Proliferation and apoptosis of smooth muscle and endothelial cells with immune inflammation in cerebrovascular diseases on atherosclerosis background

The aim – to determine the role of vascular wall cells proliferation and apoptosis with the participation of immune inflammation, and their impact on the development of cerebrovascular disease (CVD) development on the atherosclerosis (AS) background. Materials and methods. We studied 50 cases of death with ischemic stroke and 50 cases of death with hemorrhagic stroke on the cerebral vessels AS background. Outcomes. Lymphocytes are one of the atheroma components and are mainly localised at the sites of plaque rupture in close contact with macrophages and smooth muscle cells. Smooth muscle cells are able to synthesize important collagen and elastin for the vascular wall, but potentiated apoptosis of smooth muscle cells may contribute to destabilisation and plaque rupture. Smooth muscle cells apoptosis was triggered by proinflammatory factors and took place with the participation of cytotoxic T-lymphocytes (T-killers) therefore in the atherosclerotic lesions focus we registered an accumulation of multitude cytotoxic T-lymphocytes. Conclusions. The macrophages and smooth muscle cells susceptibility to apoptosis was significantly higher directly in the atheroma, but macrophage apoptosis is a useful process for the atherosclerotic plaque stability. Desquamation and endothelial cell apoptosis are interrelated processes that play an important role in atheromatous plaque formation.