July 15, 2010Open Access
View Full PaperIncreased Arterial Stiffness and Impaired Endothelial Function in Nonalcoholic Fatty Liver Disease: A Pilot Study
Key Result
Nonalcoholic fatty liver disease was associated with higher carotid-femoral pulse wave velocity (8.2 vs 6.9 m/s, P=0.001) and reduced flow-mediated dilatation (1.92% vs 4.8%, P<0.001).
Study Design
Type
Case-Control (n=51)
Structured PICO
Does the presence of nonalcoholic fatty liver disease (NAFLD) worsen arterial stiffness and endothelial function compared to matched controls?
P
Population
51 subjects, including 23 consecutive patients with biopsy evidence of nonalcoholic fatty liver disease (NAFLD) (mean age 55 ± 14 years, 11 males) and 28 control subjects matched for age, gender, body mass index, and other cardiovascular risk factors.
I
Intervention
Presence of nonalcoholic fatty liver disease (NAFLD)
C
Comparator
Control subjects matched for age, gender, body mass index, and other cardiovascular risk factors
O
Outcome
Functional arterial changes and early atherosclerosis measured by carotid-femoral pulse wave velocity (PWV), carotid intima-media thickness (IMT), and flow-mediated dilatation (FMD)surrogate
NAFLD is independently associated with increased arterial stiffness and endothelial dysfunction, providing a potential mechanism for the increased cardiovascular risk observed in these patients.
Main Result
Absolute Event Rate: 8.2% vs 6.9%
p-value: p=0.001
Abstract
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease both in the general and pediatric population and has been associated with increased cardiovascular risk. Arterial function and early atherosclerotic changes are markers of cardiovascular disease and independent predictors of the corresponding risk. Through a global approach, we investigated the relationships between NAFLD and functional arterial changes and early atherosclerosis. METHODS: A total of 23 consecutive patients (mean age 55 ± 14 years, 11 males) with biopsy evidence of NAFLD and 28 control subjects matched for age, gender, body mass index, and other cardiovascular risk factors participated in the study. RESULTS: Compared to controls, NAFLD subjects had significantly higher carotid-femoral pulse wave velocity (PWV; 8.2 ± 1.3 m/s vs. 6.9 ± 1.3 m/s, P = 0.001), higher carotid intima-media thickness (IMT; 0.79 ± 0.18 mm vs. 0.67 ± 0.13 mm, P = 0.01), and reduced flow-mediated dilatation (FMD; 1.92 ± 2.11% vs. 4.8 ± 2.43%, P < 0.001). In multivariable analysis, presence of NAFLD was an independent determinant of both PWV and FMD, whereas leptin was an independent determinant of PWV (B = 0.036, P < 0.05), and adiponectin was independently associated with FMD (B = 0.104, P < 0.05). In addition, histological activity of liver disease expressed by the global Brunt Grade was associated independently with FMD (B = -1.054, P < 0.05). CONCLUSIONS: NAFLD is associated with arterial stiffness and endothelial dysfunction. Given the important independent prognostic role of these arterial indexes, these findings have important implications for increased cardiovascular risk in patients with NAFLD.