''Mitral stenosis updates'' ''Notes on Mitral stenosis'' ''Questions regarding Mitral stenosis'' ''Echocardiographic findings for mitral stenosis'' ''Investigations for mitral stenosis'' ''Treatment for mitral stenosis'' ''Mitral stenosis in pregnancy and its treatment'' ''Cath findings in MS'' ''CXR in MS''

1. MITRAL STENOSIS
DR. ISHAABDULLAH ALI
REGISTRAR & SPECIALIST
DEPARTMENT OF CARDIOLOGY
IBRAHIM CARDIAC HOSPITAL & RESEARCH INSTITUTE

2. MITRAL STENOSIS
• A 25-YEAR-OLD LADY PRESENTED WITH MITRAL STENOSIS? POSSIBILITIES?
-RHEUMATIC
-CONGENITAL
-SLE
• A 60-YEAR-OLD MAN PRESENTED WITH MITRAL STENOSIS? POSSIBILITIES?
- RHEUMATIC
- DEGENERATIVE

3. MITRAL STENOSIS
• CAUSES OF MITRAL STENOSIS?
-RHEUMATIC
-CONGENITAL (DYSPLASIA/PARACHUTE MITRAL VALVE/SUPRAVALVULAR RING)
-MAC
-CARCINOID HEART DISEASE
-SLE, RA
-MUCOPOLYSACCHARIDOSES
-ENDOCARDIAL FIBROELASTOSIS, HEALED ENDOCARDITIS
-RADIATION INDUCED
-RESTRICTIVE MITRAL VALVE REPAIR FOR MR
- DRUG INDUCED (ANOREXIGENS (FENFLURAMINE, DEXFENFLURAMINE, AND THEIR ACTIVE METABOLITE
NORFENFLURAMINE), DOPAMINE AGONISTS (PERGOLIDE AND CABERGOLINE), MDMA, ERGOTALKALOIDS
(ERGOTAMINE, METHYSERGIDE)

4. COMPONENTS OF MV APPARATUS:
• ANNULUS
• TWO UNEQUAL LEAFLETS — AMLAND PML
• CHORDAE TENDINEAE
• TWO PAPILLARY MUSCLES (PM) — LATERAL AND MEDIAL
• ADJACENT LEFT VENTRICULAR MUSCLES

5. PATHOGENESIS:
BHS SORE THROAT : ARF — CARDITIS — VALVULITIS:
*CUSPS: FIBROUS THICKENING, SHORTENING & RETRACTION
*COMMISSURAL FUSION: NARROWING OF PRIMARY ORIFICE
*FISH MOUTH APPEARANCE OF MV ORIFICE (PSAXVIEW)
*DIASTOLIC DOMIN OF AML — RESTRICTED LEAFLET MOTION
*CHORDAE: FUSION, THICKENING, RETRACTION
*COMBINED: CALCIFICATION OF LEAFLETS, CHORDAE,COMMISSURES

6. PATHOGENESIS:
• < 3% OF STREPTOCOCCAL SORETHROAT CAUSES ARF
• > 50% PATIENTS SUFFER FROM CARDITIS CLINICALLY
• 50% CARDITIS PATIENTS DEVELOP RHD
• 50% OF PATIENTS GIVE NO PAST H/O RF
• MV AFFECTED IN > 90% CASES, THEN AV, TV, RARELY PV

7. PATHOPHYSIOLOGY
• NORMAL MVA IS 4.0 TO 5.0CM2
• WHEN MVA IS < 50% OF NORMAL OR < 2CM2’, IT IS MS
• IN DIASTOLE, LA & LV FUNCTION AS A COMMON CHAMBER
• IN MS,A GRADIENT DEVELOPS ACROSS MV (MEAN * 4 )
• LAP EXCEEDS LVPAND GRADUALLY AS MS WORSEN
• RETROGRADE TRANSMISSION OF LAP INTO P. VEIN CAUSES PULMONARY CONGESTIONAND
INTERSTITIALEDEMA
• P. VENOUS HTN - REACTIVE PAH- RVH- RV FAILURE

8. SYMPTOMS
• ASYMPTOMATIC (MILD MS)
• EXERTIONAL DYSPNEA/DYSPNEA AT REST/PND/ORTHOPNEA
• FATIGUE
• PALPITATIONS (DUE TO AF, INCIDENCE OF AF>40%)
• CHEST PAIN (DUE TO PAH AND RVH, INCIDENCE – 15%)
• HEMOPTYSIS
• HOARSENESS OF VOICE
• DYSPHAGIA
• MAY PRESENT WITH OTHER COMPLICATIONS…

9. SIGNS
• APPEARANCE: MALAR FLUSH (DUE TO REDUCED CO AND VASOCONSTRICTION)
• PULSE: MAY BE NORMAL / LOW VOLUME/ REGULAR / IRREGULARLY IRREGULAR
• BP: NORMAL / LOW
• JVP: NORMAL / RAISED WITH PROMINENTA (IF PULMONARY HTN), PROMINENT V IF ASSOCIATED WITH TR, ABSENT
A (IF PATIENT IS IN AF)
• PRECORDIUM: INSPECTION: VISIBLE APICAL IMPULSE, VISIBLE EPIGASTRIC PULSATION, ANY SCAR MARK
(CMC/OMC/MVR), PALPATION: APEX BEAT NORMALLY LOCATED, TAPPING APEX BEAT, APICAL DIASTOLIC THRILL,
LEFT PARASTERNAL HEAVE (RVH), EPIGASTRIC PULSATION (RVH), PALPABLE P2 (PAH), AUSCULTATION: LOUD S1,
LOUD P2, OPENING SNAP (+/-), LLRR MDM AT APICALAREA BEST HEARD WITH THE BELL OF STETHOSCOPE IN LEFT
LATERAL POSITION, BREATHING HOLD AFTER EXPIRATION WITH/WITHOUT PRESYSTOLIC ACCENTUATION, PSM IF
ASSOCIATED WITH TR, EDM (GRAHAM STEEL MURMUR) IF ASSOCIATED WITH PR
• LUNGS: BILATERAL FINE CREPS (PULMONARY EDEMA), COARSE CREPS/BRONCHIAL (ASSOCIATED RTI)
• ABDOMEN: TENDER HEPATOMEGALY, SPLENOMEGALY, ASCITES (IF PRESENTED WITH CCF)
• LEG EDEMA / DEPENDENT EDEMA
• CNS: EVIDENCE OF STROKE
• ANY EVIDENCE OF PERIPHERAL VASCULAR DISEASE

10. • WHY MALAR FLUSH?
-DUE TO AV ANASTOMOSIS AND VASCULAR STASIS ON CHEEKS
• IS IT PATHOGONOMIC?
-NO, MAY BE FOUND IN NORMAL, HYPOTHYROIDISM, POLYCYTHAEMIA
• HALLMARK OF MITRAL STENOSIS?
- LOUD S1 OVER APEX, OPENING SNAP?
• MECHANISM OF PULMONARY HYPTERTENSION IN MS?
-PASSIVE BACKWARD TRANSMISSION OF RAISED LA PRESSURE, REFLEX PULMONARYARTERIAL
VASOCONSTRICTION, ORGANIC OBLITERATIVE CHANGE IN PULMONARY VASCULAR BED
• WHY HEMOPTYSIS?
- DUE TO RUPTURE OF PULMONARY / BRONCHIAL VEINS WITH PHTN (PULMONARYAPOPLEXY)
- DUE TO PULMONARY INFACRTION
- ASSOCIATED WITH PNEUMONIA
- PINK FROTHY SPUTUM DUE TO RUPTURE OF ALVEOLAR CAPILLARIES

11. • WHY SYNCOPE IN MS?
-DUE TO LOW CARDIAC OUTPUT, IF ASSOCIATED WITH AF WITH FVR, PHTN, PULMONARY EMBOLISM,
CEREBRAL EMBOLISM, BALL VALVE THROMBUS
• COMPLICATIONS OF MS?
-AF, PULMONARY EDEMA, CCF, PULMONARY INFARCTION, SYSTEMIC EMBOLISM ORTNER’S SYNDROME,
DYSPHAGIA, ILD, IE (RARE)
• WHY HOARSENESS OF VOICE?
- DUE TO COMPRESSION ON RECURRENT LARYNGEAL NERVE BY ENLARGED LA / PULMONARY ARTERY
• WHY PND IN MS?
-REDISTRIBUTION OF FLUID TO CENTRE AND WITHDRAWL OF GRAVITY
-DURING SLEEP, COUGH REFLEX WORKS LESS
-DURING SLEEP, RESPIRATORY CENTER WORKS LESS
-DURING SLEEP, RESPIRATORY DRIVE REDUCES
DURING SLEEP, DIAPHRAGM RAISES, VITAL CAPACITY REDUCES
DURING SLEEP, HIGH INTRAABDOMINAL PRESSURE COMPRESSES THE LIVER – MORE BLOOD GOES TO
THE LUNGS – MORE VENOUS RETURN

12. • WHY CHEST PAIN IN MS?
-DUE TO PHTN AND MITRAL VALVE OBSTRUCTION – REDUCTION IN CO- REDUCES CORONARY
CIRCULATION
-RVH PRODUCES RELATIVE ISCHAEMIA
-PULMONARY INFARCTION
-ASSOCIATED CAD
-CORONARY ARTERY EMBOLISM (DUE TO LA THROMBUS / VEGETATION)
• WHEN HIGH BP IN MS?
-WHEN THERE IS THROMBOEMBOLISM IN RENAL ARTERY
• MECHANISM OF LOUD S1?
- SUDDEN CLOSURE OF WIDELY APART PLIABLE MITRAL VALVE LEAFLETS AGAINST HIGH LA
PRESSURE DURING VENTRICULAR SYSTOLE
• MECHANISM OF OPENING SNAP?
-SUDDEN OPENING OF TENSE AND PLIABLE MITRAL VALVE UNDER HIGH LA PRESSURE

13. • DD OF OPENING SNAP?
-SPLITTING S2
-S3
-PERICARDIAL KNOCK
• CHARACTER OF OPENING SNAP IN MS?
-HIGH FREQUENCY DIASTOLIC SOUND, COMES AFTER S2 (0.03-0.08 SECONDS), BEST HEARD WITH
DIAPHRAGM OF STETHOSCOPE BETWEEN APEX AND LOWER LEFT PSA, DOESNOT CHANGE IN
INTENSITY WITH RESPIRATION (TRANSMITRAL GRADIENT SHOULD BE MORE THAN 10 MMHG)
• RELATIONSHIP OF OS WITH AF, HEART FAILURE AND CALCIFICATION IN MS?
- IN AF AND HF – OPENING SNAP PERSISTS
- IN CALCIFICATION – OPENING SNAP DISAPPEARS
• RELATIONSHIP OF PRESYSTOLIC ACCENTUATION WITHAF IN MS?
-IN AF , PRESYSTOLIC ACCENTUATION DISAPPEARS

14. • DIFFERENTIATE OPENING SNAP FROM SPLITTING S2?
-OS – LOWER LEFT STERNAL EDGE, RADIATION TO ALL AREAS, DOESNOT CHANGE WITH
RESPIRATION
-SPLITTING S2 – LEFT 2ND ICS, RADIATION TO LEFT STERNAL EDGE, CHANGES WITH RESPIRATION
• HOW DO YOU UNDERSTAND PLIABILITY OF MITRAL VALVE CLINICALLY?
- LOUD S1, OPENING SNAP PRESENT, NOT ASSOCIATED WITH MR
• WHEN OS IS ABSENT IN MS?
- IF VALVE CUSPS ARE FIBROSED AND CALCIFIED, MILD MS (WHEN TRANSMITRAL GRADIENT<
5MMHG), VERY TIGHT MS, IF MS ASSOCIATED WITH MR
• WHAT IS SILENT MS?
-IN SEVERE MS, THERE IS NO MDM – IT IS THEN CALLED SILENT MS
• CAUSES OF MDM?
-MS, TS, ASD, VSD, PDA, SEVERE MR, CAREY COMB’S MURMUR (RF), AUSTIN FLINT (AR), BALL
VALVE THROMBUS, MAC, COR TRIATRAITUM, PARACHUTE MITRAL VALVE

15. • ADVERSE SITUATIONS FACED IN PREGNANT PATIENTS WITH MS?
-1ST TRIMESTER – CHANCE OF ABORTION
-3RD TRIMESTER – CHANCE OF PREMATURE DELIVERY
• JUVENILE MS?
-PURE OR PREDOMINANT MS OF RHEUMATIC ORIGIN UNDER THE AGE OF 20 YEARS
• HOW DO YOU CLINICALLY ASSESS A PATIENT FOR PTMC?
-LOUD S1
-OPENING SNAP PRESENT
-NO SYSTOLIC MURMUR AT THE APEX
• INDICATIONS OF OMC?
-VALVE MORPHOLOGY SUITABLE FOR PTMC / CMC BUT PERSISTENCE OF LA THROMBUS DESPITE
ADEQUATE ANTICOAGULANT THERAPY

16. • AUSCULTATORY FINDINGS AFTER PTMC/CMC?
-S1 - LOUD
-S2: LOUDNESS OF P2 DECREASED.
-ABSENCE OF OS OR THE DISTANCE BETWEEN P2 — OS IS INCREASED
-PSA IS SOFT/ABSENT IF SINUS RHYTHM IS PRESENT
-THE DURATION OF THE MDM IS LESS AND THE MURMUR IS LOW PITCHED. MURMUR MAY
DISAPPEAR EVEN
• WHAT ARE MITRAL VALVE REPAIR TECHNIQUES?
-CHORDOTOMY
-COMMISSUROTOMY
-CHORDAL RESECTION AND SHORTENING
-ANNULOPLASTY

17. INVESTIGATIONS

18. INVESTIGATIONS
• ECG
• CXR
• ECHOCARDIOGRAPHY
• CARDIAC CATHETERIZATION

19. ECG
• P MITRALE, RVH, RAE, AF WITH FVR, SINUS TACHYCARDIA, DIGOXIN EFFECT (IF ON DIGOXIN)

20. CHEST XRAY
• UPPER LOBE DIVERSION,
• STRAIGHTENING OF LEFT HEART BORDER,
• PULMONARY CONUS FULL,
• PROMINENT LAAPPENDAGE,
• PROMINENT RV APEX,
• DOUBLE RIGHT BORDER (DUE TO LA ENLARGEMENT),
• HORIZONTAL LEFT PRINCIPAL BRONCHUS,
• CARDIOMEGALY IF ASSOCIATED MR,
• PULMONARY EDEMA, PLEURAL EFFUSION,
• PULMONARY EMBOLISM,
• PULMONARY INFARCTION,
• HEMOSIDEROSIS,
• VALVULAR CALCIFICATION

22. ECHOCARDIOGRAPHY

23. ECHOCARDIOGRAPHY
PLAX VIEW: MITRAL VALVE LEAFLETS ARE THICKENED, ECHOGENIC WITH RESTRICTED
MOVEMENT. CALCIFICATION MAY BE SEEN (STARTS FROM THE TIP). DIASTOLIC DOMING OF AML
GIVING RISE TO HOCKEY STICK APPEARANCE. FLAG STAND APPEARANCE OF PML. LA-DILATED. LV-
SMALL. THROMBUS OR SEC IN LA. RVOT ENLARGEMENT IN PHTN.

24. ECHOCARDIOGRAPHY
M-MODE: (AT THE TIP OF MITRAL VALVE LEAFLETS): BOTH LEAFLETS ARE THICKENED (DUE TO
FIBROSIS), REDUCED EF SLOPE OF AML (DUE TO HIGH PRESSURE IN LA), DIASTOLIC ANTERIOR
MOTION OF PML (DUE TO COMMISSURAL FUSION)

25. ECHOCARDIOGRAPHY
PSAX VIEW AT MITRAL VALVE LEVEL: MVA BY PLANIMETRY (MID DIASTOLE). MVA REDUCED,
COMMISSURAL FUSION WITH RESTRICTED OPENING GIVING RISE TO FISH MOUTH APPEARANCE /
BUTTON HOLE APPEARANCE.
COMMISURAL FUSION – HALLMARK OF RHEUMATIC
MS.

26. • HOW DO YOU FIND OUT MITRAL VALVE AREA?
- PLANIMETRIC METHOD
- PRESSURE-HALF TIME METHOD
- CONTINUITY EQUATION
- PISA
• RHEUMATIC MS VS DEGENERATIVE MS?
-RHEUMATIC MS – MAIN MECHANISM IS COMMISSURAL FUSION. CALCIFICATION STARTS FROM
THE TIP
-DEGENERATIVE MS – MAIN MECHANISM IS ANNULAR CALCIFICATION

27. ECHOCARDIOGRAPHY
PSAX VIEW AT GREAT VESSEL LEVEL: THROMBUS IN LAA OR LA

28. MANJUNATH CLASSIFICATION

29. ECHOCARDIOGRAPHY
PSAX VIEW AT GREAT VESSEL LEVEL: LOSS OF A-DIP, REDUCED EF SLOPE, MID-SYSTOLIC NOTCH
(PULMONARY HYPERTENSION) – FLYING W SIGN

30. ECHOCARDIOGRAPHY
APICAL 4 CHAMBER VIEW: LA, RA AND RV DILATED.
COLOUR DOPPLER: MOSAIC FLOW ACROSS MITRAL VALVE WITHIN THE LV DURING DIASTOLE
(CANDLE FLAME APPEARANCE)

31. ECHOCARDIOGRAPHY
SPECTRAL DOPPLER: VELOCITY AND GRADIENT ACROSS MITRAL VALVE IS INCREASED.
MVA CALCULATION BY PRESSURE HALF TIME.
MVA = 220/PRESSURE HALF-TIME
IN AF, AVERAGE OF 3-5 CYCLES

32. ECHOCARDIOGRAPHY
• MVA MEASUREMENT BY PRESSURE HALF TIME METHOD: NOT RECOMMENDED IN IMMEDIATE
POST VALVOTOMY, SIGNIFICANT MR
• FALLACIES IN MEASURING MV AREA BY PLANIMETRY ARE:
– POOR VISUALIZATION OF MV ORIFICE
– HEAVY CALCIFICATION OF LEAFLETS
– SIGNIFICANT SUBVALVULAR DISEASE
– PRIOR COMMISSUROTOMY PROCEDURE
– LOW CARDIAC OUTPUT CONDITION

33. ECHOCARDIOGRAPHY
MORPHOLOGICAL ASSESSMENT OF MITRAL VALVE:
• ABASCAL ECHOCARDIOGRAPHIC SCORE / WILKIN SCORE (PTMC FAVOURABLE IF SCORE < 8)
• CORMIER SCORE
• 2DE SCORE BY CHEN ET AL. (MODIFIED WILKINS SCORE PARAMETER FOR SUBVALVULAR
THICKENING ACCORDING TO THE INVOLVED SEGMENT OF CHORDAL LENGTH)
• REID SCORE
• NOBUYOSHI SCORE
• NEW RT3DE MORPHOLOGY SCORE

34. MORPHOLOGICAL ASSESSMENT:

36. LIMITATIONS OF WILKIN SCORE
• ECHOCARDIOGRAPHY LIMITED IN ABILITY TO DIFFERENTIATE NODULAR FIBROSIS FROM CALCIFICATION.
• ASSESSMENT OF COMMISSURAL INVOLVEMENT IS NOT INCLUDED OR UNDERESTIMATED.
• DOESN’TACCOUNT FOR UNEVEN DISTRIBUTION OF PATHOLOGIC ABNORMALITIES.
• DOESN’TACCOUNT FOR RELATIVE CONTRIBUTION OF EACH VARIABLE (NO WEIGHTING OF VARIABLES).
• FREQUENT UNDERESTIMATION OF SUB VALVULAR DISEASE.
• DOESN’T USE RESULTS FROM TEE OR 3D ECHOCARDIOGRAPHY.

37. MORPHOLOGICAL ASSESSMENT:

38. ECHOCARDIOGRAPHY
• MVA MEASUREMENT CAN BE DONE BY 3D ECHOCARDIOGRAPHY
• ASSESSMENT OF PULMONARY HYPERTENSION

39. TOE
• THE MOST FREQUENT USE OF TOE IS TO EXCLUDE LA OR LAA THROMBUS IF A PATIENT
SUSTAINS AN EMBOLIC EVENT OR IS CONSIDERED FOR MITRAL BALLOON VALVULOPLASTY (TO
GUIDE TRANSSEPTAL PUNCTURE OR FOR POSITIONING OF THE BALLOON DURING PTMC)

40. ECHOCARDIOGRAPHY
• STRESS ECHOCARDIOGRAPHY SHOULD BE CONSIDERED IN PATIENTS WHOSE SYMPTOMS ARE
INCONGRUENT WITH ECHOCARDIOGRAPHIC DATAAND FOR RISK STRATIFICATION OF PATIENTS
WITH MS.
• A TRANSMITRAL MEAN GRADIENT >15 MMHG DURING EXERCISE ECHOCARDIOGRAPHY (OR ≥18
MMHG DURING DOBUTAMINE ECHOCARDIOGRAPHY) SHOULD BE CONSIDERED
HEMODYNAMICALLY SIGNIFICANT RHEUMATIC MS AND IDENTIFIES PATIENTS WHO MIGHT
BENEFIT FROM INTERVENTION

41. CARDIAC CATHETERIZATION
CARDIAC CATHETERIZATION FOR HEMODYNAMIC EVALUATION SHOULD BE PERFORMED FOR
ASSESSMENT OF SEVERITY OF MITRAL STENOSIS WHEN NONINVASIVE TESTS ARE INCONCLUSIVE
OR WHEN THERE IS DISCREPANCY BETWEEN NONINVASIVE TESTS AND CLINICAL FINDINGS
REGARDING SEVERITY OF MITRAL STENOSIS.

42. CARDIAC CATHETERIZATION
Pressure tracings in the left atrium (LA) and the left ventricle (LV) in an individual with severe mitral stenosis. Blue areas
represent the diastolic pressure gradient due to the stenotic valve.

43. MANAGEMENT

44. MANAGEMENT
• MEDICAL – GENERAL, PHARMACOLOGIC
• INTERVENTION
• SURGICAL

45. MEDICAL MANAGEMENT
• RESTRICTION OF ACTIVITIES IN MODERATE TO SEVERE MS
• RHEUMATIC PROPHYLAXIS
• IF PULMONARY CONGESTION: DIURETICS, BETABLOCKER, ACI/ARB, DIGITALIS
• IF AF: RATE CONTROL, RHYTHM CONTROL, ANTICOAGULATION (WARFARIN)
RATE CONTROL: BETABLOCKER, RATE LIMITING CCB, DIGOXIN, AMIODARONE
ACUTE ONSET OF AF WITH FVR, ACUTE PULMONARY EDEMA, SHOCK – DC CARDIOVERSION
**NEITHER CARDIOVERSION NOR CATHETER PULMONARY VEIN ISOLATION ARE INDICATED
BEFORE INTERVENTION IN PATIENTS WITH SIGNIFICANT MITRAL STENOSIS, AS THEY DO NOT
DURABLY RESTORE SINUS RHYTHM

46. • INDICATIONS OF WARFARIN IN MS?
- ATRIAL FIBRILLATION
- PAST H/O THROMBOEMBOLISM
- LA/LAA THROMBUS
- SEC IN LA
- ENLARGED LA (LA>50/55/65MM)

47. INTERVENTION
• INDICATIONS OF PTMC/BMV (BALLOON MITRAL VALVULOTOMY)/ PMBC (PERCUTANEOUS
MITRAL BALLOON COMMISSUROTOMY) / PMC (PERCUTANEOUS MITRAL COMMISSUROTOMY):
- IN SYMPTOMATIC PATIENTS (NYHA CLASS II, III, OR IV) WITH SEVERE RHEUMATIC MS (MITRAL
VALVE AREA ≤1.5 CM2, STAGE D) AND FAVORABLE VALVE MORPHOLOGY WITH LESS THAN
MODERATE (2+) MR* IN THE ABSENCE OF LA THROMBUS, PMBC IS RECOMMENDED (CLASS I)
- IN ASYMPTOMATIC PATIENTS WITH SEVERE RHEUMATIC MS (MITRAL VALVE AREA ≤1.5 CM2,
STAGE C) AND FAVORABLE VALVE MORPHOLOGY WITH LESS THAN 2+ MR IN THE ABSENCE OF
LA THROMBUS WHO HAVE ELEVATED PULMONARY PRESSURES (PULMONARY ARTERY SYSTOLIC
PRESSURE >50 MM HG), PMBC IS REASONABLE (CLASS IIA)

48. INTERVENTION
• IN ASYMPTOMATIC PATIENTS WITH SEVERE RHEUMATIC MS (MITRAL VALVE AREA ≤1.5 CM2,
STAGE C) AND FAVORABLE VALVE MORPHOLOGY WITH LESS THAN 2+/ MR* IN THE ABSENCE
OF LA THROMBUS WHO HAVE NEW ONSET OF AF, PMBC MAY BE CONSIDERED (CLASS IIB)
• IN SYMPTOMATIC PATIENTS (NYHA CLASS II, III, OR IV) WITH RHEUMATIC MS AND AN MITRAL
VALVE AREA >1.5 CM2, IF THERE IS EVIDENCE OF HEMODYNAMICALLY SIGNIFICANT
RHEUMATIC MS ON THE BASIS OF A PULMONARY ARTERY WEDGE PRESSURE >25 MM HG OR
A MEAN MITRAL VALVE GRADIENT >15 MM HG DURING EXERCISE, PMBC MAY BE CONSIDERED
(CLASS IIB)
• IN SEVERELY SYMPTOMATIC PATIENTS (NYHA CLASS III OR IV) WITH SEVERE RHEUMATIC MS
(MITRAL VALVE AREA ≤1.5 CM2, STAGE D) WHO HAVE A SUBOPTIMAL VALVE ANATOMY AND
WHO ARE NOT CANDIDATES FOR SURGERY OR ARE AT HIGH RISK FOR SURGERY, PMBC MAY
BE CONSIDERED (CLASS IIB)

49. INTERVENTION
- PMC SHOULD BE CONSIDERED IN ASYMPTOMATIC PATIENTS WITHOUT UNFAVOURABLE
CLINICAL AND ANATOMICAL CHARACTERISTICSC FOR PMC AND: (CLASS IIA, ESC)
• HIGH THROMBOEMBOLIC RISK (HISTORY OF SYSTEMIC EMBOLISM, DENSE SPONTANEOUS
CONTRAST IN THE LA, NEW-ONSET OR PAROXYSMAL AF), AND/OR
• HIGH RISK OF HAEMODYNAMIC DECOMPENSATION (SYSTOLIC PULMONARY PRESSURE >50
MMHG AT REST, NEED FOR MAJOR NCS, DESIRE FOR PREGNANCY).

50. ESC 2021

51. ESC 2021

52. AHA 2020

54. BALLOON MITRAL VALVOTOMY (BMV/PTMC) RESULTS:
• MVAIS INCREASED BY > 50% OF INITIALAREA (MVA >1.5 CM2)
• DECREASE IN TRANS-MITRAL GRADIENT (50%-60%), LAPRESSURE < 18MM HG, CARDIAC OUTPUT
INCREASES BY 20%
• PULMONARY ARTERY PRESSURE IS ALSO REDUCED
• SUCCESSFUL BMV: (ACHIEVED IN > 80% OF PTS) DEFINED AS:
• MVA > 1.5CM2, NO MR OR MILD MR, MV GRADIENT IS REDUCED
• DURABLE FOR A DECADE OR MORE
*COMPLICATIONS OF BMV: STROKE, SIGNIFICANT MR, CARDIAC PERFORATION, CARDIAC
TAMPONADE (HEMOPERICARDIUM), ASD, ACCIDENTAL PERFORATION OF LV/ AORTA / CORONARY
SINUS, INFECTION, AF

55. PTMC:
• CHOICE OF TECHNIQUE OF PTMC?
- INOUE BALLOON TECHNIQUE
- DOUBLE BALLOON TECHNIQUE
- MULTITRACK TECHNIQUE
- METALLIC COMMISSUROTOMY
• INOUE BALLOON SIZE?
-24 MM, 26 MM, 28 MM, 30 MM
BALOON SIZE = PATIENTS HEIGHT (CM) / 10 + 10

56. PTMC:
• HOW DO YOU LOCALIZE IAS DURING PUNCTURE WHILE DOING PTMC?
- THE PLANE OF IAS RUNS FROM 1 O CLOCK TO 7 O CLOCK
• STRUCTURES THAT CAN GET PUNCTURED DURING PTMC?
- AORTA, LA ROOF, LA FREE WALL, LV FREE WALL, PULMONARY VEIN, RA FREE WALL
• CONTRAINDICATIONS FOR TRANSSEPTAL PUNCTURE?
-PATIENTS WHO CANNOT LIE FLAT
-ANTICOAGULANT THERAPY, LOW PLATELET COUNT
-LA/RA THROMBUS
-ATRIAL MYXOMA
-IVC MASS/OBSTRUCTION
-DISTORTED CARDIAC ANATOMY
-DILATED AORTIC ROOT
-MARKED LA ENLARGEMENT
-THORACIC SKELETAL DEFORMITY

57. ROLE OF ECHO DURING PTMC:
• GUIDE THE TRANSSEPTALPUNCTURE
• HELPS IN DETECTINGACUTE COMPLICATIONS
• ATRIALORVENTRICULARPERFORATIONWITHTAMPONADE ACUTE
MITRALREGURGITATION
• VALVULAR DISRUPTION
• ASSESSMENT OF VALVE AREAAFTER PTMC
**PLANIMETRY IS IDEAL, PRESSURE HALF TIME SHOULD NOTBE USED

58. PREGNANCY ISSUES AND MS
• SEVERE MS IS POORLY TOLERATED INPREGNANCY
• DURING PREGNANCY, BLOOD VOLUME IS INCREASED
• ATRANS-MITRALGRADIENT INCREASES SEVERAL FOLDS (2ND TRIMESTERONWARD)
• CO IS DECREASED, LAV AND LAP INCREASES— PULMONARY CONGESTION
• SYMPTOMATIC STATUS FOLLOWS THE “RULE OF ONE CLASS”
• THAT IS, SYMPTOMS INCREASES BY 1 NYHA CLASS INPREGNANCY
• THUS, CLASS 1 PATIENTS DEVELOP CLASS II, CLASS II CLASS III

59. PREGNANCY ISSUES AND MS
• SYMPTOMS REACHES THEIR PEAK AT 28-32 WGESTATION
• RISK REMAINS DURING LABORAND DELIVERYALSO — DUE TO INCREASED VENOUS
RETURNAND INCREASED BLOOD VOLUME:
• AS A RESULT OF UTERINE CONTRACTION DURING LABOR AND
• AUTOTRANSFUSION OF VENOUS RETURN FROM THE LOWER EXTREMITIES
AFTER DELIVERY (RELIEF OF GRAVID UTERINE COMPRESSION ON PELVIC
VEINS)

60. PREGNANCY ISSUES AND MS
INDICATIONS OF MEDICAL THERAPY:
• SYMPTOMATIC PATIENTS
• CLINICALLY SIGNIFICANT PH (PASP ≥ 50 MMHG)
FOLLOW-UP DURING PREGNANCY:
• MODERATE TOSEVERE MS: CLINICALAND ECHO
FOLLOW-UP — MONTHLY ORBIMONTHLY
• IN MILD MS: EVERY TRIMESTER PRIOR TODELIVERY

61. PREGNANCY ISSUES AND MS
MEDICAL THERAPY
• RESTRICTION OF PHYSICALACTIVITY
• BETA-1-SELECTIVEBLOCKERS (PREFERABLYMETOPROLOL OR BISOPROLOL)
• DIURETICS- WHEN CONGESTIVE SYMPTOMS PERSIST
• ANTICOAGULATION (UFH, LMWH OR VKA)
• ALLPATIENTSWITHSIGNIFICANTMSSHOULDBE COUNSELLED AGAINST
PREGNANCY

62. PREGNANCY ISSUES AND MS
• PRE-PREGNANCY:
• PTMC IS PREFERRED
• INTERVENTION IS RECOMMENDED BEFORE PREGNANCY IN PATIENTS WITH MS AND VALVE
AREA < 1 CM2 (CLASS I) OR < 1.5 CM2 (CLASS IIA)
• DURING PREGNANCY:
INDICATIONS OF PTMC:
• NYHA CLASS III/IV
• AND/PASP ≥ 50 MM HG, DESPITE OPTIMALMEDICAL TREATMENT IN THE ABSENCE OF
CONTRAINDICATIONS

63. PREGNANCY ISSUES AND MS
• TIMING:
• PTMC IS PREFERABLY PERFORMED AFTER 20 WEEKS OF GESTATION
• TECHNICAL ASPECTS:
• MINIMAL FLUOROSCOPY USE
• ECHO GUIDANCE
• STEPWISE DILATION TECHNIQUE
• USE OF PELVIC AND ABDOMINAL SHIELD

64. PREGNANCY ISSUES AND MS
VAGINAL DELIVERY-
•MILD MS
•SIGNIFICANT MS WITH NYHACLASS I/II WITHOUTSIGNIFICANT PH
•2ND STAGE OF LABOUR (CERVIX FULL DILATATION TO DELIVERY) SHOULD BE SHORTENED BY
ASSISTED VAGINALDELIVERY, EXAMPLE-EPISIOTOMY, FORCEPS, VENTOSE
CAESAREAN SECTION-
• PATIENTS WHOARE IN NYHACLASS III/IV OR HAVE PHAND PTMC CANNOT BE PERFORMED OR
HAS FAILED

65. PREGNANCY ISSUES AND MS
• WARFARIN USE IS CONTRAINDICATED DURING 1ST TRIMESTER BECAUSE OF THE RISK OF
EMBRYOPATHY
• NOT USED IN LAST 2-3 WEEKS (BLEEDING RISK DURING LABOR)
• ANTICOAGULATION PROTOCOL:
• FIRST TRIMESTER- HEPARIN (ENOXAPARIN)
• FROM 2ND TRIMESTER UP TO36 WEEKS — WARFARIN
• FROM 36 W TO 12 HOURS BEFORE LABOR- AGAIN HEPARIN
• INR - 2.5 (RANGE 2 — 3)

66. PREGNANCY ISSUES AND MS
• SURGERY IN MS
• INDICATIONS FOR SURGERY:
• SYMPTOMATIC PATIENTS (NYHA CLASS III-IV) WHENPTMCISUNAVAILABLE OR
CONTRAINDICATED
-CLOSED MITRAL COMMISSUROTOMY(CMC)
-OPEN MITRAL COMMISSUROTOMY(OMC)
-MITRAL VALVE REPLACEMENT (MVR)

67. THANK YOU