Abstract

Introduction: Alcohol liver toxicity occurs earlier than heart toxicity, but it is unknown if markers of liver damage predict incident heart failure (HF). Methods: We studied 10,263 participants from the Atherosclerosis Risk in Communities (ARIC) study, mean age 62.2±5.5 years, free of HF, who had liver enzymes measured in 2010 from stored Visit 4 (1996-99) samples. Liver enzymes were considered elevated when alanine aminotransferase (ALT) >24 UI/L(men) and >21 UI/L(women); aspartate aminotransferase (AST) > 32 UI/L(men) and >28 UI/L(women); gama-glutamyl transpeptidase (GGT)>56 UI/L(men) and >50 UI/L(women); AST:ALT ratio ≥2. Participants were classified into 3 categories based on self-reported drinking: never (21%), former (29%), and current drinkers (50%). Multivariable Cox proportional hazards models were used to evaluate the relationship between liver enzymes and incident HF (hospitalization or death) occurring after Visit 4 through 12/31/2012. Results: During 13.2 years of follow-up, HF occurred in 1399 (13%) participants. Higher AST, GGT, and AST:ALT ratio were associated with higher alcohol intake and incident HF among current drinkers (Figure). Compared to current drinkers with normal liver enzymes, current drinkers with increased level of AST or GGT had a higher risk of HF (1.38 HR 95%CI 1.09-1.73, p=0.005 and 1.34 HR 95% CI 1.04-1.74, p=0.02, respectively). AST:ALT ratio≥2 was associated with a 35% increased risk of HF (1.35 HR 95% CI 1.01-1.82, p=0.04) in the current drinkers group, adjusting for age, sex, race, center, hypertension, BMI, LDL, smoking, diabetes, statin use, coronary disease, quantity of alcohol, and kidney function. Elevated liver enzymes were not associated with higher incidence of HF among never and former drinkers participants. Conclusion: Liver damage, as marked by elevation of AST, GGT or an AST: ALT ratio≥2, was related to a higher risk of incident HF among alcohol drinkers, independently of the quantity of alcohol intake.

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