利用 LA-LV 应变斜率评估心脏淀粉样变性中的左心房功能障碍。

European heart journal. Imaging methods and practice Pub Date : 2024-09-26 eCollection Date: 2024-07-01 DOI:10.1093/ehjimp/qyae100
Fredrik Edbom, Per Lindqvist, Urban Wiklund, Björn Pilebro, Intissar Anan, Frank A Flachskampf, Sandra Arvidsson
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引用次数: 0

摘要

目的:转甲状腺素淀粉样变性心肌病(ATTR-CM)是一种心肌浸润性疾病,细胞外淀粉样蛋白沉积会导致进行性心功能损害。我们的目的是在 ATTR-CM 患者和左心室肥厚(LVH)患者中使用 LA-LV 应变环评估左心房(LA)变形及其与左心室(LV)变形的关联。我们假设,与左心室肥厚患者相比,ATTR-CM 患者的 LA 应变异常且更独立于左心室应变:基于超声心动图数据的回顾性研究,包括30名根据舒张末期室间隔(IVSd)厚度≥14毫米诊断为ATTR-CM的患者,29名LVH患者(IVSd≥14毫米且未诊断为ATTR-CM)和30名对照组。采集左心室整体纵向应变(LV-GLS)和LA应变(评估为心房纵向应变峰值(PALS))并绘制成LA-LV应变环,使用回归线确定LA-LV应变斜率。与 LVH 患者相比,ATTR-CM 患者的 PALS 和 LA-LV 应变斜率值明显较低(分别为 P = 0.004 和 P = 0.014)。接收者操作特征(ROC)曲线显示,PALS(AUC 0.72)和LA-LV斜率(AUC 0.71)的曲线下面积(AUC)相似,两者的数值均高于LV-GLS(AUC 0.62):结论:LA变形能独立区分ATTR-CM和LVH。结合左心室应变和左心室变形分析显示了ATTR心脏淀粉样变性中机械性的左心室-左心室分离,并有可能揭示左心室淀粉样变性浸润;这有可能使ATTR-CM得到更快的诊断和治疗。
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Assessing left atrial dysfunction in cardiac amyloidosis using LA-LV strain slope.

Aims: Transthyretin amyloid cardiomyopathy (ATTR-CM) is an infiltrative disease of the myocardium in which extracellular deposits of amyloid cause progressive cardiac impairment. We aimed to evaluate left atrial (LA) deformation and its association with left ventricular (LV) deformation using LA-LV strain loops in patients with ATTR-CM and patients with LV hypertrophy (LVH). We hypothesized that LA strain in ATTR-CM patients is abnormal and more independent of LV strain, compared to LVH patients.

Methods and results: Retrospective study based on echocardiographic data including 30 patients diagnosed with ATTR-CM based on an end-diastolic interventricular septal (IVSd) thickness of ≥14 mm, and 29 patients with LVH (IVSd ≥ 14 mm and no ATTR-CM diagnosis) together with 30 controls. LV global longitudinal strain (LV-GLS) and LA strain, assessed as peak atrial longitudinal strain (PALS), were acquired and plotted to construct LA-LV strain loops and used regression line to determine a LA-LV strain slope. Significantly lower PALS and LA-LV strain slope values were detected in ATTR-CM patients compared to LVH patients (P = 0.004 and P = 0.014, respectively). A receiver operating characteristic (ROC) curve demonstrated similar area under the curve (AUC) using PALS (AUC 0.72) and LA-LV slope (AUC 0.71), with both resulting in higher values than recorded for LV-GLS (AUC 0.62).

Conclusion: LA deformation demonstrates an independent ability to differentiate ATTR-CM from LVH. Combining LV strain and LA deformation analysis displays the mechanical LA-LV dissociation in ATTR cardiac amyloidosis and potentially unmasks LA amyloid infiltration; this could potentially enable quicker diagnosis and initiation of treatment for ATTR-CM.

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