Association postprandial hypertriglyceridemia, levels of leptin and carotid intima-media thickness in patients with coronary artery disease combined with nonalcoholic liver steatosis

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Abstract Funding Acknowledgements Type of funding sources: None. Main funding source(s): - Objective To estimate the frequency of postprandial hypertriglyceridemia (PPG), levels of leptin, carotid intima-media thickness in patients with coronary artery disease (CHD) combined with nonalcoholic liver steatosis (NALS). Methods We studied 61 patients with CHD in combination with NALS mean age 57,8±2,04 (group A) and 20 patients with CHD without NALS mean age 56,6±4,6 (group B). Patients with diabetes were excluded. Studied PPG, levels of leptin and carotid intima-media thickness. Results Revealed an increase in the level of triglycerides after fat load test in group A by 57% (from 2.27 [1.74; 2.77] mmol/l to 3.56 [2.60; 4.89] mmol/l), in the group B by 203% (s 1.24 [1.05; 1.86] mmol/l to 3.76 [1.64; 5.51] mmol/l). In patients in a group A identified the highest leptin levels 20,9 [12,3; 24,6] ng/ml than in a group B- 13,2 [7,3; 16,9] ng/ml, (p <0,02). Carotid wall thickness was lower in a group A (0,14±0,02 cm) than in a group B (0,16±0,01 cm, p =0,01). Frequency of exposure of atherosclerotic carotid plaques in a group A – 82%, was higher than in a group B – 64% (p <0,05). In group A unstable plaques found significantly more often (31%, p = 0,01), than in the control group B (8%). There was correlation between PPG and unstable plaques (r=0,75, p=0,03) in a subgroup with obesity grade 2. Conclusion The incidence of unstable atherosclerotic plaques of carotid arteries in the group with CAD and NALS was higher (34%) unlike patients with CAD without NALS (5%). It has been shown for the first time that under the conditions of the combined course of CAD with liver steatosis, an increase in body weight is associated with a reduced reaction of postprandial TG levels with an increase in leptin levels. According to the results of ROC analysis of significant predictors of liver steatosis in the group of patients with CAD were levels of leptin (AUC for leptin – 0.69 (0.56-0.82)).

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