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Types of arteriosclerosis – Atherosclerosis

Arteriosclerosis:

  • Literally means ”hardening of the arteries”
  • General terms reflecting arterial wall thickening and loss of elasticity

Three patterns recognized:

  • Arteriosclerosis of small arteries and arterioles:
    • 2 variants: hyaline and hyperplastic (both associated with vessel wall thickening and luminal narrowing)
    • most often associated with hypertension and/or diabetes
  • Mönckberg medial calcific sclerosis
    • Calcific deposits in muscular arteries
    • Typically in persons older than age 50
    • Do not invade the vessel lumen
    • Usually not clinically significant
    • Microscopically: deposits of calcium salts in the media, without associated inflammation -­‐> intima and adventitia not affected
  • Atherosclerosis:
    • most frequent and clinically important

 

Atherosclerosis:

  • a specific form of arteriosclerosis affecting primarily intima of large and medium-­‐sized muscular arteries and is characterised by fibrofatty plaques or atheromas.
  • Atheromatous plaque: raised lesion with a soft, yellow, grumous core (solid mass of granular tissue) of lipid (mainly cholesterol and cholesterol esters) covered by a firm, white fibrous cap.
  • Obstruct blood flow, weaken underlying media and rupture (thrombosis)
  • Most commonly affect: aorta, coronory artery and cerebral arterial

 

Risk factors:

1. Major risks:

A) Nonmodifiable:

  • Increasing age (accumulation of atherosclerotic plaque is a progressive process, age 40-­‐60 -­‐> incidence of myocardial infarction↑fivefold)
  • Male gender (uncommon in premenopausal women unless diabetes, hyperlipidemia or severe hypertension. ↑risk after menopause)
  • Family history (multifactorial, in some hypertension/diabetes)
  • Genetic abnormalities (derangements in lipoprotein metabolism, such as familial hypercholesterolemia)

B) Potentially controllable

  • Hyperlipidemia (hypercholesterolemia, especially ↑LDL serum levels)
  • Hypertension (mechanical injury to the arterial wall due to ↑BP) CLINICAL PATHOLOGY
  • Cigarette smoking (reduced level of HDL, deranged coagulation system and accumulation of carbon monoxide in the blood -­‐> produces carboxyhemoglobin and eventually hypoxia in the arterial wall)
  • Diabetes (type 1 and 2, especially type 2 with metabolic syndrome and hyperlipidemia)
  • C-­reactive protein (inflammation is linked with atherosclerotic plaque formation and rupture)

 

2. Lesser, uncertain, or nonquantitated risks:

  • Obesity
  • Physical inactivity
  • Stress (type A behaviour pattern)
  • Postmenopausal estrogen deficiency
  • ↑carbohydrate intake
  • Lipoproteins
  • ↑unsaturated fat intake
  • Chlamydia pneumoniae infection

 

Pathogenesis:

Most widely accepted theory: response-­to-­injury hypothesis It views atherosclerosis as a chronic inflammatory response of the arterial wall to the endothelial injury.

  • Chronic endothelial injury, with resultant endothelial dysfunction, causing (among other things) increased permeability, leukocyte adhesion and thrombosis)
  • Accumulation of lipoproteins (mainly LDL and its oxidized form) in the vessel wall
  • Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
  • Platelet adhesion
  • Factor release from activated platelets, macrophages, and vascular wall cells -­‐> inducing smooth muscle cell recruitment, either from the media or from circulating precursors
  • Smooth muscle cell proliferation and extracellular matrix production
  • Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cells)

 

Morphology:

  • Early lesions in the form of diffuse intimal thickening, fatty streaks and gelatinous lesions are usually precursors in evolution of atherosclerosis

1. Fatty streaks and dots

  • Composed of lipid-­‐filled foam cells, but not significantly raised
  • Harmless
  • May be precursor lesions to atherosclerotic plaques

Gross appearance:

  • Lesions may appear flat or slightly elevated and yellow CLINICAL PATHOLOGY
  • Begin as multiple small yellow, flat spots that can develop into elongated streaks

Microscopic appearance:

  • Fatty streaks lying under the endothelium are composed of closely-­‐ packed foam cells, lipid-­‐containing elongated smooth muscle cells and a few lymphoid cells

 

2. Atherosclerotic plaques

  • A fully developed atherosclerotic lesion
  • Most often and most severely affected is abdominal aorta, though smaller lesions may be seen in descending thoracic aorta and aortic arch

Gross appearance:

  • White to yellowish-­‐white lesions
  • Vary in diameter from 1-­‐2 cm
  • Raised surface by a few mm to a cm in thickness
  • Cut section: firm luminal surface, white fibrous cap and a central core composed of yellow to yellow-­‐white, soft, porridge-­‐like (grøt) material

Microscopic appearance:

  • Superficial luminal part of the fibrous cap is covered by endothelium and is composed of smooth muscle cells, dense connective tissue and extracellular matrix containing proteoglycans and collagen
  • Cellular area under fibrous cap is comprised by a mixture of macrophages, foam cells, lymphocytes and a few smooth muscle cells which may contain lipid
  • Deeper central soft core consists of extracellular lipid material, cholesterol clefts, fibrin, necrotic debris and lipid-­‐laden foam cells
  • In older and more advanced lesions, the collagen in the fibrous cap may be dense and hyalinised, smooth muscle cells may be atrophic and foam cells fewer
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About The Author
Dr.Iqbal
Dr.Iqbal
“So be sure when you step, Step with care and great tact. And remember that life's A Great Balancing Act. And will you succeed? Yes! You will, indeed! (98 and ¾ percent guaranteed) Kid, you'll move mountains.” ― Dr. Seuss, Oh, The Places You'll Go!
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