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抗M2和抗β1自身抗体水平与恰加斯心脏病的心脏功能障碍程度无关。

Levels of anti-M2 and anti-beta1 autoantibodies do not correlate with the degree of heart dysfunction in Chagas' heart disease.

作者信息

Talvani Andre, Rocha Manoel O C, Ribeiro Antonio L, Borda Enri, Sterin-Borda Leonor, Teixeira Mauro M

机构信息

Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, UFMG, Av. Antônio Carlos 6627, Pampulha, 31270-901 Belo Horizonte, MG, Brazil.

出版信息

Microbes Infect. 2006 Aug;8(9-10):2459-64. doi: 10.1016/j.micinf.2006.06.006. Epub 2006 Jul 18.

DOI:10.1016/j.micinf.2006.06.006
PMID:16963301
Abstract

Chronic chagasic cardiomyopathy (CCC) is characterized mainly by a dilated cardiomyopathy complicated by frequent and complex ventricular arrhythmias and/or conduction defects. The aim of the present study was to evaluate functional implications of neurotransmitter receptor autoantibodies in vivo. Sera from chagasic patients were used to measure the level of autoantibodies to peptide fragments from the M2 cholinergic and beta1 adrenergic receptors. Optical density values and the frequency of anti-M2 and anti-beta1 antibodies were significantly higher in the indeterminate form and in CCC patients than in normal individuals. There was no correlation between levels of autoantibodies and clinical parameters of ventricular dysfunction, as assessed by echocardiography. Patients presenting with chronotropic insufficiency in exercise test had higher levels of anti-M2 but not anti-beta1 autoantibodies. Although anti-M2 and anti-beta1 antibodies do not appear to play a role in the pathophysiology of the heart failure that accompanies severe CCC, anti-M2 cholinergic autoantibodies may contribute to the pathogenesis of Chagas' disease dysautonomia.

摘要

慢性恰加斯病性心肌病(CCC)的主要特征是扩张型心肌病,伴有频繁且复杂的室性心律失常和/或传导缺陷。本研究的目的是评估神经递质受体自身抗体在体内的功能影响。使用恰加斯病患者的血清来测量针对M2胆碱能受体和β1肾上腺素能受体肽段的自身抗体水平。在无症状感染期和CCC患者中,抗M2和抗β1抗体的光密度值及频率显著高于正常个体。通过超声心动图评估,自身抗体水平与心室功能障碍的临床参数之间无相关性。运动试验中出现变时性功能不全的患者抗M2自身抗体水平较高,但抗β1自身抗体水平不高。虽然抗M2和抗β1抗体似乎在严重CCC伴发的心力衰竭病理生理过程中不起作用,但抗M2胆碱能自身抗体可能参与恰加斯病自主神经功能障碍的发病机制。

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