ATHEROSCLEROSIS

PRESENTED TO- DR. USHA PRESENTED BY- POONAM SONI

(210171760005)
INTRODUCTION

 Atherosclerosis (also known as Arteriosclerotic Vascular Disease or ASVD)

 The condition in which an artery wall thickens as the result of a build-up of fatty
materials such as cholesterol.
 Affecting arterial blood vessels, a chronic inflammatory response in the walls of
arteries .
 Due to the accumulation of macrophage white blood cells and promoted by Low-
density lipoproteins without adequate removal of fats and cholesterol from the
macrophages by functional high density lipoproteins.
 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.
 It can restrict blood flow. These plaques can also burst, causing a blood clot.
 Although atherosclerosis is often considered a heart problem, it can affect
arteries anywhere in your body.
 Atherosclerosis is a preventable and treatable condition.
TERMS

 Arteriosclerosis is a general term describing any

hardening (and loss of elasticity) of medium or large
arteries .
 Arteriolosclerosis is any hardening (and loss of elasticity)
of arterioles (small arteries);
 Atherosclerosis is a hardening of an artery specifically
due to an atheromatous plaque.
 Atherogenic is used for substances or processes that cause
atherosclerosis.
 Atherogenesis is the developmental process of
atheromatous plaques.
CAUSES

 Atherosclerosis starts with damage or

injury to the inner layer of an artery. The
damage may be caused by:
High blood pressure
 High cholesterol
An irritant, such as nicotine
 Certain diseases, such as diabetes
EPIDEMIOLOGY

 ATHEROSCLEROSIS is less prevalent in central

and south America, Africa, and Asia. And more
prevalent in united states and Japan.
 The mortality in U.S in 5 times higher than Japan.
 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).
PATHO-PHYSIOLOGY

 Atherosclerosis develops as a chronic inflammatory response of the

arterial wall to endothelial injury.
 Lesion progression occurs through interactions of modified
lipoproteins, monocyte-derived macrophages, T-lymphocytes, and
the normal cellular constituent of the arterial wall.
 The contemporary view of atherosclerosis is expressed by the
response-to-injury hypothesis.
 RESPONSE-TO-INJURY HYPOTHESIS

The following are the steps

involved in the hypothesis:

 Chronic endothelial injury

 Accumulation of
lipoproteins
 Monocyte adhesion to the
endothelium
 SMC proliferations and
ECM production
 factor release
 platelet adhesion
1. Chronic endothelial injury
With resultant endothelial dysfunction, causing increased permeability,
leukocyte adhesion, and thrombosis.
2. Accumulation of lipoproteins
Mainly LDL and its oxidized forms in the vessel wall. Low-density
lipoprotein molecules (LDL) becoming oxidized (ldl-ox) by free radicals,
particularly oxygen free (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. Cholesterol can move in the bloodstream
only by being transported by lipoproteins.
3. Monocyte adhesion to the endothelium
Followed by migration into the intima and transformation into
macrophages and foam cells. The body's immune system responds to the
damage to the artery wall caused by oxidized LDL by sending specialized
white blood cells (macrophages and Tlymphocytes) 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.
4. SMC proliferations and ECM production
Eventually, the artery becomes inflamed. The cholesterol plaque causes the
smooth 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.
5. Platelet adhesion &factor release
From activated platelet, macrophages and vascular wall cells, inducing SMC
recruitment, either from the media or from the circulating precursors.
6. Lipid accumulation
Both extracellularly and within cells (macrophages and SMC’s). accumulation if
lipid-containing macrophages in the intima gives rise to “fatty streaks”, with
further evolution, a fibrofatty atheroma consisting of prolifer ated SMC, foam
cells, extracellular lipid, and ECM is formed.
SYMPTOMS

Atherosclerosis develops gradually, typically begins in early adolescence, and is

usually found in most major arteries. There are usually no atherosclerosis
symptoms until an artery is so narrowed or clogged that it can't supply adequate
blood to your organs and tissues. Sometimes a blood clot completely obstructs
blood flow, or even breaks apart and causes blood clots that can trigger a heart
attack or stroke.
 Atherosclerosis symptoms depend on which arteries are affected. For example:
1. Atherosclerosis in heart arteries, have symptoms similar to those of a heart
attack, such as chest pain (angina).
2. Atherosclerosis in the arteries leading to brain, have symptoms such as sudden
numbness or weakness in your arms or legs, difficulty speaking or slurred
speech, or drooping muscles in your face.
3. Atherosclerosis in the arteries in arms and legs, produces decreased blood flow
is called peripheral artery occlusive disease (PAOD).have symptoms such as
leg pain when walking
4. Sometimes atherosclerosis causes erectile dysfunction in men.
PHYSIOLOGICAL FACTORS THAT
INCREASE RISK

 Various anatomic, physiological & behavioral risk factors for atherosclerosis are known.
These can be divided into various categories:, modifiable and non-modifiable.
1. 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 density lipoprotein (VLDL) particles, i.e., "lipoprotein
subclass analysis“
 Low serum concentration of functioning high density lipoprotein (HDL "protective if large
and high enough" particles), i.e., "lipoprotein subclass analysis"
 An LDL:HDL ratio greater than 3:1
• Tobacco smoking, 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.
2. Non modifiable 3. Lessor or uncertain

Being obese (in particular central

obesity,
A sedentary lifestyle
Advanced age Postmenopausal estrogen
deficiency
Male sex High carbohydrate intake
Having close relatives who Elevated serum levels of
have had some triglycerides
Elevated serum lev els of uric acid
complication of
(also responsible for gout)
atherosclerosis (eg. coronary Elevated serum fibrinogen
heart disease or stroke) concentrations
Genetic abnormalities, e.g. Elevated serum lipoprotein
concentrations
familial Stress or symptoms of clinical
hypercholesterolemia depression
Hyperthyroidism
 Elevated serum insulin levels
Short sleep duration
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 point.
TESTS AND DIAGNOSIS

Doctors may find signs of narrowed, enlarged or hardened

arteries during a physical exam. 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.
TESTS AND DIAGNOSIS

Depending on the results of the physical exam, doctors

may suggest one or more diagnostic tests, including:
 Blood tests.
 Doppler ultrasound
 Ankle-brachial index.
 Other imaging tests.
 Angiogram.
 Electrocardiogram (ECG).
TESTS AND DIAGNOSIS
 Blood tests. Lab tests can detect increased levels of cholesterol and blood sugar that 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-brachial index. 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 usually caused 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 attack or 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. doctor may use ultrasound, a computerized tomography (CT) scan or a
magnetic resonance angiogram (MRA) to study the arteries. These tests can often show
hardening and narrowing of large arteries, as well as aneurysms and calcium deposits in the
artery walls.
TREATMENTS AND DRUGS
 Lifestyle changes, such as eating a healthy diet and exercising , are often the first line of defense
in treating atherosclerosis. But sometimes, medication or surgical procedures may be
recommended as well.

 Various drugs can slow — or sometimes even reverse — the effects of atherosclerosis. Here are
some common choices:

• 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), can help thin

blood to prevent clots from forming.

• Blood pressure medications. Medications to control blood pressure — such as beta blockers,
angio-tensin-converting enzyme (ACE) inhibitors and calcium channel blockers — can help
slow the progression of atherosclerosis.
SURGICAL TREATMENT
 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:

1. 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 catheter to the narrowed area. The 
balloon is then inflated, compressing the deposits against 
your 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.

2. 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 carotid endarterectomy.

3. Thrombolytic therapy:- An artery  that's blocked by a blood clot, your doctor 

may insert a clot-dissolving drug into your  artery at the point of the clot to break it up.

4. Bypass surgery:- To  create a  graft bypass using a vessel from another part 

of your body or a tube made of synthetic  fabric. This allows blood to flow around the 
blocked or narrowed  artery.
 Lifestyle and home remedies

 Lifestyle changes can help prevent or slow the  progression  of atherosclerosis.

• Stop smoking. 
• Exercise most days of the week. 
• Eat healthy foods
• Manage stress
• manage the condition of high cholesterol, high blood pressure, diabetes or other chronic
disease

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 treatable  condition.
References:

 Harrison’s principle of internal medicine,
  17th edition.
 Robbins basic pathology, 8th edition.
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