12.DISEASES OF THE HEART VALVES pdf - د. صباح

DISEASES OF THE HEART VALVES

AETIOLOGY

MV orifice –

normally = 5 cm² in diastole

reduced to= 1 cm² in severe MS.

asymptomatic = stenosis < 2 cm²

Aetiology

Rheumatic-

calcification - elderly

congenital

Patholopgy

Rheumatic MS

Mitral valve orifice = slowly diminished

By -



1-progressive fibrosis



calcification of valve leaflets

2- fusion of cusps and subvalvular apparatus

Pathophysiology

Main fault=

flow of blood from LA



LV =restricted

Main chamber affected= Left Atrium

1- LA pressure



pulmonary V congestion



breathlessness.

2-Dilatation and hypertrophy -LA

left ventricular filling = dependent on LA contraction.

What makes the patient symptomatic

1-Increase in heart rate



shortens diastole (when mitral valve is open )



further rise in LA

pressure.

2-increase in cardiac output



increase LA pressure

exercise

pregnancy.

3- Reduced lung compliance ( chronic pulmonary venous congestion)



breathlessness

low cardiac output



fatigue

Atrial fibrillation (progressive dilatation of the LA )



precipitates pulmonary oedema

Pathophysiology

Outcome of MS

ACUTE



Rapid rise in LA pressure (by AF (progressive dilatation of LA)

Onset of AF



Pulmonary oedema

(tachycardia + loss of atrial contraction



marked HD deterioration)

CHRONIC



Gradual rise LA pressure



increase in PV resistance



pulmonary artery hypertension (protect from p. oedema).

Pulmonary hypertension



RV hypertrophy and dilatation



tricuspid regurgitation



right

HF.

20% = sinus rhythm= small fibrotic LA + severe pulmonary hypertension

Clinical Manifestations—ACUTE*CHRONIC

Clinical features

Symptoms

Dyspnoea-- Effort-related

Exercise tolerance – diminishes( very slowly over many years



at rest.

Haemoptysis= Acute pulmonary oedema or pulmonary hypertension =

systemic thromboembolism. (LA thrombosis) (All MS Pt. esp. AF)

SIGNS

. HS (S1)

-loud +/_ palpable (tapping apex beat).

opening snap

MURMER

low-pitched mid-diastolic murmur +/_ thrill

pre-systolic murmur

Coexisting M regurgitation



pansystolic M which radiates towards axilla.

Pulmonary hypertension supervenes



right ventricular heave +

accentuation of pulmonary component of second heart sound(S2)

Tricuspid regurgitation



systolic murmur+

systolic waves in venous pulse.

CLINICAL FEATURES OF MITRAL STENOSIS

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)

Symptoms of thromboembolic complications (e.g. stroke, ischaemic limb)

Signs

Atrial fibrillation

Mitral facies

Auscultation

Loud first heart sound, opening snap

Mid-diastolic murmur

Signs of raised pulmonary capillary pressure

Crepitations, pulmonary oedema, effusions

Signs of pulmonary hypertension

RV heave, loud P2

INVESTIGATIONS IN MITRAL STENOSIS

ECG

Chest X-ray

Echo

Doppler

Cardiac catheterisation

Assessment of coexisting coronary artery disease and mitral regurgitation

ECG

Left atrial hypertrophy (if not in AF)

Right ventricular hypertrophy

Chest X-ray

Enlarged left atrium

Signs of pulmonary venous congestion

Echo

Thickened immobile cusps

Reduced valve area

Reduced rate of diastolic filling of LV

Management

Medical management

1- anticoagulants

2-digoxin,

β-

blockers or rate-limiting calcium antagonists

3-diuretics

Mitral balloon valvuloplasty and valve replacement

Valvuloplasty

surgical closed or open mitral valvotomy

Valve replacement = substantial mitral reflux or if valve is rigid and calcified

MITRAL REGURGITATION

MITRAL APPARATUS

1-LEAFLET

2-ANNULAS

3-CHORDAE

4-PAPILLARY MUSCLES

Aetiology

Rheumatic disease

Mitral valve prolapse

Dilatation of the left ventricle and mitral valve ring

Damage to valve cusps and chordae

Damage to papillary muscle

Myocardial infarction

M valvotomy or valvuloplasty.

Pathophysiology of MR

1-Chronic =>

left atrium =gradual dilatation ( little increase in pressure)



left ventricle



dilates slowly



chronic volume overload

2- Acute

rapid rise in left atrial pressure



marked symptomatic deterioration

Clinical features of MR

SYMPTOMS

DYSPNEA

PALPITATOION

CHEST PAIN

SYNCOPE

SINGS

GENERAL

PULSE

JVP

PRECORDIUM

Clinical features

SYMPTOMS =how suddenly regurgitation develops

CHRONIC



similar to MS

ACUTE (SUDDEN) MR



Pulmonary edema

SIGNS

Regurgitant jet=SM.radiate to axilla+/- thrill

Increase flow in MV=loud S3,+/- md-M

LV overload-active rocking apex

LV dilataion-displaced apex

Clinical features (and their causes)

Symptoms

pulmonary venous congestion



Dyspnoea

low cardiac output



Fatigue

atrial fibrillation/ increased stroke volume



Palpitation

right heart failure



Oedema, ascites

Signs

Atrial fibrillation/flutter

Cardiomegaly: displaced hyperdynamic apex beat

Apical pansystolic murmur ± thrill

Soft S1, apical S3

Signs of pulmonary venous congestion (crepitations, pulmonary oedema, effusions)

Signs of pulmonary hypertension and right heart failure

(Lt.parasternal heav,Loud S2)

Investigations

ECG

Chest X-ray

Echo

Doppler

Cardiac catheterisation

Dilated LA, dilated LV, mitral regurgitation

Pulmonary hypertension

Coexisting coronary artery disease

ECG

Left atrial hypertrophy

Left ventricular hypertrophy

Chest X-ray

Enlarged left atrium

Enlarged left ventricle

Pulmonary venous congestion

Pulmonary oedema (if acute

)

Echo

Dilated LA, LV

Dynamic LV (unless myocardial dysfunction predominates

)

Structural abnormalities of mitral valve (e.g. prolapse

Doppler

Detects and quantifies regurgitation

Management

MEDICAL MANAGEMENT OF MITRAL REGURGITATION

Diuretics

Vasodilators, e.g. ACE inhibitors

Digoxin = atrial fibrillation

Anticoagulants =atrial fibrillation

SURGERICAL MANAGEMENT

reviewed at regular intervals

surgical intervention (mitral valve replacement or repair).

1- worsening symptoms,

2- progressive radiological cardiac enlargement

3- echocardiographic evidence of deteriorating LV function

Mitral valve repair

advantages when compared to mitral valve replacement.

advocated for severe regurgitation even in asymptomatic patients

results are excellent and

early repair has been shown to prevent irreversible LV damage.

Mitral valve prolapse

= 'floppy' mitral valve

1-mildest forms = valve remains competent = bulges back into the atrium during systole



mid-systolic click -no murmur.

2- regurgitant valve



click



a late systolic murmur

Progressive elongation of the chordae tendineae



increasing mitral regurgitation, => chordal

rupture

Haemodynamically significant MVP



infective endocarditis =

Associated with

1- benign arrhythmias,

2-atypical chest pain

3- a very small risk of embolic stroke or TIA

TRICUSPID VALVE DISEASE

TRICUSPID STENOSIS

TRICUSPID REGURGITATION

TRICUSPID STENOSIS

Aetiology

rheumatic 5%

Tricuspid stenosis and regurgitation - features of carcinoid syndrome

Clinical features

SYMPTOMS

associated mitral and aortic valve disease+

right heart failure

hepatic discomfort and peripheral oedema.

SIGNS

1- raised jugular venous pressure

prominent a wave, and a slow y descent (due to loss of normal rapid RV filling)

2-mid-diastolic murmur =lower left or right sternal edge; higher-pitched than murmur of MS

and is increased by inspiration.

3- Right heart failure = hepatomegaly with pre-systolic pulsation (large a wave), ascites and

peripheral oedema.

Investigations

echocardiography and Doppler=the valve has similar appearances to those of rheumatic mitral

stenosis.

Management

In patients who require surgery to other valves, tricuspid valve is either replaced or valvotomy

performed at the time of surgery.

Balloon valvuloplasty can be used to treat rare cases of isolated tricuspid stenosis

TRICUSPID REGURGITATION

Aetiology

common.

most frequent cause = 'functional' ( RV dilatation)

Primary

Rheumatic heart disease

Endocarditis, particularly in injection drug-users

Ebstein's congenital anomaly

Secondary

Right ventricular dilatation ( chronic left heart failure) ('functional tricuspid regurgitation')

Right ventricular infarction

Pulmonary hypertension (e.g. cor pulmonale)

Clinical features

Symptoms =non-specific,

relate to reduced forward flow (tiredness) and venous congestion (oedema, hepatic

enlargement).

Signs= large systolic wave in the jugular venous pulse (a cv wave replaces the normal x

descent).

pansystolic murmur at the left sternal edge and systolic pulsation of the liver.

Investigations

Echocardiography

Ebstein's anomaly

Management

right ventricular dilatation = improves when the cause of right ventricular overload is corrected

normal pulmonary artery pressure tolerate isolated tricuspid reflux well=

valves damaged by endocarditis



do not always need to be replaced.

Patients undergoing mitral valve replacement + tricuspid regurgitation ( marked dilatation of the

tricuspid annulus) benefit from repair of the valve - annuloplasty ring to bring the leaflets closer

together.

rheumatic damage = tricuspid valve replacement.

AORTIC VALVE DISEASE

AORTIC STENOSIS

AORTIC REGURGITATION

AORTIC STENOSIS

AETIOLOGY

Congenital AS=

obstruction - from birth or becomes apparent in infancy.

Bicuspid aortic valves=

take years to develop ( valve becomes fibrotic and calcified).

Rheumatic fever-

AV second most frequently affected - commonly both aortic and mitral V

Older people-

structurally normal tricuspid AV affected by fibrosis and calcification= process histologically

similar to atherosclerosis affecting the arterial wall.

TIME COARSE

Haemodynamically significant stenosis develops slowly

1- At 30-60 years in rheumatic disease

2- At 50-60 in those with bicuspid aortic valves

3-At 70-90 in those with degenerative calcific disease.

Depending on age of patient .

Infants, children, adolescents

Congenital AS

Congenital subvalvular AS

Congenital supravalvular AS

Young adults to middle-aged

Calcification & fibrosis of CBAV

Rheumatic aortic stenosis

Middle-aged to elderly

Senile degenerative AS

Calcification of bicuspid valve

Rheumatic aortic stenosis

Pathophysiology

Cardiac output - maintained at the cost of a steadily increasing

pressure gradient across the aortic valve.



hypertrophied



Coronary blood flow



inadequate



angina

(even in absence of concomitant CAD).

Fixed outflow obstruction



limits increase in CO on exercise



Syncope

LV no longer overcome OT obstruction



pulmonary oedema.

Pathophysiology

pressure gradient across the aortic valve.

LV increasingly hypertrophied

1-angina

2-effort-related hypotension and syncope

3-pulmonary oedema

AS typically remain asymptomatic for many years

death usually ensues within 3-5 years of the onset of symptoms.

patients with AS typically remain asymptomatic for many years but deteriorate rapidly when

symptoms develop, and death usually ensues within 3-5 years of these. (In contrast to mitral

stenosis, which tends to progress very slowly)

Clinical features

SYMPTOMS

Asymptomatic - routine clinical examination

symptoms - 3 cardinal



angina, breathlessness and syncope

Angina =

increased demands of hypertrophied LV working against the high-pressure outflow tract

obstruction



mismatch between oxygen demand and supply

coexisting coronary artery disease, especially in old age affects over 50%

Exertional breathlessness

=cardiac decompensation = consequence excessive pressure overload placed on LV.

Syncope = on exertion=

cardiac output fails to rise to meet demand



fall in BP.

Signs

SIGNS

Harsh ejection systolic murmur radiates to neck

(likened to a saw cutting wood +/- musical quality like 'mew' of a seagull . (especially in older

patients)

soft second heart sound, particularly with calcific valves

Severity-

difficult to gauge clinically-

older patients with a non-compliant 'stiff' arterial system have apparently normal carotid

upstroke in presence of severe aortic stenosis.

Milder degrees of stenosis - difficult to distinguish from aortic sclerosis in which the valve is

thickened or calcified but not obstructed.

careful examination - made for other valve lesions, particularly in rheumatic heart disease -

concomitant MVD

CLINICAL FEATURES

Symptoms

Mild or moderate aortic stenosis = 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

Investigation

ECG

Echocardigraphy

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



valve calcification

MRI



valve stenosis

INVESTIGATIONS IN AORTIC STENOSIS

ECG

Left ventricular hypertrophy

Left bundle branch block

Chest X-ray

Normal.

Enlarged left ventricle and dilated ascending aorta on PA view, calcified valve on lateral view

Echo

Calcified valve with restricted opening, hypertrophied LV.

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

ECG

Left ventricular hypertrophy

Left bundle branch block

Chest X-ray

Normal.

Enlarged left ventricle and dilated ascending aorta on PA view, calcified valve on lateral view

Echo

Calcified valve with restricted opening, hypertrophied LV.

Management

Asymptomatic



review,

SYMPTOMATIC=

angina, syncope, symptoms of low cardiac output or heart failure =

surgery.

Moderately severe or severe stenosis



every 1-2 years =progression

Symptomatic severe AS



aortic valve replacement.

Aortic balloon valvuloplasty

Anticoagulants = atrial fibrillation

AORTIC STENOSIS IN OLD AGE

Incidence

most common form of valve disease affecting the very old

Symptoms

common cause of syncope, angina and HF in the very old

Signs

because of increasing stiffening in central arteries, low pulse pressure and a slow rising pulse

may not be present

Surgery

can be successful in those aged 80 or more in the absence of comorbidity, but with a higher

operative mortality. prognosis without surgery is poor once symptoms have developed

Valve replacement type

biological valve is often preferable to a mechanical, (obviates need for anticoagulation, and

durability of biological valves usually exceeds t patient's anticipated life expectancy)

AORTIC REGURGITATION

AETIOLOGY AND PATHOPHYSIOLOGY

aortic valve cusps or dilatation of aortic root .

Left Ventricle



dilates and hypertrophies (compensate for regurgitation).

stroke volume of LV



doubled or trebled



major arteries conspicuously pulsatile.

LV diastolic pressure –rises



breathlessness

AORTIC REGURGITATION

Aetiology

Congenital

Bicuspid valve or disproportionate cusps

Acquired

Rheumatic disease

Infective endocarditis

Trauma

Aortic dilatation (Marfan's syndrome

aneurysm

dissection

syphilis

ankylosing spondylitis)

Clinical features ACUTE*CHRONIC

Chronic

SYMPTOMS

Awareness of heart beat esp.lying on left side (increased stroke volume).

Breathlessness, Paroxysmal nocturnal dyspnoea --peripheral oedema

angina

SIGNS

Characteristic murmur - best heard to left of sternum during held expiration - thrill - rare.

systolic murmur ( increased stroke volume )

regurgitant jet



fluttering of MV =severe,



partial closure of anterior mitral leaflet



functional mitral stenosis and a soft mid-diastolic (Austin Flint) murmur.

Acute severe regurgitation

(e.g. perforation of aortic cusp in endocarditis) - no time for compensatory LVH and

dilatation



features of heart failure

classical signs of aortic regurgitation - masked by tachycardia and an abrupt rise in left

ventricular end-diastolic pressure; ==

pulse pressure - near normal and diastolic murmur - short or even absent.

Clinical features

Symptoms

Mild to moderate AR

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

Displaced, heaving apex beat (volume overload)

Pre-systolic impulse

Fourth heart sound

Pulmonary venous congestion (crepitations

INVESTIGATIONS IN AORTIC REGURGITATION

ECG

Chest X-ray

Echo

Doppler detects reflux

Cardiac catheterisation (may not be required)

Dilated LV

Aortic regurgitation

Dilated aortic root

ECG

Initially normal, later LV hypertrophy and T-waveinversion

Chest X-ray

Cardiac dilatation+/- aortic dilatation

Features of left heart failure

Echo

Dilated left ventricle

Hyperdynamic left ventricle

Fluttering anterior mitral leaflet

Doppler detects reflux

Management

Aortic regurgitation causing symptoms



Aortic valve replacement

Chronic aortic regurgitation = asymptomatic.

Asymptomatic followed up annually

with echocardiography



increasing ventricular size;.

Systolic blood pressure = vasodilating drugs (nifedipine or ACE inhibitors).

PULMONARY VALVE DISEASE

PULMONARY STENOSIS

PULMONARY REGURGITATION

PULMONARY STENOSIS

Aetiology

usually congenital

carcinoid syndrome

Clinical features:

ejection systolic murmur +/-thrill

leans forward and breathes out.

preceded - ejection sound (click).

wide splitting of S2

Severe PS=

loud harsh murmur+ an inaudible pulmonary closure sound (P2), + increased RV heave+

prominent a waves in the jugular pulse,

Investigations

ECG

chest X-ray

Doppler echocardiography

Management

1-Mild to moderate isolated pulmonary stenosis

relatively common,

does not usually progress and does not require treatment;

Low risk lesion for infective endocarditis.

2-Severe PS (resting gradient > 50 mmHg with a normal cardiac output)

treated by percutaneous pulmonary balloon valvuloplasty or, if not available,

by surgical valvotomy.

Long-term results are very good.

Post-operative pulmonary regurgitation is common but benign.

PULMONARY REGURGITATION

* Associated with pulmonary artery dilatation

(due to pulmonary hypertension. e.g.mitral stenosis)

=early diastolic decrescendo murmur at left sternal edge (difficult to distinguish from aortic

regurgitation (Graham Steell murmur)}.

*Pulmonary hypertension =

secondary to other disease of the left side of the heart,

primary pulmonary vascular disease or

Eisenmenger's syndrome

*Trivial pulmonary regurgitation = frequent Doppler finding in normal individuals - of no

clinical significance.

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