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MITRAL
REGURGITATION
PRAVEEN RK
75
MR
• Commonest manifestation of acute as well as previous rheumatic carditis
• Loss of valvular structure and shortening of chordae tendinae
• Results in systolic leak of blood to left atrium
PATHOPHYSIOLOGY
• Chronic LV volume overload compensatory LVE initially maintaining cardiac
output
• Decompensation (increased LV wall tension) CHF
• LVE annulus dilation increased MR
• Backflow Left atrial enlargement, Atrial fibrillation, Pulmonary Hypertension
SYMPTOMS
• Dyspnea, Orthopnea
• Paroxysmal nocturnal dyspnoea
• Fatigue
• Pulmonary HTN, right sided failure
• Hemoptysis
• Systemic embolization in Atrial fibrillation
RECOGNIZING CHRONIC MR
• Pulse: – brisk, low volume, water
hammer
• Apex:
– hyperdynamic
– laterally displaced
– palpable S3, +/‐ thrill
– late parasternal lift 2o to LA
filling
• S1 soft or normal
• S2 wide split (early A2) unless LBBB
• Murmur‐Fixed MR
– pan systolic
– Loudest, apex to axilla
– no post extra‐systolic accentuation
• Murmur‐Dynamic MR(MVP)
– mid systolic
– +/‐ click
– upright
• S3 / flow rumble if severe
RECOGNIZING ACUTE SEVERE MR
• Acute severe dyspnea, CHF &
hypotension
• LV size normal
• LV may/may not be hyper dynamic
• Loud S1
• Systolic murmur may/may not be
pansystolic
• Inflow/rumble
• S3 present‐may be only abnormality
• RV lift
• Chordal or papillary muscle
rupture/tear
– Infarction with papillary
muscle ischemia or tear
– Infectious endocarditis with
leaflet perforation or
disruption or chordal tear
– Flail MV segment
• ECG:
– LA enlargement
– A fib
– LVH (50% pts. With severe
MR)
– RVH (15%)
– Combined hypertrophy (5%)
• Chest Xray
– LV
– LA
– pulmonary vascularity
– CHF
MR STAGES
LV size and function defined by echo
• Stage 1‐compensated:
• Stage 2‐transitional
• Stage 3‐decompensated
INVESTIGATION
• X‐ ray
• ECG
• Echocardiogram
• Cardiac catheterization
TREATMENT
• Rheumatic prophylaxis
• Decongestive‐ vasodilators, ACE inhibitors (digoxin increases the regurgitation)
• Infective endocarditis prophylaxis
• Valve replacement if left ventricular function is progressively reducing
MITRAL VALVE SURGERY
• Only effective treatment is valve repair/replacement
• Optimal timing determined:
– Presence/absence of symptoms
– Functional state of ventricle
– Feasibility of valve repair
– Presence of A fib/PHTN
– Preference/expectations of patient
MV REPAIR VS REPLACEMENT
VALVE REPLACEMENT
• Mortality 2‐7%
• Anti‐coagulation
• Decreased LVEF
• Tissue prosthetic valve degeneration
• Mechanical prosthetic valve
dysfunction/ thrombosis
VALVE REPAIR
• Mortality 2‐3%
• No anticoagulation (unless Afib)
• Preservation of LVEF
• Valve repair always preferable
• Feasible in 70‐90% of patients
THANK YOU

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Mitral Regurgitation in Rheumatic Heart Disease

  • 2. MR • Commonest manifestation of acute as well as previous rheumatic carditis • Loss of valvular structure and shortening of chordae tendinae • Results in systolic leak of blood to left atrium
  • 3. PATHOPHYSIOLOGY • Chronic LV volume overload compensatory LVE initially maintaining cardiac output • Decompensation (increased LV wall tension) CHF • LVE annulus dilation increased MR • Backflow Left atrial enlargement, Atrial fibrillation, Pulmonary Hypertension
  • 4. SYMPTOMS • Dyspnea, Orthopnea • Paroxysmal nocturnal dyspnoea • Fatigue • Pulmonary HTN, right sided failure • Hemoptysis • Systemic embolization in Atrial fibrillation
  • 5. RECOGNIZING CHRONIC MR • Pulse: – brisk, low volume, water hammer • Apex: – hyperdynamic – laterally displaced – palpable S3, +/‐ thrill – late parasternal lift 2o to LA filling • S1 soft or normal • S2 wide split (early A2) unless LBBB • Murmur‐Fixed MR – pan systolic – Loudest, apex to axilla – no post extra‐systolic accentuation • Murmur‐Dynamic MR(MVP) – mid systolic – +/‐ click – upright • S3 / flow rumble if severe
  • 6. RECOGNIZING ACUTE SEVERE MR • Acute severe dyspnea, CHF & hypotension • LV size normal • LV may/may not be hyper dynamic • Loud S1 • Systolic murmur may/may not be pansystolic • Inflow/rumble • S3 present‐may be only abnormality • RV lift • Chordal or papillary muscle rupture/tear – Infarction with papillary muscle ischemia or tear – Infectious endocarditis with leaflet perforation or disruption or chordal tear – Flail MV segment
  • 7. • ECG: – LA enlargement – A fib – LVH (50% pts. With severe MR) – RVH (15%) – Combined hypertrophy (5%) • Chest Xray – LV – LA – pulmonary vascularity – CHF
  • 8. MR STAGES LV size and function defined by echo • Stage 1‐compensated: • Stage 2‐transitional • Stage 3‐decompensated
  • 9. INVESTIGATION • X‐ ray • ECG • Echocardiogram • Cardiac catheterization
  • 10. TREATMENT • Rheumatic prophylaxis • Decongestive‐ vasodilators, ACE inhibitors (digoxin increases the regurgitation) • Infective endocarditis prophylaxis • Valve replacement if left ventricular function is progressively reducing
  • 11. MITRAL VALVE SURGERY • Only effective treatment is valve repair/replacement • Optimal timing determined: – Presence/absence of symptoms – Functional state of ventricle – Feasibility of valve repair – Presence of A fib/PHTN – Preference/expectations of patient
  • 12. MV REPAIR VS REPLACEMENT VALVE REPLACEMENT • Mortality 2‐7% • Anti‐coagulation • Decreased LVEF • Tissue prosthetic valve degeneration • Mechanical prosthetic valve dysfunction/ thrombosis VALVE REPAIR • Mortality 2‐3% • No anticoagulation (unless Afib) • Preservation of LVEF • Valve repair always preferable • Feasible in 70‐90% of patients