Abstract 13688: Non-Alcoholic Fatty Liver Disease is an Independent Predictor of Long-Term Incident Coronary Heart Disease Events-The Multi-Ethnic Study of Atherosclerosis

Abstract

Background: There is significant overlap between risk factors for atherosclerosis and non-alcoholic fatty liver disease (NAFLD), and studies have shown an independent association between markers of subclinical atherosclerosis and NAFLD. The current study evaluates the role of NAFLD for prediction of incident adverse coronary heart disease (CHD) events in a multi-ethnic population-based study.

Methods: The study was performed on 6,814 participants from the Multi-Ethnic Study of Atherosclerosis. Liver fat content was measured on cardiac CT scans using liver-to-spleen ratio of <1.0; this information was available in 4,384 participants (64%). Participants with heavy alcohol intake (>14 drinks/week for men and >7 for women), self-reported history of cirrhosis, on oral steroids or anti-arrhythmic medications and those with missing data were excluded (n=265). These participants were followed for the incidence of CHD events defined as myocardial infarction, angina, revascularization, resuscitated cardiac arrest, and cardiovascular death.

Results: The final study population consisted of 4,119 participants (63±10 years, 45% men). Within a median follow-up of 7.5 years, a total of 209 (5.1%) CHD events were noted. NAFLD was a strong predictor of incident adverse CHD events after adjusting for age, gender and ethnicity (hazard ratio HR, 1.73, 95% CI: 1.25-2.41, p=0.01). NAFLD remained a significant predictor of incident CHD events (HR: 1.42, 95% CI: 1.00-2.02, p=0.05) after further adjustment for risk factors (diabetes, LDL, triglycerides, HDL, cholesterol lowering medications, body mass index, hypertension, cigarette smoking), coronary artery calcium (log CAC+1) and C-reactive protein. Results from Kaplan-Meier survival curve are shown in figure 1.

Conclusion: NAFLD is an independent predictor of long-term incident adverse CHD events after adjustment for traditional risk factors as well subclinical atherosclerotic and inflammatory burden.