HSC 4555 Lecture Notes - Lecture 18: Perspiration, Stenosis, Angina Pectoris
Document Summary
Endothelial injury and inflammation, and lipid accumulation in the intima are thought to be the primary initiators of coronary plaque formation. Low-density lipoproteins (ldls) leak through the endothelium and into the vessel wall where they are oxidized by endothelial cells and macrophages. Oxidized lipids are damaging to the endothelial and smooth muscle cells, and stimulate the recruitment of macrophages into the vessel wall where they engulf the lipids. Lipid-filled macrophages are called foam cells, which release inflammatory mediators and growth factors that attract more leukocytes and stimulate smooth muscle proliferation. Progression of the coronary plaque continues as excess lipid and debris begins to accumulate within the vessel wall and coalesce into a pool called the lipid core (pgs. Factors that alter the balance between myocardial oxygen supply and demand include atherosclerotic coronary arteries, abnormalities of blood oxygen content, and poor perfusion pressure through the coronary arteries (pg.
