Cardio-vascular diseases have their roots in the slructursll and functional alterations in the vascular tree caused by the process of atherosclerosis. The term atherosclerosis indicates the collection of 'gruel' like materials inside the arteries (athero) along with hardening of the vessel wall (sclerosis). Normally the inner lining of the blood vessels (endothelium) is a smooth, glistening surface without any collection of materials and the vessel wall is in a dynamic state of contraction and relaxation depending on the metabolic demands and other influences. These maintain the smooth supply of blood to the organs according to the need. What causes the changes in the vessel wall with disruption in that demand-supply equation is a mystery, and a number of theories have been put forward to explain the process.
Basically, the mechanism of atheroma formation is thought to be related to:
i) a damage to the inner lining of blood vessels (injury theoiy) or
ii) changes in the blood lipids (lipid theory) or
iii) a combination of both, which is inore likely.
Damage to the inner lining (endothelium) makes the wall rough, irregular and dysfunctional. The changes in blood lipids with increase in bad cholesterol and its oxidation causes more damage, deposition of cholesterol rich cells, smooth muscle proliferation and fibrosis. These changes in endothelium and lipid fractions when combined together, results in atherosclerosis. Both these mechanis~ns are influenced by a number of factors or conditions, often interrelated ones and are labeled as Cardio-vascular risk factors.
Basically, the mechanism of atheroma formation is thought to be related to:
i) a damage to the inner lining of blood vessels (injury theoiy) or
ii) changes in the blood lipids (lipid theory) or
iii) a combination of both, which is inore likely.
Damage to the inner lining (endothelium) makes the wall rough, irregular and dysfunctional. The changes in blood lipids with increase in bad cholesterol and its oxidation causes more damage, deposition of cholesterol rich cells, smooth muscle proliferation and fibrosis. These changes in endothelium and lipid fractions when combined together, results in atherosclerosis. Both these mechanis~ns are influenced by a number of factors or conditions, often interrelated ones and are labeled as Cardio-vascular risk factors.
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