PATHOLOGY OF CARDIOVASCULAR SYSTEM

dr. Septi Handayani, M.Si.

OVERVIEW
Review of basics
Ischaemic heart diseases
 Coronary artery occlusions
 Myocardial infarction
Valvular heart diseases
 Degenerative valvular diseases
 Rheumatic heart disease
 Bacterial endocarditis
REVIEW
Atherosclerosis
Epidemiology of coronary artery disease
Physiology of the cardiac cycle
Anatomy of the myocardium
Vascular supply of the myocardium
Taken from Colour Atlas of Anatomy – Roden, Yokochi and Lutjen-Drecoll
Taken from Colour Atlas of
Anatomy – Roden, Yokochi and
Lutjen-Drecoll
Taken from Colour Atlas of Anatomy –
Roden, Yokochi and Lutjen-Drecoll
Taken from Colour Atlas of Anatomy – Roden, Yokochi and Lutjen-Drecoll
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 SUPPLY (PERFUSION)
The left coronary trunk gives rise to:-
 Left Anterior Descending (LAD) and the Left Circumflex (LCX)

Right Coronary Artery (RCA)

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.
Coronary atherosclerosis
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.
Three variants:-
 Stable angina
 Prinzmental angina
 Unstable angina
ANGINA PECTORIS
Stable Angina – Most common form. Chronic stenosing coronary
atherosclerosis, reaching a critical level, leaving the heart vulnerable
to increased demand.
Typically relieved by rest or a vasodilator
PRINZMENTAL ANGINA
Uncommon pattern
Occurs at rest
Documented to be due to arterial spasm
Unrelated to physical activity, heart rate or blood pressure.
Generally responds to vasodilators.
UNSTABLE ANGINA
Pattern here is the pain occurs with progressively increasing frequency
and tends to be more prolonged
Associated with disruption of the atherosclerotic plaque, with
superimposed thrombosis, embolisation or spasm.
Predictor of 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)
Varying gross appearance of
myocardial infarction
Recent and Old Myocardial Infarcts
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)
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
OTHER DIAGNOSTIC TOOLS
Electrocardiogram – Q waves
Echocardiogram
Radioisotope studies
Magnetic Resonance Imaging
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
Mitral Valves
Pulmonary
Valves
Tricuspid Valves
Taken from Colour Atlas of Anatomy – Roden, Yokochi and Lutjen-Drecoll
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 volume and Atrial dilatation

pressure

Systemic embolisation
Congestion of
Atrial thrombus
lungs

Pulmonary
Right Heart Failure Hypertension
COMMON VALVULAR DISEASES
Degenerative
 Calcific aortic stenosis
 Mitral annular calcification
 Myxomatous degeneration of mitral valves (mitral valve prolapse)

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

Aortic Valve Inlet –
Looking into the left
ventricular outlet
Note the three valvular
cusps and the three
distinct commissures
(arrows)
Calcific Aortic Stenosis – (3 cusps)
Calcific Bicuspid Aortic Valve
MITRAL ANNULAR CALCIFICATION
Degenerative calcific deposits in the ring of the mitral valve.
Generally does not affect valvular function, but can lead to mitral
regurgitation
Source of thrombi and emboli, also prone to infective endocarditis
Most common in women over 60
 Calcification of Mitral Valve Ring

Diagram from Robbins Pathologic Basis of Disease

MITRAL VALVE PROLAPSE
Myxomatous degeneration of valve.
Characteristically ballooning of the valvular cusps
with the affected leaflets thickened and rubbery.
Basis for the change unknown but believed to be
due to developmental anomaly of connective
tissue.
Association with Marfan’s syndrome (a syndrome
whereby there is a mutation in the gene encoding
fibrillin)
Mitral Valve Inlet –
Viewed from the left
atrium.
Note bicuspid valve
leaflets.
Slight tenting of the
valve leaflets
suggestive of early
mitral valve prolapse.
Mitral Valve
Prolapse
Notice tenting
of valve
leaflet
(arrow)
RHEUMATIC FEVER
Once the most common cause of valvular heart disease in Hong Kong.
It is an acute immunologically mediated , multi-system inflammatory
disease that occurs a few weeks after an episode of Group A (ß-
hemolytic) streptococcal pharyngitis.
Diagram from Robbins Pathologic Basis of Disease
 Rheumatic Valvulitis

Diagram from Robbins Pathologic Basis of Disease

 Acute Rheumatic Carditis – Aschoff Body

Diagram from Robbins Pathologic Basis of Disease

CHRONIC RHEUMATIC VALVULAR HEART
DISEASE
Most important consequence of rheumatic fever
Inflammatory deformity of valves
 Almost always involve the mitral valve
 Involvement of aortic or other valves also common
CHARACTERISTICS OF RHEUMATIC
VALVULAR DISEASE
Acute phase
 Foci of fibrinoid degeneration surrounded by lympocytes – Aschoff bodies
 Most distinctive within the heart, but widely disseminated.
 Pancarditis
 Pericarditis
 Myocarditis
 Verrucae vegetations (1-2 mm)
 Chronic Rheumatic Disease
of Aortic Valve

Diagram from Robbins Pathologic Basis of Disease

CHARACTERISTICS OF RHEUMATIC
VALVULAR DISEASE
Chronic
 Leaflet thickening
 Commissure fusion
 Shortening, thickening and fusion of chordae tendinae
 Chronic Rheumatic Disease of Mitral Valve

Vascularisation)

Diagram from Robbins Pathologic Basis of Disease

INFECTIVE ENDOCARDITIS
Colonisation or invasion of heart valves by microbiologic agent.
Formation of friable vegetations (composed of thrombotic debris and
organisms.
Leads to destruction of underlying cardiac tissue.
Source of infective embolisation
INFECTIVE ENDOCARDITIS
Most common sites involve the left heart valves
Tricuspid valves typically involved in intravenous drug abusers
Development of infective endocarditis preventable in patients with
valvular diseases by provision of antibiotic cover for any surgical or
dental procedures.
 Bacteria Endocarditis

Diagram from Robbins Pathologic Basis of Disease

 THANK YOU
FOR YOUR ATTENTION