GENERAL CONSIDERATIONS

Etiology
• Inflammatory (rheumatic)
• Infectious (postendocarditis)
• Degenerative
• Congenital
• Rare cause
Rheumatic etiology, in the developed countries is
decreasing (in 1988 in the U.S., rheumatic valvular
disease accounted for 3.4%, while the remaining
96,6% were other causes.
 DIAGNOSIS
Diagnostic evaluation
 Clinical findings
- determination of etiology
- clinical severity (NYHA class)
 Diagnostic modality:
- ECG
- Roentgenogram
- echocardiography
- cardiac catheterization ( selected cases)
 General evaluation of the pacient
 Treatment decision
 Observation the effects of the treatment
 SEVERITY EVALUATION
 Morphological criteria:
- stenosis: three grades (mild, moderate, severe)
- regurgitation: four grades (I-IV)
 Functional criteria:
- pressure gradient(stenosis)
- retrograde pressure in cavity ( regurgitation)
- morphological effects(dilatation, hipertrophy)
- functional efects on ventricles ( ventricular performance)
- circulatory efects (h sau HTA, pulmonary hypertension,
venous hypertension)
 Diagnosis and evaluation of
valvular heart disease
• Classification: The New York Heart Association – NYHA

• The diagnosis of the valvular heart disease will include:

- the valve afected (mitral, aortic, tricuspid, pulmonary)
- lezional type (stenosis sau insufficiency)
- severity (grade of severity)
- clinical severity (clasa NYHA)
- complications (embolism, fibrillation)
All this aspects will be taken in consideration for the
management of valvular heart disease
 Treatment
a) Medical treatment:
- dietary requirements
- drug therapy for cardiac insufficiency and for
the prevention of the embolic or infectious events.

The medical treatment has a palliative role. It has to be

associated with a corrective gesture.

b) Interventional treatment- corrective:

- nonsurgical - interventional(for stenosis)
- surgical :
- valve replacement
- valve repair and valve sparing
operations
Types of cardiac valve prosthesis
A. Mechanical prosthesis
 Ball and cage valve (starr-edwards)
 Tilting disc valve(medtronic-hall, sorin bicarbon)
 Bileaflet valve(st. jude, carbomedics)

B. Bioprosthesis
a) heterograft prosthesis:
- pig valves – cu stent (edwards-carpatier)
- fara stent (freestyle medtronic)
- bovine pericardium – with stent (ionescu-shiley)
- without stent (pericarbon freedom)

b) Homograft – from human corps

c) Autograft – (Ross procedure)
Tipuri de proteze valvulare
 Surgical outcome and
complications
a) Thrombebolism-thrombi form on the valve then
embolize in peripheral or cerebral circulation
b) Valve thrombosis-thrombi that form on the valve
can block the valve
c) Haemorrhages
d) Endocarditis
e) Hemolysis
f) Prosthesis dysfunction
 Complications

Late thrombosis Panus formation

 Complications

Structural failure Bacterial endocarditis

 Mitral stenosis
 Definition – incomplete opening of the MV which
restricts blood flow from LA to LV producing LA
dilatation, pulmonary hypertension and right cardiac
insufficiency.

 Etiology : adult – Rheumatic heart disease

- la copii - congenital
 NC
L

A3
A1
AL A2 PM
P1 P3

P2
 pm

al

PM AL
 Classification
Mitral stenosis

Severity MS Aria mitral orifice LA medium pressure

(pulmonary capillary)

MS mild > 1.5 cmp < 20 mmHg

MS moderate 1-1.4 cmp < 30 mmHg

MS severe < 1 cmp > 30 mmHg

 diagnosis
•Clinical - symptoms:
- dyspnea
- hemoptysis
- embolism
- Physical exam :
- mitral face
- apical diastolic thrill
- opening snap of mitral valve
- diastolic rumble
•Paraclinical tests
- ECG – Sinus rhythm with mitral
P, atrial fibrillation, right branch block.
- Chest radiography – LA
dilatation, PHT whith PA dilatation
- echocardiograhy – primary
diagnostic method. Usual transthoracic,
selectiv transesophageal
 Natural history - complications

 Progression is slow- 10-20 years.

 Complications:
- Atrial fibrillation - 60-70% incidence
- Arterial embolism (mainly cerebral 40-60%)
- endocarditis
 Indications for operation

1. Patients with moderate MS or severe

(mitral orifice area < 1.5 cmp) and
functional class III-IV NYHA.

2. Patients with severe MS (mitral orifice

area < 1 cmp) and severe PHT (PA
pressure > 60-80 mmHg) and functional
class I-II NYHA.
3. Patients with moderate or severe MS with
embolic complications or endocarditis.
 treatment
• Medical – asymptomatic patients- diuretics and salt
restriction
- if atrial fibrillation – digoxin and
anticoagulants, if necessary for reducing heart rate a
beta blocker or Ca blocker.

• Interventional – valvuloplasty ( transseptal throw

femoral vein)

• Surgical treatment:
1. On closed heart – digital or instrumental
commissurotomy . Historical.
2. Open heart:
- conservative surgery – commissurotomy
- radical intervention – valve replacement
 Surgical treatment

Monodisc valve Bidisc valve

 Mitral regurgitation

Definition

– abnormal passing of a part of the

volume of the left ventricle in systole in
the left atrium due to the impairment of
the valvular-ventricular complex.

 Chronic or acute
 etiology
 Leaflet  Chordae
rheumatic endocarditis
degenerative MI
congenital (cleft) rheumatic
endocarditis  Papillary muscle
trauma disfunction or
 Inelul valvular rupture produced by MI
dilatation of LV
calcification
destruction (absces)
 diagnosis
Clinic
a) Acute mitral regurgitation – due to the rupture of the papillary muscles and
chordae tendineae. Symptoms include intense dyspnea, caugh, sinus
tachycardia, hypotension, dilated jugular veins. Protodiastolic gallop and apical
systolic murmur can also be found.
b) Chronic mitral regurgitation– symptoms include dyspnea at exertion and fatigue.
In severe cases acute pulmonary edema . If right- sided heart failure appears
peripheral edema and ascites occure. On auscultation- apical holosistolic murmur
irradiated in axila.

Paraclinic
 ECG – mitral P, eventually AFI, LV hypertrophy.
 Th Rx – pulmonary stasis
 Echography – most important data for diagnosis
 Nuclear angiography– for the status of the LV fuction
 Cardiac chateterization– does not bring new elements to diagnosis
 Indication for surgery

1. Acute mitral regurgitation

2. Patients with symptoms NYHAclass II-IV, with

LV normal function or sightly diminished and LV
diameter< 45mm, with III-IV grade of
regurgitation.

3. Patients with or whithout syptoms with

diminished LV function(EF 30-50) and 50-55 mm
LV diameter, with II-IV grade of regurgitation.
 Surgical treatment

 Repair :
- leaflet resection
- annuloplasty with rigid or flexible
ring
- reinsertions of chordae tendineae

 Radical – valve replacement

Surgical treatment
Sef de lucrari Dr. Adrian Molnar
 Definition

 Aortic stenosis is incomplete opening of the

AV, which restrict blood flow out of the left
ventricle during systole.
 two times more frequent in male
 10-20% from the acquired valvular heart
disease.
 4% from the congenital heart disease.
 Fig.1.Normal aspect of the AV and PV

The normal surface of the AV is 2-4 cmp.

Classification :
mild - AV area < 1,5 cmp;
Moderate –AV area > 1- 1,5 cmp
Severe – AV area < 0,8-1 cmp
Etiology:
1.Rheumatic heart disease (15%)
Rheumatic Aortic Stenosis appears in the pericarditis from the acute
rheumatic arthritis.
Is characterized by diffuse fibrous leaflet thickening with fusion of one
or more commissures.
Generally all three leaflets are affected , resulting in a narrow opening
of the valve.

Fig.2
Rheumatic
Aortic
Stenosis
 2.Acquired Aortic Stenosis (73%)(fig.3.)
The most common cause of Aortic stenosis. The leaflet appear
thicker and calcificated but without the fusion of the commissures.

Fig.4.Ventricular hypertrophy
Fig.3.
3.Congenital: bicuspid aortic stenosis(fig.5.).
Bicuspid valve induces turbulent flow which injures the leaflets and
leads to fibrosis and calcification. Gradual calcification that result in
critical stenosis most often in the fifth and sixth decade

Fig.5.Bicuspid Aortic Stenosis

 hemodynamics

 Increased pressure in LV, followed by

LV hypertrophy

 Cardiac output declines in effort then

at rest
 LV end-diastolic pressure increases
and appears cardiac failure

 Pressure gradient between LV and

Aorta
 clinic
 The disease is long time well tolerated until the oriffice area is > 1
cmp/mp.
 functional syntoms:
effort dyspnea,
effort angina pectoris,
effort syncope
death, ce poate fi precipitata de effort
From the moment it becomes symptomatic , life expectancy is less
then 1,5 year

 Pulse – small-pulsus parvus and wide-pulsus tardus

 Auscultation - murmur at right upper sternal border
 Systolic blood pressure- diminished
 paraclinic

 ECG- LV hypertrophy
 Rx. Thoracic – poststenotic dilatation of the Aorta,
annular and leaflets calcification
 Echocardiography –most important data
 Doppler – mean pressure gradient, Aortic oriffice
 Cardiac catheterization and coronarography if surgical
treatment is intended in patients over 50 years old
even without angina.
 Indication for surgery

 Severe Aortic Stenosis in symptomatic patients

 Severe Aortic Stenosis in asymptomatic patients and:
- LV systolic dysfunction
- Ventricular tachycardia
-LV hypertrophy > 15 mm
-Valvular oriffice area < 0.6 cmp
 Patients with AoS moderate or severe if surgery for
ascending Aorta or coronary arteries is intended
 Surgical treatment

 Aortic valve replacement is the standard

procedure in all cases with fibrous or
calcificated leaflets.

 Aortic valve can be replace with pulmonary

valve , Aortic homograft, mechanical or
biological valve
 Technique:

Fig.6.

Transverse Aortotomy 4-6cm above the origin

of the right coronary.
The valve will be inspected and will decide what
kind of valve should be used
•Aortic Homograft:
•advantages: good hemodynamics,
no anticoagulants,
low risk of infection
•Disadvantages: complex techique
limited durability
limited availability

Fig.7.
• Pulmonary autograft: indicated in children
and young patients due to growth capacity
does not need
anticoagulant treatment.
•Bioprosthesis: limitated durability, low
thromboembolic risk, does not need
anticoagulant treatment.

Fig.8.
•Mechanical Prosthesis: high durability,
good hemodynamics, but high thromboembolic risk and
needs anticoagulant treatment

Types of mechanical prosthesis:

Fig.10. Single disk

Fig.9.CarbonMedics
 Aortic regurgitation

 Definition– diastolic reflux of blood from the

aorta into the left ventricle due to failure of
coaptation of the leflets at the onset of
diastole.

Aortic regurgitation can be acute or chronic.

 etiologiy

 Rheumatic disease  Bicuspid aortic valve

 Inflamation  Endocarditis
- spondylitis  Other causes:
- rheumatoid - Aortic valve
arthritis prolapse
 Aortic root dilatation - trauma
- Aortic dissection - siphilis
- connective
tissue disorders
 clinic
 Patients can be asymptomatic all their lives

 Symptoms : effort dyspnea

asthenia
angina pectoris
 Signs : water hammer pulse due to increased
stroke volume of the left ventricle.
 Auscultation – diastolic murmur in III-IV left
i.c space
 Paraclinic
 ECG – LV hypertrophy
 Rx. Thoracic – dilatation of the LV and
ascending aorta

 Echocardiography – anatomic modifications

of the leaflets
 Color Doppler – severity grading.

 Cardiac catheterization– not necessary for

diagnosis.
 Treatament

 Medical treatment:
 Endocarditis prophilaxis
 Vasodilator therapy
- angiotensin conversion enzyme
inhibitor

 Surgery before severe LV decompensation

 Indication for surgery

 Symptomatic patients with NYHA class III-IV

and good systolic function
 Patients NYHA class II with good systolic
function,but progressive dilatation of the LV
 Patients NYHA class II with good systolic
function , with angina pectoris and normal
coronary arteries
 Simptomatic or asymptomatic patients with
mild or moderate LV dysfunction
 Surgical treatment

 Aortic valve repair and valve-sparing

operations

 Aortic valve replacement with mechanical

or biological prosthesis