Atherosclerosis

Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form

of arteriosclerosis in which an artery wall thickens as a result of the accumulation of
calcium and fatty materials such as cholesterol and triglyceride. It reduces the
elasticity of the artery walls and therefore allows less blood to travel through. This
also increases blood pressure. It is a syndrome affecting arterial blood vessels, a
chronic inflammatory response in the walls of arteries, caused largely by the
accumulation of macrophages and white blood cells and promoted by low-density
lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without
adequate removal of fats and cholesterol from the macrophages by functional highdensity lipoproteins (HDL) (see apoA-1 Milano). It is commonly referred to as a
hardening or furring of the arteries. It is caused by the formation of
multiple plaques within the arteries. The atheromatous plaque is divided into three
distinct components

CAUSE
The atherosclerotic process is not fully understood. Atherosclerosis is initiated by inflammatory
processes in the endothelial cells of the vessel wall in response to retained low-density
lipoprotein (LDL) molecules.[14]
Lipoproteins in the blood vary in size. Some data suggests that only small dense LDL (sdLDL)
particles are able to get behind the cellular monolayer ofendothelium. LDL particles and their
content are susceptible to oxidation by free radicals,[15] and the risk may be higher while in the
bloodstream. However, LDL particles have a half-life of only a couple of days, and their content
(LDL particles carry cholesterol, cholesteryl esters, and tryglycerides from the liver to the tissues
of the body) changes with time.
Once inside the vessel wall, LDL particles get stuck and their content becomes more prone to
oxidation. The damage caused by the oxidized LDL molecules triggers a cascade of immune
responses which over time can produce an atheroma. First the immune system sends specialized
white blood cells (macrophages and T-lymphocytes) to absorb the oxidized LDL, forming
specialized foam cells. These white blood cells are not able to process the oxidized LDL. They
grow and then rupture, depositing a greater amount of oxidized cholesterol into the artery wall.
This triggers more white blood cells, continuing the cycle. Eventually, the artery becomes
inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over
the affected area. This hard cover is what causes a narrowing of the artery, reducing blood flow
and increasing blood pressure

SYMPTOMS
Atherosclerosis is often asymptomatic pending grave blockage and narrowing of an artery.
Signsand symptoms usually come out when the severe blockage impedes blood flow to different
organs.[7] Most of the time, patients realize that they have the disease only when they experience
other cardio vascular disorders such as stroke or heart attack. These symptoms, however, still
vary depending on which artery or organ is affected. [8] Typically, atherosclerosis begins as a thin
layer of white streaks on the artery wall (usually due to white blood cells) and progresses from
there. Clinically, atherosclerosis is typically associated with men over the age of 45. Sub-clinically,
the disease begins to appear at early childhood, and perhaps even at birth. Noticeable signs can
begin developing at puberty. Though symptoms are rarely exhibited in children, early screening of
children for cardiovascular diseases could be beneficial to both the child and his/her relatives.
[9]
While coronary artery disease is more prevalent in men than women, atherosclerosis of the
cerebral arteries and strokes equally affect both sexes

TREATMENT
Medical treatments often focus on alleviating symptoms. However measures which focus on
decreasing underlying atherosclerosisas opposed to simply treating symptomsare more
effective.[60] Non-pharmaceutical means are usually the first method of treatment, such as
stopping smoking and practicing regular exercise.[61][62] If these methods do not work, medicines
are usually the next step in treating cardiovascular diseases, and, with improvements, have
increasingly become the most effective method over the long term.
The key to the more effective approaches has been better understanding of the widespread and
insidious nature of the disease and to combine multiple different treatment strategies, not rely on
just one or a few approaches.[63] In addition, for those approaches, such as lipoprotein transport
behaviors, which have been shown to produce the most success, adopting more aggressive
combination treatment strategies taken on a daily basis and indefinitely has generally produced
better results, both before and especially after people are symptomatic