This document discusses various types of valvular heart disease, including rheumatic and non-rheumatic causes. It focuses on the anatomy, pathology, pathophysiology, clinical features, investigations, and management of mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid stenosis, tricuspid regurgitation, and pulmonic valve disease. Key points covered include the predominant involvement of the left side valves in rheumatic heart disease, common murmurs associated with different valve lesions, and treatments involving surgery, balloon dilation, or medication management.

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?