Valvular Heart diseases Dr: Abdulkareem Al-Othman

Lect-4(2014-2015)

1-Mitral stenosis (MS)

Case presentation

A 30 year old lady presented with left sided weakness,

PMH: Long standing history of occasional attacks of palpitation
neglected by the patient, no previous history of hypertension ,ischemic
heart disease or diabetes mellitus.
O/E Patient conscious,oriented,left sided weakness
Examination of precordium : loud S1,diatolic murmur at the
apex(Grade3/6).
ECG: Atrial fibrillation

What is the most probable cardiac diagnosis?

Transthoracic echocardiography: Markedly dilated left atrium, severe

calcified mitral valve stenosis,.mitral valve area=0.6cm.
Severe secondary pulmonary arterial hypertension, normal left
ventricular function .no evidence of thrombus in the left atrium.
Brain CT scan: Right sided ischemic stroke

What is the relation between your cardiac diagnosis and ischemic

stroke?
What is the next investigation you should send for to proof (support)
your answer (the above question)?

Etiology:
1-Rheumatic fever 2-heavy calcification of the mitral valve in the elderly 3-congenital
(rare)

Pathophysiology:
The characteristic pathological changes in rheumatic fever is fibrosis and scaring
particularly at the margins of the valve.
Normal mitral valve area-4-6cm²,when mitral valve is diminished I.e <2cm² this lead
to A- increase in left atrial pressure ,increase pulmonary venous congestion
manifested as exertional dyspnoea ,cough,haemoptysis and progress to dyspnoea at
rest
B-increase left atrial pressure lead to left atrial dilatation and atrial
fibrillation,pulmonary edema
C-Atrial fibrillation lead to stasis of blood in the left atrial appendages with the risk of
thrombus formation in this area.
D-in advanced stages of MS,pulmonary hypertension will lead to right ventricular
hypertrophy and dilatation ,tricuspid regurgitation and right ventricular failure .

Clinical features :
MS affect female more than males .
Symptoms usually develop between age 25-30
Dyspnoea ,fatigue hemoptysis,palpitation(atrial fibrillation ),systemic
embolization,pulmonary embolism.
Physical examination ;malar flush(florid congestion of the cheeks),increase JVP,right
ventricular heave (right ventricular hypertrophy ),atrial fibrillation ,diastolic thrill is
frequently present at the apex, taping apex beat.
Auscultation,loud S1,loud P2,opening snape,low pitched rumbling mid diastolic
murmur (roll the patient toward the left ),use the bell of the stethoscope,best heard at
the apex.
In later stages ankle edema ,ascitis, hepatomegaly.

Investigations

1-ECG:bifid P wave (p mitrale),atrial fibrillation ,right ventricular hypertrophy .

2-CXR: Straightening of the left heart border due to left atrial enlargement,
enlargement of upper pulmonary veins ,enlargement of pulmonary artery.
3-Transthoracic echocardiography:
4-Transesophageal echocardiography-to detect thrombus in the left atrial
appendages.
4-Cardiac catheterization

Management :

A-Medical ;digoxin,diuretics,anticoagulant(atrial fibrillation ).

Antibiotic (prophylaxis for infective endocarditis in no longer routinely
recommended.
B-Mitral balloon valvuloplasty;in symptomatic isolated not calcified MS.left atrium
free of thrombus
C-Mitral valve replacement ;in symptomatic calcified MS.
Lect.4 2014-2015 Dr.Abdulkareem Al-Othman
2-Mitral regurgitation (MR)

Definition ;leakage of blood through the mitral valve from left ventricle to left atrium
during ventricular systole.

Case-1
A 28 year old man presented with progressive increasing shortness of breath
for one year associated with palpitation.
Past medical history: unremarkable.
Risk factors for IHD: negative
On examination of the precordium: Pan-systolic murmur at the apex radiate
to the axilla
Investigations:
! ECG: Atrial fibrillation
! Transthoracic echocardiography: Moderatly dilated left atrium& left
ventricle,moderatly thickened MV,moderate MR
Mild left ventricular systolic dysfunction.

What is the most probable etiology beyond this mitral regurgitation?

Case-2
A 62 year old man admitted to the CCU with acute myocardial infarction
On admission: CV system ex within normal
Echo : normal MV,Normal LV systolic function
Third day :,sudden palpitation associated with severe dyspnea
On examination of the precordium:,new pan-systolic murmur at the apex
Echo: Severe MR,ruptur chordae tendinae
Patient died shortly in spite of intensive management

How do you explain the rapid deterioration and the death of this patient?

Etiology;

1-Leaflet abnormalities **Rheumatic heart disease **Mitral valve prolapse

2-Dilatation of mitral valve ring **Dilated cardiomyopathy **After myocardial
infarction
3-Abnormalities of chordae tendinae; **Rheumatic heart disease **Mitral valve
prolapse
**Chordal rupture(myocardial infarction)
4-Papillary muscle abnormalities **Ischemia, myocardial infarction

Pathophysiology:
A-chronic mitral regurgitation ;gradual dilatation of the left atrium with little increase
in left atrial pressure ,left ventricle dilate slowly with few symptoms .

!1
B-acute mitral regurgitation: rapid rise in left atrial pressure lead to marked
symptomatic deterioration

Clinical features ;MR occur more frequently in males .

Symptoms
:A-acute MR: Rapid deterioration with severe dyspnoea due to pulmonary edema.
B-Chronic mitral regurgitation ;fatigue,exertional dyspnoea ,orthopnea are the most
common symptoms .

PHYSICAL FINDING :Atrial fibrillation /flutter

inspection ;diffuse hyperdynamic impulse,apex beat displaced laterally,lncrease JVP.
A systolic thrill is often palpable at the apex.
Auscultation ;soft S1,wide split of S2,apical S3,pansystolic murmur extended
fromS1-S2 at the apex radiate to the axilla ,basal crepitations (crackles)
Ankle edema ,hepatomegaly .

Investigations:
1-ECG:Bifid P wave,atrial fibrillation ,left ventricular hypertrophy .
2-CXR: enlarged left atrium,left ventricle, pulmonary venous congestion ,pulmonary
edema .
3-Echo-Doppler ;diagnostic
4-MRI
5-Catheterization ;to diagnose coexisted ischemic heart disease

Management ;
A-medical ;Indicated in MR of moderate severity,
Diuretics,digoxin (atrial fibrillation ),anticoagulant(atrial fibrillation ),angiotensin
converting enzyme inhbitors in heart failure .
B-surgery;
1. Mitral valve repair:I.e in mitral valve prolapsed.
2. Mitral valve replacement
indication; progressive worsening of symptoms ,progressive cardiac
enlargement by echo or CXR ,or detorioration of left ventricular
function by echocardiography

Mitral valve prolapse

The mitral valve leaflet ,most commonly the posterior mitral valve leaflet, bulge back
into the left atrium during systole.
Etiology: **Congenital, ** Degenerative myxomatous changes ,**Marfan's
Syndrome, ** **connective tissue disease

Clinical features:
Atypical chest pain, palpitation,
Auscultation: mid systolic click, late systolic murmur
ECG: variety of benign arrhythmias
Management:

!2
 • Medical: ,Beta-blockers sometimes relieve chest pain
• Surgery: mitral valve repair.

Conclusion:

Pan-systolic murmur mostly heard at the apex , radiate to the axilla is the most
common findings on auscultation of the heart.

!3
Lect.5 (2015-2016) Dr. Abdulkareem Al-Othman

Aortic valve diseases

1-Aortic stenosis
Definition: Narrowing of the aortic valve. Normal aortic valve area=2.5-3.5cm2

Case presentation

A 25 year old man (Football player) develop sudden chest pain associated with severe
dyspnoea during his extreme exertion prior to the end of the game, followed by
syncope, cardiac arrest and death.
Past medical history: Unremarkable
no previous hypertension or diabetes mellitus, no history of ischemic heart
disease.
Risk factors for IHD: negative
Social history: not smoker, No H/O alcohol consumption
Dug history: Nil
Post mortem study: Severe left ventricular hypertrophy, severely thickened aortic
valve and severe aortic valve stenosis.

 What are the important etiologies beyond aortic stenosis in this patient?
 How do you explain the syncope and sudden death of this patient?

Etiology
A-According to the site:** Valvular **subvalvular **supravalvular
B- According to the age
1-Infants: **Congenital AS, **Congenital subvalvular AS,**Congenital
supravalvular AS.
2-Young adults to middle age: **Rheumatic AS,**Bicuspid aortic valve
3-Middle age to elderly: **Rheumatic AS,**Senile degenerative
AS,**Calcification of bicuspid valve.

Pathophysiology: The obstruction to the left ventricular outflow produces a systolic

pressure gradient between the left ventricle & the aorta, the left ventricle respond by
dilatation, the cardiac output is maintained by the presence of concentric left
ventricular hypertrophy (compensatory mechanism), cardiac output at first is within
normal but it usually fails to rise normally during exercise which lead to effort related
hypotension and syncope, the hypertrophied left ventricle will increase myocardial
oxygen requirement & compress the coronary arteries lead to ischemia even in the
absence of coronary artery disease. The patient remains asymptomatic but once
symptoms start the patient deteriorate rapidly due to left ventricular failure,
pulmonary edema. Deaths ensue with in 3-5 years of the onset of symptoms.

Clinical features: Affect male more than female, **angina pectoris **exertional
dyspnoea **syncope are characteristic symptoms of aortic stenosis ** sudden death.
On physical examination: Inspection & palpation: the peripheral pulses diminished in

1
amplitude, rises slowly to a delayed sustained peak (pulsus parvus et tardus),systolic
thrill at the base of the heart, thrusting apex beat displaced laterally.
On auscultation of the precordium: normal S1.soft A2, S4 (left ventricular
hypertrophy) and ejection click.
Diamond ejection systolic murmur (detected by the diaphragm) in the aortic area.

Investigations:
1-ECG: Left ventricular hypertrophy, left bundle branch block, sometimes normal.
2-CXR: normal ,left ventricular enlargement, poststenotic dilatation of the ascending
aorta, ??calcification of aortic valve cusp
3-Echocardiography and Doppler study
4-MRI
5-Catheterization to search for associated aortic regurgitation, ischemic heart disease.
Management:
A-Medical : asymptomatic : follow up, rest, digitalis, sodium restriction, cautious
diuretics, anticoagulant (in atrial fibrillation)

B-Surgical:
** Aortic balloon valvuloplasty: in symptomatic congenital not calcified aortic valve.
**Aortic valve replacement: symptomatic severe aortic stenosis, pressure gradient
over the aortic valve>50mmHg,calcified aortic stenosis.

Conclusion
Normal S1, soft A2, ejection click, ejection systolic murmur in the aortic area is the
main findings on auscultation of the heart

2-Aortic regurgitation

Definition: Leakage of blood from the aorta into the left ventricle during
left ventricular diastole.

Case presentation

A 36-year-old man admitted to the Emergency Department with history

of uncontrolled hypertension associated with palpitation.
Past medical history: No history of diabetes mellitus,
Social history: not smoker, no history of alcohol consumption,
Drug History: (Atenolol 100mg/d+ Valsartan 160mg/d+Hydrochothiazid
25mg/d )for more than 2 years
On examination: BMI=21,BP=220/40, PR=120BPM,large pulse
volume, Temperature 36.8°C
On examination of the precordium: Diastolic murmur at the left sternal
border with ejection systolic murmur at 2nd intercostal space (right
sternal border, referred to the neck).
Investigations:
Renal function test: Normal, Thyroid function test=Normal
Transthoracic Echocardiography (TTE): Severe AR, moderate LVH,
2
mildly dilated LV, Normal LV systolic function.

Q-How do you explain the ejection systolic murmur in this patient?

Q-What are the expected etiologies beyond this aortic regurgitation?

Aortic regurgitation
Etiology
A-Acute aortic regurgitation*
B-Chronic aortic regurgitation+
A-Valvular
• Rheumatic heart disease+
• Infective endocarditis (*or+)
• Congenital bicuspid aortic valve+
• SLE+
• Rheumatoid arthritis+
B-Aortic root disease
• Dilatation- Marfan's Syndrome+
• Dissecting aneurysm*or+
• Syphilis+
• Ankylosing spondylitis+

Trauma*or+

Pathophysiology: the left ventricle dilates & hypertrophied to compensate for the
regurgitation, the stroke volume of the left ventricle may eventually be doubled or
trebled, with increase pulse pressure & bounding peripheral pulses, as the disease
progress the left ventricular diastolic pressure rises at first only with exercise and with
progressive increasing shortness of breath.

Clinical features:
Symptoms
1-Mild to moderate aortic regurgitation: The patient may remain asymptomatic for
long periods.
2-Severe aortic regurgitation: chest pain often associated with underlying **coronary
artery disease.
** dyspnoea ,orthopnea , paroxysmal nocturnal dyspnoea. **Syncope (due to
arrhythmias).

B-Physical examination:
Inspection & palpation: **collapsing pulse , **Increase pulse pressure (high systolic
with low diastolic BP) **de-musset's sign(head nodding with the pulse) **Quinke's
sign (capillary pulsation in nail bed.
Apex beat heaving & displaced laterally & inferiorly.
Diastolic thrill often palpable at the left sternal border (LSB), sometimes systolic thrill
(LSB) due to increase blood flow.
Auscultation:**Pistol shot (femoral bruit),Duroziez's sign (to and fro murmur is
audible if the femoral artery is lightly compressed with the stethoscope).

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**Absent A2, **S3 , **occasionally S4, **early diastolic murmur best heard in the
3rd intercostal space along the left sternal border, to hear this murmur louder ask the
patient to lean forward with breath held on expiration.
Mid systolic ejection murmur best heard at the base of the heart (aortic area) and
radiate to the neck along the carotid artery.
**Austin Flint murmur is a soft mid diastolic murmur produced by diastolic
displacement of the anterior leaflet of mitral valve by aortic regurgitation.
**Chest examination: crepitations

Investigations (aortic regurgitation)

**CXR: cardiomegaly ** Echo-Doppler: diagnostic ** Catheterization ?? ischemic
heart disease.

Management:
A-Medical:
**treat underlying cause i.e endocarditis,Syphilis,
**Diuretics,angiotensin converting enzyme inhibitors,digitalis.
B-Aortic valve replacement:
indication **symptomatic patient **progressive cardiomegaly on Echo.
C-Aortic root replacement: Marfan's Syndrome with severe aortic root dilatation.
Conclusion
The main pathophysiological finding in aortic regurgitation is increase stroke volume
of the left ventricle and increase pulse pressure.

Tricuspid stenosis:
Rare
Mid diastolic murmur at lower RSB
Diagnosis: by Echo-Doppler
Treatment: surgery

Tricuspid regurgitation:
Etiology:
A:primary: ** rheumatic heart disease,**endocarditis,(drugs injection abusers)
B-Secondary:**chronic left heart failure,**right ventricular infarction,**pulmonary
hypertension.

Clinical features: symptoms & signs of primary causes

Diagnosis: Echo-Doppler
Pulmonary valve disease
A- Pulmonary stenosis (PS) :
Etiology: usually congenital **associated with tetralogy of fallot.
Clinical features: Mild PS: asymptomatic
Severe PS: fatigue, dyspnoe,right ventricular failure, syncope
On-examination: soft P2,increase JVP,harsh ejection systolic murmur & thrill at the
upper left sternal border
Echo-Doppler-diagnostic
Treatment: Mild-moderate PS: no treatment
Severe PS: Balloon valvuloplasty

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B-Pulmonary regurgitation:
Etiology
**Primary: Infective endocarditis, Rheumatic heart disease
**Secondary: to diseases of the left side of the heart
**Eisennmengers Syndrome: see congenital heart disease
Symptoms & signs of underlying causes
Graham steel murmur=Early diastolic murmur (LSB)