Non-Alcoholic Fatty Liver Disease, Heart Failure, and Long-Term Mortality: Insights From the National Health and Nutrition Examination Survey

To evaluate the association between non-alcoholic fatty liver disease (NAFLD), heart failure (HF), and all-cause mortality. Both NAFLD and HF are increasing in prevalence due to shared risk factors. We used data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 to identify non-pregnant individuals aged >= 20 years with HF and NAFLD and linked with the cause of death data from the National Center for Health Statistics. The associations between NAFLD, HF, and all-cause mortality were assessed using logistic regression and Cox proportional hazard modeling as appropriate. There were 82,358,893 weighted eligible participants of whom 3,833,667 (4.7%) had NAFLD. The mean (SE) age was 51.5 (0.35) years, 45.1% women, 63.0% Non-Hispanic White and 11.8% Non-Hispanic Black. Cardiovascular comorbidities were more common in participants with NAFLD; they were more likely to have hypertension (81.7% vs 53.5%), diabetes (65.1% vs 17.1%), stroke (7.3% vs 4.1%), coronary artery disease (14.9% vs 8.4%), or HF (10.5% v s 3.5%) compared with participants without NAFLD. In multivariate logistic regression models adjusting for age, race/ethnicity and sex, participants with NAFLD were 3.5 times more likely to have HF [aOR, 95% CI: 3.47 (1.98-6.06)]. Older age, male sex, presence of diabetes and coronary artery disease were associated with higher odds of HF in participants with established NAFLD. At the end of the follow-up period, participants with NAFLD had higher all-cause mortality compared with participants without NAFLD (HR [95% CI]: 1.93 [1.24-2.99], P < 0.001). In this analysis of US adults, ambulatory participants with NAFLD were similar to 3.5 times more likely to have HF, and twice as likely to experience mortality compared with participants without NAFLD. Further studies are needed to identify the possible linkage between NAFLD and HF beyond the shared risk factor pathogenesis.