Ischemic heart disease &

Pericarditis
II MBBS
Dr. Maitrayee Roy MD FRCPath

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The arterial supply to the heart

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Coronary arteries are end arteries, present on the surface of the
heart i.e. epicardial in location → occlusion → inner half of
myocardium is more susceptible to ischemia than outer half

Myocardium

Epicardium

Coronary artery

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Ischemic heart disease (IHD)

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 Ischemic heart disease (IHD): overview

• Also called coronary artery disease (CAD) or

coronary heart disease.

• Myocardial demand for oxygen exceeds supply

resulting in tissue hypoxia and ischemia.

• 90% of cases are because of reduced blood flow due

to obstructive atherosclerotic lesions in the
epicardial coronary arteries

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 IHD definition
• Ischemic heart disease represents a group of
pathophysiologically related syndromes resulting
from myocardial ischemia i.e. an imbalance between
myocardial supply (perfusion) and cardiac demand for
oxygenated blood.

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 IHD classification
• IHD can present as ≥1 of the following clinical syndromes:
1. Angina pectoris (literally “chest pain”) → ischemia is not
severe enough to cause myocyte necrosis → 3 types:
stable/ typical, unstable and prinzmetal angina.
2. Myocardial infarction → severe ischemia causing frank
myocardial necrosis → 2 types: subendocardial MI &
transmural MI
3. Sudden cardiac death (SCD).
4. Chronic IHD with heart failure.

Unstable angina, myocardial infarction, sudden cardiac death

→ collectively called as acute coronary syndrome
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 IHD: Etiopathogenesis
1. Coronary atherosclerosis: most common cause
2. Coronary artery thrombosis/ thromboembolism
3. Coronary artery inflammation (e.g. Takayasu arteritis)
4. Coronary artery spasm
5. Coronary artery aneurysm

Chronic, progressive atherosclerotic narrowing of the epicardial

coronary arteries → coronary stenosis (stable angina, chronic
IHD) → variable degrees of superimposed acute plaque change
like plaque rupture & thrombosis → coronary occlusion (acute
coronary syndrome i.e. unstable angina/ MI/ SCD)
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 Normal coronary artery

Coronary artery with

atherosclerotic
plaque and lumen
narrowing

Coronary artery with

atherosclerotic plaque and
superimposed thrombus
causing lumen occlusion 11
 IHD: Etiopathogenesis
Plaque Plaque-Associated
Syndrome Stenosis Disruption Thrombus
Stable angina >75% No No

Unstable angina Variable Frequent Yes, Non-occlusive

Subendocardial Variable Variable Yes, Widely variable

MI (i.e. inner half of
myocardium)
Transmural MI Variable Frequent Yes, Occlusive
(i.e. full thickness
myocardium)
Sudden cardiac Severe Frequent Often small
death (usually death due to arrhythmia)
 Angina pectoris: definition
• Angina pectoris is characterized by paroxysmal and
usually recurrent attacks of substernal/ precordial chest
discomfort caused by transient (15 seconds to 15
minutes) myocardial ischemia that is insufficient to
induce myocyte necrosis.

• 3 types
1. Stable or typical angina
2. Unstable angina
3. Prinzmetal angina

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 Stable angina
• Insufficient coronary perfusion (due to chronic
stenosing coronary atherosclerosis) compared to
increased myocardial demand caused by physical
activity, emotional excitement or psychological stress.

• Typical symptoms: heaviness or pain in the chest

during exercise/ stress, relieved by rest or vasodilator
medicine like nitroglycerine.

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 Unstable angina
• Increasingly frequent, prolonged (>20 min), or
severe chest discomfort/pain, precipitated by
progressively lower levels of physical activity or even
occurring at rest.

• Caused by the disruption of an atherosclerotic plaque

with superimposed partial thrombosis and/or
vasospasm.

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 Prinzmetal angina
• Uncommon form of episodic myocardial ischemia
caused by coronary artery spasm.

• Prinzmetal angina attacks are unrelated to physical

activity, heart rate, or blood pressure

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 Myocardial infarction (MI)
• Necrosis of cardiac myocyte due to prolonged
severe ischemia.

• Patterns of MI
1. Subendocardial MI
2. Transmural MI
3. Multifocal microinfarction (occurs when smaller
intramural vessels are involved by embolization, vasculitis,
vasospasm)

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 Patterns of MI
Subendocardial MI Transmural MI

• Necrosis involves the • Necrosis involves full

least perfused area of the
myocardium
i.e. subendocardial or
inner 1/3rd of ventricular
wall
• Atherosclerotic plaque
disruption → superimposed
thrombus causing partial
occlusion of coronary
artery lumen or patients in
shock.
thickness of myocardium.
• Atherosclerotic plaque
disruption → superimposed
thrombus causing
complete occlusion of
artery lumen.
• Area of heart infarcted
depends on the coronary
artery branch occluded.
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 Common locations of MI
• Based on coronary artery branch thrombosed.
• Most common overall location: Left ventricle.
Artery branch Frequency Most common area infarcted
Left anterior 40-50% Anterior wall of left ventricle,
descending artery apex of heart and anterior
2/3rd of inter-ventricular
septum
Right coronary artery 30-40% Posterior part of left ventricle,
posterior 1/3rd of inter-
ventricular septum, right
ventricle
Left circumflex 15-20% Lateral wall of left ventricle
coronary artery 20
 Common locations of MI

A: Anterior wall; P: Posterior wall 21

Diagnosis of MI

Clinical
ECG
features

Serum cardiac
enzymes

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 MI – clinical features
• Anterior substernal chest pain-
Crushing, stabbing, squeezing pain (caution:
diabetics may not complain of pain)
• Pain often radiates to left shoulder & upper
arm
• Rapid, weak pulse and profuse sweating
• Nausea & vomiting
• Breathlessness (due to impaired contractility
of ischemic myocardium with resultant
pulmonary congestion and edema)
• Diabetics: may not experience pain
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 MI – ECG changes Normal ECG

• Convex upward ST segment

elevation (ST elevation MI i.e.
STEMI)
• T wave inversion
• Appearance of wide deep Q waves

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Normal ECG

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 ECG showing an anterolateral STEMI

Convex upward ST segment elevation in leads I, aVL and V1-V3

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Area of heart
infarcted can be
predicted by the
leads showing MI
related changes

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 MI – cardiac enzymes
• Diagnosis is based on blood levels of enzymes that are leaked
out from irreversibly damaged myocyte.

1. Cardiac specific troponins T and I (cTnT & cTnI) : most

sensitive & specific
2. Muscle & Brain (MB) fraction of creatine kinase (CK-MB)
3. Lactate Dehydrogenase (LDH)
4. Myoglobin

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MI – cardiac enzymes

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 Complications of MI
• Arrhythmias
• Congestive heart failure
• Cardiogenic shock
• Mural thrombosis & thromboemboli
• Myocardial rupture
• Cardiac aneurysm
• Pericarditis

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 Morphological changes in MI
• Gross changes are not apparent until 4 hrs.

• Microscopic changes are not significant until 4 hrs.

• If patient died within 2 to 3 hours of MI, areas of infarction can

be highlighted by immersing tissue slices in solution of
Triphenyl tetrazolium chloride (TTC) → imparts brick red
color to viable non-infarcted myocardium while infarcted
myocardium looks pale/ unstained.

• Lactate dehydrogenase is preserved in the viable myocardium

resulting it to be stained by TTC whereas in the infracted area,
LDH enzyme leaks out of the cells due to disruption of the
membrane and hence infarcted myocardium remians unstained.

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Brick red viable myocardium Unstained infarcted myocardium

Acute MI (< 3hours): Triphenyl tetrazolium chloride stain 32

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 MI- Microscopic features
One-day-old infarct Up to 3 days duration

wavy fibers

coagulative necrosis Neutrophilic infiltrate

>3 weeks
1 -2 weeks

Granulation tissue Scar

 MI – Reperfusion injury
• Mechanisms
• Thrombolytic drugs = < 1hr after onset of MI
• PTCA/CABG = > 1hr after onset of MI

• Target = clot lysis and restoration of blood flow

• Post- reperfusion changes:

– Hemorrhagic infarcts.
– Contraction bands due to hyper contracting myocyte.
– Stunned myocardium due to transient, protective dysfunction.
– Reperfusion damage, mostly apoptosis by free radicals
(unlike MI).
MI – Reperfusion injury

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Pericarditis

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 Pericarditis: definition & etiology

• Pericarditis is the inflammation of the pericardium

which is a thin, two-layered sac that surrounds your heart.

• Etiology
1. Primary (rare): most common cause is viral infection,
tuberculosis
2. Secondary (common): secondary to cardiac disease (e.g.
complication of MI), systemic disease (e.g. SLE, renal
failure), metastatic tumor, trauma/ surgery

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 Pericarditis: morphological types
• Serous pericarditis: caused by noninfectious inflammatory
diseases e.g. rheumatic fever, SLE, scleroderma, uremia in CKD
patients
• Fibrinous pericarditis: post MI (Dressler syndrome - an
autoimmune response appearing days-weeks after an MI)
• Purulent pericarditis: Infectious etiology
• Caseous pericarditis: tuberculosis
• Hemorrhagic pericarditis: Malignant tumor, cardiac surgery,
trauma
• Chronic / healed pericarditis: plaque-like fibrous thickenings of
the serosal membranes (“soldier’s plaque”)

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 Pericarditis: clinical features
• Clinical symptoms of acute pericarditis can mimic MI.
• Sharp retrosternal chest pain, no radiation or radiates to
back; worse in supine position & deep breathing; no
increase in intensity on exertion.
• Auscultation: frictional rub.

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 Pericarditis: diagnosis
• ECG changes can also mimic acute MI.
• ECG : diffuse concave ST elevation without reciprocal
T wave changes or Q waves
• But cardiac enzymes are normal.

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Thank you

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