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Clinical approach to multi valvular heart disease

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Clinical approach to multi valvular heart disease

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Clinical approach to multi valvular heart disease

  1. 1. APPROACH TO MULTIVALVULAR HEART DISEASE Satyam Rajvanshi
  2. 2. HOW TO DEFINE MVHD
  3. 3. • Clinically significant MVHD? • Pathological MVHD? • VHD without organic valve ds?
  4. 4. • Clinically significant MVHD? • Pathological MVHD? • VHD without organic valve ds? NO STANDARD DEFINITION
  5. 5. PRACTICAL DEFINITION
  6. 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. 7. WHY IS MVHD RELEVANT
  8. 8. • Presentation • Natural history • Management
  9. 9. • Presentation • Symptoms • Physical signs • Natural history • Management
  10. 10. • Presentation • Symptoms • Physical signs • Natural history • Management Relative severity of separate lesions Order of development of separate lesions
  11. 11. WHAT CAUSES MVHD
  12. 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. 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. 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. 15. STATISTICS
  16. 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. 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. 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. 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. 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. 21. Frequency of RHD %ofpatientswithRHDat5-years Prognosis – Severity of carditis & Recurrences
  22. 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. 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. 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. 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. 26. RHD • 518 RHD cases, JIPMER Pondicherry MS+AS+TS 2.5% (Triple stenosis) Indian Heart J 1999;51:667
  27. 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. 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. 29. WHEN DO WE SUSPECT A MVHD
  30. 30. • Patient does not fit in single valve picture • By history/examination/ECG/CXR • Presentation time frame different from usual natural history
  31. 31. • Know the classical markers of significant lesions
  32. 32. HISTORY-WISE
  33. 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. 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. 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. 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. 37. TS • Never solitary • RVF – (Tender hepatomegaly, ascites, anasarca) – without disabling dyspnoea • Fatigue/Exercise intolerance more prominent than dyspnoea – d/t low CO
  38. 38. EXAMINATION-WISE
  39. 39. Severe MS • Prolonged diastolic murmur • Thrill • A2 OS gap • Pulmonary hypertension • Cardiomegaly • Congestive Heart failure
  40. 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. 41. Severe MR • Cardiomegaly • LV S3/diastolic murmur • Wide split S2 • ? Thrill • LV dysfunction • Pulmonary hypertension • Congestive Heart failure
  42. 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. 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. 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. 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. 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. 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. 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. 49. MS/MR
  50. 50. Severe MR – Is there MS? • Thrill • Prolonged MDM • Opening Snap • Loud S1 • Severe PAH
  51. 51. Pulmonary symptoms: Cough, Hemoptysis, Pulmonary Edema S2 Variable Wide split S1 Loud (mostly) Variable PAH Severe Variable OS +
  52. 52. AS/AR
  53. 53. Severe AR - is there AS? • Pulse • Systolic decapitation • Late peaking, harsher, louder murmur • Heaving apical impulse • Thrill
  54. 54. S2 Paradoxical Normal/Narrow S4 + - Apex Heaving, Not shifted Hyperkinetic, shifted Hill’s Sign
  55. 55. MS/AR
  56. 56. 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
  57. 57. MS/AS
  58. 58. In severe AS – presence of loud S1, absence of S4 - indicates MS
  59. 59. MR/AR
  60. 60. • 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
  61. 61. MR/AS
  62. 62. + TS
  63. 63. 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
  64. 64. 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
  65. 65. INVESTIGATIONAL CAVEATS
  66. 66. • 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
  67. 67. Diagnostic caveats in MVHD
  68. 68. MANAGEMENT
  69. 69. • 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
  70. 70. • 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
  71. 71. CONCLUSION
  72. 72. MVHD • Widely prevalent • Alters natural history and presentation • Requires careful evaluation • Management guidelines differ
  73. 73. La Clairvoyance, 1936 By Rene Magritte

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