Key result
NAFLD is linked to reduced flow-mediated dilation and increased carotid intima-media thickness versus healthy controls.
Why the study?
NAFLD is strongly associated with cardiovascular risk factors for atherosclerosis, but early atherosclerosis markers in NAFLD patients need evaluation.
Is nonalcoholic fatty liver disease associated with impaired flow-mediated dilation and increased carotid intima-media thickness?
Observational (n=161)
Is nonalcoholic fatty liver disease associated with impaired flow-mediated dilation and increased carotid intima-media thickness?
Absolute Event Rate: 5.9% vs 9.6%
p-value: p=<0.001
Nonalcoholic fatty liver disease is associated with impaired flow-mediated dilation and increased carotid intima-media thickness, indicating early atherogenesis.
May prompt CV risk vigilance in NAFLD; leaves open causality and need for prospective validation.
OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is characterized by the excessive accumulation of fat in the liver cells. It is strongly associated with cardiovascular risk factors for atherosclerosis. Flow-mediated dilation (FMD) and carotid intima-media thickness (CIMT) are noninvasive methods for the evaluation of endothelium. They are considered early markers of atherogenesis. The aim of this study was to evaluate early atherosclerosis markers in patients with NAFLD. METHODS: We examined 161 patients. All the patients underwent hepatic ultrasonography, transthoracic echocardiography, and brachial artery and carotid artery imaging. Fasting blood samples were drawn from all patients for the determination of lipids, insulin, C-peptide, and fasting blood glucose. HOMA-IR was calculated. RESULTS: Among the 161 patients, 44 had normal hepatic ultrasonography, 42 had stage 1 hepatosteatosis, 53 had stage 2 hepatosteatosis and 22 had stage 3 hepatosteatosis. FMD was reduced in patients with NAFLD as compared with the healthy controls (5.9 ± 3.1 vs. 9.6 ± 2.7%, P<0.001). There was a significant negative moderate correlation between ultrasonographic hepatosteatosis grade and FMD (r=-0.556, P<0.001). The mean CIMT was significantly increased in patients with NAFLD as compared with the controls (0.40 ± 0.19 vs. 0.27 ± 0.18, P<0.001). There was a significant positive weak correlation between ultrasonographic hepatosteatosis grade and mean CIMT (r=0.376, P<0.001). CONCLUSION: This study showed that NAFLD is associated with impaired CIMT and FMD, which are early markers of atherosclerosis. These findings may play a crucial role in understanding the pathophysiology of the atherosclerotic process in patients with NAFLD.
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Küçükazman et al. (2012) conducted an observational in Nonalcoholic fatty liver disease (n=161). Nonalcoholic fatty liver disease vs. Healthy controls was evaluated on Flow-mediated dilation (FMD) (p=<0.001). Nonalcoholic fatty liver disease was associated with significantly reduced flow-mediated dilation (5.9% vs. 9.6%, P<0.001) and increased carotid intima-media thickness compared to healthy controls.
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