CVS 4 PDF

Diseases of the Heart - 2
Dr. Geener .K .John

Recommended reading –
Pages 408- 419 from
Robbins – Basic Pathology 10th edition
SLO# 1 : Discuss the morphological types of aneurysms with
their causes and complications.
SLO# 2 : Discuss the pathogenesis and morphology of
Syphilitic aortitis.
SLO# 3 : Describe changes in Aortic dissection.
SLO# 4 : Discuss the clinical presentation, microscopic changes
and complications of vasculitis.
SLO# 5 : Classify the vascular tumors.
SLO# 6 : Discuss the gross and microscopic features of
capillary and cavernous hemangioma.
SLO# 7 : Discuss the aetiology gross and microscopic features
of angiosarcoma.
Ischemic heart disease (IHD)
Generic term for a group of syndromes resulting
from myocardial ischemia
Imbalance between
Cardiac Bd. supply ↔Myocardial O2 demand
Most cases – Obstruction of coronaries due to
atherosclerosis – Coronary artery disease
It is the major cause of death in industrialized
countries
Clinical syndromes of IHD
Angina pectoris – chest pain
stable & unstable
Acute myocardial infarction (Acute MI) –
ischemia is severe enough to cause cardiac
muscle death
Chronic IHD – Progressive heart failure after
MI
Sudden cardiac death (SCD) –Lethal
arrhythmia following MI
Pathogenesis
Inadequate coronary perfusion relative to
myocardial demand
In a preexisting atherosclerosis super added
thrombosis or vasospasm is the cause
>70%occlusion of cross sectional area of vessel
lumen – critical stenosis angina
When the occlusion is slow as in atherosclerosis
collaterals develops
Progression of
coronary artery
lesion
Role of acute plaque changes
Unstable angina, MI & SCD are precipitated by
abrupt plaque changes like
Rupture / fissuring  atheroembolism
Ulceration  expose thrombogenic
subendothelial BM
Hemorrhage into core of plaque  plaque
volume expansion  worsen occlusion
Angina pectoris
Chest pain due to transient, reversible
myocardial ischemia
Typical/ Stable- at particular level of exertion
-relieved by rest & drugs
Prinzmetal/variant angina- due to coronary
artery spasm- responds to vasodilators
Unstable angina- higher degree of occlusion
Present even at rest
Myocardial infarction
Necrosis of heart muscle resulting from ischemia
Frequency of MI progressively ↑ses with age –
atherosclerosis is the major cause
Men are at higher risk than women
Risk factors and epidemiology- same as coronary
atherosclerosis.
Pathogenesis- Coronary artery thrombosis due
to atheromatous plaque disruption and
thrombus formation.
Myocardial response to ischemia
Within seconds of vascular obstruction
Aerobic glycolysis ceases  ↓sed ATP
Lactic acid accumulates
Ultra structural changes – myofibrillar
relaxation, glycogen depletion &
mitochondrial swelling
If ischemia is severe & last for at least 20-40
minutes changes are irreversible 
coagulation necrosis
Vessel involvement
One or more of the 3 major trunks may be involved
Site of maximum involvement
First few cms from the
origin of
Lt. Ant. descending art.(LAD)
Lt. circumflex art.(LCX)
entire length of
Rt. coronary art.(RCA)
Frequency of occlusion and
distribution of infarction -
Left anterior Anterior wall of left ventricle including
descending apex; anterior two thirds of the
coronary artery interventricular septum
(40% to 50%)
Right coronary Posterior wall of the left ventricle;
artery (30% to posterior one third of the
40%) interventricular septum
Left circumflex Lateral wall of left ventricle excluding

coronary artery apex
(15% to 20%)
Transmural Vs Subendocardial
A transmural myocardial infarction
refers to a myocardial infarction that
infarction
involves the full thickness of the
myocardium
Involves nearly full (>50%) Necrosis limited to
thickness of ventricle inner 1/3rd to ½
More common (95%) Less common
Limited to distribution Extend beyond

territory of a single artery distribution territory
Pathogenesis – coronary Pathogenesis –
atherosclerosis & Hypoperfusion as in
Epicardial vessel occlusion shock
ST segment elevated No elevation
Morphology
Location – Most infarctions affect at least a
portion of Lt. ventricle
Even in transmural
infarction a narrow rim
of subendocardial
myocardium is preserved.
Isolated Rt. ventricular infarction is rare
Infarction of Lt. atrium is least common
Gross changes
Changes vary depending on the time interval after MI
Time interval Changes
< 12 hrs No gross changes
12-24 hrs Dark mottling
By 4th day Sharply defined with yellow
Infarcted center
End of 1st week Entire infarct is yellowish with
hyperemic border
End of 6 weeks Infarcted area replaced by
fibrous scar
Gross appearance of Myocardial
Infarction
Acute myocardial infarction Healed myocardial infarct

Microscopic changes
4-12 hrs Beginning of coagulation necrosis,
Edema, hemorrhage
12-24 hrs Coagulation necrosis progresses & is
complete by 48-72 hrs.
Followed by neutrophilic infiltration
End of 1st Necrotic fibers removed by
week macrophages, proliferation of
capillaries & fibroblasts at the margin
10-14 days Well established granulation tissue is
formed
6 weeks Dense collagenous scar is formed
Microscopy
48hr old MI
Complete coagulation necrosis
Heavy neutrophilic infiltration
contraction band necrosis
Reperfusion injury
Restoration of tissue perfusion is achieved by
thrombolysis, balloon angioplasty etc.
Sometimes reperfusion can cause greater tissue
damage
Factors involved are- Mitochondrial
dysfunction, myocyte hyper contracture, free
radicals & leucocyte aggregation
Microscopy shows contraction band necrosis
due to hyper contracted sarcomeres
Clinical features
Severe substernal crushing chest pain with
radiation- last from 20 mts to several hours
Silent MI in Diabetics
Profuse sweating
Weak & rapid pulse
Dyspnoea due to pulmonary congestion &
edema
Laboratory evaluation
ECG Changes –
ST - segment elevation, T – inversion
Appearance of new Q wave
Biochemical evidence –
Blood level of intra cellular macromolecules
that leak out of injured cell is measured -
myoglobin, cardiac troponin T & I, creatine
kinase –MB isoform, LDH etc
Biochemical evidence
Myoglobin & LDH lack specificity
Troponins (best marker) & CK – MB are highly specific
Molecule Appear Peak Disappear
TnT & TnI 2-4 hrs 48 hrs Remain elevated for 7-10 days
CK-MB 2-4 hrs 24-48 hrs Returns to normal with in 72 hrs
Complications
1. Contractile dysfunction – left ventricular pump
failure  cardiogenic shock
2. Papillary muscle dysfunction

 Mitral regurgitation
3. Arrhythmias – ischemic injury to conducting

system. Eg sinus bradycardia, heart block,
tachycardia,
Complications – Contd.
4. Myocardial rupture – most common between 3-7
days
i. Rupture of wall
Hemopericardium
& tamponade
ii. Inter-ventricular septum

Lt to Rt shunt
Complications – Contd.
5. Pericarditis –
Fibrinous or hemorrhagic
6. Mural thrombus
7. Cardiac aneurysm

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Diseases of the Heart - 2

Dr. Geener .K .John

Left circumflex Lateral wall of left ventricle excluding

Limited to distribution Extend beyond

Acute myocardial infarction Healed myocardial infarct

2. Papillary muscle dysfunction

3. Arrhythmias – ischemic injury to conducting

ii. Inter-ventricular septum

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