Contribution of neovascularization and intraplaque haemorrhage to atherosclerotic plaque progression and instability.
Atherosclerosis is a continuous pathological process that starts early in life and progresses frequently to unstable plaques. Plaque rupture leads to deleterious consequences such as acute coronary syndrome, stroke and atherothrombosis. The vulnerable lesion has several structural and functional hallmarks that distinguish it from the stable plaque. The unstable plaque has large necrotic core (over 40% plaque volume) composed of cholesterol crystals, cholesterol esters, oxidized lipids, fibrin, erythrocytes and their remnants (haeme, iron, haemoglobin), and dying macrophages. The fibrous cap is thin, depleted of smooth muscle cells and collagen, and is infiltrated with proinflammatory cells. In unstable lesion, formation of neomicrovessels is increased. These neovessels have weak integrity and leak thereby leading to recurrent haemorrhages. Haemorrhages deliver erythrocytes to the necrotic core where they degrade promoting inflammation and oxidative stress. Inflammatory cells mostly presented by monocytes/macrophages, neutrophils and mast cells extravagate from bleeding neovessels and infiltrate adventitia where they support chronic inflammation. Plaque destabilization is an evolutionary process that could start at early atherosclerotic stages and whose progression is influenced by many factors including neovascularization, intraplaque haemorrhages, formation of cholesterol crystals, inflammation, oxidative stress and intraplaque protease activity.
['Chistiakov|D A|DA|', 'Orekhov|A N|AN|', 'Bobryshev|Y V|YV|']
D000818:Animals D050197:Atherosclerosis D001808:Blood Vessels D002784:Cholesterol D018450:Disease Progression D006454:Hemoglobins D006470:Hemorrhage D006801:Humans D018836:Inflammation Mediators D007501:Iron D009389:Neovascularization, Pathologic D010447:Peptide Hydrolases D058226:Plaque, Atherosclerotic D012307:Risk Factors D012422:Rupture, Spontaneous D015398:Signal Transduction
neovascularization atherosclerotic plaque atherosclerosis inflammation arterial wall atherogenesis