835},{"VI":836},"Department of Cardiology, Piedmont Heart Institute, Atlanta, USA",[],{"title":839},{"VI":840},"Pradeep K. Yadav",{"id":842,"sortIndex":634,"researcher":22,"roles":843,"affiliations":844,"properties":851,"displayName":853,"givenName":22,"familyName":22},"eff42bef-a15b-4e7c-b3df-9b486b36a9ca",[205],[845],{"id":814,"sortIndex":23,"affiliation":846,"properties":22},{"id":814,"createTime":22,"updateTime":22,"relativeEntities":847,"slug":22,"properties":848,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":850,"statistic":22},[],{"title":849},{"VI":819},[],{"title":852,"gsAuthor":854},{"VI":853},"Lakshmi P. Dasi",{"VOID":855},"[\"CC7aZdcAAAAJ\"]",{"id":857,"sortIndex":858,"researcher":22,"roles":859,"affiliations":860,"properties":869,"displayName":871,"givenName":22,"familyName":22},"b230548e-dac3-46dc-8d4a-64062fdda3b8",3,[205],[861],{"id":862,"sortIndex":23,"affiliation":863,"properties":22},"d159839f-c614-49ab-93f3-d7d0f1418b30",{"id":862,"createTime":22,"updateTime":22,"relativeEntities":864,"slug":22,"properties":865,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":868,"statistic":22},[],{"title":866},{"VI":867},"Department of Cardiovascular Surgery, Piedmont Heart Institute, Atlanta, USA",[],{"title":870},{"VI":871},"Vinod H. Thourani",{"url":807,"publisher":873,"properties":915},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":874,"slug":10,"properties":875,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":879,"manageAffiliations":884,"indexDatabases":895,"url":22,"thumbnailPath":22,"statistic":910,"gsStatistic":22,"type":173,"analyzePriority":22},[],{"issn":876,"title":877,"eissn":878},{"VOID":15},{"EN":17},{"VOID":13},[880],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":881,"label":882,"description":883,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},[885,890],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":886,"slug":22,"properties":887,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":889,"statistic":22},[],{"title":888},{"EN":37},[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":891,"slug":22,"properties":892,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":894,"statistic":22},[],{"title":893},{"EN":44},[],[896,903],{"id":48,"indexDatabase":897,"url":61,"indexYears":22,"academicFieldIds":902,"indexDatabaseRanking":22},{"id":50,"createTime":22,"updateTime":22,"relativeEntities":898,"label":899,"description":900,"key":57,"publicationTags":901,"standard":22},[],{"EN":53,"VI":53},{"EN":55,"VI":56},[59,60],[63],{"id":65,"indexDatabase":904,"url":76,"indexYears":77,"academicFieldIds":909,"indexDatabaseRanking":80},{"id":67,"createTime":22,"updateTime":22,"relativeEntities":905,"label":906,"description":907,"key":73,"publicationTags":908,"standard":22},[],{"EN":70,"VI":70},{"EN":70,"VI":72},[75],[79],{"impactFactor":23,"impactFactorByYear":911,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":912,"totalCitation":120,"totalCitationByYear":913,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":914,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},{"pages":916,"volume":918},{"VOID":917},"33-41",{"VOID":919},"24",16,{"total":920,"publishYear":922,"statisticByYear":923},2022,{"2022":634,"2023":858,"2024":858,"2025":634,"2026":391},"2022-01-31",[80,59],{"id":927,"createTime":928,"updateTime":929,"relativeEntities":930,"slug":931,"properties":932,"entityType":194,"verifyStatus":195,"verifyTime":943,"verifyNote":197,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":944,"fullTextUrl":22,"authors":945,"publicationType":218,"publisherRelationship":974,"citationCount":23,"citationInfo":1022,"publishDate":1025,"publishYear":1023,"citationAnalyzeStatus":787,"lastCitationAnalyze":1026,"indexDatabases":1027,"openAccess":22,"references":22,"isForceReanalyzing":270},"4d57113d-2e31-4238-8160-8dd9762f71ca","2023-12-26T00:25:37.888+00:00","2026-07-20T03:01:38.620+00:00",[],"Management-of-atrial-flutter",{"abstract":933,"title":935,"gsPaper":937,"references":939,"doi":941},{"EN":934},"Typical atrial flutter is a macroreentrant arrhythmia of the right atrium. The isthmus area between the tricuspid annulus, the inferior vena cava, and the ostium of the coronary sinus is a critical zone of the reentry circle. Atrial flutter has been treated with class I and III antiarrhytmic drugs to maintain sinus rhythm, with moderate success. Catheter ablation has been highly successful in treating atrial flutter. A contiguous line of bidirectional electrical block is created in the isthmus area between the tricuspid annulus and the inferior vena cava by application of radiofrequency energy. In patients with both atrial flutter and atrial fibrillation, ablation of the atrial flutter circuit may make the atrial fibrillation more easy to control. Quality of life assessments show improvement after ablation of atrial flutter. With a probability of success of 90%, a recurrence rate of 5% to 15%, and few complications, catheter ablation emerges as the best treatment of recurrent, symptomatic flutter.",{"EN":936},"Management of atrial flutter",{"VOID":938},"[\"223331616203633410\"]",{"VOID":940},"Jolly WA, Ritchie WJ: Auricular flutter and fibrillation. Heart 1911, 2:177–221.\nKall JG, Rubenstein D, Kopp D, et al.: Atypical atrial flutter originating in the right atrial free wall. Circulation 2000, 101:270–279.\nGomes JA, Santoni-Rugiu F, Mehta D, et al.: Uncommon atrial flutter: characteristics, mechanisms, and results of ablative therapy. PACE 1998, 21:2029–2042.\nOlgin JE, Kalman JM, Lesh MD: Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy. J Cardiovasc Electrophysiol 1996, 7:1112–1126.\nSchumacher B, Jung W, Schmidt H, et al.: Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation. J Am Coll Cardiol 1999, 34:363–373.\nArenal A, Almendral J, Alday JM, et al.: Rate-dependent conduction block of the crista terminalis in patients with typical atrial flutter: influence on evaluation of cavotricuspid isthmus conduction block. Circulation 1999, 99:2771–2778.\nRoithinger FX, Karch MR, Steiner PR, et al.: Relationship between atrial fibrillation and typical atrial flutter in humans: activation sequence changes during spontaneous conversion. Circulation 1997, 96:3484–3491.\nCosio FG, Lopez-Gil M, Goicolea A, et al.: Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993, 71:705–709.\nJosephson ME: Clinical Cardiac Electrophysiology: Tehniques and Interpretations, edn 2. Philadelphia: Lea & Febinger; 1993.\nWaki K, Saito T, Becker AE: Right atrial flutter isthmus revisited: Normal anatomy favors nonuniform anisotropic conduction. J Cardiovasc Electrophysiol 2000, 11:90–94.\nCabrera JA, Sanchez-Quintana D, Ho SY, et al.: Angiographic anatomy of the inferior right atrial isthmus in patients with and without history of common atrial flutter. Circulation 1999, 99:3017–3023. A study showing a larger TA-IVC isthmus and right atrium in patients with atrial flutter compared with a control population.\nAlboni P, Scarfo S, Fuca G, et al.: Atrial and ventricular pressures in atrial flutter. PACE 1999, 22:600–604.\nBenditt DG, Williams JH, Jin J, et al.: Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and\u002For atrial flutter. d,l-Sotalol Atrial Fibrillation\u002FFlutter Study Group. Am J Cardiol 1999, 84:270–277.\nBenditt DG, Williams JH: Oral d,l-sotalol in atrial fibrillation and\u002For flutter. Am J Cardiol 2000, 85:132–133.\nChun SH, Sager PT, Stevenson WG, et al.: Long-term efficacy of amiodarone for the maintenance of normal sinus rhythm in patients with refractory atrial fibrillation or flutter. Am J Cardiol 1995, 76:47–50.\nNaccarelli GV, Dorian P, Hohnloser SH, Coumel P: Prospective comparison of flecainide versus quinidine for the treatment of paroxysmal atrial fibrillation\u002Fflutter. The Flecainide Multicenter Atrial Fibrillation Study Group. Am J Cardiol 1996, 77:53A-59A.\nAliot E, Denjoy I: Comparison of the safety and efficacy of flecainide versus propafenone in hospital out-patients with symptomatic paroxysmal atrial\u002Fflutter. Am J Cardiol 1996, 77:66A-71A.\nFeld GK, Fleck RP, Chen PS, et al.: Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques see comments]. Circulation 1992, 86:1233–1240.\nFischer B, Haissaguerre M, Garrigues S, et al.: Radiofrequency catheter ablation of common atrial flutter in 80 patients. J Am Coll Cardiol 1995, 25:1365–1372.\nKirkorian G, Moncada E, Chevalier P, et al.: Radiofrequency ablation of atrial flutter. Efficacy of an anatomically guided approach. Circulation 1994, 90:2804–2814.\nWen ZC, Chen SA, Tai CT, et al.: Temperature monitoring in radiofrequency catheter ablation of atrial flutter using the linear ablation technique. J Cardiovasc Electrophysiol 1996, 7:1050–1057.\nChen SA, Chiang CE, Wu TJ, et al.: Radiofrequency catheter ablation of common atrial flutter: Comparison of electrophysiologically guided focal ablation technique and linear ablation technique. J Am Coll Cardiol 1996, 27:860–868.\nNakagawa H, Lazzara R, Khastgir T, et al.: Role of the tricuspid annulus and the Eustachian valve\u002Fridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success. Circulation 1996, 94:407–424.\nPoty H, Saoudi N, Abdel Aziz A, et al.: Radiofrequency catheter ablation of type 1 atrial flutter. Prediction of late success by electrophysiological criteria. Circulation 1995, 92:1389–1392.\nCauchemez B, Haissaguerre M, Fischer B, et al.: Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation 1996, 93:284–294.\nIesaka Y, Takahashi A, Goya M, et al.: High energy radiofrequency catheter ablation for common atrial flutter targeting the isthmus between the inferior vena cava and tricuspid valve annulus using a super long tip electrode. PACE 1998, 21:401–409.\nTsai CF, Tai CT, Yu WC, et al.: Is 8-mm more effective than 4-mm tip electrode catheter for ablation of typical atrial flutter? Circulation.1999, 100:768–771. A study showing that the 8-mm tip ablation catheter achieves a higher succes rate than the 4-mm tip catheter.\nJais P, Haissaguerre M, Shah DC, et al.: Successful irrigated-tip catheter ablation of atrial flutter resistant to conventional radiofrequency ablation. Circulation 1998, 98:835–838.\nSchumacher B, Pfeiffer D, Tebbenjohanns J, et al.: Acute and long-term effects of consecutive radiofrequency applications on conduction properties of the subeustachian isthmus in type I atrial flutter. J Cardiovasc Electrophysiol 1998, 9:152–163. This paper shows that bidirectional isthmus conduction block predicts lower recurrence rate than termination and non-inducibility of atrial flutter.\nNabar A, Rodriguez LM, Timmermans C, et al.: Isoproterenol to evaluate resumption of conduction after right atrial isthmus ablation in type I atrial flutter. Circulation 1999, 99:3286–3291.\nShah DC, Haissaguerre M, Jais P, et al.: Simplified electrophysiologically directed catheter ablation of recurrent common atrial flutter. Circulation 1997, 96:2505–2508.\nChen J, De Chillou C, Basiouny T, et al.: Cavotricuspid isthmus mapping to assess bidirectional block during common atrial flutter radiofrequency ablation. Circulation 1999, 100:2507–2513. [This study shows that reversal of the atrial depolarization up to the line of block is a mandatory criteria of successful atrial flutter ablation.\nNakagawa H, Jackman WM: Use of a three-dimensional, nonfluoroscopic mapping system for catheter ablation of typical atrial flutter. PACE 1998, 21:1279–1286.\nPaydak H, Kall JG, Burke MC, et al.: Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course. Circulation 1998, 98:315–322.\nPhilippon F, Plumb VJ, Epstein AE, Kay GN: The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter. Circulation 1995, 92:430–435.\nNabar A, Rodriguez LM, Timmermans C, et al.: Effect of right atrial isthmus ablation on the occurrence of atrial fibrillation: observations in four patient groups having type I atrial flutter with or without associated atrial fibrillation. Circulation 1999, 99:1441–1445. This paper shows that TA-IVC isthmus ablation reduces recurrences of atrial fibrillation in patients with typical atrial flutter as the predominant clinical arrhythmia.\nAnselme F, Saoudi N, Poty H, et al.: Radiofrequency catheter ablation of common atrial flutter: significance of palpitations and quality-of-life evaluation in patients with proven isthmus block. Circulation 1999, 99:534–540. A study showing improvement in functional status after successful catheter ablation of typical atrial flutter.\nNabar A, Rodriguez LM, Timmermans C, et al.: Radiofrequency ablation of “class IC atrial flutter” in patients with resistant atrial fibrillation. Am J Cardiol 1999, 83:785–787.\nSchumacher B, Jung W, Lewalter T, et al.: Radiofrequency ablation of atrial flutter due to administration of class IC antiarrhythmic drugs for atrial fibrillation. Am J Cardiol 1999, 83:710–713.\nTai CT, Chiang CE, Lee SH, et al.: Persistent atrial flutter in patients treated for atrial fibrillation with amiodarone and propafenone: electrophysiologic characteristics, radiofrequency catheter ablation, and risk prediction. J Cardiovasc Electrophysiol 1999, 10:1180–1187.\nLee SH, Tai CT, Yu WC, et al.: Effects of radiofrequency catheter ablation on quality of life in patients with atrial flutter. Am J Cardiol 1999, 84:278–283.\nBathina MN, Mickelsen S, Brooks C, et al.: Radiofrequency catheter ablation versus medical therapy for initial treatment of supraventricular tachycardia and its impact on quality of life and healthcare costs. Am J Cardiol 1998, 82:589–593.\nLuchsinger JA, Steinberg JS: Resolution of cardiomyopathy after ablation of atrial flutter. J Am Coll Cardiol 1998, 32:205–210.",{"VOID":942},"10.1007\u002Fs11886-000-0087-1","2024-06-26T09:05:06.809+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-000-0087-1",[946,961],{"id":947,"sortIndex":23,"researcher":22,"roles":948,"affiliations":949,"properties":958,"displayName":960,"givenName":22,"familyName":22},"8811e25d-988a-4288-9efc-b7111e4b5992",[205],[950],{"id":951,"sortIndex":23,"affiliation":952,"properties":22},"b7571a29-1525-4fd6-adbf-e572ac616003",{"id":951,"createTime":22,"updateTime":22,"relativeEntities":953,"slug":22,"properties":954,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":957,"statistic":22},[],{"title":955},{"VI":956},"Department of Cardiology, Rikshospitalet, University Hospital of Oslo, Oslo, Norway",[],{"title":959},{"VI":960},"Erik Kongsgaard",{"id":962,"sortIndex":391,"researcher":22,"roles":963,"affiliations":964,"properties":971,"displayName":973,"givenName":22,"familyName":22},"0d76b562-c679-4f0f-bac4-47d8638c12c6",[205],[965],{"id":951,"sortIndex":23,"affiliation":966,"properties":22},{"id":951,"createTime":22,"updateTime":22,"relativeEntities":967,"slug":22,"properties":968,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":970,"statistic":22},[],{"title":969},{"VI":956},[],{"title":972},{"VI":973},"Halfdan 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studies have highlighted that dyspneic patients comprise a high-risk subgroup of patients referred for cardiac stress testing. Even after adjusting for the presence and degree of coronary artery disease the risk of cardiac and all-cause mortality is at least three- to fivefold higher in dyspneic patients compared to asymptomatic or those with chest pain. Stress echocardiography is uniquely positioned to characterize all potential cardiovascular etiologies of dyspnea from global and regional systolic dysfunction, myocardial ischemia to valvular heart disease, pulmonary hypertension and diastolic dysfunction. Various data point to diastolic dysfunction and associated heart failure as the major potential etiology for dyspnea as well as the likely cause of the heightened mortality risk. Doppler echocardiography at rest and with stress can now characterize the hemodynamics of diastolic dysfunction and close the loop on the comprehensive assessment of the patient who has exertional shortness of breath. This review discusses the role of the Doppler echocardiographic diastolic stress test in the evaluation of patients with cardiac dyspnea.",{"EN":1038},"Diastolic Stress Test for the Evaluation of Exertional Dyspnea",{"VOID":1040},"[\"4276360243784592352\"]",{"VOID":1042},"Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary-artery disease. N Engl J Med. 1979;300:1350–8.\nJones RC, Francis GS, Lauer MS. Predictors of mortality in patients with heart failure and preserved systolic function in the Digitalis Investigation Group trial. J Am Coll Cardiol. 2004;44(5):1025–9.\nGibbons RJ, Balady GJ, Bricker JT, et al. ACC\u002FAHA 2002 guideline update for exercise testing: summary article A report of the American College of Cardiology\u002FAmerican Heart Association task force on practice guidelines (committee to update the 1997 exercise testing guidelines). J Am Coll Cardiol. 2002;40:1531–40.\nAbidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I, Friedman JD, Germano G, Berman DS. Prognostic significance of dyspnea in patients referred for cardiac stress testing. N Engl J Med. 2005;353(18):1889–98.\nSenni M, Tribouilloy CM, Rodeheffer RJ, Jacobsen SJ, Evans JM, Bailey KR, Redfield MM. Congestive heart failure in the community: a study of all incident cases in Olmsted County, Minnesota, in 1991. Circulation. 1998;98:2282–9.\nOwan TE, Hodge DO, Herges RM, et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006;355:251–9.\nRedfield MM, Jacobsen SJ, Burnett Jr JC, et al. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289(2):194–202.\n•• Kane GC, Karon BL, Mahoney DW, Kane GC, Karon BL, Mahoney DW, et al. Progression of left ventricular diastolic dysfunction and risk of heart failure. JAMA. 2011;306(8):856–63. This is the first large study to demonstrate the association of the presence or progression of diastolic dysfunction in community subjects with the risk of future heart failure.\nWann LS, Faris JV, Childress RH, Dillon J, Weymann AE, Feigenbaum H. Exercise cross-sectional echocardiography in ischemic heart disease. Circulation. 1979;60:1300–8.\nOh JK, Appleton CP, Hatle LK, et al. The noninvasive assessment of left ventricular diastolic function with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 1997;10:246–70.\nOh J. Echocardiography as a noninvasive Swan-Ganz catheter. Circulation. 2005;111:3192–4.\nOh J, Hatle L, Tajik A, Little W. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol. 2006;47:500–6.\n• Ha JW, Choi D, Park S, et al. Left ventricular diastolic functional reserve during exercise in patients with impaired myocardial relaxation at rest. Heart. 2009;95:399–404. This is an important study addressing the significance of changes of myocardial tissue velocity with stress.\nNagueh S, Middleton K, Kopelen H, Zoghbi W, Quinones M. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;30:1527–33.\n•• Oh JK, Park SJ, Nagueh SF. Established and novel clinical applications of diastolic function assessment by echocardiography. Circ Cardiovasc Imaging. 2011;4:444–55. This is a review highlighting current, emerging, and future applications in the assessment of diastolic function.\nNagueh S, Mikari I, Kopelen H, Middleton K, Quinones M, Zoghbi W. Doppler estimation of left ventricular filling pressure in sinus tachycardia. A new application of tissue Doppler imaging. Circulation. 1998;98:1644–50.\nSohn D, Song J, Zo J, Chai I, Kim H, Chun H, Kim H. Mitral annulus velocity in the evaluation of left ventricular diastolic function in atrial fibrillation. J Am Soc Echocardiogr. 1999;12:927–31.\nOmmen S, Nishimura R, Appleton C, Miller Jr F, Oh J, Redfield M, Tajik A. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures. Circulation. 2000;102:1788–94.\n•• Grewal J, McCully RB, Kane GC, et al. Left ventricular function and exercise capacity. JAMA. 2009;301(3):286–94. Shows a notable association of abnormalities in diastolic function with impairment in exercise capacity in a large cohort of patients without ischemia.\nOtto MEB, Pereira MM, Beck AL, Milani M. Correlation between diastolic function and maximal exercise capacity on exercise test. Arq Bras Cardiol. 2011;96(2):107–13.\nHa JW, Lulic F, Bailey KR, et al. Effects of treadmill exercise on mitral inflow and annular velocities in healthy adults. Am J Cardiol. 2003;91(1):114–5.\n•• Holland D, Prasad S, Marwick T. Prognostic implications of left ventricular filling pressure with exercise. Circ Cardiovasc Imaging. 2010;3:149–56. This is a seminal study demonstrating the prognostic value of the E\u002Fe′ ratio with exercise, which is incremental over clinical data and the degree of myocardial ischemia.\nKane GC, Ammash NM, Villarraga HR, Behrenbeck T, Oh JK, McGoon MD, Pellikka PA, McCully RB. Exercise changes in pulmonary artery systolic pressure: normative values from a prospective evaluation of 457 Subjects. Am J Respir Crit Care Med. 2009;179:A4129.\nHa JW, Choi D, Park S, et al. Determinants of exercise-induced pulmonary hypertension in patients with normal left ventricular ejection fraction. Heart. 2009;95:490–4.\nShim CY, Kin SA, Coi D, et al. Clinical outcomes of exercise-induced pulmonary hypertension in subjects with preserved left ventricular ejection fraction: implication of an increase in left ventricular filling pressure during exercise. Heart. 2011;97:1417–24.\nHa JW, Oh JK, Pellikka PA, et al. Diastolic stress echocardiography: a novel noninvasive diagnositic test for diastolic dysfunction using supine bicycle exercise Doppler echocardiography. J Am Soc Echocardiogr. 2005;18:63–8.\nTalreja DR, Nishimura RA, Oh JK. Estimation of left ventricular filling pressure with exercise by Doppler echocardiography in patients with normal systolic function: a simultaneous echocardiographic-cardiac catheterization study. J Am Soc Echocardiogr. 2007;20(5):477–9.\nBurgess MI, Jenkins C, Sharman JE, Marwick TH. Diastolic stress echocardiography: hemodynamic validation and clinical significance of estimation of ventricular filling pressure with exercise. J Am Coll Cardiol. 2006;47:1891–900.\nHatle L. How to diagnose diastolic heart failure: a consensus statement. Eur Heart J. 2007;28:2421–3.\nHolland DJ, Prasad SB, Marwick TH. Contribution of exercise echocardiography to the diagnosis of heart failure with preserved ejection fraction (HFpEF). Heart. 2010;96(13):1024–8.\nDokainish H, Nguyen JS, Sengupta R, et al. Do additional echocardiographic variables increase the accuracy of E\u002Fe′ for predicting left ventricular filling pressure in normal ejection fraction? An echocardiographic and invasive hemodynamic study. J Am Soc Echocardiogr. 2010;23:156–61.\nDokainish H, Nguyen JS, Bobeck J, et al. Assessment of the American society of echocardiography-European association of echocardiography guidelines for diastolic function in patients with depressed ejection fraction: an echocardiographic and invasive haemodynamic study. Eur J Echocardiogr. 2011;12:857–64.\nDevereux RB, Wachtell K, Gerdts E, et al. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA. 2004;292:2350–6.\n• Lam CS, Borlaug BA, Kane GC, Enders FT, Rodeheffer RJ, Redfield MM. Age-associated increases in pulmonary artery systolic pressure in the general population. Circulation. 2009;119(20):2663–70. Shows the prognostic implications of elevated pulmonary artery pressure by echocardiography in a community population.\nLam CS, Grewal J, Borlaug BA, et al. Size, shape and stamina. The impact of left ventricular geometry on exercise capacity. Hypertension. 2010;55:1143–9.\nTsang TS, Barnes ME, Gersh BJ, et al. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol. 2002;90(12):1284–9.\nMcCully RB, Roger VL, Mahoney DW, Karon BL, Oh JK, Miller Jr FA, Seward JB, Pellikka PA. Outcome after normal exercise echocardiography and predictors of subsequent cardiac events: follow-up of 1,325 patients. J Am Coll Cardiol. 1998;31(1):144–9.\nMyers J, Prakash M, Froelicher V, et al. Exercise capacity and mortality among men referred for exercise testing. N Engl J Med. 2002;346:793–801.\nKane GC, Hepinstall MJ, Kidd GM, Kuehl CA, Murphy AT, Nelson JM, Schneider L, Stussy VL, Warmsbecker JA, Miller Jr FA, Pellikka PA, McCully RB. Safety of stress echocardiography supervised by registered nurses: results of a 2-year audit of 15,404 patients. J Am Soc Echocardiogr. 2008;21(4):337–41.",{"VOID":1044},"10.1007\u002Fs11886-012-0269-7","2024-06-23T05:31:26.431+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11886-012-0269-7",[1048,1063],{"id":1049,"sortIndex":23,"researcher":22,"roles":1050,"affiliations":1051,"properties":1060,"displayName":1062,"givenName":22,"familyName":22},"6dccedce-0a6c-458e-a8a4-da78983d92ad",[205],[1052],{"id":1053,"sortIndex":23,"affiliation":1054,"properties":22},"29905476-5b17-4221-a885-f02095aad3d9",{"id":1053,"createTime":22,"updateTime":22,"relativeEntities":1055,"slug":22,"properties":1056,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":1059,"statistic":22},[],{"title":1057},{"VI":1058},"Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, USA",[],{"title":1061},{"VI":1062},"Garvan C. Kane",{"id":1064,"sortIndex":391,"researcher":22,"roles":1065,"affiliations":1066,"properties":1073,"displayName":1075,"givenName":22,"familyName":22},"80ba958f-eb5d-4e5a-90dd-39e1121f0cc8",[205],[1067],{"id":1053,"sortIndex":23,"affiliation":1068,"properties":22},{"id":1053,"createTime":22,"updateTime":22,"relativeEntities":1069,"slug":22,"properties":1070,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":1072,"statistic":22},[],{"title":1071},{"VI":1058},[],{"title":1074,"gsAuthor":1076},{"VI":1075},"Jae K. Oh",{"VOID":1077},"[\"iHEZPO8AAAAJ\"]",{"url":1046,"publisher":1079,"properties":1121},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1080,"slug":10,"properties":1081,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":1085,"manageAffiliations":1090,"indexDatabases":1101,"url":22,"thumbnailPath":22,"statistic":1116,"gsStatistic":22,"type":173,"analyzePriority":22},[],{"issn":1082,"title":1083,"eissn":1084},{"VOID":15},{"EN":17},{"VOID":13},[1086],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":1087,"label":1088,"description":1089,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},[1091,1096],{"id":33,"createTime":22,"updateTime":22,"relativeEntities":1092,"slug":22,"properties":1093,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":1095,"statistic":22},[],{"title":1094},{"EN":37},[],{"id":40,"createTime":22,"updateTime":22,"relativeEntities":1097,"slug":22,"properties":1098,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":1100,"statistic":22},[],{"title":1099},{"EN":44},[],[1102,1109],{"id":48,"indexDatabase":1103,"url":61,"indexYears":22,"academicFieldIds":1108,"indexDatabaseRanking":22},{"id":50,"createTime":22,"updateTime":22,"relativeEntities":1104,"label":1105,"description":1106,"key":57,"publicationTags":1107,"standard":22},[],{"EN":53,"VI":53},{"EN":55,"VI":56},[59,60],[63],{"id":65,"indexDatabase":1110,"url":76,"indexYears":77,"academicFieldIds":1115,"indexDatabaseRanking":80},{"id":67,"createTime":22,"updateTime":22,"relativeEntities":1111,"label":1112,"description":1113,"key":73,"publicationTags":1114,"standard":22},[],{"EN":70,"VI":70},{"EN":70,"VI":72},[75],[79],{"impactFactor":23,"impactFactorByYear":1117,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":1118,"totalCitation":120,"totalCitationByYear":1119,"totalCitationPerPublication":146,"totalCitationPerPublicationByYear":1120,"hindexLast5Year":172,"hindex":172},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"1999":99,"2000":100,"2001":101,"2002":102,"2003":101,"2004":103,"2005":104,"2006":105,"2007":106,"2008":104,"2009":107,"2010":108,"2011":108,"2012":103,"2013":109,"2014":110,"2015":111,"2016":112,"2017":113,"2018":114,"2019":115,"2020":116,"2021":117,"2022":118,"2023":116,"2024":119},{"1999":122,"2000":123,"2001":124,"2002":125,"2003":126,"2004":127,"2005":128,"2006":129,"2007":130,"2008":131,"2009":132,"2010":133,"2011":105,"2012":134,"2013":135,"2014":136,"2015":137,"2016":138,"2017":139,"2018":140,"2019":141,"2020":142,"2021":143,"2022":144,"2023":145},{"1999":148,"2000":149,"2001":150,"2002":151,"2003":152,"2004":153,"2005":154,"2006":155,"2007":156,"2008":157,"2009":158,"2010":159,"2011":160,"2012":161,"2013":162,"2014":163,"2015":164,"2016":165,"2017":166,"2018":167,"2019":168,"2020":169,"2021":170,"2022":171,"2023":83},{"pages":1122,"volume":1124},{"VOID":1123},"359-365",{"VOID":693},21,{"total":1125,"publishYear":695,"statisticByYear":1127},{"2013":391,"2014":858,"2015":634,"2016":634,"2017":634,"2018":634,"2019":858,"2021":391,"2022":634,"2024":634,"2025":391},"2012-05-03",[80,59],{"id":1131,"createTime":1132,"updateTime":1133,"relativeEntities":1134,"slug":1135,"properties":1136,"entityType":194,"verifyStatus":195,"verifyTime":1147,"verifyNote":197,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":1148,"fullTextUrl":22,"authors":1149,"publicationType":218,"publisherRelationship":1178,"citationCount":576,"citationInfo":1226,"publishDate":1229,"publishYear":1227,"citationAnalyzeStatus":787,"lastCitationAnalyze":1230,"indexDatabases":1231,"openAccess":22,"references":22,"isForceReanalyzing":270},"2cc8d1a8-ba90-4654-8160-cafcece059c8","2024-02-16T08:02:13.049+00:00","2026-07-19T19:00:45.845+00:00",[],"Calcific-aortic-stenosis-New-pathophysiologic-insights-and-possible-new-medical-therapy",{"abstract":1137,"title":1139,"gsPaper":1141,"references":1143,"doi":1145},{"EN":1138},"Aortic stenosis is a progressive disease of aging with serious complications. A common disease of the elderly, it may inexorably progress to stenosis. Recent retrospective studies have correlated risk factors commonly associated with coronary and vascular atherosclerosis with an accelerated rate of aortic valve stenosis. Although hydroxymethyl glutaryl co-enzyme A reductase inhibitor (statin) treatment therapy has been shown to delay the rate of progression of valvular aortic stenosis, the salutary mechanism of the statin may be cholesterol-lowering and\u002For anti-inflammatory. Further prospective studies are warranted to investigate the mechanism and medical therapy of aortic sclerosis and stenosis.",{"EN":1140},"Calcific aortic stenosis: New pathophysiologic insights and possible new medical therapy",{"VOID":1142},"[\"18338667643831414611\"]",{"VOID":1144},"Carabello BA: Aortic stenosis. N Engl J Med 2002, 346:677–681. A succinct review with clinical algorithm.\nSchoen FJ: Evaluation of natural and prosthetic heart valves. In Cardiovascular Pathology. Edited by Virmani R, Atkinson JB, Fenoglio JJ. Philadelphia: WB Saunders; 1991:399–418.\nRoss J Jr, Braunwald E: Aortic stenosis. Circulation 1968, 38(Suppl V):V61-V67. A classic natural history paper of patients with aortic stenosis.\nPellikka PA, Nishimura RA, Bailey KR, Tajik AJ: The natural history of adults with asymptomatic, hemodynamically significant aortic stenosis. J Am Coll Cardiol 1990, 15:1012–1017.\nConnolly HM, Bakman KV, Roger V, Tajik J: Aortic stenosis: no more hemodynamic cardiac catheterization [letter]. Mayo Clin Proc 2001, 76:961.\nAmerican College of Cardiology\u002FAmerican Heart Association Guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology\u002FAmerican Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 1998, 32:1486–1588. Pronouncement of standard of care for valvular heart disease.\nOtto CM, Burwash IG, Legget ME, et al.: Prospective study of asymptomatic valvular aortic stenosis. Circulation 1997, 95:2262–2270. Describes the natural history of patients with aortic stenosis determined by baseline Doppler gradient.\nNassimiha D, Aronow WS, Ahn C, Goldman ME: Rate of progression of valvular aortic stenosis in patients > 60 years of age. Am J Cardiol 2001, 87:807–809.\nOtto CM, Lind BK, Kitzman DW, et al.: Association of aorticvalve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999, 341:142–147. Aortic stenosis is not necessarily a benign finding\nUS Bureau of the Census, Population Division: Summary of Reportable Diseases and Conditions. 2001, 20:2–3.\nLarkin M: Robert Butler: championing a healthy view of aging. Lancet 2001, 357:48.\nStewart BF, Siscovick D, Lind B, et al.: Clinical factors associated with calcific aortic valve disease. J Am Coll Cardiol 1997, 29:630–634.\nAronow WS, Schwartz KS, Koenigsberg M: Correlation of serum lipids, calcium, and phosphorous diabetes and history of hypertension with presence or absence of calcified or thickened aortic cusps or root in elderly patients. Am J Cardiol 1987, 59:998–999.\nAronow WS, Ahn C, Kronzen I, Goldman ME: Association of coronary risk factors and usual statins with progression of mild valvular aortic stenosis in older persons. Am J Cardiol 2001, 88:693–695. A retrospective study demonstrating the benefit of statins to slow the rate of progression of aortic stenosis.\nPalta S, Pai AM, Gill KS, Pai RG: New insights into the progression of aortic stenosis: implications for secondary prevention. Circulation 2000, 101:2497–2502.\nPohle K, Maffert R, Ropers D, et al.: Progression of aortic valve calcification: association with coronary atherosclerosis and cardiovascular risk factors. 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Lancet 2000, 356:524–525.\nRidker PM, Rifai N, Rose L, et al.: Comparison of C-reactive protein and low density lipoprotein cholesterol levels in the predictors of first cardiovascular events. New Engl J Med 2002, 347:1557–1565. C-reactive protein is a marker of vascular inflammation that when elevated may be an ominous marker of future cardiovascular events.\nGalante A, Pietriusti A, Vellini M, et al.: C-reactive protein is increased in patients with degenerative aortic valvular stenosis. J Am Coll Cardiol 2001, 38:1078–1082.\nWilklund O, Mattsson-Hulten L, Hurt-Camejo E, Oscarsson J: Effects of simvastatin and atorvastatin on inflammation markers in plasma. J Intern Med 2002, 251:338–347.\nBudoff MJ, Lane KL, Bakhsheshi H, et al.: Rates of progression of coronary calcium by electron beam tomography. Am J Cardiol 2000, 86:8–11.\nSharelle DM, Takasu J, Budoff MJ, et al.: HMG CoA reductase inhibitor (statin) and aortic valve calcium. 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