Abstract P224: Association of Nonalcoholic Fatty Liver Disease With Left Ventricular Geometry and Remodeling: the Coronary Artery Risk Development in Young Adults (CARDIA) Study
Background: Nonalcoholic fatty liver disease (NAFLD) is associated with high cardiovascular mortality, including heart failure (HF). Left ventricular hypertrophy (LVH) increases the risk of future HF. The relationship between NAFLD and LV geometry is unknown. In a large prospective population-based sample of black and white adults free from liver or heart disease, we examined the relationship between NAFLD and markers of LV remodeling.
Methods: Participants from the CARDIA study (Y25 exam; age 43-55 years) with concurrent CT quantification of liver fat and tissue Doppler echocardiography were included (n=2,576). Echocardiography was repeated at Y30 follow up (age 47-62 years). LV geometry was classified into normal and abnormal geometry by integrating relative wall thickness and LV mass index. NAFLD was defined as CT liver attenuation ≤ 40 Hounsfield units after excluding other causes of liver fat. Logistic and polytomous regression models were used to test associations.
Results: NAFLD prevalence was 9.6%. NAFLD participants were more likely to be male (57.7% vs. 40.0%), white (57.3% vs. 50.2%), and had higher BMI (36.0 vs. 29.9 kg/m2) than non-NAFLD. At Y30 NAFLD participants had higher LV mass, left atrial diameter, and LV relative wall thickness compared to non-NAFLD (p<0.01). Those with NAFLD had higher prevalence of LVH (31.9% vs. 18.2%), concentric remodeling (15.3% vs. 13.1%), concentric hypertrophy (12.9% vs. 7.9%) and eccentric hypertrophy (18.9% vs. 10.1%, p<0.0001). In multivariable analyses NAFLD was independently associated with prevalent LV remodeling (Table). Associations were attenuated after adjustment for HF risk factors. In contrast, NAFLD was associated with incident LVH independent of HF risk factors. Adjustment for BMI attenuated this association. There was no interaction by race or sex.
Conclusion: NAFLD is associated with subclinical changes in LV geometry and remodeling, a precursor to HF. The role of NAFLD in LV remodeling as a potential therapeutic target warrants further investigation.
Author Disclosures: L.B. VanWagner: B. Research Grant; Modest; Novartis. D. Speakers Bureau; Modest; Valeant (Salix) Pharmaceuticals. G. Consultant/Advisory Board; Modest; American Liver Foundation Medical Advisory Committee. J.E. Wilcox: None. H. Ning: None. C.E. Lewis:None. S.J. Shah: None. J.J. Carr: None. M.E. Rinella: None. J.A.C. Lima: None. D.M. Lloyd-Jones: None.
- © 2017 by American Heart Association, Inc.