短期胺碘酮治疗可减弱C反应蛋白诱导的单核细胞细胞因子和趋化因子的产生，并改善特发性扩张型心肌病合并室性心动过速患者的心脏功能。

Short-term amiodarone treatment attenuates the production of monocyte cytokines and chemokines by C-reactive protein and improves cardiac function in patients with idiopathic dilated cardiomyopathy and ventricular tachycardia.

作者信息

Hirasawa Yasuhiro, Nakagomi Akihiro, Kobayashi Yoshinori, Katoh Takao, Mizuno Kyoichi

机构信息

First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.

出版信息

Circ J. 2009 Apr;73(4):639-46. doi: 10.1253/circj.cj-08-0794. Epub 2009 Feb 19.

DOI:10.1253/circj.cj-08-0794

PMID:19225199

Abstract

BACKGROUND

Increased expression of cytokines and chemokines has been observed in chronic heart failure (CHF). Amiodarone reduces circulating cytokine levels, so it may attenuate the production of monocyte cytokines and chemokines by C-reactive protein (CRP) and thus improve the left ventricular ejection fraction (LVEF) in dilated cardiomyopathy (DCM) patients with ventricular tachycardia (VT).

METHODS AND RESULTS

Peripheral blood mononuclear cells (PBMCs) were stimulated by 25 microg/ml CRP in 23 patients with DCM, who were divided into 2 groups based on whether or not amiodarone was included in their treatment (Amiodarone group n=8; No amiodarone group n=15). Tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein (MCP)-1 on monocytes at baseline and after 4 weeks of treatment was measured by ELISA and expressed as mean+/-SD (pg.ml(-1)x10(-6) PBMCs). The LVEF and the CRP-induced monocyte cytokine and chemokine production were unchanged in the No amiodarone group after 4 weeks; however, LVEF in the Amiodarone group was increased (32.7+/-6.9 to 39.2+/-6.9%; P=0.005), and TNF-alpha and MCP-1 production in the Amiodarone group were decreased (P=0.012, respectively).

CONCLUSIONS

Amiodarone attenuates the production of monocyte cytokines and chemokines by CRP, and improves LVEF in CHF patients with VT.

摘要

背景

在慢性心力衰竭（CHF）中已观察到细胞因子和趋化因子的表达增加。胺碘酮可降低循环细胞因子水平，因此它可能通过C反应蛋白（CRP）减弱单核细胞细胞因子和趋化因子的产生，从而改善患有室性心动过速（VT）的扩张型心肌病（DCM）患者的左心室射血分数（LVEF）。

方法与结果

23例DCM患者的外周血单个核细胞（PBMC）用25μg/ml CRP刺激，根据治疗中是否包含胺碘酮将患者分为2组（胺碘酮组n = 8；无胺碘酮组n = 15）。通过酶联免疫吸附测定法（ELISA）测量基线时和治疗4周后单核细胞上的肿瘤坏死因子（TNF）-α和单核细胞趋化蛋白（MCP）-1，并表示为平均值±标准差（pg.ml⁻¹×10⁻⁶ PBMC）。4周后，无胺碘酮组的LVEF以及CRP诱导的单核细胞细胞因子和趋化因子产生未发生变化；然而，胺碘酮组的LVEF增加（从32.7±6.9增至39.2±6.9%；P = 0.005），胺碘酮组的TNF-α和MCP-1产生减少（分别为P = 0.012）。