{"title":"梗死后早期室性心律失常基质的演变:猪缺血再灌注模型的启示","authors":"","doi":"10.1016/j.jacep.2024.06.016","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>The evolution of myocardial scar and its arrhythmogenic potential postinfarct is incompletely understood.</div></div><div><h3>Objectives</h3><div>This study sought to investigate scar and border zone (BZ) channels evolution in an animal ischemia-reperfusion injury model using late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).</div></div><div><h3>Methods</h3><div>Five swine underwent 90-minute balloon occlusion of the mid-left anterior descending artery, followed by LGE-CMR at day (d) 3, d30, and d58 postinfarct. Invasive electroanatomic mapping (EAM) was performed at 2 months. Topographical reconstructions of LGE-CMR were analyzed for left ventricular core and BZ scar, BZ channel geometry, and complexity, including transmurality, orientation, and number of entrances/exits.</div></div><div><h3>Results</h3><div>LVEF reduced from 48.0% ± 1.8% to 41.3% ± 2.3% postinfarct. Total scar mass reduced over time <em>(P =</em> 0.008), including BZ <em>(P =</em> 0.002) and core scar <em>(P =</em> 0.05). A total of 72 BZ channels were analyzed across all animals and timepoints. Channel length <em>(P =</em> 0.05) and complexity <em>(P =</em> 0.02) reduced progressively from d3 to d58. However, at d58, 64% of channels were newly formed and 36% were midmyocardial. Conserved channels were initially longer and more complex. All LGE-CMR channels colocalized to regions of maximal decrement on EAM, with significantly greater decrement (115 ± 31 ms vs 83 ± 29 ms; <em>P</em> < 0.001) and uncovering of split potentials (24.8% vs 2.6%; <em>P</em> < 0.001) within channels. In total, 3 of 5 animals had inducible VT and tended to have more channels with greater midmyocardial involvement and functional decrement than those without VT.</div></div><div><h3>Conclusions</h3><div>BZ channels form early postinfarct and demonstrate evolutionary complexity and functional conduction slowing on EAM, highlighting their arrhythmogenic potential. Some channels regress in complexity and length, but new channels form at 2 months’ postinfarct, which may be midmyocardial, reflecting an evolving, 3-dimensional substrate for VT. LGE-CMR may help identify BZ channels that may support VT early postinfarct and lead to sudden death.</div></div>","PeriodicalId":14573,"journal":{"name":"JACC. Clinical electrophysiology","volume":null,"pages":null},"PeriodicalIF":8.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Evolution of Substrate for Ventricular Arrhythmias Early Postinfarction\",\"authors\":\"\",\"doi\":\"10.1016/j.jacep.2024.06.016\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>The evolution of myocardial scar and its arrhythmogenic potential postinfarct is incompletely understood.</div></div><div><h3>Objectives</h3><div>This study sought to investigate scar and border zone (BZ) channels evolution in an animal ischemia-reperfusion injury model using late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).</div></div><div><h3>Methods</h3><div>Five swine underwent 90-minute balloon occlusion of the mid-left anterior descending artery, followed by LGE-CMR at day (d) 3, d30, and d58 postinfarct. Invasive electroanatomic mapping (EAM) was performed at 2 months. Topographical reconstructions of LGE-CMR were analyzed for left ventricular core and BZ scar, BZ channel geometry, and complexity, including transmurality, orientation, and number of entrances/exits.</div></div><div><h3>Results</h3><div>LVEF reduced from 48.0% ± 1.8% to 41.3% ± 2.3% postinfarct. Total scar mass reduced over time <em>(P =</em> 0.008), including BZ <em>(P =</em> 0.002) and core scar <em>(P =</em> 0.05). A total of 72 BZ channels were analyzed across all animals and timepoints. Channel length <em>(P =</em> 0.05) and complexity <em>(P =</em> 0.02) reduced progressively from d3 to d58. However, at d58, 64% of channels were newly formed and 36% were midmyocardial. Conserved channels were initially longer and more complex. All LGE-CMR channels colocalized to regions of maximal decrement on EAM, with significantly greater decrement (115 ± 31 ms vs 83 ± 29 ms; <em>P</em> < 0.001) and uncovering of split potentials (24.8% vs 2.6%; <em>P</em> < 0.001) within channels. In total, 3 of 5 animals had inducible VT and tended to have more channels with greater midmyocardial involvement and functional decrement than those without VT.</div></div><div><h3>Conclusions</h3><div>BZ channels form early postinfarct and demonstrate evolutionary complexity and functional conduction slowing on EAM, highlighting their arrhythmogenic potential. Some channels regress in complexity and length, but new channels form at 2 months’ postinfarct, which may be midmyocardial, reflecting an evolving, 3-dimensional substrate for VT. LGE-CMR may help identify BZ channels that may support VT early postinfarct and lead to sudden death.</div></div>\",\"PeriodicalId\":14573,\"journal\":{\"name\":\"JACC. Clinical electrophysiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":8.0000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JACC. Clinical electrophysiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2405500X24004900\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JACC. Clinical electrophysiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2405500X24004900","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Evolution of Substrate for Ventricular Arrhythmias Early Postinfarction
Background
The evolution of myocardial scar and its arrhythmogenic potential postinfarct is incompletely understood.
Objectives
This study sought to investigate scar and border zone (BZ) channels evolution in an animal ischemia-reperfusion injury model using late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).
Methods
Five swine underwent 90-minute balloon occlusion of the mid-left anterior descending artery, followed by LGE-CMR at day (d) 3, d30, and d58 postinfarct. Invasive electroanatomic mapping (EAM) was performed at 2 months. Topographical reconstructions of LGE-CMR were analyzed for left ventricular core and BZ scar, BZ channel geometry, and complexity, including transmurality, orientation, and number of entrances/exits.
Results
LVEF reduced from 48.0% ± 1.8% to 41.3% ± 2.3% postinfarct. Total scar mass reduced over time (P = 0.008), including BZ (P = 0.002) and core scar (P = 0.05). A total of 72 BZ channels were analyzed across all animals and timepoints. Channel length (P = 0.05) and complexity (P = 0.02) reduced progressively from d3 to d58. However, at d58, 64% of channels were newly formed and 36% were midmyocardial. Conserved channels were initially longer and more complex. All LGE-CMR channels colocalized to regions of maximal decrement on EAM, with significantly greater decrement (115 ± 31 ms vs 83 ± 29 ms; P < 0.001) and uncovering of split potentials (24.8% vs 2.6%; P < 0.001) within channels. In total, 3 of 5 animals had inducible VT and tended to have more channels with greater midmyocardial involvement and functional decrement than those without VT.
Conclusions
BZ channels form early postinfarct and demonstrate evolutionary complexity and functional conduction slowing on EAM, highlighting their arrhythmogenic potential. Some channels regress in complexity and length, but new channels form at 2 months’ postinfarct, which may be midmyocardial, reflecting an evolving, 3-dimensional substrate for VT. LGE-CMR may help identify BZ channels that may support VT early postinfarct and lead to sudden death.
期刊介绍:
JACC: Clinical Electrophysiology is one of a family of specialist journals launched by the renowned Journal of the American College of Cardiology (JACC). It encompasses all aspects of the epidemiology, pathogenesis, diagnosis and treatment of cardiac arrhythmias. Submissions of original research and state-of-the-art reviews from cardiology, cardiovascular surgery, neurology, outcomes research, and related fields are encouraged. Experimental and preclinical work that directly relates to diagnostic or therapeutic interventions are also encouraged. In general, case reports will not be considered for publication.