Professional Documents
Culture Documents
S
BY:
MAYURI MISHRA
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 plaqueswithin
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:
5. factor release
• from activated platelet,
macrophages and vascular wall
cells, inducing SMC recruitment,
either from the media or from the
circulating precursors
Response-to-injury hypothesis
6. 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.
Response-to-injury hypothesis
7. 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
proliferated SMC, foam cells, extracellular
lipid, and ECM is formed.
Micrograph of an artery that supplies the heart With
significant atherosclerosis and marked luminal narrowing
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.
Symptoms
Atherosclerosis symptoms depend on which arteries are
affected. For example:
• Atherosclerosis in heart arteries, have symptoms similar
to those of a heart attack, such as chest pain (angina).
• 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.
• 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
• Sometimes atherosclerosis causes erectile dysfunction in
men.
Symptoms
Symptoms
Physiologic 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
Physiologic factors that increase risk
3. Lesser or uncertain
2. Non modifiable • Being obese (in particular central
• Advanced age obesity,
• A sedentary lifestyle
• Male sex • Postmenopausal estrogen deficiency
• Having close relatives •
•
High carbohydrate intake
Elevated serum levels of
who have had some triglycerides
complication of • Elevated serum levels of uric acid
(also responsible for gout)
atherosclerosis (eg. • Elevated serum fibrinogen
coronary heart disease concentrations
•
or stroke) Elevated serum lipoprotein
concentrations
• Genetic abnormalities, • Stress or symptoms of clinical
depression
e.g. familial • Hyperthyroidism
hypercholesterolemia • Elevated serum insulin levels
• Short sleep duration
• Chlamydia pneumoniae infection
Table 1.Conditions That Accelerate the Progression of Atherosclerosis and the Mechanisms
Responsible.
Condition Mechanism
Male gender (and females Estrogen increases cholesterol removal by the liver, and the progression of
after menopause) atherosclerosis is less rapid in premenopausal women that in men