Scientists studying atherosclerosis know that the build-up of atheroma is an inflammation and thickening due to an immune defense mechanism gone wrong.
32.
Regarding atheroma development and progression as opposed to regression, the key issue has always been cholesterol transport patterns, not cholesterol concentration itself.
33.
Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen.
34.
The most promising since the early 1990s has been EBT, detecting calcification within the atheroma before most individuals start having clinically recognized symptoms and debility.
35.
Historically, arterial wall fixation, staining and thin section has been the gold standard for detection and description of atheroma, after death and autopsy.
36.
In contrast, HDL particles ( especially large HDL ) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma.
37.
The concentration of these other components, which may cause atheroma, is known as the "'non-HDL-C " '.
38.
Macklin, who conducted the postmortem, concluded that the cause of death was atheroma of the coronary arteries exacerbated by " overstrain during a period of debility ".
39.
Methods to increase high-density lipoprotein ( HDL ) particle concentrations, which in some animal studies largely reverses and remove atheromas, are being developed and researched.
40.
From human clinical trials, it has become increasingly evident that a more effective focus of treatment is slowing, stopping and even partially reversing the atheroma growth process.
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