Rano B. Alieva
Republican Specialized Scientific & Practical Medical Center of Cardiology, Uzbekistan
Abstract Title:
CD36 and PCSK9 Levels in Patients with Chronic Coronary Syndrome
Biography:
Rano Alieva is a cardiologist. Her areas of expertise include imaging, cardio-oncology and lipid metabolism disorders. She is PhD, DSc, a senior research fellow at the Laboratory of Chronic coronary syndrome and Atherosclerosis at the Republican Specialized Scientific and Practical Medical Center of Cardiology. She is the author of 96 articles and 3 monographs. Member of the editorial board of the Journal of Cardiology of Uzbekistan
Research Interests:
Introduction: The interaction between CD36 and PCSK9 forms a vicious cycle in the pathogenesis of chronic coronary syndrome (CCS): PCSK9-mediated hypercholesterolemia increases the uptake of oxidized LDL via the CD36 scavenger receptor into macrophages, while inflammation within the plaque further stimulates the expression of both proteins. Aim of the study – to compare the levels of CD36 and PCSK9 in patients with CCS (Group 1) and in healthy individuals (Group 2), and to identify the relationship between these markers. Material and methods: A total of 108 subjects were prospectively enrolled in the study: 80 patients with CCS and 28 healthy individuals. All participants underwent clinical examination, as well as laboratory and instrumental investigations, including measurement of CD36 and PCSK9 levels. Results: The mean age was 65.4 ± 6.2 years in Group 1 and 41.2 ± 4.2 years in Group 2. The groups were comparable with respect to sex distribution. The CD36 level in Group 1 was 22.6 ± 5.2 ng/mL, whereas in Group 2 it was 14.7 ± 3.1 ng/mL, representing a statistically significant difference (p = 0.038). The PCSK9 level was 561.5 ± 202.1 ng/mL in Group 1 and 217 ± 96.4 ng/mL in Group 2 (p = 0.021). The Pearson correlation coefficient between these two parameters was 0.17 (p < 0.05). Conclusions: Thus, in our study, CD36 and PCSK9 levels were significantly higher in patients with CCS compared with healthy individuals; however, the correlation between these markers was weak. These findings require validation in large‑scale clinical studies.
