1. VALVULAR HEART
DISEASE
RHEUMATIC AND NON-RHEUMATIC
Samuel Ngigi K.
KMTC

2. PREAMBLE
 Predominantly rheumatic in this environment
 Most important cause of cardiac disease in
teenagers, young adults
 Epidemiology reflects Rh. Fever
 Disease of under privilege
 Yet management expensive, risky
 Other causes:
- Congenital
-Degenerative
-Ischaemic, CCF, inflammatory

3. PATTERN OF
INVOLVEMENT
 Rheumatic, predominantly left side,
mitral > aortic
 Rarely tricuspid, almost never
pulmonic
 May present as stenosis regurgitation
or both
 May be multivalvular

5. Common Murmurs and
Timing
Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis
S1 S2 S1

6. MITRAL STENOSIS
 FUNCTIONAL ANATOMY:
-Leaflets, commissures, chordea tendinae
-MVA – Normal 4-6 cm2
- 1-2cm2 significant stenosis
- < 1cm2 critical stenosis
 AETIOLOGY:
- Almost invariably rheumatic
- Others; - Congenital, Annular calc., Atrial myxoma, Ball
thrombus
 PATHOLOGY:
- Fibrosis, calcification of leaflets > immobility
- Commissural fusion
- Fibrosis, distortion and shortening of chordae

7. FISH MOUTH DEFORMITY
OF MITRAL VALVE

8. MITRAL STENOSIS
PATHOPHYSIOLOGY
 Impaired opening of MV
- Inadequate emptying of LA
- Inadequate filling of LV
 Inadequate LA emptying
- Increased LA pressures PULMONARY HYPERTENSION
- Increased LA size
>LA thrombosis
>Atrial fibrillation
- Inadequate LV filling
- Low cardiac output

9. Right Heart Failure:
Hepatic Congestion
JVD
Tricuspid Regurgitation
RA Enlargement
 Pulmonary HTN
Pulmonary Congestion
LA Enlargement
Atrial Fib
LA Thrombi
 LA Pressure
RV Pressure Overload
RVH
RV Failure LV Filling
Mitral Stenosis
Pathophysiology

10. Mitral Stenosis Symptoms
 Fatigue
 Palpitations
 Cough
 SOB
 Left sided failure
– Orthopnea
– PND
 Palpitation
 AFib
 Systemic embolism
 Pulmonary infection
 Hemoptysis
 Right sided failure
– Hepatic Congestion
– Edema
 Worsened by conditions
that  cardiac output.
– Exertion,fever, anemia,
tachycardia, Afib,
intercourse, pregnancy,
thyrotoxicosis

11. MITRAL STENOSIS
CLINICAL FEATURES
SYMPTOMS
 Exertional dyspnoea, fatigue
 Palpitations, maybe at rest
 Cough, haemoptysis
 Orthopnea ± PND
 Abd discomfort

12. MITRAL STENOSIS
CLINICAL FEATURES
SIGNS
 Mitral facies
 Low volume pulse, rapid ± irregular
 Apex not displaced, tapping
 Palpable P2
 Right parasternal heave
 Auscultation;
- Loud S1, P2.
- Opening snap, mid diastolic murmur, presystolic
accentuation
- Features of TR
- Pulmonary EDM (Graham Steele)

13. Recognizing Mitral
Stenosis
Palpation:
 Small volume pulse
 Tapping apex-palpable
S1
 +/- palpable opening
snap (OS)
 RV lift
 Palpable S2
ECG:
 LAE, AFIB, RVH, RAD
Auscultation:
 Loud S1- as loud as S2 in
aortic area
 A2 to OS interval inversely
proportional to severity
 Diastolic rumble: length
proportional to severity
 In severe MS with low flow-
S1, OS & rumble may be
inaudible

14. MITRAL STENOSIS
COMPLICATIONS
 Heart Failure
 Atrial Fibrillation
 Thromboembolism
 Infective Endocarditis

15. MITRAL STENOSIS
INVESTIGATIONS
 CXR – features of LA enlargement;
- double shadow, filling of pul. bay, widened
carina
 ECG – LAE, RVH, RAD
- Atrial Fibrillation
 ECHO – Morphology
- Doppler – valve area, gradients, pul
pressures
- Secondary changes – LAE, RVH etc

16. MITRAL STENOSIS
MANAGEMENT
PHARMACOLOGICAL
 Limited
 Diuretics
 HR slowing – Beta blockers
 No role for usual ‘anti CCF’
management
 Management of Complications; A.fib,
thromboembolism, infective end.

17. MITRAL STENOSIS
MANAGEMENT
DEFINITIVE
 Surgical;
- Valvotomy – closed, open
- Valve replacement/repair
 Interventional;
- Percutaneous balloon dilatation

18. Mitral Regurgitation:
Etiology
 Valvular-leaflets
– Myxomatous MV Disease
– Rheumatic
– Endocarditis
– Congenital-clefts
 Chordae
– Fused/inflammatory
– Torn/trauma
– Degenerative
– IE
 Annulus
– Calcification, IE (abcess)
 Papillary Muscles
– CAD (Ischemia,
Infarction, Rupture)
– HCM
– Infiltrative disorders
 LV dilatation &
functional regurgitation
 Trauma

19. MR Pathophysiology
 Chronic LV volume overload -»
compensatory LVE initially maintaining
cardiac output
 Decompensation (increased LV wall
tension) -»CHF
 LVE – » annulus dilation – » increased
MR
 Backflow – » LAE, Afib, Pulmonary
HTN

20. MR Symptoms
 Similar to MS
 Dyspnea, Orthopnea, PND
 Fatigue
 Pulmonary HTN, right sided failure
 Hemoptysis
 Systemic embolization in A Fib
 Features of CCF

21. MITRAL REGURGITATION
CLINICAL FEATURES
SIGNS
 Pulse maybe large volume
 Apex, displaced, heaving
 Muffled S1, S3+
 Apical pansystolic murmur radiating
to axilla

22. MITRAL REGURGITATION
COMPLICATIONS
 CCF
 Infective endocarditis
 A.Fib
 Thromboembolism

23. MITRAL REGURGITATION
INVESTIGATIONS
 CXR- cardiomegaly
- pul congestion
 ECG- LAE, LVH, A.Fib
 ECHO- Morphology
- Quantification
- LV function
- Secondary changes

24. MITRAL REGURGITATION
MANAGEMENT
 Pharmacological;
- Management of CCF
- Complications
- Rh fever prophylaxis
 Definitive;
- Surgery – valve replacement,
repair

25. AORTIC STENOSIS
 ANATOMY – Cusps, commissures ,(sub,
supravalvular)
 AETIOLOGY/PATHOLOGY;
- Congenital- unicuspid, bicuspid, tricuspid
- Acquired;
-Rheumatic
-Degenerative(senile), calcific
-Atherosclerotic

26. AORTIC STENOSIS
PATHOPHYSIOLOGY
 Obstruction to LV emptying
 Pressure overload
 Marked concentric hypertrophy
 Increased oxygen demand(LV mass)
 Elevated LV diastolic pressures
(diastolic failure)

27. Severity of Stenosis
 Normal aortic valve area 2.5-3.5 cm2
 Mild stenosis 1.5-2.5 cm2
 Moderate stenosis 1.0-1.5 cm2
 Severe stenosis < 1.0 cm2
 Onset of symptoms
~0.9 cm2 with CAD
~0.7 cm2 without CAD

28. AORTIC STENOSIS
CLINICAL FEATURES
SYMPTOMS
 Long latent period
 Once symptoms supervene, rapid progression
 Classical triad;
- Dyspnoea
- Angina
- Syncope
 Sudden death (ventricular arrhythmias)

29. AORTIC STENOSIS
CLINICAL FEATURES
SIGNS
 Slow rising, sustained pulse, small
volume
 Apex usually displaced, sustained
heave
 Ejection click
 Ejection systolic murmur > carotids
 S4

30. AORTIC STENOSIS
COMPLICATIONS
 LV systolic failure
 Ventricular arrhythmias

31. AORTIC STENOSIS
INVESTIGATIONS
 CXR- Maybe normal, normal CTR
- Calcification
- Post stenotic dilatation
 ECG- Marked LVH with ST depression, T wave
inversion
 ECHO- Valve morphology
- Doppler – valve area, gradients
- LVH, LV function

32. AORTIC STENOSIS
MANAGEMENT
 Medical;
- Limited
- Cautious diuresis
- “CCF” management only in systolic dysfunction
- Management of complications
 Definitive
- Surgery
- Balloon dilatation

33. AORTIC REGUGITATION
 ANATOMY/PATHOLOGY:
- Root dilatation
- Valve cusps

34. AORTIC REGURGITATION
AETIOLOGY
 Congenital
 Acquired
-Rheumatic
-Syphilis
-Dissecting aneurysm
-Inflammatory disorders
-Degenerative

35. AORTIC REGURGITATION
PATHOPHYSIOLOGY
 Regurgitant fraction > high SV
 Volume overload
 However entire SV into high pressure
area-aorta( cf. MR)
 Hence more stress > massive
dilatation( cor bovis)
 Hyperdynamic circulation

36. AORTIC REGURGITATION
CLINICAL FEATURE
SYMPTOMS
 Long latency
 Features of hyperdynamic state;
-Pounding in chest, head,
palpitations
 Features of heart failure

37. Aortic Regurgitation:
Symptoms
 Dyspnea, orthopnea, PND
 Chest pain.
– Nocturnal angina >> exertional angina
– ( diastolic aortic pressure and increased LVEDP
thus  coronary artery diastolic flow)
 With extreme reductions in diastolic
pressures (e.g. < 40) may see angina

38. Peripheral Signs of
Severe
Aortic Regurgitation
 Quincke’s sign:
capillary pulsation
 Corrigan’s sign: water
hammer pulse
 Bisferiens pulse (AS/AR
> AR)
 De Musset’s sign:
systolic head bobbing
 Mueller’s sign: systolic
pulsation of uvula
 Durosier’s sign:
femoral retrograde
bruits
 Traube’s sign: pistol
shot femorals
 Hill’s sign:BP Lower
extremity >BP Upper
extremity by
– > 20 mm Hg - mild AR
– > 40 mm Hg – mod AR
– > 60 mm Hg – severe
AR

39. Aortic Regurgitation:
Physical Exam
 Widened pulse pressure
– Systolic – diastolic =
pulse pressure
 High pitched, blowing,
decrescendo diastolic
murmur at LSB
 Best heard at end-
expiration & leaning
forward
 Hands & Knee position
S1 S2 S1

40. Central Signs of Severe
Aortic Regurgitation
 Apex:
– Enlarged
– Displaced
– Hyper-dynamic
– Palpable S3
– Austin-Flint
murmur
 Aortic diastolic
murmur
– length correlates
with severity
(chronic AR)
– in acute AR
murmur shortens
as Aortic
DP=LVEDP
– in acute AR - mitral
pre-closure

41. AORTIC REGURGITATION
SIGNS (CONT)
 Soft S1, A2
 Early diastolic murmur (decrescendo)
 Apical mid diastolic murmur( Austin
Flint)

42. AORTIC REGURGITATION
INVESTIGATIONS
 ECG - LVH, marked ST, T changes
 CXR – Massive cardiomegaly
 ECHO – Morphology
- Quantification
- LV size, function

43. AORTIC REGURGITATION
MANAGEMENT
 PHARMACOLOGICAL
- Management of CCF
- ?Afterload reduction – CCBs, ACEIs
 DEFINITIVE
- Surgical- mainly valve replacement

44. TRICUSPID STENOSIS
 Predominantly rheumatic
 Usually occurs with MS, masks presentation
 Other causes:- Tricuspid atresia, tumours,
carcinoid synd.
 Pathophysiology:
- RV-RA gradient > elevated RA pressure >
systemic venous congestion
- Impaired RV filling > low output

45. TRICUSPID STENOSIS
SYMPTOMS
 Low output:- fatigue etc
 Systemic congestion:- abd swelling,
discomfort; leg swelling; fluterring in
the neck
 Absence of chest symptoms( even
with MS)

46. TRICUSPID STENOSIS
SIGNS
 Prominent “a” waves on JVP
 Low volume pulse
 Negatives – No PHT, RVH and clear
lung fields in MS
 Auscultation - LSE opening snap,
MDM- increased on inspiration

47. TRICUSPID STENOSIS
INVESTIGATIONS
 CXR – Marked “cardiomegaly’- RA
enlargement ,with clear lung fields
 ECG – RAH, ? Biatrial hypertrophy
with NO RVH
 ECHO – Confirm stenosis, gradient
- Coexistent MS

48. TRICUSPID STENOSIS
 MANAGEMENT:
- Medical – Sodium restriction, diuresis
- Surgical – Valvotomy(open/closed),
prosthetic valve

49. TRICUSPID
REGURGITATION
 Aetiology – most often secondary to
RV dilatation ( functional)
- Others – Rheumatic, various-cong,
inflammatory etc
 Pathophysiology – RV volume overload
- Primary pathology esp PHT

50. TRICUSPID
REGURGITATION
 CLINICAL:
- Usually well tolerated in absence of PHT
- With PHT features of RV failure - low
output, systemic venous congestion
- Cachexia, pulsatile liver, ascites
- Elevated JVP with prominent “v” wave
- Left parasternal heave, LLSE thrill
- LLSE pansystolic murmur
- Loud P2

51. TRICUSPID
REGURGITATION
 INVESTIGATIONS:
- ECG – Non specific, RVH
- ECHO – Morphology
- Quantification,Pul pressures
- RVH, primary pathology
- CXR – Cardiomegaly due to RVH

52. TRICUSPID
REGURGITATION
 MANAGEMENT:
- Mainly surgical – annuloplasty,
prosthetic valve
- Primary condition

53. PULMONIC VALVE
 STENOSIS – Almost always congenital
 REGURGITATION – Secondary to
pulmonary hypertension
- Presentation, management is of
primary disease

54. QUESTIONS?