Vessels are the conduits by which blood is distributed to and from the organs. Obstruction or occlusion of vessels leads to ischemia of the organs, which causes cell death (necrosis). The most common cause of obstruction or occlusion of vessels is arteriosclerosis (“hardening of the arteries”).
Pressure within the vessels is determined by a combination of contraction of cardiac muscle and resistance created by the vessels themselves. Changes in this system (e.g., increased vascular resistance) can lead to hypertension, which can cause irreversible damage of the vessels. Examples of structural changes include narrowing of the lumen and dilations of vessels (i.e., aneurysms). Other disorders (e.g., vasculitis) as well as hypertension can cause vascular injury. This chapter will discuss arteriosclerosis and atherosclerosis, systemic hypertension, aortic dissection, pulmonary hypertension, aneurysms, vasculitis, and vascular proliferations.
Overview: Arteriosclerosis is also known as “hardening” or sclerosis of the arteries and occurs in three main forms, Mönckeberg medial calcification, arteriolosclerosis, and atherosclerosis.
Mönckeberg medial calcification: A condition of little clinical significance because the changes are nonstenotic. It is characterized by medial calcification (“pipestem rigidity”) of the muscular arteries (often radial and ulnar arteries) in elderly men.
Arteriolosclerosis: Thickening of arterioles (see the discussion below on systemic hypertension).
Pathogenesis of atherosclerosis
Chronic endothelial cell injury by hyperlipidemia, hypertension, toxins in cigarette smoke, elevated levels of homocysteine, and hemodynamic forces (e.g., turbulent blood flow) leads to endothelial cell dysfunction.
Endothelial cells regulate vasodilation and constriction, promote hemostasis, and otherwise prevent thrombosis. Endothelial dysfunction promotes thrombosis and increased permeability as well as allows monocytes and lymphocytes to adhere to the surface and migrate into the intima.
Low-density lipoproteins (LDL) can move into and out of the intima; however, the presence of macrophages (derived from blood monocytes) results in production of enzymes that oxidize LDL. Oxidized LDL is engulfed by macrophages through scavenger receptors.
Finally, smooth muscle cells migrate into the intima: The smooth muscle cells convert from a contractile role in the media to a secretory role in the intima, where they produce extracellular matrix. Smooth muscle cells secrete extracellular matrix components (e.g., collagen) that contribute to the development of plaque. Smooth muscle cells, like macrophages, are capable of engulfing oxidized LDL.
Important points regarding atherosclerosis
- Atherosclerosis begins as an intimal process; the changes in the media occur secondary to changes in the intima.
- Macrophages that engulf LDL die and release oxidized LDL, causing intracellular and extracellular lipid to accumulate within plaque.
- Elevated levels of high-density lipoproteins (HDL) are protective. HDL removes LDL from the wall of the vessel. Moderate alcohol consumption and exercise have been demonstrated to increase HDL levels.
Risk factors for atherosclerosis
- Major and modifiable risk factors (i.e., modifiable through changes in lifestyle): Smoking, diabetes mellitus, hypertension, and hyperlipidemia. The term “metabolic syndrome” describes a group of metabolic risk factors that includes ...
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