Post-graduate presentation on Mitral Valve Lesions - Mitral Stenosis & Mitral Regurgitation

1. Mitral Valve
Disorders
(MS & MR)
Dr. Abdul Kareem
First Year DNB Resident
Department of General Medicine
Rohini Super-Speciality Hospital

2. Heart
Valves

3. Mitral Valve
Anatomy

4. Valvular Heart Disease
▪ Stenosis
▪ Failure of a valve to open completely, which impedes forward flow.
▪ Regurgitation (also called Insufficiency or Incompetence)
▪ Failure of a valve to close completely, thereby allowing reversed flow.
▪ Functional regurgitation is due to surrounding structure abnormalities
▪ Can co-exist in the same valve & across other valves.

5. Mitral Stenosis

7. Etiology

8. Etiology
▪ 40% of all patients with Rheumatic Heart disease and history of
rheumatic fever will have MS.
▪ RHD can also cause MR, AS & AR. Tricuspid & pulmonary
involvement is rare.
▪ Chronic inflammation leads to narrowing of valve (‘fish-mouth
valve’) and calcification
▪ Thrombo-embolism may occur especially in AF patients

9. Pathophysiology
Degree of mitral stenosis Mean gradient Mitral valve area
Progressive mitral stenosis <5 mmHg >1.5 cm2
Severe mitral stenosis 5 - 10 mmHg 1.0 - 1.5 cm2
Very severe mitral stenosis > 10 mmHg < 1.0 cm2

10. Pathophysiology
Severe MS
↑ LA pressure
↑ Pulmonary arterial & venous wedge pressures
↓ Pulmonary compliance
Exertional dyspnea

11. Pathophysiology

12. Pathophysiology
▪ Cardiac output:
▪ Severe MS → Normal CO, ↓ rise during exertion
▪ Very severe MS → ↓ at rest, ↓ rise or ↓ CO on exertion
▪ Pulmonary Hypertension (↑):
▪ Causes:
1. Backward transmission of LA pressure
2. ‘Second stenosis’ → PA constriction secondary to ↑ LA & PV pressure
3. Interstitial edema of pulmonary vessel walls
4. End stage obliterative changes in pulmonary vascular bed
▪ Pul. HTN leads to RV enlargement, secondary TR, PR & Rt. Heart failure

13. Clinical Features

14. Symptoms
▪ Duration:
▪ Initial attack of rheumatic carditis to MS symptoms → 20 years
▪ Smaller interval around 10 years in tropical & developing countries
▪ Common presentation in fourth decade of life
▪ Dyspnea & cough
▪ Precipitated by exertion
▪ ↑ severity of MS → Easier precipitation, PND develops
▪ Atrial fibrillation (AF) may develop

15. Symptoms (contd.)
▪ Hemoptysis:
▪ Due to pulmonary venous hypertension
▪ Recurrent pulmonary emboli
▪ Important cause of morbidity and mortality
▪ Recurrent pulmonary infections
▪ Especially in winters
▪ Pulmonary changes:
▪ Fibrosis of capillary & alveoli walls
▪ ↓ Vital capacity, TLC, O2 uptake, compliance (with ↑capillary pressure)

16. Symptoms (contd.)
▪ Thrombo-embolism:
▪ Thrombi formed in LA, especially in enlarged atrial appendage
▪ 10-20% incidence
▪ High risk in patient with AF, age > 65, ↓ cardiac output
▪ Important cause of morbidity & mortality

17. Physical Findings
▪ Inspection & Palpation:
▪ Face:
▪ Malar flush & pinched blur facies → Severe MS
▪ JVP:
▪ If P. HTN + or TS + → prominent ‘a’ waves
▪ Enlarged RV → Parasternal lift
▪ Diastolic thrill rarely at cardiac apex in left lateral position

18. Physical Findings (contd.)
▪ Auscultation:
▪ S1 accentuated and slightly delayed in early stages
▪ P2 of S2 prominent, close split
▪ Opening Snap (OS) of mitral valve readily audible, at apex
▪ Interval between A2 & OS inversely related to severity of
MS.
More severe MS ≫ earlier OS

19. Murmur

20. Physical Findings (contd.)
▪ Diastolic murmur
▪ Low-pitched, rumbling diastolic murmur
▪ Follows OS
▪ Best heard at apex in left lateral position
▪ Accentuated with mild exercise
▪ Correlates with severity (in preserved CO)
▪ Has pre-systolic accentuation (increased before S1)
▪ Better heard with bell of stethoscope
▪ Other murmurs of associated valve disorders may be heard
▪ May be absent in ↓CO (Silent MS)

21. Physical Findings (contd.)
▪ Other organs:
▪ Hepatomegaly, ankle edema, ascites, and pleural effusion,
particularly in the right pleural cavity, may occur in patients
with MS and RV failure.
▪ Associated lesions:
▪ Sev. Pul. HTN → functional TR → Pansystolic murmur
(along left sternal border)
▪ Louder during inspiration,
disappears during forced expiration → Carvallo sign
▪ MS + Sev. Pul. HTN high-pitched, diastolic, decrescendo
blowing murmur along the left sternal border (Graham Steell
mumur of PR)

22. Laboratory Examination
▪ ECG:
▪ P wave suggests
LA enlargement
▪ If Pul. HTN develops:
▪ RA enlargement
▪ RV hypertrophy &
Rt. Axis deviation
may be seen

23. Laboratory Examination
▪ Echocardiography:
▪ Gives mitral valve area, severity of MS
▪ Also gives LV, RV function, chamber sizes & PA
systolic pressure
▪ Chest X-ray:
▪ Earliest change is flattening of upper left heart
border.
▪ Prominence of main PAs, upper lobe PVs, and
esophagus diaplcement by enlarged LA
▪ Kerley B lines (due to prominent lymphatics) may
be seen if LA pressure > 20 mmHg

24. Differential Diagnosis

25. Heart Murmurs in various
conditions

27. Differential Diagnosis
▪ Severe MR
▪ Also has diastolic murmur at apex but no OS or prominent P2
▪ S3 will be present
▪ LV will be enlarged
▪ Severe AR
▪ Austin-Flint murmur → short mid-diastolic murmur at apex
▪ No pre-systolic accentuation, ↓ on amyl nitrite
▪ TS
▪ Diastolic murmur increases with inspiration, delayed y descent in
JVP

28. Differential Diagnosis
▪ ASD
▪ Both ASD & MS may have RV enlargement
▪ But in ASD there will be no LA enlargement, Kerley B lines
▪ ASD will have fixed S2 split & a mid-systolic murmur over left sternal
border
▪ Left atrial myxoma
▪ Can cause mechanical obstruction mimicking MS
▪ Will have systemic symptoms like weight loss, fever, ↑IgG & ↑IL-6
▪ Auscultatory findings change with body position
▪ Echo shows a mass

29. Treatment

30. Treatment
▪ Penicillin prophylaxis of group A β-hemolytic streptococcal
infections for secondary prevention of rheumatic fever is
important for at-risk patients with rheumatic MS
▪ Infective endocarditis prophylaxis
▪ Asymptomatic patients don’t need any treatment.
▪ Symptomatic rx:
▪ ↓ Sodium intake
▪ Oral diuretics

31. Treatment
▪ Management of AF:
▪ Rate control → Beta blockers, Non-DHP CCBs, digitalis
▪ Warfarin therapy with INR maintained at 2-3
▪ Direct oral anticoagulants not yet approved
▪ Cardioversion after 3 weeks of Warfarin or TTE thrombus
clearance & heparin.

33. Mitral Valvotomy
▪ Percutaneous or surgical
▪ Percutaneous → PMBV
(Percutaneous mitral balloon valvuloplasty)
▪ Results same as surgical but lesser peri-procedural
complications
▪ Mitral valve replacement (MVR) is indicated in patients with
associated significant MR

35. Mitral Regurgitation

37. Etiology

38. Pathophysiology
▪ May be acute or chronic
▪ Acute MR:
▪ High LA pressure
▪ Pulmonary edema
▪ Chronic MR
▪ Dilated LA with normal pressure
▪ LV also enlarges (ventricular remodelling)
▪ Total stroke volume increases

39. Clinical Features

40. Symptoms
▪ Chronic Mild to Moderate → Asymptomatic
▪ Chronic severe MR
▪ Fatigue, exertional dyspnea, orthopnea
▪ If AF develops → palpitations
▪ If Pul HTN present → Right-sided heart failure, painful hepatic
congestion, ankle edema, distended neck veins, ascites, secondary
tricuspid regurgitation (TR)
▪ Acute severe MR → Acute pulmonary edema

41. Auscultation
▪ Characteristic Holosystolic murmur is present
▪ Most prominent at apex, radiates to axilla
▪ Increased in handgrip, reduced in Valsalva (d/t ↓LV preload)
▪ S1 absent or soft or buried in the murmur
▪ S3 present due to sudden tensing of papillary muscles & leaflets
▪ Mid-diastolic murmur may be present even without MS
▪ Acute severe MR → S4 may be heard
▪ Acute severe MR → Holosystolic murmur is decrescendo

43. Laboratory Examination
▪ ECG:
▪ LA enlargement seen
▪ RA enlargement if significant
pul. HTN
▪ AF is frequently associated

44. Laboratory Examination
▪ Echocardiography:
▪ LV function can be assessed. MR jet area and
intensity can be seen
▪Chest X-ray:
▪ LA enlargement on left heart border
▪ Calcification of mitral annulus can be seen
especially in lateral view
▪ Acute severe MR → Pulmonary edema

45. Treatment

46. Medical Management
▪ Management of AF
▪ Warfarin or Direct acting anticoagulants
▪ Cardioversion
▪ Antibiotic prophylaxis for Infective endocarditis
▪ Acute severe MR
▪ Urgent stabilisation & preparation for surgery
▪ Diuretics, vasodilators (esp. sod. nitroprusside)

48. Surgical Management
▪ Two types:
▪ Mitral valve repair
▪ Mitral valve replacement
▪ Repair has lower risk
▪ Indicated for symptomatic patients.
▪ Minimally invasive - Transcatheter mitral valve repair &
replacement is also available.

49. Thank you