Quantifying the contribution of alcohol to cardiomyopathy: A systematic review

Jürgen Rehm1, Omer Syed Muhammad Hasan2, Sameer Imtiaz3

  • 1Institute for Mental Health Policy Research, CAMH, 33 Russell Street, Toronto, ON, M5S 2S1, Canada; Campbell Family Mental Health Research Institute, 250 College Street, Toronto, ON, M5T 1R8, Canada; Institute of Medical Science (IMS), University of Toronto, Faculty of Medicine, Medical Sciences Building, 1 King's College Circle, Room 2374, Toronto, ON, M5S 1A8, Canada; Institute for Clinical Psychology and Psychotherapy, Technische Universität Dresden, Chemnitzer Str. 46, 01187 Dresden, Germany; Department of Psychiatry, University of Toronto, 250 College Street, 8th Floor, Toronto, ON, M5T 1R8, Canada; Dalla Lana School of Public Health, University of Toronto, 155 College Street, 6th Floor, Toronto, ON, M5T 3M7, Canada.

Insights

Heavy alcohol consumption over years significantly increases cardiomyopathy risk. Quantifying alcohol-attributable cardiomyopathy burden requires new methods beyond traditional population-attributable fractions.

Area of Science:

  • Cardiology
  • Toxicology
  • Epidemiology

Background:

  • Alcohol consumption is a known cardiotoxin.
  • Alcoholic cardiomyopathy has an ICD code, but its population burden is unclear.
  • Estimating burden typically uses population-attributable fractions, requiring dose-response data.

Purpose of the Study:

  • To systematically review and establish dose-response relationships between alcohol consumption and cardiomyopathy risk.
  • To assess the feasibility of quantifying alcohol-attributable cardiomyopathy burden using existing data.

Main Methods:

  • Systematic literature search for studies on alcohol consumption and cardiomyopathy dose-response relationships.
  • Inclusion of direct studies and reviews.
  • Attempted meta-analysis to pool estimates.

Main Results:

  • Meta-analysis was not feasible due to data limitations.
  • Heavy drinking (≥80 g/day) over years is linked to high cardiomyopathy risk.
  • Increased lifetime alcohol exposure correlates with higher risk; drinking patterns may also play a role.

Conclusions:

  • Current data does not permit conventional burden estimation methods.
  • Heavy and prolonged alcohol intake poses significant cardiomyopathy risk.
  • Novel methodologies are needed for global quantification of alcohol-attributable cardiomyopathy.

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