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.
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 cardiomyopathypatients 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.
Authors: H T Aretz; M E Billingham; W D Edwards; S M Factor; J T Fallon; J J Fenoglio; E G Olsen; F J Schoen Journal: Am J Cardiovasc Pathol Date: 1987-01
Authors: L C Archard; N E Bowles; L Cunningham; C A Freeke; E G Olsen; M L Rose; B Meany; H J Why; P J Richardson Journal: Eur Heart J Date: 1991-08 Impact factor: 29.983
Authors: M Grasso; E Arbustini; E Silini; M Diegoli; E Percivalle; G Ratti; M Bramerio; A Gavazzi; M Vigano; G Milanesi Journal: Am J Cardiol Date: 1992-03-01 Impact factor: 2.778