Atherosclerosis and MI

1. 1
Cardiac Disorders
Hizbullah Khan
BScN, MScN
Asst. Professor (CNM)

2. Objectives
Review the A & P of the heart
Review the following structure that support the cardiac
metabolism i.e.
Coronary circulation ( collateral arteries)
Heart action i.e. conduction system ,myocardial contraction
and relaxation
Briefly discuss the normal function of lipoprotein
List the vessels most commonly effected by
atherosclerosis.
List the risk factors in atherosclerosis.
Describe the possible mechanism involved in the
development of atherosclerosis.
Explain the physiological changes in patients with
ischemic heart diseases
2

3. 3
Location of the heart

4. 4
Chambers of the heart

5. 5

6. 6

7. 7
Blood flow through heart

8. Conducting System of Heart
Groups of autorhythmic cells are found at the:
Sinoatrial node – located near the opening of the SVC.
Atrioventricular node – located in the inferior interatrial
septum near the tricuspid orifice.
Atrioventricular bundle – found in the superior
interventricular septum.
Right and left bundle branches – travel through the
interventricular septum to the apex of the heart.
Purkinje fibers – cells that wind their way throughout the
ventricles.
8

9. 9
Conduction system of the heart

10. 10

11. Factors regulating stroke volume
Stroke volume is regulated by the three factors.
Preload
Afterload
 Myocardial contractility

12. Factors regulating stroke volume
Preload:
Reflects the loading conditions of the ventricle at the
end of diastole, just before the onset of systole.
Volume of blood stretching the myocardial muscle at
end of diastole, also known as end-diastolic volume
Within certain limits if the end-diastolic volume or
preload increases, the stoke volume also increases.

13. Factors regulating stroke volume
Afterload:
The force that the contracting heart muscle must
generate to eject blood from the filled heart.
Increased peripheral vascular resistance(PVR)
increases the afterload and decreases stroke volume

14. Factors regulating SV.
Myocardial contractility
The ability of the contractile cells of the heart muscle to
contract effectively
Depends on the availability of ATP and Calcium ions
and the integrity of heart muscles itself.
The more effective the heart muscles contract,
greater the blood ejected from the heart.

15. 15
Coronary circulation

16. Coronary circulation
The left and the right coronary artries, arise from the
coronary sinus of aorta just above the aortic valve.
The left coronary artery supplies blood flow to the
anterior and left lateral portions of the LV.
The left main coronary artery divides into the left
anterior descending and circumflex branches.
The left anterior descending artery supply the LV, the
anterior portion of the interventricular septum and the
anterior papillary muscle of the LV
The circumflex artery supply the left lateral wall of the
LV.
16

17. Coronary circulation
The right coronary artery supply most of the right
ventricle and the posterior part of the LV.
Posterior descending artery, a branch of the right
coronary artery supplies the posterior portion of the
heart, interventricular septum, sinoatrial (SA) and
atrioventricular (AV) nodes, and posterior papillary
muscle.
Beside main branches of coronary arteries there are
smaller arteries that form collateral circulation.
 With gradual occlusion of the larger vessels, the
smaller collateral vessels increase in size and provide
alternative channels for blood flow. 17

18. A & P of blood vessels:
18
A & P of blood vessels

19. Tunica interna: (the inner most coat)
Consists of a layer of simple squamous epithelium
called endothelium, a basement membrane and a layer
of elastic connective tissue called the internal elastic
lamina.
The endothelial is a continuous layer and line the
entire cardiovascular system.
The tunica interna is closest to the lumen, the hollow
center through which blood flow.
19

20. Tunica media: (The middle coat)
It is usually the thickest layer
This layer consists of elastic fibers (smooth
muscle) that extend circularly( in ring)
around the lumen.
Due to there plentiful elastic fibers the wall
of arteries easily stretch and expend without
tearing in response to small increase in
pressure.
Tunica externa: ( the external coat)
It is composed mainly of elastic and collagen
fibers
20

21. Lipoprotein:
Particles found in plasma that transport lipids
including cholesterol
Lipoprotein classes
Chylomicrons: take lipids from small intestine
through lymph cells
Very low density lipoproteins (VLDL)
Intermediate density lipoproteins (IDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)
21

22. Function of lipoprotein::
Chylomicrons transport dietary triglycerides and cholesterol
absorbed by intestinal epithelia.
LDL and HDL transport both dietary and endogenous
cholesterol in the plasma.
LDL is the main transporter of cholesterol and makes up
more than half of the total lipoprotein in plasma.
LDL bind to macrophages and form foam cell.
HDL causes reverse transport of cholesterol, it carry
cholesterol away from the artery and it removes lipid from
atherosclerotic plaque and transport it to liver for excretion
in bile.
Increase HDL decrease the rate of IHD.
22

23. 23

24. Arteriosclerosis vs
Atherosclerosis
Arteriosclerosis – natural changes in the intimal
layer, connective tissue and diameter of the artery
resulting in thickening & hardening of the arterial
walls.
Atherosclerosis – pathologic phenomenon occurring
in the coronary (thus causing coronary artery disease),
carotid, iliac, and femoral arteries as well as the aorta.
Atherosclerosis is a specific form of arteriosclerosis
affecting primarily the intima (the innermost layer) of
large and medium-sized arteries and is characterized by
the presence of fibro-fatty plaques or atheromas.

25. Atherosclerosis
 An atheroma consists mainly of macrophages cells or
debris, containing lipids (cholesterol and fatty acids),
calcium and a variable amount of fibrous connective
tissue (collagens, proteoglycans).
The term atherosclerosis is derived from “athero”
referring to “a paste” the soft lipid-rich material and
“sclerosis” or scarring is referred to “hardness” denotes
the formation of fibro fatty lesions in the intimal lining of
arteries.

26. Atherosclerosis
Most commonly affected arteries by atherosclerosis
include large & medium sized arteries like aorta,
coronary, popliteal and cerebral arteries.
Major complications that result from ischemia due to
atherosclerosis include myocardial infarction leading to
heart attacks & cerebral infarction leading to strokes.
Less common complications include peripheral vascular
disease, aneurysmal dilatation due to weakened arterial
wall and chronic ischemic heart disease.

27. Atherosclerosis is an abnormal accumulation of lipid, or
fatty and fibrous substances in the vessel wall.
Coronary artery disease (CAD).
Coronary atherosclerosis is the most common heart disease
in the United States.
 This is when plaque builds up in the coronary arteries,
narrowing the vessels and reduces blood flow to the heart.
 When blood flow to the heart is reduced or blocked, it can
lead to ischemia, chest pain and heart attack(MI).
27

28. Carotid artery disease.
This happens when plaque builds up in the carotid
arteries. These arteries supply oxygen-rich blood to your
brain.
When blood flow to the brain is reduced or blocked, it
can lead to stroke.
Peripheral arterial disease (PAD).
 This occurs when plaque builds up in the major arteries
that supply oxygen-rich blood to the legs, arms, and
pelvis.
When blood flow to these parts of the body is reduced
or blocked, it can lead to numbness, pain, and
sometimes dangerous infections 28

29. Risk Factors for CAD
29
Uncontrollable/non modifiable
•Sex: Heart disease occurs three times more often in
men than in premenopausal women
•Hereditary: Family history of coronary heart disease
•Genetic factors
•Race: higher incidence of heart disease in African
Americans than in Caucasians
•Increasing age

30. Risk Factors for CAD
30
Controllable/ modifiable
•High blood cholesterol level
•Cigarette smoking, tobacco use
•Hypertension
•Diabetes mellitus
•Lack of estrogen in women
•Physical inactivity
•Obesity

31. Major Constitutional Risk Factors
AGE
 Atherosclerosis is an age-related disease.
 Clinically significant lesions are found
with increasing age.
 Fully-developed atheromatous plaques
usually appear in 40s and beyond.
 Evidence in support comes from the high
death rate from IHD in this age group.

32. Major Constitutional Risk Factors
SEX
 Incidence and severity of atherosclerosis is more in
men than in women.
 Prevalence of atherosclerotic IHD is about three times
higher in men than in women.
 Lower incidence of IHD in women, especially in
premenopausal age is probably due to high levels of
estrogens & high-density lipo- proteins, both of which
have anti-atherogenic influence.

33. Major Constitutional Risk Factors
GENETIC FACTORS
 Hereditary genetic derangements of lipoprotein metabolism
predispose the individuals to high blood lipid level.
FAMILIAL AND RACIAL FACTORS
 Familial predisposition to atherosclerosis may be related to other
risk factors like diabetes, hypertension and hyperlipoproteinemia.
 Racial differences too exist. Blacks have less severe
atherosclerosis than Whites.

34. Major Acquired Risk Factors
HYPERLIPIDAEMIA
Hypercholesterolemia has directly
proportionate relationship with
atherosclerosis & IHD because:
The atherosclerotic plaques contain cholesterol
largely derived from the lipoproteins in the blood.
Individuals with hypercholesterolemia have
increased risk of developing atherosclerosis and IHD.
Individuals with hypercholesterolemia have higher
death rates (mortality)from IHD.
Dietary control & administration of cholesterol-
lowering drugs have beneficial effect on reducing the
risk of IHD.

35. Major Acquired Risk Factors
HYPERLIPIDAEMIA CONT…
An elevation of serum cholesterol levels above 260mg/dl
in men and women between 30 and 50 years of age has
three times higher risk of developing IHD as compared to
people with normal serum cholesterol levels (140-200
mg/dl).
Low-density lipoproteins (LDL) is richest in cholesterol
and has maximum association with atherosclerosis. HDL
is protective good cholesterol against atherosclerosis.
Diet rich in saturated fats e.g., eggs, meat, milk, butter etc,
raises the plasma cholesterol level while diet rich in poly-
unsaturated fats and omega-3 fatty acids e.g., fish, fish oils
etc lowers its level.

36. Major Acquired Risk Factors
HYPERTENSION
Hypertension causes mechanical injury to the arterial
wall due to increased blood pressure leading to
atherosclerotic IHD and cerebrovascular disease.
Endothelial injury due to persistent high B.P leads to
plaque formation.
A systolic pressure of over 160 mmHg or a diastolic
pressure of over 95 mmHg leads to 5 times higher risk
of developing IHD than in people with normal B.P.
(140/90 mmHg or less).

37. Major Acquired Risk Factors
SMOKING
Cigarette smoking is associated with higher risk of
atherosclerosis, IHD and sudden cardiac death.
Increased risk is due to the accumulation of carbon
monoxide in the blood that produces carboxy-
hemoglobin and eventually hypoxia in the arterial wall
favoring atherosclerosis.
Smoking also promotes atherosclerosis by increased
platelet adhesiveness, raised endothelial permeability,
sympathetic nervous system stimulation by nicotine.

38. Major Acquired Risk Factors
DIABETES MELLITUS
Atherosclerosis develops at an early age in people with
both insulin-dependent & non-insulin dependent diabetes
mellitus.
The risk of cerebrovascular disease is high and frequency
to develop gangrene of foot is about 100 times increased.
Causes of increased severity of atherosclerosis with DM
are complex & include increased aggregation of platelets,
increased LDL and decreased HDL.

39. Minor Risk Factors
1. Higher incidence of atherosclerosis in developed countries is
primarily because of environmental influences.
2. Obesity: Risk is increased if a person is overweight by 20%
or more.
3. Use of exogenous hormones (e.g. oral contraceptives) by
women or endogenous estrogen deficiency e.g., in post-
menopausal women leads to increased risk.
4. Physical inactivity and lack of exercise increase the risk
5. Stressful life style led by aggressiveness, a sense of urgency
& over-ambitiousness is associated with the risk of IHD.

40. Minor Risk Factors
6. Infections particularly clamydia pneumonia and viruses
such as herpes virus and cytomegalovirus increases
coronary atherosclerotic lesions.
7. Moderate consumption of alcohol has slightly beneficial
effect by causing vasodilatation.
However persistent consumption of alcohol in large
quantities causes more damage. The direct toxic effect
of alcohol results in fat deposition in the liver that
becomes a constant source of low-grade asymptomatic
fat emboli. Fat emboli become hydrolyzed to free fatty
acids, which cause endothelial cells damage.

41. Mechanism of development of atherosclerosis
Endothelial injury by (Agents such as smoking, elevated
LDL levels, immune mechanisms, and mechanical stress
associated with hypertension)
 Monocytes attach to endothelium, penetrate to sub-
endothelial spaces and converted to macrophages
Activated macrophages release free radicals that oxidize
LDL
Oxidized LDL is toxic to the endothelium, causing
endothelial loss and exposure of the sub-endothelial
tissue to blood components.
This leads to platelet adhesion and aggregation
and fibrin deposition.
41

42. Mechanism of development of atherosclerosis
Platelets and activated macrophages release various
factors that leads to proliferation of smooth muscle cells
and deposition of extracellular matrix( collagen and
elastic fibers).
Activated macrophages also ingest oxidized LDL to
become foam cells.
The necrotic foam cells release lipids to form a lipid
core.
Fatty streaks and proliferated smooth muscles form
fibrous plaque
A fatty streak consists of lipid-containing foam cells in
the arterial wall just beneath the endothelium.

43. Mechanism of development of atherosclerosis
Endothelial necrosis and luminal narrowing occurs
 Sometimes Plaque is ulcerated or ruptures, more
platelet aggregation occurs that leads to thrombus
formation.
Rupture, ulceration, or erosion of an unstable or
vulnerable fibrous cap may lead to hemorrhage into
the plaque or thrombotic occlusion of the vessel
lumen.
Occlusion or narrowing of the vessel may then lead
to ischemic heart diseases or myocardial infarction.

44. 44

45. 45

46. Ischemic heart Disease
46

47. Ischemic Heart Disease
o Leading cause of death in industrialized countries
o Leads to angina, myocardial infarction, sudden
cardiac death, and chronic heart failure
o It results from coronary arteries atherosclerosis
o Narrowing and hardening of the arteries leads to
imbalance between supply and demand of blood
for cardiac muscles = Ischemia.
o Ischemia is either detected by a symptom
(angina) or indirectly by electrocardiogram and
other non-invasive (e.g. echo) & invasive
diagnostic techniques (e.g. cardiac enzymes).

48. Causes:
Atherosclerosis
Congenital defects
Coronary artery spasm
Dissecting aneurism
Infectious vasculitis
Syphilis
High blood levels of C reactive protein
49

49. Myocardial Ischemia
 Ischemia is inadequate blood flow to a tissue or part
of the body.
 Myocardial ischemia occurs when the blood flow
demands of the heart muscles exceed the blood supplied
by the coronary arteries.
Pathophysiology of Myocardial Ischemia
 Under resting conditions, myocardial oxygen supply
and delivery of nutrients through the coronary arteries
should match the metabolic requirements of the heart.
 When the metabolic needs of the heart increase, the
coronary blood flow must increase accordingly.

50.  With age and progressive occlusion
of coronary arteries, smaller
collateral vessels may begin to
carry a greater proportion of blood
and thus provide an alternate means
of perfusion for an area of
myocardium.
 These collateral blood vessels may
run parallel to the larger coronary
arteries & be connected to other
small coronary vessels by vascular
connections called anastomoses.
Pathophysiology of Myocardial
Ischemia

51.  Development of collateral circulation may
reduce or delay the occurrence of
symptoms from myocardial ischemia until
the blockage is very progressed.
 The presence of extensively developed
collateral circulation might also explain
why many older individuals often survive
serious heart attacks, while younger
individuals have not yet developed
collateral circulation, often do not.
Pathophysiology of Myocardial
Ischemia

52. Symptoms of Coronary Artery
Disease
Most common symptom is Angina Pectoris
also known as chest discomfort.
Quality - "squeezing," "grip like," "pressure like,"
"suffocating" and "heavy”; or a "discomfort" but not
"pain." Angina is almost never sharp or stabbing,
and usually does not change with position or
respiration.
Duration - angina episode is typically minutes in
duration. Feeling discomfort or a dull ache lasting
for hours is rarely angina.
53

53. Angina
Angina is a symptom of a condition called
myocardial ischemia
Other symptoms that can occur with coronary artery
disease include:
Decrease peripheral pulse
Nausea and vomiting
Fainting
Sweating
Cool extremities
Shortness of breath
54

54. Angina
55

55. Angina Pectoris
Usually substernal, but radiation to the neck, jaw,
epigastrium, or arms can occur.
Pain above the mandible, below the epigastrium, or
localized to a small area over the left lateral chest is
rarely angina.
Provocation - angina is generally precipitated by
exertion or emotional stress and commonly relieved
by rest. Sublingual nitroglycerin also relieves
angina, usually within 30 seconds to several minutes.
56

56. Angina Pectoris
Location
57

57. Ischemia
Ischemia is most likely to occur when the heart
demands extra oxygen. This is most common during
one or more of the four E’s:
• Exertion (activity)
• Eating
• Excitement
• Exposure to cold
58

58. Myocardial Ischemia
Types of angina
Stable Angina Pectoris
Unstable Angina
Prinzmetal’s or Variant angina
(coronary spasm)
59

59. Stable Angina Pectoris
A type of angina brought on by an imbalance between
the heart’s need for oxygen-rich blood and the amount
available.
Episodic chest pain
Stress or exertion
 Fix atherosclerotic plaque (75%)
Crushing, squeezing, suffocating, sub sternal sensation
Pain intensity increase at onset and end of attack
It is relieved by rest and/or oral medications
(nitroglycerin)
60

60. Unstable Angina
When a change in status of angina occurs (e.g. new
onset; angina of increasing severity, duration or
frequency; or angina occurring at rest for the first
time). feel more severe, or last longer.
Unstable angina is usually triggered by minor
injury to atherosclerotic plaque.
Plaque disruption may occur with or with out
thrombosis, it increase the degree of coronary
artery obstruction
61

61. Additionally there is a release of vasoconstricting
factors i.e thromboxane, serotonine, and platelet
derived growth factors from platelets that
aggregate at the site of injury.
These platelets factors contribute even at rest the
episode of reduce coronary blood flow.
 Close observation and intensive therapy is
required; more serious clinical situation as may be
a precursor of MI.
62

62. Prinzmetal’s Angina/Variant angina
(or coronary spasm)
Variant angina are first describe by prinzmetal
in 1959.
A coronary artery can go into spasm,
disrupting blood flow to the heart muscle
(ischemia).
The hallmark is ST segment elevation on the
ECG during angina attack.
Usually associated with fixed atherosclerotic
lesion, but not always.
63

63. This type of angina is not common usually occurs
at rest (often at night), and episodes are frequently
associated with ventricular arrhythmias.
The mechanism of coronary vasospasm is
unclear.
It has been suggested that it may result from
hyper active sympathetic nervous system response
from a defect in handling of calcium in vascular
smooth muscle and reduces production of
prostaglandin I2.
64

64. 65

65. 66

66. Pain is caused by :
Build up of lactic acid or abnormal stretching of
the ischemic myocardium irritates myocardial
nerve fibers.
Afferent sympathetic fibers enter the spinal cord
from levels C3 to T4 accounting for the variety of
locations and radiation pattern of anginal pain.
Dysrhythmias occurs in severe pain
67

67. Coronary angioplasty
68

68. Coronary Bypass Surgery:
69

69. Myocardial Infarction:
Myocardial Infarction (MI) is the condition of
irreversible necrosis of heart muscle that results
from prolonged ischemia or may be defined as
Ischemic death of myocardium.
Prolonged Ischemia longer than 30-45 minutes
causes irreversible cellular damage and muscle
death or necrosis.
70

70. Myocardial infarction is the medical term for heart
attack.
Heart attack means there has been death of heart
cells.
This is the result of a complete blockage of one of
the blood vessels that feeds the heart muscle
(coronary artery).
Cell death does not occur immediately once the
artery is blocked. It takes several minutes to start
the injury process and this continues for several
hours unless the artery is opened, restoring blood
flow.
71

71. Cardiac muscle requires about 1.3 ml of oxygen
per 100 gm of muscle tissue per minute just to
remain alive.
At resting state normally left ventricle receive
8 ml of blood per 100 gm of tissue.
If there is 15-30% of normal resting coronary
blood flow the muscle will not die.
72

72. Site of MI
Anterior MI-involves the anterior wall of the left
ventricle.
Other sites of infarction are:
Inferior
Posterior
Lateral (anterolateral)
Septal ( Anteroseptal)
73

73. Anterior wall infarctions result from lesions in
the left coronary anterior artery.
Inferior wall infarction results of right coronary
artery lesions.
Anterioseptal result from left anterior
descending.
Lateral MI involves circumflex and Lt anterior
descending.
Posterior wall infarction results from Rt.
Coronary artery and circumflex.
74

74. Are there different types of heart
attacks?
The location of the blockage, the length of time the
blockage persisted and the amount of damage will
determine the type of heart attack that occurs.
75

75. Types of Heart Attacks
Pathologically there are two patterns of MI:
Transmural (Q wave infarction)
 Subendocardial (non Q wave infarction)
76

76. Q-wave MI
A MI or heart attack that is caused by a prolonged
period of blocked blood supply.
A large area of the heart muscle is affected, causing
changes on the ECG as well as chemical markers in the
blood.
Involves the entire depth of the ventricular wall.
77

77. Non-Q-wave MI
A MI or heart attack that does not cause changes
on the electrocardiogram (ECG) however, chemical
markers in the blood indicate that damage has
occurred to the heart muscle.
78

78. Symptoms of a Heart Attack
Chest pain or discomfort in the center of the chest;
a “squeezing,” heaviness” or “crushing” feeling that
lasts for more than a few minutes or goes away and
comes back.
Fullness, indigestion, or choking feeling (may feel like
“heartburn”)
• Nausea or vomiting
• Light-headedness
• Extreme weakness or anxiety
• Rapid or irregular heart beats
79

79. 1. Electrocardiograph (ST segment depression T-wave
flattening or inversion)
2. Holter monitoring — 24 ambulatory
electrocardiograph
3. Stress testing with electrocardiograph(ETT)
4. Nuclear imaging
5. Cardiac catheterization (angiography)
Myocardial Ischemia
Diagnosis of myocardial ischemia:

80. Cardiac markers:
Cardiac markers are proteins that leak out of
injured myocardial cells through their
damaged cell membranes into the
bloodstream.
Until the 1980s, the enzymes SGOT and LDH
were used to assess cardiac injury.
 Now, the markers most widely used in
detection of MI are MB subtype of the enzyme
creatine kinase, and cardiac troponins T and I
as they are more specific for myocardial injury.
81

81. The cardiac troponins T and I which are
released within 4–6 hours of an attack of MI
and remain elevated for up to 2 weeks, have
nearly complete tissue specificity and are now
the preferred markers for assessing myocardial
damage.
 Elevated troponins in the setting of chest pain
may accurately predict a high likelihood of a
myocardial infarction in the near future.
New markers such as glycogen phosphorylase
isoenzyme BB are under investigation.
82

82.  Treatment of myocardial ischemia and the resulting
angina can involve two strategies:
1. Increase coronary blood flow by dilating coronary
arteries.
2. Reduce cardiac workload by reducing heart rate
and/or force of contraction.
Rationale for the Treatment of Myocardial Ischemia
Treatment of Myocardial
Ischemia

83. The treatment regimen may include:
1. Non-pharmacologic treatment
2. Pharmacologic therapies.
Treatment of myocardial ischemia:
 Pacing of physical activity.
 Avoidance of stress (emotional, physiologic,
cold).
 Reduction of risk factors for ischemic heart
disease, (hyperlipidemia, obesity,
hypertension, diabetes, smoking, etc.)
Non-pharmacologic Treatment
Treatment of Myocardial
Ischemia

84. Mechanism of Action
 Dilate coronary arteries and increase myocardial
blood flow.
 Dilate peripheral arteries and reduce afterload.
 Dilate peripheral veins and reduce preload.
Examples
 Amyl nitrate, nitroglycerine, isosorbide dinitrite
Pharmacologic Treatment
Treatment of Myocardial
Ischemia
Nitrates

85. Mechanism of action
 Block myocardial β-adrenergic receptors.
 Reduce heart rate and cardiac output (reduced myocardial
workload and oxygen demand).
Examples of β-Adrenergic Receptor Antagonists
 May be selective β1 (atenolol), or
 Nonselective β1 and β2 blockers (propranolol)
Pharmacologic Treatment
β-Adrenergic Blockers
Treatment of Myocardial
Ischemia

86. Mechanism of action
 Block calcium channels in vascular smooth muscles.
 Dilate coronary arteries and increase myocardial blood flow.
 Dilate peripheral arteries and reduce afterload.
Examples
Dihydropyridines (nifedipine), verapamil, diltiazem
 Dihydropyridines have greater specificity for
relaxing vascular smooth muscle.
Calcium Channel Blockers
Treatment of Myocardial
Ischemia

87. Mechanism
Prevent platelet aggregation.
Used for prophylaxis of blood clots
particularly in unstable angina.
Aspirin
Surgical Treatment
Coronary Angioplasty
Uses a balloon catheter to open occluded blood
vessels
Usually performed under local anesthesia
Use of metal “stents” in opened vessel reduces rate of
occlusion
Metal Stent
Treatment Cont…

88. Treatment of Myocardial
Ischemia
Coronary artery bypass graft
Revascularization procedure in which a blood vessel
is taken from elsewhere in the body & surgically
sutured around a blocked coronary artery.
May involve multiple (one to five) blood vessels.
Re-occlusion of transplanted vessel is possible.
Surgical Treatment

89. 5. β -Blockers: Reduce the effect of catecholamine release
on
the myocardium, reduce heart rate and myocardial work.
6. Pain management: Sublingual nitroglycerin, morphine if
necessary.
7. Antiarrhythmic drugs: To treat and prevent a number of
potentially life-threatening arrhythmias that might arise
following a myocardial infarction.
8. ACE inhibitors: the negative effects of vasoconstriction
and salt and water retention on the myocardium.
Treatment for myocardial
infarction
Myocardial Infarction

90. 1. Streptokinase: Derived from β -hemolytic streptococcus
bacteria; involved in the activation of plasmin.
2. Anistreplase (APSAC): Complex of human lys-
plasminogen and streptokinase.
3. Urokinase: Endogenous human enzyme that converts
plasminogen to active plasmin
4. Routes of administration: Intravenous for all of the
above.
5. Major unwanted effects: Internal bleeding,
gastrointestinal bleeding, stroke, allergic reactions
Myocardial Infarction
Thrombolytic Agents Used Clinically

91. 1. Sublingual nitroglycerin: A potent vasodilator
of coronary arteries, also dilates peripheral
arteries & veins to reduce preload and afterload
on the heart.
2. Morphine sulfate: Powerful opioid analgesic
that also provides a degree of sedation &
vasodilatation.
Although the opioid analgesics have little effect on
the myocardium, they are powerful respiratory
depressants.
Myocardial Infarction
Pain Management in Myocardial Infarction

92.  Inhibits the cyclo-oxygenase pathway for the
synthesis of prostaglandins, prostacyclins &
thromboxanes.
 Inhibits aggregation of platelets and is effective in
reducing myocardial infarction, stroke and
mortality in high-risk patients.
Myocardial Infarction
Aspirin

93. Key terms
 Cardiac tamponade: Excessive pressure that
develops from the accumulation of fluid in the
pericardium.
 Pericarditis: Inflammation of the pericardium.
 Stroke volume: Volume of blood ejected from
each ventricle per beat.
Myocardial Infarction

94. 1. Danish MI. Short text book of pathology. 4th
edition;
2010. Johar Publications, Karachi-Pakistan.
2. Emanuel Rubin & John L. Farber, Essential Pathology,
Philadelphia, 1990.
3. Kumar, Vinay; Abbas, Abul K; Aster, Jon. (2009).
Robbins & Cotran pathologic basis of diseases (8th ed.).
St. Louis, Mo: Elsevier Saunders. ISBN 1-4160-3121-9.
3. Porth CM. Pathophysiology: Concepts of altered Health
States. 7th
edition; 2005. Lippincott Williams & Wilkins.
Reference
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