Cardio-rheumatology: present and future. Part I

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Abstract

Patients suffering from rheumatic diseases are at high risk of the development and accelerated progression of cardiovascular due to inflammation as one of the etiological factors of atherogenesis and heart failure. To choose the rational and safe treatment, especially in comorbid patients, it is necessary to have a comprehensive and complete understanding of the mechanisms of these relationships, as well as the most accurate determination of cardiovascular risk using modern validated scales. The first part of the review presents the results of current experimental and clinical studies on the effect of the chronic inflammatory and its biomarkers on the development, course and prognosis of cardiovascular diseases.

About the authors

Yi Ma

The third Xiangya Hospital of the Central South University

Email: mayi2908@yandex.ru
ORCID iD: 0000-0002-2339-4263

MD, Cand. Sci. (Medicine)

China, Changsha

Zhuo Wang

The third Xiangya Hospital of the Central South University

Email: wangzhuo1008@yandex.ru
ORCID iD: 0000-0002-2415-4982

MD, Cand. Sci. (Medicine)

China, Changsha

Vadim I. Mazurov

North-Western State Medical University named after I.I. Mechnikov; Clinical Rheumatology Hospital No. 25

Email: maz.nwgmu@yandex.ru
ORCID iD: 0000-0002-0797-2051
SPIN-code: 6823-5482

MD, Dr. Sci. (Medicine), Professor, Academician of the RAS, Honored Scientist of the Russian Federation

Russian Federation, Saint Petersburg; Saint Petersburg

Evgeniy A. Trofimov

North-Western State Medical University named after I.I. Mechnikov

Email: evgeniy.trofimov@szgmu.ru
ORCID iD: 0000-0003-3236-4485
SPIN-code: 4358-1663

MD, Dr. Sci. (Medicine)

Russian Federation, Saint Petersburg

Roman A. Bashkinov

North-Western State Medical University named after I.I. Mechnikov; Clinical Rheumatology Hospital No. 25

Author for correspondence.
Email: bashkinov-roman@mail.ru
ORCID iD: 0000-0001-9344-1304
SPIN-code: 5169-5066

assistant of the department

Russian Federation, Saint Petersburg; Saint Petersburg

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2. Figure. The role of inflammation in the formation of atherosclerotic plaque [1]. At the early stage, endothelial dysfunction and subintimal accumulation of cholesterol crystals initiate an inflammatory reaction. At the same time, an increase in the expression of cell adhesion molecules (ICAM, VCAM) and various selectins promotes the migration of immunocompetent cells to the sites of early formation of atherosclerotic plaques. Hypoxia and phagocytosis by macrophages of cholesterol in the form of oxidized low-density lipoprotein (Ox-LDL) are accompanied by the assembly of the NLRP3 inflammasome, which results in the activation of interleukin-1β (IL-β) and interleukin-18 (IL-18). In turn, pro-inflammatory cytokines induce procoagulant activity, increased adhesion to endothelium, proliferation of smooth muscle cells (SMC), increase the production of reactive oxygen species (ROS) and potentiate the inflammatory cascade with the production of interleukin-6 (IL-6) in the vascular wall. T cells, mast cells and dendritic cells support the transmission of signals modulating the formation and growth of atherosclerotic plaques, including by increasing the synthesis of tumor necrosis factor alpha (TNF-α), while the accumulation of foam cells is complicated by the formation of a necrotic lipid core. Moreover, interleukin-1β activates the production of matrix metalloproteinases (MMP) that damage collagen in the atherosclerotic plaque cap. Finally, in the process of increasing the size of the lipid core, the thinning of the fibrous capsule leads to its instability, and also raises the likelihood of rupture and subsequent thrombosis

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