川崎病的心肌应变和应变率:范围、恢复和与全身炎症/冠状动脉扩张的关系。

Benjamin Frank, Jesse Davidson, Suhong Tong, Blake Martin, Heather Heizer, Marsha S Anderson, Mary P Glode, Samuel R Dominguez, Pei-Ni Jone
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引用次数: 15

摘要

背景:川崎病(Kawasaki Disease, KD)是一种中等大小血管的系统性血管炎,是发达国家儿童获得性心脏病的最常见原因。一些KD患者表现出心肌力学下降的超声心动图证据。然而,KD患者异常力学的发生率、病因和可逆性仍不明确。方法和结果:回顾性分析41例KD患者,采用治疗前和恢复期超声心动图的速度矢量成像测量心肌应变和应变率。对所有患者进行治疗前降钙素原、c反应蛋白(CRP)和冠状动脉z-评分,并比较保留急性期机制组和抑制急性期机制组之间的差异。急性期和恢复期的力学变化也进行了评估。最初低纵向应变的患者在恢复期得到改善(平均差- 4.0%;结论:在我们的队列中发现的菌株范围很大。平均应变的改善主要是由较低的初始应变患者驱动的。低应变与全身性炎症标志物增加有关,但与近端冠状动脉改变无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Myocardial Strain and Strain Rate in Kawasaki Disease: Range, Recovery, and Relationship to Systemic Inflammation/Coronary Artery Dilation.

Myocardial Strain and Strain Rate in Kawasaki Disease: Range, Recovery, and Relationship to Systemic Inflammation/Coronary Artery Dilation.

Myocardial Strain and Strain Rate in Kawasaki Disease: Range, Recovery, and Relationship to Systemic Inflammation/Coronary Artery Dilation.

Myocardial Strain and Strain Rate in Kawasaki Disease: Range, Recovery, and Relationship to Systemic Inflammation/Coronary Artery Dilation.

Background: Kawasaki Disease (KD), a systemic vasculitis of medium sized vessels, is the most common cause of acquired heart disease among children in the developed world. Some KD patients demonstrate echocardiographic evidence of depressed myocardial mechanics. However, the incidence, etiology, and reversibility of abnormal mechanics in KD patients remain undefined.

Methods and results: We retrospectively studied 41 KD patients and measured myocardial strain and strain rate by velocity vector imaging from pre-treatment and convalescent echocardiograms. Pre-treatment procalcitonin, C-reactive protein (CRP), and coronary artery z-scores were obtained in all patients and compared between the groups with preserved versus depressed acute phase mechanics. The change in mechanics between the acute and convalescent phases was also assessed. Patients with initially low longitudinal strain improved by the convalescent period (mean difference - 4.0%; p<0.005) with the greatest improvement occurring in patients with the lowest initial strain (-7.3%; p<0.05). Patients with higher initial strain did not change significantly by the convalescent period. Patients with lower longitudinal and circumferential strain demonstrated higher median procalcitonin levels (1.2 vs. 0.3 ng/mL; p<0.05 and 1.8 vs. 0.4 ng/mL; p<0.05 respectively) and a trend towards higher CRP, but no difference in coronary artery z-scores. Strain rate was not associated with inflammatory markers or coronary artery z-scores.

Conclusions: The range of strain found in our cohort was large. Improvement in mean strain was driven primarily by patients with lower initial strain. Lower strain was associated with increased markers of systemic inflammation, but not proximal coronary artery changes.

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