Valvular heart disease

Mitral stenosis
.Almost all MS is due to RHD
The single most common valve lesion due to rheumatic fever is pure MS ( at least 50% ).
Mitral & aortic valves ( 40% ), MV, AV & TV ( 5%) , AV alone ( 2% ) all valves combinations
.( 3% )
.Rheumatic MS is more common in woman
Pathological process results in : valve thickening , cusp fustion , calcium deposition,
.stenotic valve orifice & progressive immobility of valve cusps
:Other causes
.Lutembachers, syndrome( acquired MS & ASD) -
.Congenital MS ( rare ) -
Calcification & fibrosis ( MS ) in elderly pt -
Carcinoid tumors -
 Pathophysiology
When the normal valve area ( 5cm2) reduced to 1cm2 , severe MS is present . In order •
sufficent COP is maintained, LAP is increase & LAH & dilatation occur, pul arterial & venous
.pressure & Rt side pressure also increase
Increase pul capillary pressure …… pul odeama •
. Reactive pul HTN , lead to RVH, dilatation & failure •
.RHF results in TR •
: Complications of MS •
Afib - •
systemic embolization - •
pul HTN- •
Pul infarction - •
chest infection - •
IE ( rare) - •
TR - •
Rt ventricular failure - •
 Symptoms

No symptoms until the valve orifice is moderately stenosis ( MVA = 2cm2) •

Symptoms of pul venous congestion •
Symptoms Rt HF •
Palpitation ( Afib) •
Systemic emboli ( Afib) •
:Sings •
Face: ( mitral facies or malar flush) •
Pulse : early small volume regular pulse , later on may develop •
.Afib … irregularity irregular pules
JVP: distended vein & raised JVP •
.If pul HTN or TS present … prominent a wave •
:Palpation •
a tapping impulse at Lt parasternal area- •
Sustained parastenal impulse ( RVH) •
:Auscultation •
aloud S1- •
An opening snap - •
Low pitched rumbling mid diastolic murmur at apex with pt at - •
Lt side with the bell of stethoscope
:Severity of MS clinically depend on the following criteria •
pul HTN ( by RV heave, loud pul component of S2, signs of Rt HF, - •
early diastolic murmur ( PR) heard at pul area called agraham steal
.murmur )
closeness of OS to 2nd heart sound - •
Length of mid diastolic m - •
soften the loud S1 & disappear the OS ( when the cusps become - •
immobile.)
Due to pul HTN the pul component of S2 is increase in intensity & •
.mitral diastolic murmur become quiet
 Investigations
CXR , ECG •
: Imaging •
.Echo( TTE) , TEE, CMR & cardiac catheterization ( seldom required ) •
: Treatment •
.Mild MS no treatment
.early dyspnea in MS …. Small dose diuresis
Afib …..digoxin & OAC
.If pul HTN develops or signs of pul congestion persist despite med # , surgery is indicated
: There are 4 type of operations
Trans –septal balloon valvotomy •
Closed valvotomy •
Open valvotomy •
: Mitral valve replacement •
If MR is present •
.Badly calcified stenotic valve •
.Severe MS or symptomatic moderate MS , both with LA thrombus despite anticoagulation •
•
 Mitral regurgitation
Causes : RHD ( 50% ) & MVP are the most common •
: Others •
AV disease •
Acute RF •
Myocarditis •
DCM •
HHD •
IHD •
IE •
HCM •
Rheumatic autoimmune ( e.g SLE) •
Collagen abnormalities ( marfan syndrome ) •
Degeneration of valve cusps or mitral annular calcification •
Rupture of cordae tendinae •
Drugs : e.g centrally acting appetite suppressants e.g fenfluramine •
•
 Pathophysiology
.LA dilatation •
In acute MR there is no much dilatation , but increase LAP, increase PVP •
. & pul odeama
: Symptoms •
Palpiation •
Symptoms of pul venous congestion •
Fatigue •
Symptoms of RHF •
Cardiac cachexia •
Thromboembolism ( less common) •
Subacute IE •
 Signs
Laterally displaced apex beat & systolic thrill ( if severe) •
Soft S1 •
Pan systolic murmur •
Prominent S3 •
Signs of Afib •
Signs of pul venous congestion •
Signs of RHF •
.Investigations : CXR, ECG, ECHO & TOE, cardiac catheterization & CMR •
: Treatment •
# Mil MR may no need •
Med # include ACI, diuresis & possible OAC •
Evidence of progressive cardiac enlargement & no response to •
.med # surgery is indicated with MV repair or MVR
In acute MR & acute rupture of chordae tendinae or papillary •
muscle or IE. o
 Mitral Valve prolapse ( MVP)
This is also known as Barlow’s syndrome or floppy mitral valve •
,Causes : excessively large mitral valve leaflets •
an enlarged mitral annulus, abnormally long chordae or •
.disordered papillary muscle contraction •
:Histology •
.myxomatous degeneration of the mitral valve leaflets •
It is more commonly seen in young women than .
.in men or older women and it has a familial incidence •
Its cause is unknown but it is associated with Marfan’s •
syndrome, thyrotoxicosis, rheumatic or ischaemic heart •
disease. It also occurs in association with atrial septal defect •
and as part of hypertrophic cardiomyopathy. Mild mitral valve •
prolapse is so common that it should be regarded as a normal variant •
 Pathophysiology
During ventricular systole, a mitral valve leaflet (most commonly •
the posterior leaflet) prolapses into the left atrium. This •
may result in abnormal ventricular contraction, papillary •
muscle strain and some mitral regurgitation. Usually the syndrome •
is not haemodynamically serious. Thromboembolism occurs •
: Symptoms •
atypical chest pain- •
palpitation- •
SCD - •
: Signs •
mid systolic click, followed by late systolic murmur ( MR) - •
with more MR .. pan systolic murmur - •
Investigation : by echo •
: Treatment •
BB , antiarrhythmic drug ( sometime ), MVP + Afib ( OAC), severe MR ( MV repair Vs MVR)- •
 Aortic stenosis
:Causes •
Congenital aortic stenosis ( most commonly bicuspid aortic valve) - •
Rheumatic heart disease - •
Calcific valvular disease - •
Valvular aortic stenosis should be distinguished from •
:other causes of obstruction to left ventricular emptying, include •
. supra aortic obstruction ( williams syndrome) - •
HOCM - •
Subvalvular AS - •
•
 Pathophysiology
Obstructed left ventricular emptying leads to increased left •
.ventricular pressure and compensatory left ventricular hypertrophy •
In turn, this results in relative ischaemia of the left •
ventricular myocardium, and consequent angina, arrhythmias •
and left ventricular failure. The obstruction to left ventricular •
. emptying more severe on exercise
:Symptoms •
. usually no symptoms unless moderate to severe AS - •
.Exercise induced syncope, angina & dyspnea - •
 Signs
.Pulse: carotid pulse is small volume, slow rising or platue in nature •
 Investigations
CXR, ECG , ECHO , CMR, & cardiac cathetertization •
: Treatment •
asymptomatic pts need echo follow up - •
.all symptomatic pts need AVR - •
Balloon valvuloplasty - •
percutaneous valve replacement ( TAVI) - •
Aortic regurgitation
 Pathophysiology
volume over load * •
decrease diastolic pressure of LV … decrease coronary perfusion … * •
.cardiac ischemia
: Symptoms •
symptoms of LVF - •
Pounding of the heart & vigorous pulsation - •
Angina pectoris - •
dyspnea - •
arrhythmias ( uncommon) - •
 :Signs
•

The signs of aortic regurgitation are due to the The following hyperdynamic circulation •

. •
. The pulse is bounding or collapsing •

: The following signs, which are rare, also indicate a hyperdynamic circulation •
:
Quincke’s sign – capillary pulsation in the nail beds ■ •
De Musset’s sign – head nodding with each heart beat ■ •
Duroziez’s sign – a to-and-fro murmur heard when the ■ •
femoral artery is auscultated with pressure applied •
distally (if found, it is a sign of severe aortic •
)regurgitation •
pistol shot femorals – a sharp bang heard on ■ •
auscultation over the femoral arteries in time with each •
.heart beat •
 Investigation
CXR, ECG, ECHO & cardiac catheterization •
: Treatment •
Treat the underlying cause - •
.surgery before symptoms appear- •
Timing of op depend on hemodynamic, echo & •
angiographic criteria
Antibiotic IE prophylaxis - •
 Tricuspid stenosis
This uncommon valve lesion, which is seen much more often •
in women than in men, is usually due to rheumatic heart disease •
.tricuspid stenosis is also seen in the carcinoid syndrome •
:Pathophysiology •
Tricuspid valve stenosis results in a reduced cardiac •
output, which is restored towards normal when the right •
atrial pressure increases. The resulting systemic venous •
congestion produces hepatomegaly, ascites and dependent •
.oedema •
 S& S
Symptoms of associated Lt side rheumatic valve disease - •
abd pain & swelling - •
peripheral odeama - •
: Signs •
Prominent a wave- •
presystolic pulasation also felt on the liver - •
Rumbling mid systolic murmur - •
Opening snap - •
hepatomegaly , ascites & dependent edema - •
 Investigation
CXR,ECG, ECHO & cardiac catheterization •
: Treatment •
Medical management consists of diuretic therapy and salt •
restriction. Tricuspid valvotomy is occasionally possible, but •
tricuspid valve replacement is often necessary. Other valves •
usually also need replacement because tricuspid valve stenosis •
.is rarely an isolated lesion •
 Tricuspid regurgitation
Functional tricuspid regurgitation may occur whenever the •
right ventricle dilates, e.g. in cor pulmonale, myocardial •
infarction or pulmonary hypertension •
Organic tricuspid regurgitation may occur with rheumatic •
,heart disease, infective endocarditis, carcinoid syndrome •
Ebstein’s anomaly (a congenitally malpositioned tricuspid •
valve) and other congenital abnormalities of the atrioventricular •
.valves •
 S& S
.Symptoms of RHF •
.Signs include : large JV ( cv) wave, palpable liver that pulsating in systole - •
RV impulse at Lt sternal edge - •
A blowing pan systolic murmur - •
Afib is common - •
: Treatment •
Functional tricuspid regurgitation usually disappears with •
medical management. Severe organic tricuspid regurgitation •
may require operative repair of the tricuspid valve (annuloplasty •
or plication). Very occasionally, tricuspid valve replacement •
may be necessary. In drug addicts with infective •
endocarditis of the tricuspid valve, surgical removal of the •
valve is recommended to eradicate the infection. This is usually •
well tolerated in the short term •
 Pulmonary stenosis
This is usually a congenital lesion, but it may rarely result •
from rheumatic fever or from the carcinoid syndrome. Congenital •
pulmonary stenosis may be associated with an intact •
ventricular septum or with a ventricular septal defect (Fallot’s •
.)tetralogy •
Pulmonary stenosis may be valvular, subvalvular •
or supravalvular. Multiple congenital pulmonary arterial •
stenoses are usually due to infection with rubella during •
.pregnancy •
 S&S
RVH & RAH - •
Fatigue , syncope & symptoms of RHF - •
Mild PS is asymptomatic - •
: Physical signs •
Harsh mid ejection systolic murmur - •
pul closure sound delay & soft - •
.Rt S 4 * prominent JV a wave - •
RV heave ( sustained impulse may be felt - •
 Investigations

CXR, ECG , ECHO & cardiac catheterization •

: Treatment •
Treatment of severe pulmonary stenosis requires pulmonary •
.valvotomy (balloon valvotomy or direct surgery) •
 Pulmonary regurgitation
This is the most common acquired lesion of the pulmonary •
,valve. It results from dilatation of the pulmonary valve ring •
which occurs with pulmonary hypertension. It is characterized •
by a decrescendo diastolic murmur, beginning with the •
pulmonary component of the second sound, that is difficult •
to distinguish from the murmur of aortic regurgitation. Pulmonary •
regurgitation usually causes no symptoms and treatment •
.is rarely necessary •