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CVS Lecture 1

The document provides an overview of the pathology of the cardiovascular system, covering ischaemic heart diseases, valvular heart diseases, and shock. It details the anatomy and vascular supply of the myocardium, the effects of ischaemia, and the clinical manifestations of myocardial infarction. Additionally, it discusses the anatomy of heart valves and the impacts of valvular diseases, including common conditions like calcific aortic stenosis.

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AHMAD Ali
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13 views40 pages

CVS Lecture 1

The document provides an overview of the pathology of the cardiovascular system, covering ischaemic heart diseases, valvular heart diseases, and shock. It details the anatomy and vascular supply of the myocardium, the effects of ischaemia, and the clinical manifestations of myocardial infarction. Additionally, it discusses the anatomy of heart valves and the impacts of valvular diseases, including common conditions like calcific aortic stenosis.

Uploaded by

AHMAD Ali
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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Pathology of Cardiovascular

System
Overview
• Review of basics
• Ischaemic heart diseases
– Coronary artery occlusions
– Myocardial infarction
• Valvular heart diseases
– Degenerative valvular diseases
– Rheumatic heart disease
– Bacterial endocarditis
• Shock
– Hypovoleamic shock
– Cardiogenic shock
– Septiceamic shock
– Anaphylactic shock
Taken from Colour
Atlas of Anatomy –
Roden, Yokochi and
Lutjen-Drecoll
Anatomy of the myocardium
• Cardiac muscle cells form a collection of
branching and anastamosing striated muscles.
They make up 90% of the volume of the
myocardium.
• Unlike skeletal muscles, they contain ten times
more mitochondria per muscle cell. This reflects
their extreme dependence on aerobic metabolism.
They do not need to rest!!
Vascular supply of the
myocardium
• Predominant blood supply is from the coronary
arteries, which arises from the aorta and runs
along an epicardial route before penetrating the
myocardium as intramural arteries. Effectively a
“one-way street” flow and supply.
• Coronary arterial blood flow to the myocardium
occurs during ventricular diastole; when the
microcirculation in the myocardium is not
compressed by cardiac contraction. The “one^way
street” only flows within a fixed time span.
Coronary Angiography

L = Left main trunk


A= Anterior descending
C= Circumflex
R= Right coronary
P=Posterior descending
Areas of perfusion
• Left anterior descending (LAD) – supplies most of
the apex of the heart, the anterior wall of the left
ventricle and the anterior two-thirds of the
ventricular septum.
• Left circumflex branch supplies the lateral wall of
the left ventricle.
• The right coronary artery in 80% of the population
supplies the right ventricle, the posterior third of
the ventricular septum and the posterior-basal wall
of the left ventricle. (Right dominant circulation)
Ischaemic Heart Diseases
• This is a generic name for a group of
closely related syndromes that result from
myocardial ischaemia.
• In over 90%, this is due to a reduction in
coronary blood flow. (Decrease in supply)
• Other conditions arise as a result of
increases in demand e.g. hypertrophy,
shock, increase heart rate, etc.
Diminished Coronary Perfusion
• Fixed coronary obstruction
– More than 90% of patients with IHD
– One or more lesions that causes at least 75%
reduction of the cross-sectional area of at least
one of the major epicardial arteries.
Coronary atherosclerosis
Coronary atherosclerosis
Coronary atherosclerosis
Taken from Robbins Pathologic Basis of Disease
Clinical Manifestations
• Angina Pectoris
• Myocardial Infarction
• Chronic ischaemic heart disease
– Progressive heart failure consequent to previous
myocardial infarction.
• Sudden Cardiac Death
Angina Pectoris
• This is a symptom complex. Symptoms
caused by transient myocardial ischaemia
that falls short of inducing the cellular
necrosis that defines myocardial infarction.
Effects of ischaemia on myocytes
• Onset of ATP Depletion • Seconds
• Loss of contractility • < 2 minutes
• ATP reduced
– to 50% of normal • 10 minutes
– To 10% of normal • 40 minutes
• Irreversible injury • 20-40 minutes
• Microvascular injury • > 1 hour
Myocardial Infarction
Transmural Infarction
– The ischaemic necrosis involves the full or
nearly the full thickness of the ventricular wall
in the distribution of a single coronary artery.
– Usually associated with chronic coronary
atherosclerosis, acute plaque change and
superimposed completely obstructive
thrombosis.
Myocardial Infarction
• Subendocardial infarct
– Limited to the inner one-third or at most one
half of the ventricular wall
– May extend laterally beyond the perfusion
territory of a single coronary artery
– In a majority of cases, there is diffuse stenosing
coronary atherosclerosis.
Gross changes of myocardial
infarction
• Gross changes
– None to occasional mottling (up to 12 hours)
– Dark mottling (12-24 hours)
– Central yellow tan with hypereamic border (3-7
days)
– Gray white scar (2-8 weeks)
Microscopic changes of
myocardial infarct
• Early coagulation necrosis and oedema;
haemorrhage (4-12 hours)
• Pyknosis of nucleic, hypereosinophilia,
early neutrophilic infiltrate (12-24 hours)
• Coagulation necrosis, interstitial infiltrate of
neutrophils (1-3 days)
• Dense collagenous scar (> 2 months)
Coagulative necrosis
Interstitial infiltration of neutrophils
Laboratory detection of
myocardial infarction
• This is based on the measurement of
intracellular macromolecules leaked from
the damaged myocytes into the circulation
• Creatine kinase – particularly the MB
isoenzyme
• Lactate dehydrogenase
• Troponin – Troponin 1 and Troponin T
Electrocardiogram (ECG) changes
Acute effects of myocardial
infarction
• Contractile dysfunction
• Arrhythmias
• Cardiac rupture
• Pericarditis
• Sudden death
– Invariably this would be due to a lethal
arrhythmia (asystole or ventricular fibrillation)
Pathological complications of
myocardial infarction
• Infarct extension
• Mural thrombus
• Ventricular aneurysm
• Myocardial rupture
– Ventricular free wall
– Septal
– Papillary muscle
Infarct extension

Diagram from Robbins Pathologic Basis of Disease


Ruptured
Myocardial
Infarct
Ruptured Papillary muscle
Old myocardial infarct showing evidence of
thinning of ventricular wall replaced by fibrous scar
Fibrous scarring with compensatory hypertrophy of
unaffected ventricular wall
Ventricular wall
aneurysm
Anatomy of Heart Valves
• Aortic valve – Commonly tricuspid semi lunar
valves. Can be congenitally bicuspid.
• Mitral valve – Bi-cuspid flaps supported by
chordae tendinae attached to papillary muscles
• Pulmonary valves – Tricuspid semi lunar valves
• Tricuspid valves – Tri-cuspid flaps supported by
chordae tendinae.
Aortic Valves
Response to injury
• Mechanical injury – superficial fibrous
thickening over preserved architecture.
• Inflammation – invariably leads to
vascularisation of structure, fibrosis leads to
decrease in size/surface area.
• Degenerative changes – distortion and
increase in size due to deposits of material
such as calcium salts, cholesterol, etc.
Effects of valvular disease
• Stenosis – tightening of the valvular
opening resulting in decreased flow of
blood through the opening.
• Incompetence – incomplete closure of the
valvular opening, allowing backflow of
blood through the valvular opening
• Mixed.
Effects of valvular disease

Mitral Stenosis

Increased atrial Atrial


volume and pressure dilatation

Systemic
embolisation Atrial thrombus Congestion
of lungs

Pulmonary
Right Heart Hypertension
Failure
Common valvular diseases
• Degenerative
– Calcific aortic stenosis
– Mitral annular calcification
• Rheumatic fever and rheumatic heart
disease
Calcific Aortic Stenosis
• Most frequent of all valvular abnormalities
• Calcification induced by wear and tear
• Onset in the elderly
– 50’s and 60’s in congenital bicuspid individuals
– 70’s and 80’s in those with previous normal
valves
• Heaped up calcified masses
Calcific Aortic Stenosis – (3 cusps)

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