CONTEXT: Nonalcoholic fatty liver disease (NAFLD) is associated with coronary artery calcification (CAC) in cross-sectional studies. However, whether NAFLD itself affects CAC development or progression remains unknown. OBJECTIVE: This study investigated the longitudinal association between NAFLD and CAC score. DESIGN AND SETTING: This study is a longitudinal cohort study performed in a healthcare center. PARTICIPANTS: Among 1732 subjects who underwent serial CAC evaluation, we evaluated 846 subjects with NAFLD and 886 subjects without NAFLD, as diagnosed via ultrasonography. MAIN OUTCOME MEASURES: CAC score was compared at baseline and follow-up. In subjects without calcification (CAC score = 0) at baseline, any incidental calcification (CAC score >0) at follow-up was defined as development of CAC. In subjects with CAC (CAC score > 0) at baseline, confirmed CAC aggravation was defined as progression. Logistic regression analysis was performed. RESULTS: More subjects with NAFLD than without showed CAC development or progression (48.8 vs 38.4%; P < .001). The impact of NAFLD on a change in CAC score significantly differed according to the CAC score at baseline. In subjects without calcification at baseline, NAFLD significantly affected the development of calcification (odds ratio, 1.49; 95% confidence interval, 1.01-2.21; P = .045) after adjusting for traditional metabolic risk factors. However, in subjects with baseline CAC, NAFLD did not significantly affect progression (P = .734). Additionally, the severity of NAFLD was important. The severity of NAFLD was dose-dependently associated with the development of CAC (P for trend = .043). CONCLUSIONS: NAFLD plays a role in the early development of CAC, but not the progression. Ultrasonographic severity of NAFLD is dose-dependently associated with CAC development in subjects with a CAC score of 0 at baseline, independent of traditional risk factors.
CONTEXT: Nonalcoholic fatty liver disease (NAFLD) is associated with coronary artery calcification (CAC) in cross-sectional studies. However, whether NAFLD itself affects CAC development or progression remains unknown. OBJECTIVE: This study investigated the longitudinal association between NAFLD and CAC score. DESIGN AND SETTING: This study is a longitudinal cohort study performed in a healthcare center. PARTICIPANTS: Among 1732 subjects who underwent serial CAC evaluation, we evaluated 846 subjects with NAFLD and 886 subjects without NAFLD, as diagnosed via ultrasonography. MAIN OUTCOME MEASURES: CAC score was compared at baseline and follow-up. In subjects without calcification (CAC score = 0) at baseline, any incidental calcification (CAC score >0) at follow-up was defined as development of CAC. In subjects with CAC (CAC score > 0) at baseline, confirmed CAC aggravation was defined as progression. Logistic regression analysis was performed. RESULTS: More subjects with NAFLD than without showed CAC development or progression (48.8 vs 38.4%; P < .001). The impact of NAFLD on a change in CAC score significantly differed according to the CAC score at baseline. In subjects without calcification at baseline, NAFLD significantly affected the development of calcification (odds ratio, 1.49; 95% confidence interval, 1.01-2.21; P = .045) after adjusting for traditional metabolic risk factors. However, in subjects with baseline CAC, NAFLD did not significantly affect progression (P = .734). Additionally, the severity of NAFLD was important. The severity of NAFLD was dose-dependently associated with the development of CAC (P for trend = .043). CONCLUSIONS: NAFLD plays a role in the early development of CAC, but not the progression. Ultrasonographic severity of NAFLD is dose-dependently associated with CAC development in subjects with a CAC score of 0 at baseline, independent of traditional risk factors.
Authors: Rosemay A Remigio-Baker; Matthew A Allison; Nketi I Forbang; Rohit Loomba; Cheryl A M Anderson; Matthew Budoff; Jeffrey B Schwimmer; Roger S Blumenthal; Pamela Ouyang; Michael H Criqui Journal: Atherosclerosis Date: 2016-11-17 Impact factor: 5.162
Authors: Lindsay T Fourman; Michael T Lu; Hang Lee; Kathleen V Fitch; Travis R Hallett; Jakob Park; Natalia Czerwonka; Julian Weiss; Takara L Stanley; Janet Lo; Steven K Grinspoon Journal: Physiol Rep Date: 2017-10-16