Atherosclerosis pdf - شكري فائز

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
myocardial infarction

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

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

Do not smoke

Aim for ideal body weight

Take regular exercise (exercise up to, but not

beyond, the point of chest discomfort is beneficial
and may promote collateral vessels)

Avoid severe unaccustomed exertion, and

vigorous exercise after a heavy meal or in very
cold weather

Take 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
I

channel antagonist

INVASIVE THERAPY : PCI AND CABG

COMPARISON OF PCI AND CABG

PCI

CABG

Death

0.5

1.5

Myocardial infarction*

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
Vascular damage related to
access site

Diffuse myocardial damage
Infection (chest, wound)
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

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

Echocardiogram in mitral

Desktop

SHOKRY

Users

YouTube.flv

stenosis

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

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