The association between impaired collateral circulation and non-alcoholic fatty liver in patients with severe coronary artery disease

Background and purpose: Coronary collateral circulation (CCC) has been demonstrated to be impaired in patients with type 2 diabetes mellitus which is characterized by insulin resistance. In this study, our purpose was to find out a possible relationship between CCC and non-alcoholic fatty liver disease (NAFLD), which is also characterized by insulin resistance, in non-diabetic patients with severe coronary artery disease. Methods: One hundred and fifty-one consecutive non-diabetic patients with stable angina pectoris who were found to have >95% stenosis of at least one major coronary artery were enrolled. Abdominal ultrasonography (USG) was performed after coronary angiography to determine the presence or absence of NAFLD. Results: According to Cohen-Rentrop method, 81 (53.7%) patients had good and 70 (46.3%) patients had poor collateral development. NAFLD was present in 98 patients (64.9% of study population) and more prevalent in patients with poor collateral development [58 of 70 patients (82.9%) vs. 40 of 81 patients (49.4%), p < 0.001]. Mean Rentrop collateral score was significantly lower in patients with NAFLD (1.2 +/- 1.2 vs. 2.1 +/- 0.9, p < 0.001). Shorter angina time, metabolic syndrome, presence of insulin resistance, less severe coronary artery disease, and female sex were also associated with poor collateral development. When the logistic regression analysis was performed using these factors, NAFLD was still significantly related to poor collateral development. Conclusions: Presence of NAFLD is associated with poor coronary collateral development in non-diabetic patients with severe coronary artery disease independent from other variables, especially metabolic syndrome and insulin resistance. Which mechanisms play role in this association is needed to be cleared with further studies. (C) 2012 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.