V.М. Kovalenko, T.V. Talaieva, A.S. Kozlyuk, V.V. Bratus. Mechanisms of development of cardiovascular pathology in osteoarthrosis

The aim – to study the pathogenetic specificity of the vascular injury in patients with OA, the role of the traditional cardiovascular risk factors and, especially, factors linked to the systemic inflammation.

Material and methods. There were investigated 3 groups of patients – 1st group (main) – 83 patients with osteoartritis (OA), 2nd group (reference group) – 20 patients with metabolic syndrome without OA, 3rd group (control group) – 25 healthy persons. All groups were comparable by age and sex. In all patients vascular Doppler study was performed; besides, we determined endothelial dependent relaxation of the brachial artery with evaluation of intraluminar diameter and blood flow velocity, ankle-brachial index, lipid and lipoprotein blood spectrum, glucose and glycated hemoglobin blood content. The extent of the systemic inflammation was elaluated by C-reactive protein and malone dialdehyde blood content.

Results. The obtained data witness that OA even in early stages is accompanied with significant vascular damage on background of systemic inflammation and proatherogenic metabolic changes, such as insulin resistance, diabetic dyslipidemia, hyperglycemia, modification of LDL and VLDL. Nevertheless, vascular damages corresponded more to arteriosclerotic type, were generalized and appeared as morpho-functional remodelling of both systemic vessels and micro-circulatory vessels. The signs of the vascular damage were related to the indexes of systemic inflammation, but not to the traditional factors of atherogenesis.

Conclusions. Pronounced increase of cardiovascular risk in patients on the early stages of OA is related to the development of generalized arteriosclerosis, but not to the coronary atheroslerosis. Morpho-functional vascular disturbances in patients with OA are the consequences of mainly systemic inflammation. This should be taken into account in diagnosis, treatment and prevention of acute coronary syndrome.

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