Keeling P J, Jeffery S, Caforio A L, Taylor R, Bottazzo G F, Davies M J, McKenna W J
Department of Cardiological Sciences, St George's Hospital Medical School, London.
Br Heart J. 1992 Dec;68(6):554-9. doi: 10.1136/hrt.68.12.554.
To assess the prevalence and significance of enteroviral genome within myocardial biopsy specimens taken from patients with idiopathic dilated cardiomyopathy and from controls.
Prospective evaluation of myocardial tissue for the presence of an enteroviral genome by the polymerase chain reaction.
A tertiary referral centre for patients with idiopathic dilated cardiomyopathy.
Tissue for the study came from 50 consecutive patients with dilated cardiomyopathy, 41 with other forms of heart disease and 34 from coroners' necropsy cases.
Enteroviral genome was detected in 6/50 (12%) patients with dilated cardiomyopathy and 13/75 (17%) of the controls (not significant). No differences were seen between dilated cardiomyopathy patients with or without myocardial enteroviral genome in respect of age; duration of symptoms; proportion of patients with a premorbid acute viral illness, excess alcohol consumption, or hypertension; New York Heart Association functional class; measures of left ventricular function; or endomyocardial histology. Within the control group enteroviral genome was detected in 3/15 (20%) patients with ischaemic heart disease, 2/19 (10.5%) with valvar heart disease, 1/5 (20%) with specific heart muscle disease, 0/2 (0%) with congenital heart disease, and 7/34 (20.6%) cases of sudden death. During 2-52 month follow up (mean 22) 15/44 (34%) patients without myocardial enteroviral genome and 2/6 (33%) with myocardial enteroviral genome died suddenly or required orthotopic heart transplantation for progressive heart failure.
These findings do not support the hypothesis that persistent enteroviral infection is of pathogenic or prognostic importance in dilated cardiomyopathy but they are consistent with enterovirus being a common environmental pathogen.
评估从特发性扩张型心肌病患者及对照组获取的心肌活检标本中肠道病毒基因组的患病率及意义。
通过聚合酶链反应对心肌组织中肠道病毒基因组的存在情况进行前瞻性评估。
一家特发性扩张型心肌病患者的三级转诊中心。
研究用组织来自50例连续的扩张型心肌病患者、41例其他形式心脏病患者以及34例验尸病例。
在6/50(12%)的扩张型心肌病患者及13/75(17%)的对照组中检测到肠道病毒基因组(无显著差异)。在年龄、症状持续时间、病前有急性病毒感染、过量饮酒或高血压的患者比例、纽约心脏协会心功能分级、左心室功能指标或心内膜组织学方面,有或无心肌肠道病毒基因组的扩张型心肌病患者之间未见差异。在对照组中,3/15(20%)的缺血性心脏病患者、2/19(10.5%)的瓣膜性心脏病患者、1/5(20%)的特异性心肌病患者、0/2(0%)的先天性心脏病患者以及7/34(20.6%)的猝死病例中检测到肠道病毒基因组。在2至52个月的随访期间(平均22个月),无心肌肠道病毒基因组的患者中有15/44(34%)、有心肌肠道病毒基因组的患者中有2/6(33%)突然死亡或因进行性心力衰竭需要原位心脏移植。
这些发现不支持持续性肠道病毒感染在扩张型心肌病中具有致病或预后重要性的假说,但与肠道病毒是一种常见的环境病原体相一致。