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Cardiovascular - atherosclerosis (RISK FACTORS (Hypertension, Immune…
Cardiovascular - atherosclerosis
C-reactive protein (CRP)
increases the expression of cell adhesion molecules
C-reactive protein causes down-regulation of endothelial nitric oxide synthase (eNOS)
Angiotensin II
induces significant leukocyte rolling, adhesion, and emigration,
Monocytes and macrophages
monocytes are activated and recruited to the developing lesion of
the arterial wall
monocytes increase the production of cytokines such as IL-8, IL-1β, and TNFα that
further contribute to the local inflammation
Once inflammation is established in the affected tissue, the second phase
described for the classical monocytes is the production and release of anti-inflammatory mediators such as TGF-β, IL-10, IL-
13, IL-4 and prostaglandin E2 in an effort to counteract ongoing inflammation
Nitrous oxide
As the disease progresses and the artery thickens, it becomes
increasingly difficult for NO to reach the smooth muscle that is still able to relax
The feedback effect of NO (together with prostacyclin) on platelet aggregation decreases steadily,
Dietary Impact
saturated fat and refined carbohydrates
induces oxidative and inflammatory stress
Type of plaque
Soft plaque
can rupture leading
to ischemic strokes
Hard plaque
may elicit up to 90%
blockage of the intima without a
person exhibiting any symptoms
RISK FACTORS
Hypertension
Immune mediated inflammatory disease
Lp(a) - a type of apoB lipoprotein
Increased inflammatory markers
Diabetes / Insulin resistance
Visceral adiposity
Endothelial dysfunction
Elevated homocysteine
Low omega 3 status / poor absorption
Chronic stress
Decreased oestrogen in women
Gut microbiota
engage in the metabolism of phospholipids
to yield a product (trimethylamine) that is further metabolized (to TMAO) in the host and that can
contribute to atherogenesis.