Atherosclerosis
From Anvita Health Wiki
Contents |
More Specific Terms
Introduction
Etiology
- Risk factors: (also see coronary artery disease)
- male age > 45 years
- female age > 55 years
- estrogen deficiency
- elevated LDL cholesterol (> 160 mg/dL)
- low HDL cholesterol (< 35 mg/dL)
- smoking
- hypertension
- elevated homocysteine
- elevated insulin
- diabetes mellitus
- immune complexes (i.e. lupus erythematosus)
- stress
- depression
- low plasma antioxidants
- physical inactivity
- elevated triglycerides
- dietary saturated fat
- small, dense LDL particles
- increased Lp<a>
- increased VLDL remnants
- increased IDL
- leukocytosis
- thrombocytosis & increased platelet activity
- increased fibrinogen
- increased factor VIIa
- increased C-reactive protein
Pathology
- hemodynamic injury
- hypertension
- wall shear stress
- chemical injury
- infection/immune mediated injury
- atheromatous plaque formation
- lipid infiltration through injured endothelium
- invasion of monocytes that mature into resident macrophages
- coalescence into fatty streaks
- macrophage rupture forming lipid core of maturing atheromatous plaque
- fibrous tissue produced by migrating smooth muscle cells
- participation of:
- hydroxyapatite crystals are present in early lesions
- atheromatous plaque growth
- growth is slow, averaging 3% reduction in luminal diameter yearly of 0.03-0.05 mm/year
- atheromatous plaques generally do not narrow the coronary lumen until after 3-4 decades
- rapid growth can occur from intraplaque hemorrhage & intimal injury with incorporation of thrombotic material
- mature plaque is eccentric
- 2 dominant forms, may be present in same patient
- gradually occlusive fibrous plaque
- plaque with soft lipid core & thin fibrous cap
- prone to rupture
- responsible for most acute ischemic events
- rupture or fissure of atheromatous plaque
- weakening of the fibrous cap
- rupture of fissure of a relatively soft, lipid-rich atherosclerotic plaque exposes subendothelial structures
- platelet activation
- thrombosis
- procoagulant state 6 AM-11 AM
- peak incidence of stroke, MI, sudden cardiac death in this time interval
- relative resistance to thrombolytic therapy in this time interval
- * oxidized choline glycerophospholipids activate platelet CD36, promote platelet activation, impair endothelial function & increase foam cell concentration within atherosclerotic plaques [3]
Genetics
Laboratory
- regression of atherosclerosis associated with reduction in LDL cholesterol & increase in HDL cholesterol
More General Terms
Additional Terms
- coronary artery disease (CAD)
- endothelin-1 (ET-1)
- peripheral vascular disease; PVD; peripheral arterial disease; PAD
Internet Database
OMIM: 108725
References
- Medical Knowledge Self Assessment Program (MKSAP) 11, American College of Physicians, Philadelphia 1998
- Nicholls SJ et al, Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis. JAMA 2007, 297:499
- Podrez EA, Byzova TV, Febbraio M, Salomon RG, Ma Y, Valiyaveettil M, Poliakov E, Sun M, Finton PJ, Curtis BR, Chen J, Zhang R, Silverstein RL, Hazen SL. Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype. Nat Med. 2007 Sep;13(9):1086-95. Epub 2007 Aug 26. PMID: [1]
- Jackson SP, Calkin AC. The clot thickens-oxidized lipids and thrombosis. Nat Med. 2007 Sep;13(9):1015-6. <PubMed> PMID: [2] <Internet> [3] - What is Atherosclerosis? [4]
- National Guideline Clearinghouse
- Atherosclerosis ngc-guideline: [5]
- Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. ngc-guideline: [6]
