In Russia, the prevalence of obesity is detected in all age groups and is commonly revealed in more than 50% of the examined cases; the same trend exists in other countries of the world [1]. Within the framework of the epidemiological study ESSE-RF 2, significant associations of cardiac ischemia coronary with obesity, especially abdominal obesity, were noted without gender specificities [2][3]. Obesity is a serious challenge to the quality and longevity of life. Obese people live an average of 15.4 years less than people with normal weight [4]. Body mass index (BMI) is considered the gold standard for diagnosing obesity but it is not a reliable indicator of body constitution since it cannot show the distribution of fat tissue in the body. Indices such as waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WC/HC) are more associated with progressing myocardial infarction risk [5]. Obesity promotes the accumulation of epicardial fat and fatty infiltration of the myocardium [6]. Increased epicardial adipose tissue (EAT) becomes a source of free fatty acids contributing to the clinical and metabolic complications caused by obesity [7].

The purpose of the study was to assess the dynamics of EAT thickness and lipid profile in patients with different BMIs over 48 months of their monitoring.

The study was approved by the local ethics committee. According to the inclusion and exclusion criteria, 121 men were selected for the prospective open-label study. The average age of the subjects was 59.4 ± 8.5 years. Inclusion criteria were the following: informed consent signed by the patient, age of men over 18 years and under 74 years, percutaneous coronary intervention with lesions of no more than two vessels, and no more than two stents installed. Exclusion criteria involved recurrent acute myocardial injury, the presence of clinical concomitant pathology, and a history of type 2 diabetes mellitus.

Three main test groups were separated: group I included 24 patients with normal BMI (20%), group II consisted of 35 patients with excess BMI (29%), and group III consisted of 62 patients with obesity (51%). The control group (IV) included 27 apparently healthy men. Three stages of prospective examination of patients were defined: the first one was at the time of hospitalization, and then in 12 and 48 months (±2 weeks) from the index event. At each examination at the research center, in addition to measuring BMI, WC, and WC/HC, the EAT thickness was determined by ultrasound, as well as blood lipid levels were tested. Calculation of the linear thickness of EAT was carried out in the B-mode of the echocardiography (EchoCG) technique in the standard left parasternal position along the long and short axis of the left ventricle with a sensor Philips Epiq 7. WC and height were measured, and BMI was calculated according to the WHO classification. Throughout the study, patients took at least 80% of the obligatory medication groups, according to the Morisky-Green questionnaire of adherence to therapy.

Statistical analysis and processing of collected data were performed using the R Project for Statistical Computing (version 3.2, R Foundation for Statistical Computing, Vienna, Austria) and Statistica 10.0.228.8 (InstallShield Software Corp., Chicago, IL, USA) software. A comparison of variables in groups was carried out using the Mann-Whitney and Kruskal-Wallis tests. The differences were considered statistically significant at the p<0.05 level.

Adherence to therapy was assessed using the Morisky–Green Scale (MMAS-4), which implies the total intake of at least 80% of prescribed medications. At the stage of 12 months (n=108 people), 103 patients (95.37%) received lipid-lowering therapy; at the end of 48 months (n=102 people), 83 patients (81.37%) received lipid-lowering therapy. Patients of different BMI groups were comparable in terms of lipid-lowering therapy.

EAT thickness measured by echocardiography in patients with an acute ST-elevation myocardial infarction (STEMI) correlated with BMI and WC measuring data throughout all stages of the study (Figs. 1–3). WC correlated with epicardial tissue thickness with a strong positive relation, in contrast to BMI, where the correlation was moderate.

In Figure 4, one can see that EAT thickness in patients with STEMI increased in two groups, namely in patients with over-BMI and in patients with obesity, at all stages from the beginning to the end of the study (p<0.05), and was significantly higher than in the control group and the group of patients with normal BMI.

EAT thickness through all stages of the study had a weak positive correlation with the levels of blood triglycerides (TGs), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) and did not have a correlation with high-density lipoprotein cholesterol (HDL-C) (Table 1).

Increased TC, hypertriglyceridemia, and decreased HDL-C were significantly more common in the group of patients with obesity. At the time of hospitalization, the values of LDL-C, TGs, and total blood cholesterol in the patients were augmented along with an increase in BMI and were significantly higher in the group of patients with obesity; the HDL-C level, on the contrary, dropped as BMI increased. At the outpatient stage, in groups with different BMIs, no significant decreases in lipid profile parameters were detected compared to the hospital stage. Hypertriglyceridemia and an increase in LDL-C as well as the TC level persisted in patients with an increased BMI. Besides, a corresponding decrease in HDL-C was also kept (Table 2).

Obesity and endothelial injuries contribute to progressive lipid metabolism disorders and accelerate the atherosclerosis process [8]. The increase in LDL-C in patients with obesity is accounted for by the endocrine dysfunction of the adipose tissue and the disorders of the synthesis and metabolism of atherogenic lipoproteins [9]. In patients with STEMI included in this study, the level of LDL-C was higher than in the control group. Patients with obesity maintained elevated LDL-C and TG levels through all stages of the study, which did not contradict data presented by other researchers [10]. HDL-C in the index group was within the normal range, but the consideration of the obtained data by BMI values in the groups revealed a significant drop in the HDL-C level as BMI increased; these data were also consistent with the results presented in other works [11].

Epidemiological investigations confirmed the association of EAT thickness with atherosclerosis [12]. Dönmez described an elevation of the LDL-C and TC levels upon increasing the EAT thickness in patients with and without familial hypercholesterolemia [13]. Manno drew attention to the fact of an increase in LDL-C in patients with excess BMI and obesity upon increasing EAT thickness [14]. Wu described a negative relationship between EAT thickness and HDL-C [15]. Goeller found negative relationships between EAT volume and HDL-C levels and positive relationships with LDL and TGs in patients with early atherosclerosis. What deserves special attention in his work is the fact that EAT density, unlike its thickness, had inverse relationships with lipid profile parameters in those patients [16]. In the geriatric population, the accumulation of EAT along with obesity was determined by the TC and LDL-C levels [17]. Upon cardiac ischemia coronary, EAT increased to a greater extent at unstable angina compared with exertional angina [17]. An increase in EAT thickness has been shown in visceral obesity and augmenting of BMI [6][18]. Positive correlations between EAT thickness and BMI and WC have been identified in patients with cardiac ischemia [19]. In the patients included in the study, EAT thickness was positively correlated with BMI and WC through all stages of the examination.

The failure to achieve target lipid levels in examined patient groups may be stipulated by the insufficient titration of lipid-correcting therapy doses.

With an increase in BMI in men who had suffered a STEMI, the thickness of the EAT increased and became significantly higher by the 48th month of observation in groups of patients with excess BMI and patients with obesity. Patients with obesity and excess BMI had significantly higher levels of TC, LDL-C, and TGs but significantly lower levels of HDL-C in the blood serum. Positive correlations between EAT and the levels of TC, LDL-C, and TGs were established during the 48-month monitoring.