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| Slide Lecture Programs |
| Postintervention Continuum of Care: Focus on Lipids |
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November 1, 1999
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Achievements and challenges in medical interventional approaches
- Immediately after the intervention, there is deposition of proteins and platelets. This is a natural response and is intended to ?passivate? (render inert) the injured surface.
- Platelet aggregation and release of platelet-derived growth factor (PDGF) lead to formation of a white, platelet-rich thrombus.8 If passivation is successful, the extent of thrombus formation is limited, leaving an adequate lumen. However, while thrombus formation may not be significant in terms of lumen encroachment, it serves as a locus for the second phase of repair.
- The second phase is an inflammatory reaction involving mononuclear and polymorphonuclear leukocytes, which adhere to the injury site and secrete many mediators, including interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF a) and basic fibroblast growth factor (Basic FGF).12
- The inflammatory response stimulates smooth muscle cell migration from the media to the intima. These cells proliferate, secrete matrix material and become intermixed with the monocytes. This third phase peaks approximately 1 week after angiography and continues for some weeks after.12
- The final phase involves collagen deposition and remodeling of the arterial wall. Expansion of the matrix causes progressive narrowing and (within 6 to 12 months) restenosis. The arterial wall may expand and grow (remodel), thus facilitating maintenance of the lumen, or it may shrink and contribute to restenosis.
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