C J McKenna1, M B Codd, H A McCann, D D Sugrue. 1. Department of Clinical Cardiology, National Cardiac Centre, Mater Misericordiae Hospital, Dublin, Ireland.
Abstract
BACKGROUND: Alcohol has been implicated as a risk factor for idiopathic dilated cardiomyopathy (DCM), but a causal relation has not been established. The objective of this study was to determine the association between alcohol consumption and DCM. METHODS: Questionnaires detailing average weekly intake of alcohol, total lifetime consumption, and alcohol abuse were administered in a cohort of well-defined patients with DCM and a randomly selected, population-based control group. RESULTS: Significantly more of the 100 patients with DCM than the 211 members of the control group drank greater than the recommended weekly intake of alcohol (40% vs 24%; p < 0.01) and were alcohol abusers according to the CAGE questionnaire (27% vs 16%; p < 0.05). The average total lifetime consumption measured in units of alcohol was also significantly greater in cases than in the control group (31,200 vs 7,904; p < 0.01). Patients with familial DCM were not significantly more likely to consume alcohol above recommended limits or to be alcohol abusers compared with nonfamilial cases. CONCLUSIONS: This study confirms previous suspicion of a causal association between alcohol and DCM, with significantly more patients than members of the control group either abusing alcohol or drinking it in excess of recommended limits.
BACKGROUND:Alcohol has been implicated as a risk factor for idiopathic dilated cardiomyopathy (DCM), but a causal relation has not been established. The objective of this study was to determine the association between alcohol consumption and DCM. METHODS: Questionnaires detailing average weekly intake of alcohol, total lifetime consumption, and alcohol abuse were administered in a cohort of well-defined patients with DCM and a randomly selected, population-based control group. RESULTS: Significantly more of the 100 patients with DCM than the 211 members of the control group drank greater than the recommended weekly intake of alcohol (40% vs 24%; p < 0.01) and were alcohol abusers according to the CAGE questionnaire (27% vs 16%; p < 0.05). The average total lifetime consumption measured in units of alcohol was also significantly greater in cases than in the control group (31,200 vs 7,904; p < 0.01). Patients with familial DCM were not significantly more likely to consume alcohol above recommended limits or to be alcohol abusers compared with nonfamilial cases. CONCLUSIONS: This study confirms previous suspicion of a causal association between alcohol and DCM, with significantly more patients than members of the control group either abusing alcohol or drinking it in excess of recommended limits.
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