Rolul inflamaţiei sistemice în evoluţia afecţiunilor cardiovasculare

Abstract

Background: Growing clinic-experimental evidences suggest notable systemic inflammation implication in the pathogenesis of multiple cardiovascular diseases. This article is aimed at underlying the most important referred to inflammation mechanisms causing circulatory disorders and proven predictors of their diagnosis and prognosis. It has been established that crucial triggering factor of inflammatory response is the nuclear transcription factorkappaB whose activation leads to increased quantity and expression of a lot of inflammation mediators, like C reactive protein, cytokines (TNF-alpha, interleukins), chemokines (MCP-1) and intercellular adhesion molecules (selectins, integrins) which basically guide the sequestration of circulatory leukocytes. These mediators are responsible for inflammation sustaining and dissemination. On the other hand IL-10 is defined as a cytokine having anti-inflammatory action. The common effects of inflammation are endothelial dysfunction associated with NO synthesis impairment, oxidative stress boosting, extracellular matrix reorganization resulted from metalloproteinase activation, cell migration proliferation and apoptosis, neointima hyperplasia and plaque destabilization. Conclusions: Recent studies indicate the inflammation pathogenic value in the major adverse cardiovascular events development in patients undergone primary coronary revascularization by angioplasty, inclusive in-stent restenosis. Diabetes mellitus, smoking, dislipidemia, metabolic syndrome, hyperhomocysteinemia, arterial hypertension are main cardiovascular risk factors leading to inflammatory response augmentation.