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

IF 8 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS JACC. Clinical electrophysiology Pub Date : 2024-10-01 DOI:10.1016/j.jacep.2024.06.016
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引用次数: 0

摘要

背景:心肌梗死后心肌瘢痕的演变及其致心律失常潜能尚不完全清楚:本研究试图利用晚期钆增强心脏磁共振(LGE-CMR)研究动物缺血再灌注损伤模型中瘢痕和边界区(BZ)通道的演变:方法:5 头猪接受了 90 分钟的左前降支中动脉球囊闭塞术,然后在梗塞后第 3 天、第 30 天和第 58 天进行了 LGE-CMR。2 个月后进行有创电解剖图绘制(EAM)。对LGE-CMR的地形重建进行分析,以确定左心室核心和BZ瘢痕、BZ通道的几何形状和复杂性,包括透射性、方向和入口/出口的数量:梗死后 LVEF 从 48.0% ± 1.8% 降至 41.3% ± 2.3%。随着时间的推移,瘢痕总质量减少(P = 0.008),包括BZ(P = 0.002)和核心瘢痕(P = 0.05)。在所有动物和时间点上共分析了 72 个 BZ 通道。通道长度(P = 0.05)和复杂性(P = 0.02)从第3 d到第58 d逐渐减少。然而,在 d58 时,64% 的通道是新形成的,36% 是心肌中段通道。保留通道最初更长、更复杂。所有 LGE-CMR 通道都集中在 EAM 的最大衰减区域,衰减显著增大(115 ± 31 ms vs 83 ± 29 ms;P < 0.001),通道内的分裂电位也明显增大(24.8% vs 2.6%;P < 0.001)。总之,5只动物中有3只发生了诱发性VT,与没有发生VT的动物相比,这些动物的心肌中段受累更多,功能减退的通道也更多:结论:BZ通道在梗死后早期形成,在EAM上表现出进化的复杂性和功能性传导减慢,突显了其致心律失常的潜力。一些通道的复杂性和长度有所减退,但在梗死后 2 个月又形成了新的通道,这些通道可能位于心肌中段,反映了 VT 的三维基底在不断演变。LGE-CMR 可帮助识别可能在梗死后早期支持 VT 并导致猝死的 BZ 通道。
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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.
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来源期刊
JACC. Clinical electrophysiology
JACC. Clinical electrophysiology CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
10.30
自引率
5.70%
发文量
250
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.
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