Kühl Uwe, Pauschinger Matthias, Noutsias Michel, Seeberg Bettina, Bock Thomas, Lassner Dirk, Poller Wolfgang, Kandolf Reinhard, Schultheiss Heinz-Peter
Charite-University Medicine Berlin, Campus Benjamin Franklin, Department of Cardiology and Pneumology, Hindenburgdamm 30, 12200 Berlin, Germany.
Circulation. 2005 Feb 22;111(7):887-93. doi: 10.1161/01.CIR.0000155616.07901.35. Epub 2005 Feb 7.
For a long time, enteroviruses have been considered to be the most common cause of acute viral myocarditis (MC), with possible transition from MC to dilated cardiomyopathy (DCM). Recent investigations have shown, however, that other viruses are also frequently encountered in MC patients, suggesting that persistence of various virus species may play a pathogenic role in the transition from MC to DCM. The purpose of this study was to screen endomyocardial biopsies (EMBs) from patients with "idiopathic" DCM for the presence of viral genomes by using polymerase chain reaction (PCR) to assess the frequency of cardiac viral infections that may be involved in the pathogenesis of the disease.
EMBs were obtained for PCR analysis from 245 consecutive patients (median left ventricular ejection fraction, 35.0%; range, 9% to 59%). PCR and reverse transcription-PCR were performed to detect the genomic sequences of enterovirus (EV), adenovirus (ADV), human cytomegalovirus (HCMV), herpes simplex virus, Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), parvovirus B19 (PVB19), and influenza A and B viruses. Myocardial inflammation was assessed by histological and immunohistological analyses. Viral genomes could be amplified from EMBs of 165 (67.4%) of the 245 DCM patients: EV=23 (9.4%), ADV=4 (1.6%), PVB19=126 (51.4%), HHV-6=53 (21.6%), EBV=5 (2.0%), HCMV=2 (0.8%), including n=45 cases (27.3%) with multiple infections. Active or borderline myocarditis according to the Dallas classification did not exist in any case. Lymphocyte and macrophage infiltrates were not significantly different in virus-positive versus virus-negative patients.
Viral genomes were frequently detected in EMBs of patients with systolic left ventricular dysfunction. Our data suggest that myocardial persistence of various viruses, often presenting as multiple infections, may play a role in the pathogenesis of DCM far more frequently than suspected so far.
长期以来，肠道病毒一直被认为是急性病毒性心肌炎（MC）最常见的病因，且可能从MC转变为扩张型心肌病（DCM）。然而，最近的研究表明，MC患者中也经常发现其他病毒，这表明多种病毒的持续存在可能在从MC转变为DCM的过程中起致病作用。本研究的目的是通过聚合酶链反应（PCR）筛查“特发性”DCM患者的心内膜心肌活检（EMB）中病毒基因组的存在情况，以评估可能参与该疾病发病机制的心脏病毒感染频率。
对245例连续患者（左心室射血分数中位数为35.0%；范围为9%至59%）进行EMB获取并进行PCR分析。进行PCR和逆转录PCR以检测肠道病毒（EV）、腺病毒（ADV）、人巨细胞病毒（HCMV）、单纯疱疹病毒、爱泼斯坦-巴尔病毒（EBV）、人疱疹病毒6型（HHV-6）、细小病毒B19（PVB19）以及甲型和乙型流感病毒的基因组序列。通过组织学和免疫组织学分析评估心肌炎症。在245例DCM患者中，165例（67.4%）的EMB中可扩增出病毒基因组：EV=23例（9.4%），ADV=4例（1.6%），PVB19=126例（51.4%），HHV-6=53例（21.6%），EBV=5例（2.0%），HCMV=2例（0.8%），其中45例（27.3%）为多重感染。根据达拉斯分类法，无一例存在活动性或临界性心肌炎。病毒阳性患者与病毒阴性患者的淋巴细胞和巨噬细胞浸润无显著差异。
在收缩期左心室功能障碍患者的EMB中经常检测到病毒基因组。我们的数据表明，多种病毒在心肌中的持续存在，通常表现为多重感染，可能在DCM的发病机制中发挥比迄今所怀疑的更为频繁的作用。
