Now Reading
Types of arteriosclerosis – Atherosclerosis


  • 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



  • 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



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)



  • 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
What's your reaction?
Nice Theme
About The Author
“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!
Leave a response

Leave a Response