ATHEROSCLEROSIS

ATHEROSCLEROSIS

Atherosclerosis can affect any artery in the body

Occult coronary artery disease is common in those

who present with other forms of atherosclerotic
vascular disease
PATHOPHYSIOLOGY
Type I ( initial lesion) : isolated macrophage ,foam
cells
Type II ( fatty streak) : intracellular lipid
Type III (intermediate lesion); type II+ small
extracellular lip[id pool
Type IV (atheroma lesion) :type II + core of
extracellular lipid pool
Type V (fibroatheroma): Lipid core + fibrotic layer
Type VI (complicated): surface defect , hematoma
;hemorrhage ; thrombus
 EARLY ATHEROSCLEROSIS
Atherosclerosis begins early in life

Early atherosclerotic lesions have been found in the

arteries of victims of accidental death in the second
and third decades of life
Fatty streaks tend to occur at sites of altered arterial
shear stress
They develop when inflammatory cells, predominantly
monocytes, bind to receptors expressed by
endothelial cells, migrate into the intima, take up
oxidised low-density lipoprotein (LDL) particles and
become lipid-laden macrophages or foam cells
 ADVANCED
ATHEROSCLEROSIS
In an established atherosclerotic plaque,
macrophages mediate inflammation and smooth
muscle cells promote repair.

Any breach in the integrity of the plaque will

expose its contents to blood, and trigger platelet
aggregation and thrombosis that extend into the
atheromatous plaque and the arterial lumen
'Vulnerable' plaques are characterised by a lipid-rich
core, a thin fibrocellular cap and an increase in
inflammatory cells that release specific enzymes to
degrade matrix proteins. In contrast, stable plaques are
typified by a small lipid pool, a thick fibrous cap,
calcification and plentiful collagenous cross-struts

Atherosclerosis may induce complex changes in the

media that lead to arterial remodelling ( posative and
negative)
 RISK FACTORS
Age and sex.
Family history.
Smoking.
Hypertension
Hypercholesterolaemia
Diabetes mellitus.
Haemostatic factors.
Physical activity.
Obesity
Alcohol.
Other dietary factors.
Personality.
Social deprivation.
PREVENTION

Primary prevention

Secondary prevention
 CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is the most common form

of heart disease

By 2020, it is estimated that it will be the major

cause of death in all regions of the world.

Occasionally, the coronary arteries are involved in other

disorders such as aortitis, polyarteritis and other
connective tissue disorders.
CORONARY ARTERY DISEASE: CLINICAL
MANIFESTATIONS AND PATHOLOGY
Stable angina Ischaemia due to fixed atheromatous
stenosis of one or more coronary arteries
Unstable angina Ischaemia caused by dynamic
obstruction of a coronary artery due to plaque rupture or
erosion with superimposed thrombosis
Myocardial infarction Myocardial necrosis caused by
acute occlusion of a coronary artery due to plaque rupture
or erosion with superimposed thrombosis
Heart failure Myocardial dysfunction due to infarction or
ischaemia
Arrhythmia Altered conduction due to ischaemia or
infarction
Sudden death Ventricular arrhythmia, asystole or massive
 STABLE ANGINA
is the symptom complex caused by transient
myocardial ischaemia and constitutes a clinical
syndrome rather than a disease.

imbalance between myocardial oxygen supply and

demand

may be a manifestation of other forms of heart

disease, particularly aortic valve disease and
hypertrophic cardiomyopathy
FACTORS INFLUENCING MYOCARDIAL OXYGEN SUPPLY AND
DEMAND

Oxygen demand: cardiac work

Heart rate
BP
Myocardial contractility
Left ventricular hypertrophy
Valve disease, e.g. aortic stenosis

Oxygen supply: coronary blood flow

Duration of diastole
Coronary perfusion pressure (aortic diastolic minus coronary sinus or right
atrial diastolic pressure)
Coronary vasomotor tone
Oxygenation
Haemoglobin
Oxygen saturation
 ACTIVITIES PRECIPITATING
ANGINA
Common
Physical exertion
Cold exposure

Heavy meals
Intense emotion

Uncommon
Lying flat (decubitus angina)

Vivid dreams (nocturnal angina)

INVESTIGATIONS

Resting ECG

Exercise ECG
EXERCISE ECG
OTHER FORMS OF STRESS
TESTING

Stress echocardiography

Myocardial perfusion scanning

Coronary arteriography
STRESS ECHO
MYOCARDIAL PERFUSION
SCANNING
CORONARY ANGIO.
RISK STRATIFICATION IN STABLE ANGINA

High risk Low risk

Post-infarct angina Predictable exertional angina

Poor effort tolerance Good effort tolerance

Ischaemia at low workload Ischaemia only at high workload

Left main or three-vessel disease Single-vessel or two-vessel disease

Poor LV function Good LV function

MANAGEMENT: GENERAL
MEASURES

a careful assessment of the likely extent and

severity of arterial disease
the identification and control of risk factors
such as smoking, hypertension and
hyperlipidaemia
the use of measures to control symptoms
the identification of high-risk patients for
treatment to improve life expectancy.
 ADVICE TO PATIENTS WITH STABLE
ANGINA

ØDo not smoke

ØAim for ideal body weight
ØTake regular exercise (exercise up to, but not
beyond, the point of chest discomfort is beneficial
and may promote collateral vessels)
ØAvoid severe unaccustomed exertion, and
vigorous exercise after a heavy meal or in very
cold weather
ØTake sublingual nitrate before undertaking
exertion that may induce angina
 PHARMACOLOGICAL THERAPY
Antiplatelet therapy

Anti-anginal drug treatment

Nitrates
Beta-blockers
Calcium channel antagonists
Potassium channel activators
If channel antagonist
INVASIVE THERAPY : PCI AND CABG
 COMPARISON OF PCI AND CABG
PCI CABG
Death %0.5 > %1.5 >

Myocardial infarction* %2 %10

Hospital stay 12-36 hrs 5-8 days

Return to work 2-5 days 6-12 wks

Recurrent angina 15-20% at 6 mths 10% at 1 yr

Repeat revascularisation 10-20% at 2 yrs 2% at 2 yrs

Neurological complications Rare Common (see text)

Other complications Emergency CABG Diffuse myocardial damage

Vascular damage related to Infection (chest, wound)
access site Wound pain
 PROGNOSIS
Symptoms are a poor guide to prognosis

Exercise testing and other forms of stress testing

are much more powerful predictors of mortality

In general, the prognosis of coronary artery

disease is related to the number of diseased
vessels and the degree of left ventricular
dysfunction.
ANGINA WITH NORMAL CORONARY
ARTERIES

Coronary artery spasm

Syndrome X
ACUTE CORONARY SYNDROME

Unstable Angina

MI

The culprit lesion is usually a complex ulcerated or

fissured atheromatous plaque with adherent platelet-rich
thrombus and local coronary artery spasm
 CLINICAL FEATURES
Symptoms
Prolonged cardiac pain: chest, throat, arms, epigastrium or back
Anxiety and fear of impending death
Nausea and vomiting
Breathlessness
Collapse/syncope

Physical signs
Signs of sympathetic activation: pallor, sweating, tachycardia
Signs of vagal activation: vomiting, bradycardia
Signs of impaired myocardial function
• Hypotension, oliguria, cold peripheries
• Narrow pulse pressure
• Raised JVP
• Third heart sound
• Quiet first heart sound
• Diffuse apical impulse
• Lung crepitations
Signs of tissue damage: fever
Signs of complications: e.g. mitral regurgitation, pericarditis
 DIAGNOSIS AND RISK
STRATIFICATION
The differential diagnosis is wide

The assessment of acute chest pain depends heavily on an

analysis of the character of the pain and its associated
features

ECG and Biochemical markers

Risk stratification is important because it guides the use of

more complex pharmacological and interventional
treatment ( GRACE )
INVESTIGATIONS : ECG
NON STEMI
ANTERIOR STEMI
INFEROLATERAL STEMI
PLASMA CARDIAC BIOMARKERS
Other blood tests

Chest X-ray

Echocardiography
 IMMEDIATE MANAGEMENT: THE
FIRST
12 HOURS
Addmission

Analgesia

Antithrombotic therapy

Anti-anginal therapy

Reperfusion therapy
PRIMARY PCI
 CONTRAINDICATIONS
Absolute
•ICH
•Structural cerebral vascular lesion
•Ischaemic strok within 3 months
•Malig. Intracranial neoplasm
•Active bleeding and bleeding diathesis
•Aortic dissection
•Significant closed –head or facial trauma within 3 months

Relative
•Poorly controlled HT. ( SBP ≥ 180)
•Ischaemic strok ≥ 3 months
•Dementia
•Prolonged traumatic resuscitation ( ≥ 10 min)
•Recent internal bleeding ( within 2-4 weeks)
•Non compressible vascular puncture
•Active peptic ulcer
•Current use of anticoagulants
•Pregnancy
•Prior exposure ( for streptokinase)
 COMPLICATIONS OF ACUTE
CORONARY SYNDROME
Arrhythmias
Ischaemia
Acute circulatory failure
Pericarditis
Mechanical complications
Embolism
Impaired ventricular function, remodelling and ventricular aneurysm
LATE MANAGEMENT OF ML
Valvular heart
diseases
Mitral Stenosis
 AETIOLOGY

1- Congenital

2- acquired
Rheumatic
Degenerative
pathophysiology
PATHOPHYSIOLOGY
DEFINITIONS OF SEVERITY OF
MITRAL STENOSIS

Valve Area:
• <1.0 cm2 è Severe
• 1.0-1.5 cm2 è Moderate
• >1.5-2.5 cm2 è Mild

Mean gradient:
• >10 mmHg è Severe
• 5-10 mmHg è Moderate
• <5 mmHg è Mild
 CLINICAL FEATURES
Symptoms
Breathlessness (pulmonary congestion)
Fatigue (low cardiac output)
Oedema, ascites (right heart failure)
Palpitation (atrial fibrillation)
Haemoptysis (pulmonary congestion, pulmonary embolism)
Cough (pulmonary congestion)
Chest pain (pulmonary hypertension)
Thromboembolic complications (e.g. stroke, ischaemic limb)

Signs
Atrial fibrillation
Mitral facies
Auscultation
Loud first heart sound, opening snap
Mid-diastolic murmur
Crepitations, pulmonary oedema, effusions (raised PCWP)
RV heave, loud P2 (pulmonary hypertension)
Investigations
ECG
P mitrale or atrial fibrillation
Right ventricular hypertrophy: tall R waves in V1-V3

CXR
Enlarged LA and appendage
Signs of pulmonary venous congestion

Echo
Thickened immobile cusps
Reduced valve area
Reduced rate of diastolic filling of LV
Enlarged LA

Doppler
Pressure gradient across mitral valve
Pulmonary artery pressure
Left ventricular function

Cath
Coronary artery disease
Mitral stenosis and regurgitation
Pulmonary artery pressure
C:\Users\SHOKRY\Desktop\Echocardiogram in mitral
stenosis - YouTube.flv
 MANAGEMENT
1- Medical management
Anticoagulation
Rate control
Diuretics
2- Mitral balloon valvuloplasty
Significant symptoms
Isolated mitral stenosis
No (or trivial) mitral regurgitation
Mobile, non-calcified valve ( Wilkins score )
LA free of thrombus
3- Valvotomy and Valve replacement
 MITRAL REGURGITATION
Causes of mitral regurgitation
Mitral valve prolapse

Dilatation of the LV and mitral valve ring (e.g.

coronary artery disease,cardiomyopathy)

Damage to valve cusps and chordae (e.g. rheumatic heart

disease,endocarditis)

Ischaemia or infarction of the papillary muscle

MI
 MITRAL VALVE
PROLAPSE

Congenital anomalies

Degenerative myxomatous changes

Marfan syndrom
CLINICAL FEATURES
INVESTIGATIONS
 MANAGEMENT
Medical management of MR
Diuretics
Vasodilators, e.g. ACE inhibitors
Digoxin if atrial fibrillation is present
Anticoagulants if atrial fibrillation is present

Surgical management
Repair
Replacement
 AORTIC STENOSIS
Infants, children, adolescents
Congenital aortic stenosis
Congenital subvalvular aortic stenosis
Congenital supravalvular aortic stenosis

Young adults to middle-aged

Calcification and fibrosis of congenitally bicuspid aortic valve
Rheumatic aortic stenosis

Middle-aged to elderly
Senile degenerative aortic stenosis
Calcification of bicuspid valve
Rheumatic aortic stenosis
 CLINICAL FEATURES
Symptoms
Mild or moderate stenosis: usually asymptomatic
Exertional dyspnoea
Angina
Exertional syncope
Sudden death
Episodes of acute pulmonary oedema

Signs
Ejection systolic murmur
Slow-rising carotid pulse
Narrow pulse pressure
Thrusting apex beat (LV pressure overload)
Signs of pulmonary venous congestion (e.g. crepitations)
 INVESTIGATIONS IN AORTIC STENOSIS
ECG
Left ventricular hypertrophy (usually)
Left bundle branch block

Chest X-ray
May be normal; sometimes enlarged LV and dilated ascending aorta on PA view,
calcified valve on lateral view
Echo
Calcified valve with restricted opening, hypertrophied Left ventricle
Doppler
Measurement of severity of stenosis
Detection of associated aortic regurgitation

Cardiac catheterisation
Mainly to identify associated coronary artery disease
May be used to measure gradient between LV and aorta
MANAGEMENT

Conservative

AVR

Balloon dilatation

TAVI
 AORTIC REGURGITATION
Congenital
Bicuspid valve or disproportionate cusps

Acquired
Rheumatic disease
Infective endocarditis
Trauma
Aortic dilatation (Marfan's syndrome, aneurysm, dissection,
syphilis,ankylosing spondylitis)
 CLINICAL FEATURES
Mild to moderate AR
Often asymptomatic
Awareness of heart beat, 'palpitations'
Severe AR
Breathlessness
Angina
Signs Pulses
Large-volume or 'collapsing' pulse
Low diastolic and increased pulse pressure
Bounding peripheral pulses
Capillary pulsation in nail beds: Quincke's sign
Femoral bruit ('pistol shot'): Duroziez's sign
Head nodding with pulse: de Musset's sign
Murmurs
Early diastolic murmur
Systolic murmur (increased stroke volume)
Austin Flint murmur (soft mid-diastolic)
Other signs
 INVESTIGATIONS
ECG
Initially normal, later left ventricular hypertrophy and T-wave inversion
Chest X-ray
Cardiac dilatation, maybe aortic dilatation
Features of left heart failure
Echo
Dilated LV
Hyperdynamic LV
Fluttering anterior mitral leaflet
Doppler detects reflux
Cardiac catheterisation (may not be required)
Dilated LV
Aortic regurgitation
Dilated aortic root
 MANAGEMENT

underlying conditions

Systolic BP should be controlled with vasodilating

drugs such as nifedipine or ACE inhibitors

Surgery
 INFECTIVE ENDOCARDITIS

This is due to microbial infection of a heart

valve (native or prosthetic), the lining of a
cardiac chamber or blood vessel, or a
congenital anomaly
 PATHOPHYSIOLOGY

occurs at sites of pre-existing endocardial damage

Many acquired and congenital cardiac lesions are
vulnerable to endocarditis
Infection tends to occur at sites of endothelial damage
vegetations composed of organisms, fibrin and platelets
grow and may become large enough to cause obstruction
or embolism
Valve regurgitation may develop or increase
Extracardiac manifestations such as vasculitis and skin
lesions are due to emboli or immune complex deposition
Mycotic aneurysms may develop in arteries at the site of
infected emboli
 MICROBIOLOGY
Over three-quarters of cases are due to streptococci or
staphylococci (viridans group )
Other organisms Enterococcus faecalis, E. faecium and
Strep. Bovis
Staph. aureus has now overtaken streptococci
Post-operative endocarditis: coagulase-negative
staphylococcus (Staph. epidermidis , Staph. Lugdenensis )
Q fever endocarditis due to Coxiella burnetii
HACEK group and Brucella
Yeasts and fungi (Candida, Aspergillus)
INCIDENCE
5 to 15 cases per 100 000 per annum
rheumatic heart disease in 24%
congenital heart disease in 19%
other cardiac abnormality (e.g. calcified aortic
valve, floppy mitral valve) in 25%.
32% not have a pre-existing cardiac
abnormality
CLINICAL FEATURES

Subacute endocarditis

Acute endocarditis

Post-operative endocarditis
INVESTIGATIONS

Blood culture
Echocardiography
ESR, anaemia, and leucocytosis
CRP ; Proteinurea ; microscopic haematuria
ECG
CXR
 MANAGEMENT
The case fatality 20%
A multidisciplinary approach
Empirical treatment
A 2-week treatment regimen may be sufficient for fully
sensitive strains of Strep. viridans and Strep. Bovis

Cardiac surgery
Heart failure due to valve damage
Failure of antibiotic therapy
Large vegetations on left-sided heart valves
Abscess formation