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Atherosclerosis
Various immunodeficiencies
Clinical
Fever > 38.5
Splenomegaly
Laboratory
Cytopenia of => 2/3 cell lines
Hypertriglyceridemia and/or
hypofibrinogenemia
Histopathology
Hemophagocytosis in bone marrow
or spleen or liver or lymphnode
Prognosis
Arteriosclerosis
Thickening and loss of elasticity of arterial
walls
Hardening of the arteries
Prevalence
In US there are 6 million with CAD
3 million Americans have had strokes
Mortality
1.5 million deaths/yr in US due to
myocardial infarction
0.5 million deaths/yr in US due to strokes
Three patterns of arteriosclerosis
Atherosclerosis
The dominant pattern of arteriosclerosis
Primarily affects the elastic (aorta, carotid,
iliac) and large to medium sized muscular
arteries (coronary, popliteal)
Monckeberg medial calcific sclerosis
Arteriolosclerosis small arteries and
arterioles (hypertension and DM)
Non-Modifiable Risk Factors
Age
A dominant influence
Atherosclerosis begins in the young, but does not
precipitate organ injury until later in life
Gender
Men more prone than women, but by age 60-70
about equal frequency
Family History
Familial cluster of risk factors
Genetic differences
Modifiable Risk Factors
(potentially controllable)
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes Mellitus
Elevated Homocysteine
Factors that affect hemostasis and
thrombosis
Infections: Herpes virus; Chlamydia
pneumoniae
Obesity, sedentary lifestyle, stress
AHA Classification of atherosclerosis
Fig. 11.7
Normal Artery
Normal Artery
Atherosclerosis
A disease of the intima
A disease of the intima
A disease of the intima
Atheromas, atheromatous/fibrofatty
plaques, fibrous plaques
Narrowing/occlusion; weakness of wall
Major components of plaque
Cells (SMC, macrophages and other WBC)
(Often calcification)
Two major processes in plaque
formation
Lipid accumulation
Consequences of plaque
formation
Generalized
Narrowing/Occlusion
Rupture
Emboli
Cause?
Current hypothesis: Response to Injury
Initiated by endothelial dysfunction
Disease of the intima
Intimal thickening
Intra- and extra-cellular lipid accumulation
Chronic Inflammation
Basic Lesion: is termed atheroma, fibro-fatty
plaque, or atheromatous plaque
Response to injury hypothesis
* Injury to the endothelium
(dysfunctional endothelium)
* Chronic inflammatory response
* Migration of SMC from media to intima
* Proliferation of SMC in intima
Excess production of ECM
Enhanced lipid accumulation
Response to injury hypothesis (I)