Atherosclerosis by neha

Project
on
ATHEROSCLEROSIS
By
Neha vishwakarma

INTRODUCTION
Cardiovascular disorders have been the major cause of death in western societies. In India, due to industrialization
and a change in the living pattern during the past three to four decades, the incidence of cardiovasculardisorders
has been on the increase. It is thus, becoming a major cause of death especially in the adult male population.
Cardiovascular disorders include the diseases of heart and blood vessels such as atherosclerosis leading to coronary
heart disease (CHD) and hypertension.
Atherosclerosis is a pathological process in the coronary arteries, cerebral arteries and aorta that are responsible
for coronary heart disease and stroke.
The term atherosclerosis has been derived from the Greek word athere meaning gruel, as the lesions formed have a
deposit of yellow porridge like material. Atherosclerosis begins during childhood in the intima of the large elastic
and muscular arteries with deposits of lipids, principally cholesterol and its esters, triglycerides, ceroid, deposits of
calcium and iron,red blood cells and fibrous tissue in macrophages and smooth muscle cells. These result in
lesions called fattystreaks, which produce only minimal intimal thickening and cause no disturbances in blood
flow during early childhood, but they rapidly become more extensive during adolescence.

In the young adults more lipid is deposited at some
sites, and a core of lipid and necrotic debris become
covered by a cap of smooth muscle and fibrous
tissue. These changes produce elevated lesions
called fibrous plaque that project into the
lumen and begin to disturb blood flow. Such
lesions in the coronary arteries lead to coronary
heart disease, which is the most common and
the most serious manifestation of atherosclerotic
cardiovascular disease in the middle aged adults.
The fatty degeneration and the thickening
narrows the lumen of the blood vessel and this plaque
is highly susceptible to rupture which then promotes
blood clot formation within artery (thrombosis). A blood clot
(thrombus) can enlarge in time and ultimately obstruct blood flow. A portion of a clot may also break
free (embolus) and travel through the circulatory system until it lodges in a narrowed artery and shuts off blood
flow to the surrounding tissue (embolism). If this occurs in a major coronary blood vessel the tissue area supplied
by this artery is deprived of its vital oxygen and nutrient supply(ischemia) and the cells die. Thelocalised area of
dying or dead tissue is called an infarct. Since this occurs in the cardiac muscle or myocardium, the end result is
called myocardial infarction.

Afterwards, the dead or necrotic tissue is replaced by connective tissue. The patient may recover cardiac function
as the remaining heart hypertrophies to compensate for myocardium lost by infarction. At any stage, the patient
may die from failure of the heart to pump sufficient blood due to the condition of congestive heart failure.
Stenosis of the coronary arteries sometimes is sufficient to cause ischemic pain, but not infarction, especially on
exertion. This condition is called angina pectoris. It indicates the presence of severe lesions and high risk of
myocardial infarction. All these syndromes (angina pectoris, MI, sudden cardiac death) are included in the term
CHD.

Pathophysiology
ASCVD involves the accumulation of
plaque within the walls of the
arteries. It starts with injury to the
endothelial cells with an associated
inflammatory response involving
phagocytes and monocytes. Once in
the tissue, monocytes evolve into
macrophages that ingest oxidized
cholesterol and become foam cells
and then fatty streaks in these
vessels. Intracellular
microcalcification occurs, forming
deposits within the
vascular smooth muscle cells of the
surrounding muscular layer.

A protective fibrin layer (atheroma) forms between the fatty deposits and the artery lining. Atheromas produce
enzymes that cause the artery to enlarge over time, thus compensating for thenarrowing caused by the
plaque. This “remodeling” of the shape and size of the blood vessel may result in an aneurysm.
Atheromas can rupture or break off, forming a thrombus (blood clot), where theyattract blood platelets and
activate the clotting system in the body. This response can result in a block-age and restricted blood flow.
Only high-risk or vulnerable plaque forms thrombi. Vulnerable plaque are lesions with a thin fibrous cap, few
smooth muscle cells, many macrophages (inflammatory cells), and a large lipid core (see Figure 33-2). Arterial
changes begin in infancy and progress asymptomatically throughout adulthood .
The clinical outcome of impaired arterial function arising from atherosclerosis depends on the location of the
impairment. In the coronary arteries atherosclerosis can cause angina (chest pain), MI, and sudden death; in
the cerebral arteries it causes strokes and transient ischemic attacks; and in the peripheral circulation it
causes intermittent claudication, limb ischemia (inadequate blood supply), and gangrene. Thus atherosclerosis
is the underlying cause of many forms of CVD.Dyslipidemia refers to a blood lipid profile that increases the risk of
developing atherosclerosis. Three important biochemical measurements in ASCVDinclude lipoproteins, total
cholesterol, and triglycerides. Cholesterol is delivered into cell walls by low-densitylipoprotein (LDL),
especially smaller particles. To attract and stimulate the macrophages, the cholesterol must be released from the
LDL particles and oxidized, a key step in the ongoing inflammatory process. Additionally, macrophages must move
excess cholesterol quickly into high-densitylipoprotein (HDL) particles to avoid becoming foam cells and dying.
The typical dyslipidemic condition is one in which LDL levels are elevated (hyperlipidemia) and HDL levels are
low.

CAUSES
Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidized (LDL-ox) by free
radicals, particularly oxygen free radicals (ROS).
When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair the damage to the
artery wall caused by oxidized LDL. The LDL molecule is globular shaped with a hollow core to carry
cholesterol throughout the bodyto generate brain tissues, vitamin D, and so on. Cholesterol does not dissolve in
water. Blood is 70% water. Cholesterol can move in the bloodstreamonly by being transported byLDL.
The body's immune systemresponds to the damage to the artery wall caused by oxidized LDL by sending
specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming
specialized foam cells. Unfortunately, these white blood cells are not able to process the oxidized-LDL, and
ultimately grow 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, reduces the blood
flow and increases blood pressure. Some researchers believe that atherosclerosis may be caused by an infection
of the vascularsmooth muscle cells. Chickens, for example, develop atherosclerosis when infected with the
Marek's disease herpesvirus.. Herpesvirus infection of arterial smooth muscle cells has been shown to cause
cholesteryl ester (CE) accumulation. Cholesteryl ester accumulation is associated with atherosclerosis. Also,
cytomegalovirus (CMV) infection is associated with cardiovascular diseases.

SYMPTOMS
Atherosclerosis typically begins in early adolescence, and is usually found in most major arteries, yet is
asymptomatic and not detected by most diagnostic methods during life. Atheroma in arm, or more often in leg
arteries, which produces decreased blood flow is called peripheral artery occlusive disease (PAOD). According to
United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of
atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of
onset of the symptom). Most artery flow disrupting events occur at locations with less than 50% lumen narrowing
(~20% stenosis is average). Cardiac stress testing, traditionally the most commonly performed non-invasive testing
method for blood flow limitations, in general, detects only lumen narrowing of ~75% or greater, although some
physicians claim that nuclear stress methods can detect as little as 50%.
The list of signs and symptoms mentioned in
various sources for Atherosclerosis includes
the 20 symptoms listed below:
• No early symptoms
• Symptoms of coronary artery disease
o Angina
o Heart attack

o Coronary thrombosis
• Symptoms of brain artery disease
O Stroke
 Transient ischemic attack
• Symptoms of leg artery disease
o Leg blood clot
o Leg pain
o Leg cramps
o Intermittent claudication
• Other symptoms
o Erectile dysfunction
Atherosclerosis usuallydoesn't cause signs and symptoms until it severely narrows or totally blocks
an artery.

• Angina may feel like pressure or a squeezing pain in your chest. You also may feel it in your shoulders, arms,
neck, jaw, or back. This pain tends to get worse with activity and go away when you rest. Emotional stress also can
trigger the pain.
• Shortness of breath
• Arrhythmias (irregular heartbeats).
• Sudden numbness, weakness, and dizziness.
Signs and symptoms of atherosclerosis are not visible until the arteries are severely narrowed or blocked. Signs and
symptoms differ depending on the arteries affected by atherosclerosis.
Coronary Artery Disease(CAD):
Once the arteries supplying blood to heart are blocked, the cells in the heart begin to die and a heart attack may
occur. Themost common symptoms of Coronary Artery Disease (CAD) are:
1. Chest pain with a heavy, squeezing or crushing sensation with possible burning or stabbing pain
2. Abdominal, neck, back, jaw or shoulder and arm pain
3. Nausea and vomiting sensation
4. Fatigue

5. Weakness
6. Perspiration
7. Shortness of breath
8. Depression and anxiety
Carotid Artery Disease or CerebrovascularDisease:
Cerebrovascular disease is caused due to reduced supply of oxygen rich blood to brain leading to transient
ischemic attack (meaning sudden loss of brain function and complete recovery within a day) and stroke. Some
of the symptoms include:
1. Paralytic stroke on one side of the body
2. Inability to comprehend speech, or to have garbled speech
3. Loss of vision in one of the eyes
4. Muscle weakness
5. Impairment of facial muscles
6. Poor coordination
7. Involuntary and jerky movements on one side of the body
8. Rapid and iterative involuntary eye movement

9. Vertigo
Peripheral Artery Disease (PAD):
Accumulation of plaque in the arteries supplying blood to the hands and feet lead to PAD. Some of the symptoms
of PAD include:
1. Pain, cramps, numbness and sense of fatigue in muscles of limbs
2. Diminished pulses in the hands and feet
3. Reduced muscle mass
4. Blowing sounds that can be heard with the help of a stethoscope indicating turbulence in blood flow (also
called as “Bruits”)
5. Loss of hair
6. Thickening of nails
7. Smooth and shiny skin surface
8. Gangrene
AbdominalAngina and Bowel Infarction:
Narrowing of intestinal arteries leads to abdominal angina and bowel infarction.
Some of the symptoms are:

1. Cramping pain in the middle of the abdomen
2. Severe abdominal pain with vomiting and diarrhea or abdominal swelling

RISKFACTORSFORATHEROSCLEROSIS
Coronary artery disease is the leading cause of death in the United States and while the exact cause of
atherosclerosis remains unknown, certain traits, conditions, or habits may raise a person's chance of developing it.
These conditions are known as risk factors and a person's chances of developing atherosclerosis increase with the
number of risk factors they have - most risk factors can be controlled and atherosclerosis can be prevented or
delayed - these include high Cholesterol and low-density lipoprotein (LDL) in the blood, low level of high-
density lipoprotein (HDL) in the blood, Hypertension (high blood pressure), tobacco smoke, Diabetes
Mellitus, Obesity, inactive lifestyle, age - a family history of heart disease is also a risk factor and the one which
cannot be controlled.

Unhealthy blood cholesterol levels - this includes high LDL cholesterol (sometimes called bad cholesterol)
and low HDL cholesterol (sometimes called good cholesterol).
High blood pressure - blood pressure is considered high if it stays at or above 140/90 mmHg over a period of time.
Smoking - this can damage and tighten blood vessels, raise cholesterol levels, and raise blood pressure - smoking
also doesn't allow enough oxygen to reach the body's tissues.
Insulin resistance - Insulin is a hormone that helps move blood sugar into cells where it's used and insulin
resistance occurs when the bodycannot use its own insulin properly.

Diabetes - this is a disease in which the body's blood sugar level is high because thebody doesn't make enough
insulin or does not use its insulin properly.
Overweight or obesity - overweight is having extra body weight from muscle, bone, fat, and/or water - obesityis
having a high amount of extra body fat.
Lack of physical activity - lack of activity can worsen other risk factors for atherosclerosis.
Age - as the body ages the risk for atherosclerosis increases and genetic or lifestyle factors cause plaque to
gradually build in the arteries - by middle-age or older, enough plaque has built up to cause signs or symptoms, in
men, the risk increases after age 45, while in women, the risk increases after age 55.
Family history of early heart disease - the risk for atherosclerosis increases if a father or a brother was diagnosed
with heart disease before 55 years of age, or if a mother or a sister was diagnosed with heart disease before 65
years of age but though age and a family history of early heart disease are risk factors, it does not mean
that you will develop atherosclerosis if you have one or both. Making lifestyle changes and/ortaking medicines to
treat other risk factors can often lessen the genetic influences and prevent atherosclerosis from developing, even in
older adults.
Emerging Risk Factors
Scientists continue to study other possible risk factors for atherosclerosis and have found that high levels of a
protein called C-reactive protein (CRP) in the blood may raise the risk for atherosclerosis and heart attack -

high levels of CRP are proof of inflammation in the body which is the body's response to injury or infection -
damage to the arteries' inner walls appears to trigger inflammation and help plaque grow.
People with low CRP levels may get atherosclerosis at a slower rate than people with high CRP levels and research
is currentlyunder way to establish whether reducing inflammation and lowering CRP levels also can reduce the
risk of atherosclerosis.
High levels of fats called triglycerides in the blood also may raise the risk of atherosclerosis, particularlyin
women.
Other Factors That AffectAtherosclerosis
Other risk factors also may raise your risk for developing atherosclerosis include:
Sleep apnoea - a disorder in which the breathing stops or gets very shallow while a person is sleeping -
untreated sleep apnoea can raise the chances of high blood pressure, diabetes, and even a heart attack or stroke.
Stress - research shows that the most commonly reported "trigger" for a heart attackis an emotionally upsetting
event-particularlyone involving anger.
Alcohol - heavy drinking can damage the heart muscle and worsen other risk factors for atherosclerosis - men
should have no more than two drinks containing alcohol a day, while women should have no more than one
drink containing alcohol a day.
Modifiable
• Having diabetes or Impaired glucose tolerance (IGT) +

• Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats & cholesterol)
 High serum concentration of low-density lipoprotein (LDL, "bad if elevated concentrations and small"),
and / or very low densitylipoprotein (VLDL) particles, i.e., "lipoprotein subclass analysis" .
o Low serum concentration of functioning high density lipoprotein (HDL "protective if large and high
enough" particles), i.e., "lipoprotein subclass analysis"
o An LDL:HDL ratio greaterthan 3:1
• Tobaccosmoking, increases risk by 200% after several pack years
• Having high blood pressure +, on its own increasing risk by 60%
• Elevated serum C-reactive protein concentrations
Non modifiable
• Advanced age
• Male sex
• Having close relatives who have had some complication of atherosclerosis (e.g. coronary heart disease or
stroke)
• Genetic abnormalities, e.g. familial hypercholesterolemia
Lesser or uncertain

The following factors are of relatively lesser importance, are uncertain or non-quantitated :
• Being obese (in particularcentral obesity, also referred to as abdominal or male-type obesity)
• A sedentary lifestyle
• Postmenopausalestrogen deficiency
• High carbohydrate intake
• Intake of trans -fat
• Elevated serum levels of triglycerides +
• Elevated serum levels of homocysteine
• Elevated serum levels of uric acid (also responsible for gout)
• Elevated serum fibrinogen concentrations
• Elevated serum lipoprotein (a) concentrations
• Chronic systemic inflammation as reflected by upper normal WBC concentrations, elevated hs-CRP and
many other blood chemistry markers, most only research level at present, not clinically done.
• Stress or symptoms of clinical depression
• Hyperthyroidism(an over-active thyroid).

• Elevated serum insulin levels
• Short sleep duration
• Chlamydia pneumonia infection
Dietary risk factors
The relation between dietary fat and atherosclerosis is a contentious field. The USDA, in its food pyramid,
promotes a low-fat diet, based largely on its view that fat in the diet is atherogenic.
The role of dietary oxidized fats / lipid peroxidation (rancid fats) in humans is not clear.
Laboratory animals fed rancid fats develop atherosclerosis. Rats fed
DHA-containing oils experienced marked disruptions to their
antioxidant systems, as well as accumulated significant amounts of
peroxide in their blood, livers and kidneys.
In another study, rabbits fed atherogenic diets containing
various oils were found to undergothe greatest amount of
oxidative susceptibilityof LDL via polyunsaturated oils. In a study
involving rabbits fed heated soybean oil, "grossly induced
atherosclerosis and marked liver damage were histologically and
clinically demonstrated".

Rancid fats and oils taste very bad even in small amounts; people avoid eating them. It is very difficult to measure
or estimate the actualhuman consumption of these substances.
In addition, the majority of oils consumed in the United States are refined, bleached, deodorized and degummed
by manufacturers. The resultant oils are colourless , odourless, tasteless and have a longer shelf life than their
unrefined counterparts. This extensive processing serves to make peroxidated , rancid oils much more
elusive to detection via the various human senses than the unprocessed alternatives.

COMPLICATIONS
The complications of atherosclerosis depend on the location of the blocked arteries. For example:
• Coronary artery disease. When atherosclerosis narrows the arteries close to your heart, you may develop coronary
artery disease, which can cause chest pain (angina) or a heart attack.
• Carotid artery disease. When atherosclerosis narrows the arteries close to your brain, you may develop carotid
artery disease, which can cause a transient ischemic attack (TIA) or stroke.
* Peripheral artery disease. When atherosclerosis narrows the arteries in your arms or legs, you may develop
circulation problems in your arms and legs called peripheral arterial disease. This can make you less sensitive to
heat and cold, increasing your risk of burns or frostbite. In rare cases, poor circulation in your arms or legs can
cause tissue death (gangrene).

• Aneurysms. Atherosclerosis can also
cause aneurysms, a serious complication that
can occur anywhere in your body. An aneurysm
is a bulge in the wall of your artery. Pain and
throbbing in the area of an aneurysm is a common
symptom. If an aneurysm bursts, you may face life-
threatening internal bleeding. Although this is
usually a sudden, catastrophic event, a slow
leak is possible. If a blood clot within an aneurysm
dislodges, it may obstruct an artery at some distant

Tests and diagnosis
Doctors may find signs of narrowed, enlarged or hardened arteries during a physicalexam. These include:
• A weak or absent pulse below the narrowed area of the artery
• Decreased blood pressure in an affected limb
• Whooshing sounds (bruits) over the arteries, heard with a stethoscope
• Signs of a pulsating bulge (aneurysm) in the abdomen or behind knee
• Evidence of poor wound healing in the area where blood flow is restricted.
Depending on the results of the physicalexam, doctors may suggest one or more diagnostic tests, including:
• Blood tests.
• Doppler ultrasound
• Ankle-brachialindex.
• Other imaging tests.
• Angiogram.
• Electrocardiogram(ECG).

• Blood tests. Lab tests can detect increased levels of cholesterol and blood sugarthat may increase the risk of
atherosclerosis.
• Doppler ultrasound. Uses a special ultrasound device (Doppler ultrasound) to measure blood pressure at various
points along arm or leg. These measurements can help doctor gauge the degree of any blockages, as well as the
speed of blood flow in the arteries.
• Ankle-brachialindex. This test can tell if one have atherosclerosis in the arteries in your legs and feet. Doctor
may compare the blood pressure in ankle with the blood pressure in the arm. This is known as the ankle-brachial
index. An abnormal difference may indicate peripheral vascular disease, which is usuallycaused by atherosclerosis
.• Electrocardiogram (ECG). An electrocardiogram records electrical signals as they travel through your heart. An
ECG can often reveal evidence of a previous heart attackor one that's in progress. If signs and symptoms occur
most often during exercise,
• Angiogram. To better view blood flow through heart, brain, arms or legs, doctor may inject a special dye into
your arteries before an X-ray. This is known as an angiogram. The dye outlines narrow spots and blockages on the
X-ray images.
• Other imaging tests. doctormay use ultrasound, a computerized tomography(CT) scan or a magnetic resonance
angiogram (MRA) to studythe arteries. These tests can often show hardening and narrowing of large arteries, as
well as aneurysms and calcium deposits in the artery walls.

MEDICAL TREATMENT
Medical treatments often focus on alleviating symptoms. However measures which focus on decreasing underlying
atherosclerosis—as opposed to simply treating symptoms—are more effective. Non-pharmaceuticalmeans are
usually the first method of treatment, such as stopping smoking and practicing regular exercise. 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 is to combine multiple different treatment strategies. In addition, for
those approaches, such as lipoprotein transport behaviours, 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 betterresults, both before and especially after people are symptomatic.
Diet
Changes in diet may help prevent the development of atherosclerosis.
Tentative evidence suggests that a diet containing dairy products has no
effect on or decreases the risk of cardiovasculardisease.
A diet high in fruits and vegetables decreases the risk of cardiovascular
disease and death. Evidence suggests that the Mediterranean
diet may improve cardiovascular results. There is also evidence that
a Mediterranean diet may be betterthan a low-fat diet in

bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure).
medications
For many people, making changes to diet and lifestyle doesn’t do enough to lower
blood pressure to a healthy range. Fortunately, there are many medications that
can help. They each work in different ways to help lower your blood pressure.
Not all blood pressure medications work the same way for everyone, so you
and your healthcare provider may need to work togetherto try different
medications until you find the best one for you.
Cholesterol medications. Aggressively lowering low-density
lipoprotein (LDL) cholesterol, the "bad" cholesterol, can slow, stop or
even reverse the buildup of fatty deposits in arteries. Boosting your high-
density lipoprotein (HDL) cholesterol, the "good" cholesterol, may help,
too. cholesterol medications includes drugs known as statins and
fibrates.
Anti-platelet medications. Doctors may prescribe anti-platelet medications, such as
aspirin, to reduce the likelihood that platelets will clump in narrowed arteries, form a blood clot and cause further
blockage.
• Anticoagulants. An anticoagulant, such as heparin or warfarin (Coumadin), which inhibit clot formation by
interfering with Vitamin K metabolism, may actually promote arterial calcification in the long term despite
reducing clot formation in the short term.
High blood pressure medications

**Diuretics :- Often the first medication tried with a person newly diagnosed high blood pressure, diuretics work
by removing excess salt and water from your body, which is passed through urine. Diuretics are enough for some
people, but others need more help to lower blood pressure to a healthy range. In these cases, a healthcare provider
may prescribe an additional medication or a medication that contains a diuretic and an additional medication.
Diuretics can have side effects. These can include reduced potassiumin the body(which can be supplemented),
increased blood sugarlevels (a potential problem for diabetics), and in some cases, flare-ups of gout or impotence.
**ACE inhibitors :- These medications work by expanding blood vessels and reducing resistance inside them. By
doing this, ACE inhibitors allow blood to flow more easily and reduce the workload on the heart. Side effects can
include skin rash, loss of taste, and a chronic, dry hacking cough. In rare instances, kidney damage can result. ACE
inhibitors should not be taken by pregnant women, and are not recommended for most women of child-bearing
age.
**Angiotensin II receptor antagonists :- These medications stop a hormone called angiotensin II from narrowing
the blood vessels. These can cause occasional dizziness. They should not be used in pregnant women.
**Beta blockers :- These reduce the heart rate and decrease cardiac output, which both help lower blood
pressure. Side effects can include insomnia, cold hands or feet, tiredness or depression, asthma symptoms, or a
slow heartbeat. For people with diabetes who take insulin, beta blockers have to be monitored carefully.
Women receiving beta blockers who are or may become pregnant should consult with their healthcare providers
to determine the safest treatment strategy.
**Calcium channel blockers :- These interrupt the movement of calcium into the heart and blood vessel cells.
These can cause palpitations, swollen ankles, constipation, headache, and dizziness. Side effects can vary
depending on the specific calcium channel blocker prescribed.
**Central agonists :- These work by limiting the ability of blood vessels to expand and contract, thus lowering
blood pressure. These can cause a rapid drop in blood pressure while standing or moving, which can make you feel
weak or faint. They can also cause drowsiness or sluggishness, drymouth, constipation, fever, or anaemia.
**Peripheral and energic inhibitors :- These lower blood pressure by blocking the chemical message the brain
sends to the blood vessels to make them constrict.

These medications are typically only prescribed if other medications don’t help. Stuffynose, diarrhea, or heartburn
can be side effects from this medication.
**Blood vessel dilators :- These cause the blood vessel walls to relax, which helps them expand more easily and
allow blood to flow more freely. These can cause headaches , swelling around the eyes, heart palpitations, or aches
and pains in the joints
Statins
The group of medications referred to as statins are widely prescribed for
treating atherosclerosis. They have
shown benefit in reducing cardiovascular disease and mortality in those with high cholesterol with few side effects.
These data are primarily in middle-age men and the conclusions are less clear for women and people over the age
of 70.

Monocyte counts, as well as cholesterol markers such as LDL:HDL ratio and apolipiprotein B: apolipoprotein A-1
ratio can be used as markers to monitor the extent of atherosclerotic regression which proves useful in guiding
patient treatments.
Other medications
Doctor may suggest certain medications to control specific risk factors for atherosclerosis, such as diabetes. Someti
mes medications to treat symptomsof atherosclerosis, such as leg pain during exercise, are prescribed.
SURGERY
Sometimes more aggressive treatment is needed. If you have severe symptoms or a blockage that threatens muscle
or skin tissue survival, you may be a candidate for one of the following surgical procedures:
Angioplasty.
In this procedure, your doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of your artery.

A wire with a deflated balloon is
passed through the catheterto the narrowed area. The balloon is then inflated, compressing the deposits against y
our artery walls. A mesh tube (stent) is usually left in the artery to help keep the artery open. Angioplasty may also
be done with laser technology.
Endarterectomy. In some cases, fatty deposits must be surgically removed from the walls
of a narrowed artery. When the procedure is done on arteries in the neck (the carotid arteries), it's known as carot
id endarterectomy.
Thrombolytic therapy. If you have an artery that's blocked by a blood clot, your doctor may
insert a clotdissolving drug into your artery at the point of the clot to break it up.

Bypass surgery
. Your doctor may create a graft bypass using a vessel from another part of your body or a tube made of synthetic f
abric. This allows blood to flow around the blocked or narrowed artery.

PREVENTION
Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Medical
management of atherosclerosis first involves modification to risk factors–forexample, via smoking cessation and
diet restrictions. Additionally, a controlled exercise program combats atherosclerosis by improving circulation and
functionality of the vessels. Exercise is also used to manage weight in patients who are obese, lower blood pressure,
and decrease cholesterol. Often lifestyle modification is combined with medication therapy. For example, statins
help to lower cholesterol, anti-platelet medications like aspirin help to prevent clots, and a variety of
antihypertensive medications are routinely used to control blood pressure. If the combined efforts of risk factor
modification and medication therapyare not sufficient to control symptoms, or fight imminent threats of ischemic
events, a physician may resort to interventional or surgical procedures to correct the obstruction.
DIETARY MANGEMENT –
Objectives =
 Maximum rest to the heart.
 Maintenance of good nutrition
 Acceptabilityof the programme
PRINCIPLES OF DIET-Diet therapy remains the first line of treatment for patients with high blood cholesterol
levels. Low calorie, low fat particularly low saturated fat, low cholesterol, high in PUFA withn-6 to n-3 ratio 4-
10: 1, low carbohydrate and normal protein, minerals and vitamins are suggested.

High fibre diet with increased amount of anti oxidants is also recommended.
Conclusion
Although atherosclerosis is considered a heart disease it can happen in

any part of the bodies.Atherosclerosis can be prevented by life style factor and home remidies by eating healthy
diet. Atherosclerosis is a preventable and treatablecondition.

Atherosclerosis by neha

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