Contribution of neovascularization and intraplaque @entity548 to XXXX plaque progression and instability.

@entity1187 @entity32 @entity64 @entity68 @entity39 @entity548 @entity397 @entity731 @entity8557 @entity165
UNASSIGNED: @entity731 is a continuous pathological process that starts early in life and progresses frequently to unstable plaques. @entity397 leads to deleterious consequences such as @entity1187 , @entity64 and atherothrombosis. The vulnerable lesion has several structural and functional hallmarks that distinguish it from the stable plaque. The unstable plaque has large @entity39 core (over 40% plaque volume) composed of @entity165 crystals, @entity8557 , oxidized lipids, fibrin, erythrocytes and their remnants (haeme, @entity68 , 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 @entity548 . @entity548 deliver erythrocytes to the @entity39 core where they degrade promoting @entity32 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 @entity32 . Plaque destabilization is an evolutionary process that could start at early @entity731 stages and whose progression is influenced by many factors including neovascularization, intraplaque @entity548 , formation of @entity165 crystals, @entity32 , oxidative stress and intraplaque protease activity.
