Why the study?
Does the prevalence of myocardial enteroviral genome differ between patients with idiopathic dilated cardiomyopathy and controls?
Does the prevalence of myocardial enteroviral genome differ between patients with idiopathic dilated cardiomyopathy and controls?
The presence of enteroviral genome in the myocardium is similar between patients with idiopathic dilated cardiomyopathy and controls, suggesting it is a common environmental pathogen rather than a specific pathogenic factor for DCM.
Similar enteroviral detection in DCM and controls should not change practice; leaves open any causal role in pathogenesis.
OBJECTIVE: To assess the prevalence and significance of enteroviral genome within myocardial biopsy specimens taken from patients with idiopathic dilated cardiomyopathy and from controls. DESIGN: Prospective evaluation of myocardial tissue for the presence of an enteroviral genome by the polymerase chain reaction. SETTING: A tertiary referral centre for patients with idiopathic dilated cardiomyopathy. PATIENTS: 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. RESULTS: 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. CONCLUSIONS: 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.
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Keeling et al. (1992) studied this question.
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