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Nonalcoholic fatty liver disease is associated with coronary artery disease in Koreans
Dae Hee Choi1, Sung Joon Lee, Chang Don Kang
1Dae Hee Choi, Sung Joon Lee, Chang Don Kang, Myoung Ok Park, Dong Wook Choi, Tae Suk Kim, Wonho Lee, Byung Ryul Cho, Yong Hoon Kim, Bong-ki Lee, Dong Ryeol Ryu, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon 200-701, South Korea.
Insights
Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for coronary artery disease (CAD), with severity correlating to disease progression. Adiponectin may play a role in the pathogenesis of NAFLD and CAD.
Area of Science:
- Cardiology
- Hepatology
- Metabolic Syndrome
Background:
- Nonalcoholic fatty liver disease (NAFLD) is a growing health concern.
- Coronary artery disease (CAD) remains a leading cause of mortality worldwide.
- The relationship between NAFLD and CAD requires further investigation.
Purpose of the Study:
- To determine if NAFLD is associated with CAD.
- To identify potential mediators linking NAFLD and CAD.
- To assess the grade-dependent relationship between NAFLD and coronary artery stenosis.
Main Methods:
- 134 patients undergoing coronary angiography were classified by coronary artery stenosis.
- Abdominal ultrasonography diagnosed and graded NAFLD.
- Serum levels of insulin, HOMA-index, adiponectin, IL-6, TNF-α, and hs-CRP were measured.
Main Results:
- 61.2% of patients had NAFLD; 80.4% of CAD patients had NAFLD.
- NAFLD was significantly associated with CAD in a grade-dependent manner (P=0.025).
- NAFLD independently predicted CAD (P=0.03, OR=1.685). Adiponectin showed a trend towards lower levels with CAD progression (P=0.071).
Conclusions:
- NAFLD is an independent, grade-dependent risk factor for CAD.
- Adiponectin may be involved in the pathogenesis of NAFLD and its association with CAD.
Aim:
To investigate whether nonalcoholic fatty liver disease (NAFLD) affects coronary artery disease (CAD) and identify candidate mediators.
Methods:
Patients who underwent coronary angiography were consecutively recruited. The patients were classified into four groups by coronary artery stenosis: A, insignificant; B, one-vessel disease; C, two-vessel disease; and D, three-vessel disease. Abdominal ultrasonography was performed to determine the presence of a fatty liver and categorize by grade: 0, no evidence; 1, mild; 2, moderate; and 3, severe. We measured not only known CAD risk factors, but also serum insulin, HOMA-index, adiponectin, interleukin-6, tumor necrosis factor-α and high-sensitivity C-reactive protein levels.
Results:
Of the 134 patients who met the inclusion criteria, 82 (61.2%) had ultrasonographically diagnosed NAFLD. Among the 46 patients with CAD, 37 (80.4%) had evidence of a fatty liver. The two groups (A vs B-D) were significantly different in terms of age, total cholesterol, triglycerides, low-density lipoprotein levels and fatty liver. Coronary artery stenosis was strongly associated with fatty liver in a grade-dependent manner (P = 0.025). In binary logistic regression, NAFLD was a significant independent predictor of CAD (P = 0.03, OR = 1.685; 95%CI: 1.051-2.702). Among the candidate mediators, the serum adiponectin level showed a trend toward lowering based on CAD progression (P = 0.071).
Conclusion:
NAFLD is an independent risk factor for CAD in a grade-dependent manner. Moreover, adiponectin might be related to the pathogenesis of NAFLD.
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