The article gives details information about the mechanism of atherosclerosis and arteriosclerosis. In particular, it states that atherosclerosis affects medium and large arteries, with the formation of focal thickening, and in most severe cases are clogging the arteries. Arteriosclerosis - a disease in which the small arteries of muscular type, as well as in large vessels develop hypertrophy of the muscular layer and sub intimal fibrosis with hyaline degeneration.

Arteriosclerosis vs atherosclerosis

Arteriosclerosis - generalized disease in which a small muscular arteries (arteriolosclerosis), as well as in large vessels develop hypertrophy of the muscular layer and sub intimal fibrosis with hyaline degeneration. With age, there are fibrosis and a thickening of the intima with a decrease in the number and disruption of the structure of elastic fibers in the walls of large arteries (e.g. aorta and its major branches). Come some atrophy of the medial (smooth muscle layer) and an increase in the lumen of the aorta and one or more of its branches (ecstasies) with the possible formation of an aneurysm. This process may have a genetic origin.

Develops diffuse calcification with loss of elasticity of the vascular wall. Hemodynamically, these changes are manifested an increase in pulse and systolic blood pressure. In the elderly, in some cases there is degeneration of the smooth muscle media (arteriosclerosis Menkeberg). May develop damage and ulceration of the intima with subsequent formation of clots that lead to embolism or thrombosis.

Atherosclerosis affects medium and large arteries, for it characterized by the formation of focal intramural sub intimal thickenings, which act in the lumen of the artery and in the most severe cases clog it. Atherosclerotic plaque consists of an accumulation of intra-and extracellular lipids, smooth muscle cells, connective tissues and glycosaminoglycans.

The earliest atherosclerotic changes are fat strips (consisting of lipid-laden foam cells - macrophages, represented by monocytes migrating from the bloodstream to the sub endothelial layer of the intima) and later converted into fat strips of the fibrous plaque (consisting of intimal smooth muscle cells surrounded by connective tissue and intra-and extracellular lipids).

Strains affected by atherosclerosis during systole are reduced, and pulse wave velocity is pathologically enlarged. Elasticity modified arteriosclerosis of the arteries in patients with hyper-tensor is also reduced and it becomes even less if associated atherosclerosis. Diabetes leads to extensive atherosclerosis, which develops at a younger age and appears as a manifestation of generalized metabolic disorder that includes dyslipidemia, and glycosylation of connective tissue.

Proposed two main hypotheses to explain the pathogenesis of atherosclerosis: the lipid hypothesis and the hypothesis of chronic endothelial damage.

According to the lipid hypothesis, elevated levels of low density lipoprotein (LDL) in plasma promote their penetration into the arterial wall and accumulate in the smooth muscle cells and macrophages (foam cells). LDL increase as hyperplasia of smooth muscle cells caused by growth factors. In the presence of endothelial cells, oxidized LDL and acquire properties that increase their atherogenicity. Thus, oxidized LDL chemotactically attracts monocytes and in the early stages of atherosclerosis may contribute to their appearance in the strips and the accumulation of fat under the intima in the form of macrophages. Oxidized LDL also have cytotoxic properties towards endothelial cells, and it is possible that they are responsible for the disappearance of the endothelium of atherosclerotic plaques in the later stages of atherosclerosis.