A 64-year-old man presents to the Emergency Department complaining of substernal chest pain. An acute coronary event is suspected and a coronary catheterization procedure reveals an atherosclerotic plaque in the patient’s left anterior descending artery. In the formation of an atherosclerotic plaque, which of the following pairings is correct?
1.Fibroblasts foam cells
2.Smooth muscle cells ECM deposition
3.Endothelial cells downregulation VCAM-1
4.Smooth muscle cells migration from intima to media
5.LDL chemical reduction ednothelial dysfunction
sol:
In the formation of an atherosclerotic plaque, smooth muscle cells (SMCs) are responsible for the deposition of extracellular matrix (ECM) in the intima. SMC proliferation and SMC-mediated ECM deposition are major processes leading to intimal thickening.
There are several mechanisms leading to endothelial dysfunction, including dyslipidemia and inflammation. This dysfunction allows for the deposition of LDL in the intima and the recruitment of monocytes. Factors released by injured endothelial cells and monocytes contribute to SMC migration and proliferation. Combined, these processes lead to the formation of an atheroma (atherosclerotic plaque).
Hall et al. discuss the usefulness of lipid reduction in secondary prevention of further coronary artery disease. They note that the reduction of cholesterol levels decreases the risk of recurrent coronary events and that this may be achieved by using statins, for example.
Rivard et al. describe the proliferation of vascular smooth muscle cells as a major player in the formation of atherosclerotic plaques. The authors note that “targeted specific cell-cycle control genes or growth regulatory molecules” that inhibit SMC proliferation, might prove beneficial in preventing neointimal formation.
Illustration A displays several hallmarks of atherosclerosis including intimal thickening (black arrow), lipid deposition, and narrowing of the lumen (red arrow).
Illustration B shows the process of plaque formation.