1. ATHEROSCLEROSIS
&
MYOCARDIAL INFARCTION
MARYAM JAMILAH BINTI ABDUL HAMID
082013100002
IMS BANGALORE

2. LEARNING OUTCOME
 Student should be able to give the definition of
atherosclerosis and myocardial infarction.
 Student should be able to explain the process of
atherosclerosis and myocardial infarction.
 Student should be able to list the causes of
atherosclerosis and myocardial infarction.

3. ATHEROSCLEROSIS
Definition:
Hardening of the arteries, and caused by plaque building up in
the vessel. Over time the plaque causes thickening of the walls
of the artery. Stiffness and a loss of elasticity also result.

5. Endothelial injury
Monocytes adhere to
endothelial cells & move to
subendothelial (intima)
Scavenger receptor
Superoxide
Nitric oxide
Hydrogen
peroxide
Other oxidants
1)highly specific and regulated receptor mediated pathway for LDL uptake
macrophages possess high levels of
scavenger receptor activity; can bind to a
broad range of ligands (non-specific) and
mediate the endocytosis of chemically
modified LDL in which the lipid components
or apo B have been oxidized.
Transformed into
macrophages
LDL
+
Oxidized LDL
Vitamin E
Ascorbic acid
B-Carotene
Other
Macrophages consumes antioxidants
2)Unlike the LDL receptor, the
excess modified (oxidized)
scavenger receptor is not downlipoprotein & become foam
cells
regulated in response to increased
Foam cells accumulate,
intracellular cholesterol.
release growth factors and
cytokines; stimulate migration 3)Cholesteryl esters (CE) accumulate
of smooth muscle cells from
in macrophages and cause their
media to intima
transformation into “foam” cells,
Smooth muscle cells
proliferate, produce collagen & which participate in the formation of
take up lipid, potentially
atherosclerotic plaque
becoming foam cells.

6. Smooth muscle cells
proliferate, produce collagen &
take up lipid, potentially
becoming form cells.
Diameter of the lumen
Blood become turbulence
Activation of clot formation
Produce thrombus
Stop at the line if you are
discussing about
atherosclerosis, go beyond
the line for myocardial
infarction
Thrombus get calcified
Calcified thrombus is the
atherosclerotic plaque
Block the coronary
artery/arteries
Myocardium not supplied
by oxygen
Anaerobic glycolysis
Lactic acid produce (lactic
acidosis), pH

7. Lactic acid produce (lactic
acidosis), pH
Less ATP production/no
ATP production
Inefficient contraction of
myocardium (heart
muscles)
Heart muscles supplies by
this artery dies
Pain at that area
Myocardial infarction

11. MYOCARDIAL INFARCTION
Definition:
Irreversible necrosis of heart muscle secondary to prolonged
ischemia

12. Causes of Myocardial Infarction
 Presence of atherosclerosis.
 High Lipoprotein (a) in the plasma.

13. Presence of atherosclerosis
 Presence of atherosclerotic plaque in coronary artery will
decrease the oxygen delivery to the heart.
 This leads to ischemia of myocardium (cardiac muscle)
and lastly causes dead to the myocardium.
 Degree of blockage of coronary artery: Partially blockage
 Fully blockage
 In early stage of atherosclerosis, drugs will be given to
dilute the plaque in the coronary arteries but in later stage,
angioplasty cam be done. However, if the blockage is too
much, bypass surgery should be done to create new
pathway for the oxygen in red blood cell to be taken by
myocardium

16. Lipoprotein (a) in heart disease
 Present in large quantities in the plasma, is
associated with an increased risk of coronary
heart disease.
 Lp(a) is nearly identical in structure to an LDL
particle.
 Lp(a) has additional apo(a), that is covalently linked
at a single site to apo B-100.
 Apo(a) is structurally homologous to

17.  Elevated Lp(a) slows the breakdown of blood clots
that trigger heart attacks because it competes with
plasminogen for binding to fibrin.
 Circulating levels of Lp(a) are determined primarily
by genetics.

18. Factors influencing level of Lp(a)
 Trans fatty acids have been shown to
increase Lp(a)
 Estrogen decreases both LDL and
Lp(a).
 Niacin reduces Lp(a) and raises HDL.

19. (MI)
 Type 1 – spontaneous MI related to ischemia due to a
primary coronary event such as plaque erosion and/or
rupture, fissuring(split), or dissection
 Type 2 – MI secondary to ischemia due to either
increased oxygen demand or decreased supply, e.g.
coronary artery spasm, coronary embolism, anaemia,
arrhythmias, hypertension, or hypotension
 Type 3 – sudden unexpected cardiac death, including
cardiac arrest, often with symptoms suggestive of
myocardial ischaemia, accompanied by new ST
elevation, or new LBBB, or evidence of fresh thrombus
in a coronary artery by angiography and/or at autopsy,
but death occurring before blood samples could be
obtained, or at a time before the appearance of cardiac
biomarkers in the blood
 Type 4 – associated with coronary angioplasty or
stents:
 Type 4a – MI associated with percutaneous coronary
intervention (PCI)

20. CONCLUSION
Atherosclerosis:
Hardening, stiffness and lost of elasticity of the arteries
because
formation of plaque inside the artery
Myocardial infarction:
Irreversible necrosis of myocardium
―So, as a human being, we should take optimum amount of lipid.
This is because some of the food will cause harm to our body when
we take
them excessively.‖

21. REFERENCES
 Lippincott’s Illustrated Reviews: Biochemistry Fifth




Edition, Richard A. Harvey, PhD and Denise R.
Ferrier, PhD, Lippincott Williams & Wilkins,
Philadelphia, USA.
http://surgery.about.com/od/beforesurgery/f/Arterioscl
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http://emedicine.medscape.com/article/155919overview
https://www.google.com/search?q=fibrilysis&oq=fibrily
sis&aqs=chrome..69i57j0l5.5118j0j7&sourceid=chrom
e&espv=210&es_sm=93&ie=UTF-8
http://www.heart.org/HEARTORG/Conditions/HeartAtt
ack/AboutHeartAttacks/About-HeartAttacks_UCM_002038_Article.jsp