Clinical approach to multi valvular heart disease

1. APPROACH TO
MULTIVALVULAR HEART DISEASE
Satyam Rajvanshi

2. HOW TO DEFINE MVHD

3. • Clinically significant MVHD?
• Pathological MVHD?
• VHD without organic valve ds?

4. • Clinically significant MVHD?
• Pathological MVHD?
• VHD without organic valve ds?
NO STANDARD DEFINITION

5. PRACTICAL DEFINITION

6. • Involvement of more than one heart valve
• Clinically significant – alters natural history,
management
• Valve may or may not be pathological but
must be grossly dysfunctional

7. WHY IS MVHD RELEVANT

8. • Presentation
• Natural history
• Management

9. • Presentation
• Symptoms
• Physical signs
• Natural history
• Management

10. • Presentation
• Symptoms
• Physical signs
• Natural history
• Management
Relative severity of
separate lesions
Order of development
of separate lesions

11. WHAT CAUSES MVHD

12. • Rheumatic Heart Disease
• Infective endocarditis
• Myocardial Dysfunction (Remodelled heart – MR, PR, TR)
• Aging, Degenerative (calcific)
• Disorders of other Organs – ESRD, Carcinoid
• Myxomatous diseases – Marfan, EDS
• CTDs – SLE, APLA, RA
• Congenital diseases – Discrete Subaortic stenosis, HOCM,
Shone’s complex, Trisomy (13-15-18), Alkaptonuria
• Endocardial Disorders
• Thoracic/Mediastinal radiation therapy
• Drugs – Ergotamine/Fen-Phen/Methysergide

13. • Significant stenosis at multiple valves are
usually Rheumatic
• Significant regurgitation at multiple valves are
likely Non Rheumatic
• Significant stenosis and regurgitation together
are usually Rheumatic

14. • Quadrivalvular disease is most likely due to
combination of causes – Rheumatic, infective,
congenital, inflammatory or degenerative
disease
• A unitary cause for quadrivalvular disease is
either rheumatic or myxomatous
degeneration

15. STATISTICS

16. ARF with carditis
MV 70-75%
MV+AV 20-25%
AV 5-8%
TV 1-2%
PV Rare
Ann Indian Acad Med Sci 1972;8:47-52

17. ARF with carditis
CLINICAL
MV 70-75%
MV+AV 20-25%
AV 5-8%
TV 1-2%
PV Rare
Ann Indian Acad Med Sci 1972;8:47-52

18. ARF with carditis
CLINICAL
MV 70-75%
MV+AV 20-25%
AV 5-8% HISTOPATHOLOGICAL
TV 1-2% 30-35%
PV Rare 15-20%
Ann Indian Acad Med Sci 1972;8:47-52

19. ARF with carditis
MV 70-75% MC is MR
MV+AV 20-25% 90-95%
AV 5-8%
TV 1-2%
PV Rare
Ann Indian Acad Med Sci 1972;8:47-52

20. ARF with carditis
MV 70-75%
MV+AV 20-25% 2nd MC is AR
AV 5-8% 20-40%
TV 1-2%
PV Rare
Ann Indian Acad Med Sci 1972;8:47-52

21. Frequency of RHD
%ofpatientswithRHDat5-years
Prognosis – Severity of carditis & Recurrences

22. RHD
• 378 cases of juvenile RHD (<19 yr), Orrissa
MS 34.9%
MR 14.8%
AR 6.1%
MS+MR 11.9%
MS+AR 21.1%
MS+MR+TS 4.8%
MS+MR+TS+TR 6.4%
Indian Heart J 1999;51:653

23. RHD
• 378 cases of juvenile RHD (<19 yr), Orrissa
MS 34.9%
MR 14.8%
AR 6.1%
MS+MR 11.9%
MS+AR 21.1% >40% MVHD
MS+MR+TS 4.8%
MS+MR+TS+TR 6.4%
Indian Heart J 1999;51:653

24. RHD
• >9000 RHD cases, Orrissa
MS 35%
MR 10%
AR or AS 3%
MS+MR 15%
MV+AV 25%
MV+TV 12%
Indian Heart J 2003;55:152-157

25. RHD
• >9000 RHD cases, Orrissa
MS 35%
MR 10%
AR or AS 3%
MS+MR 15%
MV+AV 25% >50% MVHD
MV+TV 12%
Indian Heart J 2003;55:152-157

26. RHD
• 518 RHD cases, JIPMER Pondicherry
MS+AS+TS 2.5%
(Triple stenosis)
Indian Heart J 1999;51:667

27. RHD
• NIMS, Hyderabad 2002
MS+MR 12.9%
AS+AR 4.4%
MS+AR 13.9%
MS+MR+AR 2.0%
MS+MR+TR 8%
MS+AR+TR 8%

28. RHD
• 434 RHD AUTOPSY cases, Mumbai
MV 21%
AV 2%
MV+AV 21%
MV+AV+TV 27%
MV+TV 5%
MV+TV+PV 2%
MV+AV+TV+PV 19%
Indian Heart J 2002;54:676-80

29. WHEN DO WE SUSPECT A MVHD

30. • Patient does not fit in single valve picture
• By history/examination/ECG/CXR
• Presentation time frame different from usual
natural history

31. • Know the classical markers of significant
lesions

32. HISTORY-WISE

33. MS
• Exertional dyspnoea – 1st and MC symptom
– PND
– Orthopnea
– 5-10 yrs from ARF to symptoms (15-20 yrs in
western population)
– Progresses over 3-5 yrs from NYHA II to IV
(5-10 yrs in western population)
• Hemoptysis
• Systemic embolism
• RVF – but after NYHA IV state

34. MR
• History
– Long asymptomatic period – 10-20 yrs from ARF
to symptoms (a decade longer than MS)
– Once severe MR – Symptomatic within 6-10 yrs
– Symptoms herald LVSD or AF – Rapid decline in
survival
• Chronic weakness/Fatigue/Exercise
Intolerance – MC
• Dyspnoea – less common and late

35. AS
• History
– Long asymptomatic period – 10-20 yrs from ARF to
symptoms (a decade longer than MS)
– 10-15 yrs from Mild to Severe AS
– Once severe AS – Symptomatic within 2 yrs
– Symptoms – Rapid decline in survival
– 2 HF/3 Syncope/5 Angina
• Exercise intolerance and dyspnoea – MC
• Exertional Angina
• Exertional Presyncope (> than Syncope)

36. AR
• Long (perhaps longest!) asymptomatic period
– After ARF
– After development of AR
– Once symptomatic – course similar to AS
• Exercise intolerance and dyspnoea - MC
• Palpitations – exertional and resting – even
painful! – may precede other symptoms by
months-yrs
• Nocturnal (and exertional) angina

37. TS
• Never solitary
• RVF – (Tender hepatomegaly, ascites,
anasarca) – without disabling dyspnoea
• Fatigue/Exercise intolerance more prominent
than dyspnoea – d/t low CO

38. EXAMINATION-WISE

39. Severe MS
• Prolonged diastolic murmur
• Thrill
• A2 OS gap
• Pulmonary hypertension
• Cardiomegaly
• Congestive Heart failure

40. A2-OS Gap
• Inversely proportional to severity
• 40 – 120 msec
• HR, LAP, LV EDP, LV compliance, mobility
• Narrow always tight MS
• Widened (falsely)
– Bradycardia
– AR
– Low output (Sev PAH, TR, CHF)
– Inc LV EDP (LV dysfunction)

41. Severe MR
• Cardiomegaly
• LV S3/diastolic murmur
• Wide split S2
• ? Thrill
• LV dysfunction
• Pulmonary hypertension
• Congestive Heart failure

42. Severe AS
• Pulsus parvus et tardus
• Peaking of systolic murmur
• Paradoxical split S2
• LV S4
• Apico-carotid delay (often neglected)
• Thrill
• Cardiomegaly
• LV dysfunction (S3)
• Pulmonary hypertension
• Congestive Heart failure

43. Severe AR
• Hill’s Sign
• Duration of diastolic murmur
• Austin Flint murmur
• Thrill (rare)
• Cardiomegaly
• LV S3
• LV dysfunction
• Pulmonary hypertension
• Congestive Heart failure

44. Things that Stand are
• AV disease
– Pulse
– Hill’s sign
• Murmur characteristic (except MR)
• Diastolic thrill
• S2
– Paradoxical spilt – AS
– Wide split – MR
• A2 OS gap - mostly

45. HOW TO APPROACH
MS/MR/AS/AR
SEVERE?
MVHD
SUSPECTED?
EXAMINE
ECG/ECHO/CATH
WHICH ONE IS
DOMINANT?
MODIFYING /
PRECIPITATING
FACTORS?
DIAGNOSIS
PROGNOSTICATE
MANAGEMENT
GDM

46. Non valvular Factors
Modify/Precipitate presentation
– Arrhythmias
– Infective endocarditis
– RF recurrence – valvulitis and myocarditis
– Volume overload states – Anemia, worsening
Renal failure, Dietary non-compliance
– Pressure overload states – Uncontrolled HTN
– Ischemia – CAD/ACS, Respiratory illness, altitude
– SIRS – Infection, MC Pneumonia

47. Non valvular Factors
Modify/Precipitate presentation
– Arrhythmias
– Infective endocarditis
– RF recurrence – valvulitis and myocarditis
– Volume overload states – Anemia, worsening
Renal failure, Dietary non-compliance
– Pressure overload states – Uncontrolled HTN
– Ischemia – CAD/ACS, Respiratory illness, altitude
– SIRS – Systemic Infection, MC Pneumonia

48. Some Rules of Combined Valve Lesions
Severe
lesions
dominate
Proximal
lesions
dominate
Multivalvular
disease – 1+1
may not be 2
• Ability to
compensate

49. MS/MR

50. Severe MR – Is there MS?
• Thrill
• Prolonged MDM
• Opening Snap
• Loud S1
• Severe PAH

51. Pulmonary symptoms: Cough, Hemoptysis, Pulmonary Edema
S2 Variable Wide split
S1 Loud (mostly) Variable
PAH Severe Variable
OS +

52. AS/AR

53. Severe AR - is there AS?
• Pulse
• Systolic decapitation
• Late peaking, harsher, louder murmur
• Heaving apical impulse
• Thrill

54. S2 Paradoxical Normal/Narrow
S4 + -
Apex Heaving, Not shifted Hyperkinetic, shifted
Hill’s Sign

55. MS/AR

57. MS Vs. Austin Flint
Characteristic MS Austin Flint
Diastolic Murmur Prolonged with thrill Soft/shorter
Apex RV
Tapping
LV
Hyperkinetic
Added sounds OS S3
PAH Severe mild
S1 Loud (mostly) -
AF Suggestive -
Hand grip

58. MS/AS

59. In severe AS – presence of loud S1, absence of S4 - indicates MS

60. MR/AR

62. • Exception to proximal distal rule – AR usually
predominates in physical signs
• In Severe MR, mild-mod AR well tolerated
• In Severe AR, even mild-mod MR worsens
symptoms as LV dilates further

63. MR/AS

65. + TS

66. TS
• Easily escapes detection
• More fatigue, CHF/RVF - Less PND orthopnea
• Distal lesions SYMPTOMS masked, signs may
remain prominent
• JVP is the key
– Giant a waves
– Slow Y descent
• Pulsatile liver
• Murmur of TS
– Location
– Pre systolic or mid diastolic
– Inspiratory augmentation

68. TR
Characteristic High pressure Low pressure
Murmur PSM Early systolic with
variable duration
Pitch High low
Shape PSM Decrescendo
P2 Loud Normal
JVP CV waves Variable

69. INVESTIGATIONAL CAVEATS

70. • Doppler-echocardiographic methods have
been validated in single valve disease but not
in multivalve disease
• Interactions between different valve lesions.
• Methods that depend less on loading
conditions are preferred, such as direct
planimetry of the stenotic valves

71. Diagnostic caveats in MVHD

72. MANAGEMENT

76. • In the EuroHeart Survey, the operative risk ranged from
0.9% to 3.9% for single valve interventions and rose to
6.5% in cases of multiple valve disease
Ann Thorac Surg 1999;67:943-51
• In the Society of Thoracic Surgeons National Database,
mortality was 4.3% and 6.4% for isolated aortic and
mitral valve replacement, respectively, to 9.6% for
multiple valve replacement (Doubles)
Eur Heart J 2003;24:1231-43

77. • TVR: overall operative mortality was 22 %
Ann Thorac Surg 2005;80:845-850
• Operative mortality was similar for TVR 13%
vs. repair 18% p = 0.64.
• Higher mortality for higher NYHA class
Ann Thorac Surg 2009;87:83-89

78. CONCLUSION

79. MVHD
• Widely prevalent
• Alters natural history and presentation
• Requires careful evaluation
• Management guidelines differ

80. La Clairvoyance, 1936 By Rene Magritte