RELATIONSHIP BETWEEN TELOMERE LENGTH AND MARKERS OF INFLAMMATION IN THE PRE- AND POSTOPERATIVE PERIOD OF PATIENTS WITH CORONARY ARTERY DISEASE

Highlights Telomere length in patients with coronary artery disease is shorter compared to the telomere length of healthy individuals. Telomeric regions of DNA in patients with coronary artery disease do not recover over time. Telomere length in atherogenesis negatively correlates with markers of cardiovascular diseases and inflammatory process. Aim. To assess the impact of changes in the length of telomeric regions of chromosomes on the course of coronary artery disease caused by coronary artery atherosclerosis in the population of residents of a coal-mining region. Methods. The study included 60 patients with coronary artery disease (before surgery and five years after) and 52 healthy participants. We isolated the DNA using the standard phenol-chloroform extraction method. We used the quantitative PCR method to measure the relative length of leukocyte telomeres and analyzed biochemical parameters using standard methods, selecting cytokine proteins as markers of the inflammatory process. Results. Telomeres in healthy participants were seven times longer compared to patients with coronary artery disease. At the same time, the length of telomeric regions of DNA did not differ in patients before surgery and after 5 years of rehabilitation. We used ROC analysis to determine the effectiveness of measuring telomeres as a marker of atherosclerosis. The area under the ROC curve was 0.998 ± 0.002. We found an inverse correlation between the telomere length and such parameters as the total body sodium, triglycerides and high-density lipoproteins. We noted a significant inverse correlation between such indicators of the lipid profile as triglycerides and high-density lipoproteins only in patients before surgery. The study results revealed direct and inverse dependence of the length of telomeres and cytokines such as IL-33 and IL-10, respectively. Conclusion. Supposedly, inflammatory processes and oxidative stress, complementing each other, are the causes of irreparable damage to telomeres, accelerating the aging process and leading to irreversible consequences in atherogenesis.