OBJECTIVES: The objective of this study was to identify the presence of non-alcoholic fatty liver disease (NAFLD) in patients with coronary artery disease (CAD). METHODS: 149 patients were selected, who had been referred to the Institute of Cardiology, Banglore, India, between January 2007 and June 2009 and diagnosed with CAD. Four patients did not participate in the study. Venous blood samples were taken from these cases, and agematched healthy controls who came for a master health check-up (N = 100). All were subjected to routine liver function tests including serum transaminases, enzyme immunoassays for plasminogen activator inhibitor I (PAI-I), C reactive protein (CRP), and tumour necrosis factor-alpha (TNF-α). Using ultrasonography and serum alanine aminotransferase (ALT) levels, the presence of NAFLD in CAD patients was reported. RESULTS: CAD patients with NAFLD had significantly higher liver enzymes and marginally higher A1C levels compared to control subjects. Levels of TNF-α and PAI-I were higher in CAD patients with NAFLD compared to both female and male controls (P <0.1 and P <0.05). Levels of CRP (P <0.01 in both groups) and uric acid were increased in both group of patients (P <0.05 and P <0.01 in male and female patients, respectively). Levels of adiponectin were significantly reduced in the patients compared to the controls (P <0.05 and P <0.001) in male and female patients respectively. CONCLUSION: The increased serum levels of PAI-I and TNF-α reflected the proinflammatory status in these CAD patients which may be due to the presence of NAFLD. This could contribute additively to the development of cardiovascular events (CVD).
OBJECTIVES: The objective of this study was to identify the presence of non-alcoholic fatty liver disease (NAFLD) in patients with coronary artery disease (CAD). METHODS: 149 patients were selected, who had been referred to the Institute of Cardiology, Banglore, India, between January 2007 and June 2009 and diagnosed with CAD. Four patients did not participate in the study. Venous blood samples were taken from these cases, and agematched healthy controls who came for a master health check-up (N = 100). All were subjected to routine liver function tests including serum transaminases, enzyme immunoassays for plasminogen activator inhibitor I (PAI-I), C reactive protein (CRP), and tumour necrosis factor-alpha (TNF-α). Using ultrasonography and serum alanine aminotransferase (ALT) levels, the presence of NAFLD in CAD patients was reported. RESULTS: CAD patients with NAFLD had significantly higher liver enzymes and marginally higher A1C levels compared to control subjects. Levels of TNF-α and PAI-I were higher in CAD patients with NAFLD compared to both female and male controls (P <0.1 and P <0.05). Levels of CRP (P <0.01 in both groups) and uric acid were increased in both group of patients (P <0.05 and P <0.01 in male and female patients, respectively). Levels of adiponectin were significantly reduced in the patients compared to the controls (P <0.05 and P <0.001) in male and female patients respectively. CONCLUSION: The increased serum levels of PAI-I and TNF-α reflected the proinflammatory status in these CAD patients which may be due to the presence of NAFLD. This could contribute additively to the development of cardiovascular events (CVD).
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