Abstract P009: The Association of Liver Enzymes with Subclinical Myocardial Damage
Background: Nonalcoholic fatty liver disease (NAFLD) is present in up to 30% of the US population and is strongly associated with obesity and diabetes. While a number of studies support an association between NAFLD and cardiovascular disease, limited evidence exists for the association with subclinical myocardial injury.
Objective: To test the hypothesis that elevated liver enzymes (Alanine aminotrasferase [ALT], Aspartate aminotranferase [AST] and Gamma-glutamyl transpeptidase [GGT]) in the absence of significant alcohol consumption are independently associated with subclinical myocardial injury, defined by elevated cardiac troponin-T measured using a highly-sensitive assay (hs-cTnT).
Methods: We conducted a cross-sectional analysis of 9351 participants from the Atherosclerosis Risk in the Communities (ARIC) Study with information on ALT, AST and GGT , hs-cTnT, and no evidence of coronary heart disease or elevated alcohol consumption (>14 and >21 drinks/week for women and men, respectively). We used logistic regression models to examine the association between liver enzymes and elevated hs-TnT (hs-TnT >0.014 μ g/L ) defined in a healthy reference population. Our secondary outcome was detectable hs-TnT (>0.003 μ g/L ).
Results: In this community-based population (mean age 63 years, 60% women, 78% white), 7.2% and 66.1% had elevated and detectable hs-TnT, respectively. Medians [range] of ALT, AST and GGT were 13 [1-381], 18 [5-358] and 21 [2-1277], respectively. Higher levels of ALT, AST and GGT, even within the normal range, were independently associated with elevated hs-TnT (Figure). ALT and AST were also independently associated with detectable hs-TnT. After excluding participants with heart failure, the results remained consistent.
Conclusions: In this sample, elevated livers enzymes were independently associated with subclinical myocardial damage suggesting that NAFLD may contribute to myocardial injury beyond its effects on development of clinical atherosclerotic coronary disease.
- © 2012 by American Heart Association, Inc.