Cardiovascular Pathophysiology Coronary Artery Disease (CAD)/ Ischaemic Heart Disease (IHD)

1. Cardiovascular Pathophysiology
Coronary Artery Disease (CAD)/
Ischaemic Heart Disease (IHD)
Dr. Vishal Balakrushna Jadhav
Assistant Professor (Pharmacology)
School of Pharmaceutical Sciences (SOPS), SUN
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2. Content
 Definition of CAD/IHD
 Clinical manifestations of IHD
1. Angina pectoris
2. Myocardial infarction (MI)
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3. Definition of CAD/ IHD
 An acute or chronic form of cardiac disability arising from imbalance
between myocardial supply and demand for oxygenated blood.
 Narrowing or obstruction of coronary arterial system is the most common
cause of myocardial anoxia (deficiency of oxygen in body tissues), the
alternate term coronary artery disease (CAD) is used synonymously with
IHD.
 IHD or CAD is the leading cause of death in most of the industrialized
countries and somewhat low incidence is observed in developed
countries.
 Men develop IHD earlier than women and death rates are also slightly
higher for men than women until the menopause.
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4. Clinical manifestations of IHD
1. Angina pectoris
 A clinical syndrome of IHD may result from transient myocardial ischaemia
characterized by the paroxysmal pain in the substernal or precordial region of the
chest which is provoked by an increase in the demand of heart for oxygenated
blood and relieved by the decrease in the work of the heart.
 Pain of the angina often radiates to the left arm, neck, jaw or right arm.
Classification of angina pectoris
A) Stable or typical angina
B) Prinzmetal’s Variant angina
C) Unstable or Crescendo angina
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5. A) Stable or typical angina
 Synonyms- Angina of efforts or Meberdeen’s angina.
 It is the most common type of the angina characterized by attack of pain
following the physical exertion or emotional excitement and is relieved by
rest.
 Causes-
a) Severe atherosclerosis of the larger coronary arteries leads to coronary stenosis,
b)Release of catecholamines (Adrenaline or Nor-adrenaline), and
c) Re-distribution of the blood from coronary to splanchic circulation after meal and
certain drug therapies, e.g. sulphonamides and histamine etc.
 ECG Signs- ST segment depression.
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6. B) Prinzmetal’s Variant angina
 It is characterized by the pain at rest and has no relationship with the physical
activity.
 Causes-
Exact pathogenesis is not known, it may occurs due to-
a) sudden vasospasm of the coronary trunk induced by coronary atherosclerosis, and
b) release of humoral vasoconstrictors by mast cells located in coronary adventitial
layer.
 ECG Signs- ST Segment elevation.
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7. C) Unstable or Crescendo angina
 Synonyms- Pre-infarction angina or acute coronary insufficiency.
 It is the most serious form of angina characterized by frequent onset of pain
of prolonged duration which occurs often at rest, and is an indication of
upcoming myocardial infarction.
 Causes-
a) Stenosing coronary atherosclerosis,
b) Complicated coronary plaques
c) Platelet thrombi over atherosclerotic plaques, and
d) Vasospasm of coronary arteries.
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Diagram of discomfort caused by coronary artery
disease. Pressure, fullness, squeezing or pain in
the center of the chest. Can also feel discomfort
in the neck, jaw, shoulder, back or arm.
Illustration representing angina

9. 2. Myocardial infarction (MI)
 MI is the medical emergency due to ischaemic necrosis (death) of the
myocardium. (Infarct- A small localized area of dead tissue resulting from failure of
blood supply).
 The term heart-attack is often used alternatively to MI.
 Incidence of MI-
In industrialized countries, MI accounts for 10-25% of all the deaths. The
incidence of MI correlates well with the incidence of coronary atherosclerosis in
geographical areas.
a) Age- MI may virtually occur at all the ages- though its incidence is high in elderly.
About 5% heart attacks occurs in younger peoples under the age of 40 years,
particularly with major risk factors to develop coronary atherosclerosis like
hypertension, diabetes mellitus, cigarette smoking, familial hypercholesterolaemia etc.
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10. b) Sex-
Males throughout their life are more susceptible than females to develop MI. Women
during reproduction period have low remarkable incidence of MI, probably due to
protective influence of estrogen. The use of oral contraceptives is associated with high
risk of developing MI. After menopause, the risk of developing MI is gradually
declines.
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11. Pathogenesis of MI-
 Coronary angiography and autopsy reveals that coronary atherosclerosis is
an important etiological factor in the development of about 90 % cases of
acute MI.
 Myocardial ischaemia due to decreased blood flow, increased myocardial
oxygenated blood demand, and hypertrophy of heart without simultaneous
increase in the blood flow complicates coronary atherosclerosis.
 Platelet aggregation, activation and release reaction leads to platelet mass/
plug formation leads to the formation of emboli (clot) in coronaries.
 Non-atherosclerotic causes such as coronary vasospasm, arteritis, coronary
arterial stenosis, embolism, thrombotic diseases, trauma and outside
compression develops MI.
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12. Pathological changes-
 The gross and microscopic changes in MI vary according to the age of
infarct.
 Grossly, most of the myocardial infarcts occurs singly and vary in size from
4 to 10 cm. The infarcts are most common in the left ventricle are- a)
transmural infarcts, which involve the entire thickness of the ventricular
wall, and b) subendocardial infarcts which affect the inner subendocardial
half of the myocardium.
 The frequency of AMI in the three major branch of coronary arteries are-
Left anterior descending (40-50%), Right coronary (30-40%), and Left
circumflex (15-20%).
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Sr. No. Time Gross changes Microscopic changes
1 0-30 min. Nil Ultramicroscopic changes
2 1-2 Hrs Nil Wavy fibers, Contraction band
3 4-12 Hrs Insignificant
Coagulative necrosis, Edema,
Hemorrhages, Neutrophilic infiltration
4 18-24 Hrs Pallor
Coagulative necrosis, Contraction band,
Marginal necrosis
5 24-72 Hrs Pallor with hyperemic margin
Total necrosis in hyperemic margins,
Affected areas with hyperemia
6 3-7 days
Hyperemic border with central
softening
Repair process starts with fibrovascular
response
7 10 days
Depressed areas with vascularized
margins
Prominent fibrovascular marginal
reactions
8 7th week Completion of scarring Fibrosis
The gross and microscopic features of AMI depend upon the time duration from onset

14. Clinical features-
 Pain,
 Indigestion,
 Anxiety due to fear of death,
 Shock,
 Oliguria,
 Low grade fever accomplished with
leucocytosis and elevated ESR,
 Acute pulmonary edema, and
 ECG changes- a) ST-segment elevation,
b) T-wave inversion, and c) appearance of
deep Q-wave
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15. Complications-
 Arrhythmias- Sinus tachycardia or sinus bradycardia, atrial fibrillation, premature systole,
and the most serious ventricular fibrillation leading to sudden cardiac death,
 Congestive heart failure (CHF),
 Cardiogenic shock,
 Mural thrombosis and thromboembolism,
 Rupture of the heart,
 Cardiac aneurysm in left ventricle,
 Pericarditis
 Post-myocardial infarction syndrome characterized by pneumonitis.
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Figure- Diagram of a myocardial infarction (2) of the tip of
the anterior wall of the heart (an apical infarct) after
occlusion (1) of a branch of the left coronary artery (LCA).
In the diagram, RCA is the right coronary artery.
Figure- Rough diagram of pain zones in
myocardial infarction; dark red: most typical
area, light red- other possible areas; view of the
chest.

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Figure- Back View.
Figure- A myocardial infarction occurs when
an atherosclerotic plaque slowly builds up in the inner lining
of a coronary artery and then suddenly ruptures, causing
catastrophic thrombus formation, totally occluding the artery
and preventing blood flow downstream.

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