LDL infiltrates intimat of arteriol wall, modified by oxidation and enzymes which cause release of leukocytes which leads to inflammatory proteins (cytokines, TNF, IL-6, C-reactive protein)
reversible by diet
response to injury/infection, nonspecific stress response, capillaries become more permeable to allow phagocytes to destroy.
norepinephrine and epinephrine, increase metabolic rate, glycogen breakdown in liver and muscle, glucose production from amino acids, release of fatty acids from adipose tissue, glucagon secretion from pancreas.
glycogen breakdown in liver, glucose production from amino acids, release of fatty acids from adipose tissue.
protein degradation, enhancement of glucagons action on liver glycogen, glucose production from amino acids, release of fatty acids from adipose tissue.
hormone involved in retention of stodium
hormone involved in retention of water
additional immune response to atherosclerosis
T cells patrol arteries for antigens, if found produce cytokines for inflammation. promote atherosclerosis in response to infection.
acute phase protein produced by liver and increased in systemic infection. may be additional test for CVD risk. highly sensitive in increased risk of heart attack, sudden death, peripheral artery disease.
Test suggestions for CRP using global risk assessment
factors increasing release of chemicals and activation of immune cells
cigarette smoking, hypertension, atherogenic lipoproteins, hyperglycemia, all give rise to variety of noxious stimuli that cause release of chemicals and activation of cells involved in inflammatory process which can cause formation of plague and clots causing CHD.
Modifiable Risk Factors in CVD
markers in blood, lipoprotein profile, inflammatory markers, lifestyle risk factors, related diseases.
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