Martí V, Coll P, Ballester M, Obrador D, Carrió I, Moya C, Lama E, Augè J M, Archard L C
Department of Cardiology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Eur Heart J. 1996 Apr;17(4):545-9. doi: 10.1093/oxfordjournals.eurheartj.a014907.
Patients with dilated cardiomyopathy in whom enteroviruses in the myocardium are detected are more likely to die than those in whom no viruses have been demonstrated. The presence of enterovirus RNA in the myocardium at endomyocardial biopsy has been shown to be the strongest predictor of reduced survival. These results raise the question as to whether persistent virus might be responsible for continuing myocardial damage. Detection of myocardial cell damage is assessed using 111Indium-labelled monoclonal antimyosin antibodies. The present study was undertaken to address the question of whether the presence of myocardial cell damage by such antibodies in patients with dilated cardiomyopathy can be correlated with enterovirus persistence.
A series of 19 consecutive patients diagnosed as having chronic dilated cardiomyopathy who were referred for evaluation for heart transplantation were studied with 111Indium labelled monoclonal antimyosin antibodies. These patients and 10 controls were screened for enterovirus RNA sequences in endomyocardial biopsy tissue by hybridization with an enterovirus group-specific cDNA probe.
Antimyosin uptake, indicative of myocardial cell damage, was observed in 16 of 19 patients (84%), with dilated cardiomyopathy, and enterovirus RNA sequences were detected in endomyocardial biopsies from four of these 16 patients (25%), but not in myocardium from the remaining three patients with a negative antimyosin scan, nor from any of 10 controls.
Although these data do not establish a causal relationship between virus persistence in the myocardium and myocardial damage, the results obtained in the preliminary study support the hypothesis that enterovirus persistence is associated with continuing myocardial damage in patients with dilated cardiomyopathy.
在扩张型心肌病患者中，检测到心肌中有肠道病毒的患者比未检测到病毒的患者更易死亡。心内膜心肌活检时心肌中存在肠道病毒RNA已被证明是生存时间缩短的最强预测指标。这些结果提出了一个问题，即持续存在的病毒是否可能导致心肌持续损伤。使用铟-111标记的单克隆抗肌球蛋白抗体评估心肌细胞损伤的检测情况。本研究旨在探讨扩张型心肌病患者中此类抗体检测到的心肌细胞损伤是否与肠道病毒持续存在相关。
对19例连续诊断为慢性扩张型心肌病并被转诊进行心脏移植评估的患者，用铟-111标记的单克隆抗肌球蛋白抗体进行研究。通过与肠道病毒组特异性cDNA探针杂交，对这些患者和10名对照的心内膜心肌活检组织进行肠道病毒RNA序列筛查。
19例扩张型心肌病患者中有16例（84%）观察到抗肌球蛋白摄取，提示心肌细胞损伤，这16例患者的心内膜心肌活检中4例（25%）检测到肠道病毒RNA序列，但抗肌球蛋白扫描结果为阴性的其余3例患者的心肌以及10名对照的心肌中均未检测到。
虽然这些数据并未确立心肌中病毒持续存在与心肌损伤之间的因果关系，但初步研究结果支持这样的假说，即肠道病毒持续存在与扩张型心肌病患者的心肌持续损伤有关。
