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Common Congenital Heart Lesions - page 33 / 126





33 / 126

33 of 126

  • This process is mediated by substances secreted by foam cells, activated platelets, and endothelial cells. Examples of this include:

    • o

      PDGF, which is secreted by foam cells and helps to stimulate the migration of SMCs into the subendothelial space.

      • o

        Cytokines (ie. TNF-a, IL-1, TGF-b), which are secreted by foam cells and along with activating WBCs, induces SMC proliferation and ECM protein synthesis.

*Altogether, it is the migration of SMCs from the media to the intima, the

accumulation of WBCs and foam cells, and the formation of the ECM-derived fibrous cap that generates the fibrous plaque characteristic of advanced atherosclerosis.

Fibrous Plaque

  • Localized in the same sites as fatty streaks

  • Appear as firm, gray lesions

  • May project into the lumen, and if large enough, create a significant stenosis or obstruction to blood flow

  • Has a necrotic core of cellular debris, as a result of the toxic effects of mLDL and of free oxygen radicals & hydrolytic enzymes derived from foam cells and T cells

  • Thrombogenic due to its necrotic core. This is attributed to:

    • o

      Production of TF by foam cellsÆ activation of coagulation

      • o

        Release of PDGF by activated plateletsÆ degradation of heparin sulfate, a compound normally involved in the inhibition of SMC migration and proliferation.

3. Differentiate the clinical presentation and pathophysiology of coronary artery stenosis from coronary artery thrombosis

...So, I couldn’t find any specifics in the book about this nor was there anything specific in the powerpoint lectures…I’ll email Dr. Smith for key points and get back to you…

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