Pathophysiology of LV Remodeling Following STEMI,JACC: Cardiovascular Imaging

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Pathophysiology of LV Remodeling Following STEMI
JACC: Cardiovascular Imaging ( IF 12.8 ) Pub Date : 2022-06-15 , DOI: 10.1016/j.jcmg.2022.04.002
Arka Das ₁ , Christopher Kelly ₁ , Irvin Teh ₁ , Christian T Stoeck ₂ , Sebastian Kozerke ₂ , Noor Sharrack ₁ , Peter P Swoboda ₁ , John P Greenwood ₁ , Jürgen E Schneider ₁ , Sven Plein ₁ , Erica Dall'Armellina ₁

Affiliation

Background

Adverse LV remodeling post–ST-segment elevation myocardial infarction (STEMI) is associated with a poor prognosis, but the underlying mechanisms are not fully understood. Diffusion tensor (DT)-cardiac magnetic resonance (CMR) allows in vivo characterization of myocardial architecture and provides unique mechanistic insight into pathophysiologic changes following myocardial infarction.

Objectives

This study evaluated the potential associations between DT-CMR performed soon after STEMI and long-term adverse left ventricular (LV) remodeling following STEMI.

Methods

A total of 100 patients with STEMI underwent CMR at 5 days and 12 months post-reperfusion. The protocol included DT-CMR for assessing fractional anisotropy (FA), secondary eigenvector angle (E2A) and helix angle (HA), cine imaging for assessing LV volumes, and late gadolinium enhancement for calculating infarct and microvascular obstruction size. Adverse remodeling was defined as a 20% increase in LV end-diastolic volume at 12 months.

Results

A total of 32 patients experienced adverse remodeling at 12 months. Compared with patients without adverse remodeling, they had lower FA (0.23 ± 0.03 vs 0.27 ± 0.04; P < 0.001), lower E2A (37 ± 6° vs 51 ± 7°; P < 0.001), and, on HA maps, a lower proportion of myocytes with right-handed orientation (RHM) (8% ± 5% vs 17% ± 9%; P < 0.001) in their acutely infarcted myocardium. On multivariable logistic regression analysis, infarct FA (odds ratio [OR]: <0.01; P = 0.014) and E2A (OR: 0.77; P = 0.001) were independent predictors of adverse LV remodeling after adjusting for left ventricular ejection fraction (LVEF) and infarct size. There were no significant changes in infarct FA, E2A, or RHM between the 2 scans.

Conclusions

Extensive cardiomyocyte disorganization (evidenced by low FA), acute loss of sheetlet angularity (evidenced by low E2A), and a greater loss of organization among cardiomyocytes with RHM, corresponding to the subendocardium, can be detected within 5 days post-STEMI. These changes persist post-injury, and low FA and E2A are independently associated with long-term adverse remodeling.

中文翻译：

STEMI 后 LV 重塑的病理生理学

背景

不利的 LV 重塑后 ST 段抬高心肌梗死 (STEMI) 与不良预后相关，但其潜在机制尚不完全清楚。扩散张量 (DT)-心脏磁共振 (CMR) 允许对心肌结构进行体内表征，并提供对心肌梗死后病理生理变化的独特机制洞察。

目标

本研究评估了 STEMI 后不久进行的 DT-CMR 与 STEMI 后长期不良左心室 (LV) 重塑之间的潜在关联。

方法

共有 100 名 STEMI 患者在再灌注后 5 天和 12 个月接受了 CMR。该协议包括用于评估分数各向异性 (FA)、二次特征向量角 (E2A) 和螺旋角 (HA) 的 DT-CMR、用于评估 LV 体积的电影成像以及用于计算梗塞和微血管阻塞大小的晚期钆增强。不良重塑定义为 12 个月时 LV 舒张末期容积增加 20%。

结果

共有 32 名患者在 12 个月时经历了不良重塑。与没有不良重塑的患者相比，他们的 FA 较低（0.23 ± 0.03 vs 0.27 ± 0.04；P < 0.001），E2A 较低（37 ± 6° vs 51 ± 7°；P < 0.001），并且在 HA 图上，a在急性梗死的心肌中，右手方向 (RHM) 的肌细胞比例较低（8% ± 5% 对比 17% ± 9%；P < 0.001）。在多变量逻辑回归分析中，梗塞 FA（比值比 [OR]：<0.01；P = 0.014）和 E2A（OR：0.77；P = 0.001）是调整左心室射血分数 (LVEF) 后不良 LV 重构的独立预测因子和梗塞面积。两次扫描之间的梗塞 FA、E2A 或 RHM 没有显着变化。