Department of Pediatrics and Medicine, Rady Children's Hospital, University of California San Diego, School of Medicine, La Jolla, CA, United States.
Int J Cardiol. 2013 Mar 20;164(1):58-63. doi: 10.1016/j.ijcard.2011.06.065. Epub 2011 Jul 20.
Endomycocardial biopsies have demonstrated that subclinical myocarditis is a universal feature of acute Kawasaki disease (KD).
We investigated biochemical evidence of myocardial strain, oxidative stress, and cardiomyocyte injury in 55 acute KD subjects (30 with paired convalescent samples), 54 febrile control (FC), and 50 healthy control (HC) children by measuring concentrations of cardiovascular biomarkers.
Levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble ST2 (sST2) were elevated in acute vs. convalescent KD, FC, and HC (p≤0.002), while γ-glutamyl transferase and alanine amino transferase as measures of oxidative stress were increased in acute vs. FC (p≤0.0002). Cardiac troponin I (cTnI) levels, using a highly sensitive assay, were elevated in 30% and 40% of paired acute and convalescent KD subjects, respectively, and normalized within two years of disease onset. NT-proBNP and sST2 negatively correlated with deceleration time, but only NT-proBNP correlated with MV E:A ratio and internal diameter of the coronary arteries (RCA/LAD Zworst).
NT-proBNP and sST2 were elevated in acute KD subjects and correlated with impaired myocardial relaxation. These findings, combined with elevated levels of cTnI, suggest that both cardiomyocyte stress and cell death are associated with myocardial inflammation in acute KD.
心肌内膜活检显示亚临床心肌炎是急性川崎病(KD)的普遍特征。
我们通过测量心血管生物标志物的浓度,研究了 55 例急性 KD 患者(30 例有配对恢复期样本)、54 例发热对照组(FC)和 50 例健康对照组(HC)儿童的心肌应变、氧化应激和心肌细胞损伤的生化证据。
与恢复期 KD、FC 和 HC 相比,急性 KD 患者的 N 末端脑利钠肽前体(NT-proBNP)和可溶性 ST2(sST2)水平升高(p≤0.002),而丙氨酸氨基转移酶和γ-谷氨酰转移酶作为氧化应激的指标在急性 KD 患者中升高(p≤0.0002)。使用高灵敏度检测法,在 30%和 40%的急性和恢复期 KD 患者中,心脏肌钙蛋白 I(cTnI)水平升高,并且在疾病发病后两年内恢复正常。NT-proBNP 和 sST2 与减速时间呈负相关,但只有 NT-proBNP 与 MV E:A 比值和冠状动脉(RCA/LAD Zworst)内径相关。
NT-proBNP 和 sST2 在急性 KD 患者中升高,并与心肌舒张功能受损相关。这些发现,加上 cTnI 水平升高,表明在急性 KD 中,心肌细胞应激和细胞死亡与心肌炎症有关。