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M I T R A L V A L V E
D I S E A S E
D E P A R T M E N T O F C A R D I A C A N D V A S C U L A R S U R G E R Y
M E D I C A L U N I V E R S I T Y P L O V D I V
H R I S T O R A H M A N
M I T R A L R E G U R G I T A T I O N
N A T U R A L H I S T O R Y
ā€¢ ASYMPTOMATIC PATIENTS HAVE LONG LATENT
PERIOD BEFORE ONSET OF SYMPTOMS
ā€¢ CHRONIC MR - WELL TOLERATED IF LV
FUNCTION IS WELL PRESERVED
M I T R A L R E G U R G I T A T I O N
N A T U R A L H I S T O R Y
ā€¢ POOR PROGNOSTIC FEATURES OF MR:
ā€¢ - SYMPTOMS >1 YEAR;
ā€¢ - ATRIAL FIBRILLATION;
ā€¢ - AGE >60 YEARS;
ā€¢ - EF <50%
ā€¢ - LVEDV >100 mL/m2; LVESV >60 mL/m2;
ā€¢ - LVESD >5 cm; LVEDD >7cm
M I T R A L R E G U R G I T A T I O N
P A T H O P H Y S I O L O G Y
ā€¢ CHRONIC LV VOLUME OVERLOAD ASSOCIATED WITH MR
LEADS TO LV HYPERTROPHY
ā€¢ STROKE VOLUME INITIALLY MAINTAINED BY THE FRANK-
STARLING MECHANISM
ā€¢ EVENTUALLY LV CONTRACTILE FUNCTION DECLINES
PRODUCING:
ā€¢ - INCREASED LVESV;
ā€¢ - RAISED LV FILLING PRESSURES;
ā€¢ - RAISED LA AND PULMONARY FILLING PRESSURES;
R E S U L T
I N R E S U L T
P U L M O N A R Y
O E D E M A
&
C H F
M I T R A L R E G U R G I T A T I O N
P A T H O P H Y S I O L O G Y
ā€¢ ONCE LV EJECTION FRACTION FALLS BELOW
APPROX. 60%, LV SYSTOLIC DYSFUNCTION IS
ALMOST CERTAINLY PRESENT AS SOME OF THE
EJECTED VOLUME FLOWS BACK INTO LA (
AFTERLOAD-REDUCING EFFECT OF MR)
M I T R A L R E G U R G I T A T I O N
C L A S S I F I C A T I O N
ā€¢ CARPENTIERā€™S FUNCTIONAL CLASSIFICATION
D Y S F U N C T I O N L E S I O N
T Y P E I
N O R M A L L E A F L E T
M O T I O N
A N N U L A R D I L A T A T I O N ,
L E A F L E T P E R F O R A T I O N
T Y P E I I
E X C E S S L E A F L E T
M O T I O N
M YX O M A T O U S
D E G E N E R A T I O N ,
C H O R D A L R U P T U R E
T Y P E I I I
R E S T R I C T E D L E A F L E T
M O T I O N
I I I A R E S T R I C T E D O P E N I N G R H E U M A T I C F E V E R
I I I B R E S T R I C T E D C L O S U R E I S C H A E M I C C A R D I O M YO P A T H Y
M I T R A L R E G U R G I T A T I O N
C L A S S I F I C A T I O N
ā€¢ CARPENTIERā€™S FUNCTIONAL CLASSIFICATION
T Y P E I
N O R M A L L E A F L E T M O T I O N
C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
T Y P E I I
E X C E S S L E A F L E T M O T I O N
C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
T Y P E I I
E X C E S S L E A F L E T M O T I O N
C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
T Y P E I I I A ( D I A S T O L I C )
R E S T R I C T E D L E A F L E T O P E N I N G
C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
T Y P E I I I B ( S Y S T O L I C )
R E S T R I C T E D L E A F L E T C L O S U R E
C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
W H A T A R E T H E C A U S E S O F
C H R O N I C M I T R A L R E G U R G I T A T I O N ?
ā€¢ 1. MYXOMATOUS DEGENERATION ( TYPE II )
ā€¢ 2. RHEUMATIC FEVER ( TYPE IIIA )
ā€¢ 3. ISCHAEMIC CARDIOMYOPATHY ( TYPE IIIB & TYPE I
)
1 2 3
+
W H A T A R E T H E C A U S E S O F
A C U T E M I T R A L R E G U R G I T A T I O N ?
ā€¢ 1. CHORDAL RUPTURE ( TYPE II )
ā€¢ 2. INFECTIVE ENDOCARDITIS ( TYPE I )
ā€¢ 3. PAPILLARY MUSCLE RUPTURE AFTER MI ( TYPE II
)
1 & 3 2
I N F E C T I V E
E N D O C A R D I T I S
T Y P E I
N O R M A L L E A F L E T M O T I O N
E T I O L O G Y
I S C H A E M I C M I T R A L R E G U R G I T A T I O N
ā€¢ ACUTE
ISCHAEMIC MR
IS USUALLY
CAUSED BY:
ā€¢ - INFARCTED;
ā€¢ - RUPTURED;
ā€¢ - NON-RUPTURED
PAPILLARY
MUSCLE
T Y P E I I
E X C E S S
L E A F L E T
M O T I O N
E T I O L O G Y
I S C H A E M I C M I T R A L R E G U R G I T A T I O N
ā€¢ CHRONIC ISCHAEMIC
MR IS CAUSED BY:
ā€¢ COMBINATION OF:
ā€¢ - RESTRICTED MOVEMENT OF
P2 & P3 SCALLOPS OF
POSTERIOR MITRAL VALVE
LEAFLET (PML) DUE TO
VENTRICULAR DILATATION
DISPLACING PAPILLARY
MUSCLES;
ā€¢ - FUNCTIONAL DILATATION OF
MITRAL VALVE ANNULUS
C O M B I N A T I O N O F :
T Y P E I I I B + T Y P E I
R E S T R I C T E D
C L O S U R E
+
N O R M A L L E A F L E T
M O T I O N
E T I O L O G Y
I S C H A E M I C M I T R A L R E G U R G I T A T I O N
ā€¢ REDUCED CONTRACTION OF MV ANNULUS
ā€¢ +
ā€¢ REDUCED VENTRICULAR CLOSING FORCES ON
MV DUE TO POOR LV FUNCTION
ā€¢ = CONTRIBUTE TO ISCHAEMIC MR
S Y M P T O M S
M I T R A L R E G U R G I T A T I O N
ā€¢ MR IS PROGRESSIVE DISEASE AND PATIENTS
CAN BE ASYMPTOMATIC FOR MANY YEARS
ā€¢ FATIGUE AND WEAKNESS RELATED TO LOW
CARDIAC OUTPUT
ā€¢ DYSPNOEA, ORTHOPNOEA AND PAROXYSMAL
NOCTURNAL DYSPNOEA
ā€¢ EVENTUALLY PATIENTS MAY DEVELOP
PULMONARY HYPERTENSION AND RIGHT HEART
FAILURE
S I G N S
M I T R A L R E G U R G I T A T I O N
ā€¢ DISPLACES VOLUME-LOADED APEX BEAT
ā€¢ APICAL THRILL
ā€¢ 3RD HEART SOUND
ā€¢ APICAL PANSYSTOLIC MURMUR - RADIATING TO THE AXILLA (
INTENSITY OF MURMUR DOES NOT NECESSARILY CORRELATE
WITH SEVERITY OF MR )
ā€¢ APICAL DIASTOLIC MURMUR ( DUE TO INCREASED FLOW ACROSS
MV IN DIASTOLE )
ā€¢ RIGHT VENTRICULAR HEAVE AND INCREASED PULMONARY
COMPONENT OF 2ND HEART SOUND ( IF PULMONARY
HYPERTENSION IS PRESENT )
H O W I S M R Q U A N T I F I E D
E C H O C A R D I O G R A P H I C A L L Y
ā€¢ ACCORDING TO AMERICAN HEART ASSOCIATION
( AHA ) THERE ARE 5 MAIN CRITERIA
A H A G U I D E L I N E S F O R S E V E R I T Y O F M R
M I L D M O D E R A T E S E V E R E
J E T A R E A
( % L A A R E A ) < 2 0 % 2 0 - 4 0 % > 4 0 %
V E N A C O N T R A C T A ( C M .
) < 0 , 3 0 , 3 - 0 , 7 > 0 , 7
R E G U R G I T A N T V O L U M E (
M L . ) < 3 0 3 0 - 6 0 > 6 0
R E G U R G I T A N T F R A C T I O N
( % ) < 3 0 3 0 - 5 0 > 5 0
E F F E C T I V E
R E G U R G I T A N T O R I F I C E
A R E A ( C M 2 )
< 0 , 2 0 , 2 - 0 , 4 > 0 , 4
H O W I S M R Q U A N T I F I E D
E C H O C A R D I O G R A P H I C A L L Y
ā€¢ INFORMATION REGARDING:
ā€¢ - LEFT ATRIAL SIZE;
ā€¢ - VALVE MORPHOLOGY;
ā€¢ - FLOW REVERSAL IN PULMONARY VEINS;
ā€¢ - UNDERLYING ETIOLOGY OF MR;
ā€¢ - CHANGES OF LV FUNCTION AND SIZE
ā€¢ ALSO IMPORTANT WHEN ASSESSING SEVERITY OF
MR
H O W I S M R Q U A N T I F I E D
E C H O C A R D I O G R A P H I C A L L Y
ā€¢ FOR ISCHAEMIC MR:
ā€¢ - REGURGITANT
VOLUME >30 ML;
ā€¢ - EFFECTIVE REGURG.
ORIFICE AREA >0,2
CM2
S E V E R
E
VENA CONTRACTA REFERS TO NARROWEST PART
OF REGURG. JET JUST AFTER VALVE ORIFICE
I N D I C A T I O N S F O R M I T R A L V A L V E
S U R G E R Y I N P A T I E N T S W I T H M R
ā€¢ AHA GUIDELINES
G U I G E L I N E S
C L A S S I
S E V E R E M R W I T H S Y M P T O M S ( N Y H A I I - I V ) O R
L V C H A N G E S ( L V E S D > 4 0 M M O R E F < 6 0 % )
C L A S S I I A
S E V E R E M R I N A S Y M P T O M A T I C P A T I E N T S W I T H G O O D
L V F U N C T I O N A N D S I Z E , W H E R E L I K E L I H O OD O F
R E P A I R I N O P E R A T I N G C E N T R E I S > 9 0 %
C L A S S I I A
S E V E R E M R W I T H A F I B . O R P U L M O N A R Y
H Y P E R T E N S I O N ( > 5 0 M M H G A T R E S T O R 6 0 M M H G
W I T H E X E R C I S E )
C L A S S I I B
S E V E R E M R , P O O R L V E F < 3 0 % A N D S Y M P T O M S ( N Y H A
I I I - I V ) D E S P I T E M A X . A N T I - F A I L U R E M E D I C A L
T H E R A P Y A N D B I V E N T R I C U L A R P A C I N G )
S H O U L D T R A N S O E S O P H A G E A L E C H O C A R D I O G R A P H Y
( T E E ) B E P E R F O R M E D I N P A T I E N T S W I T H S E V E R E
M R ?
ā€¢ CLASS I : INTRAOPERATIVE TEE, PRE-CPB TO
ASSESS FEASIBILITY OF REPAIR AND POST-CPB
TO ASSESS SUCCESS OF REPAIR;
ā€¢ CLASS IIA: PRE-OPERATIVE TO GUIDE WHETHER
ASYMPTOMATIC PATIENTS HAVE >90% CHANCE
OF REPAIR
M I T R A L V A L V E P R O L A P S E D U E T O
B A R L O W ā€™ S D I S E A S E
ā€¢ MITRAL VALVE PROLAPSE IS DEFINED AS >2
MM BILLOWING OF AML OR PML BEYOND
ANNULAR PLANE INTO LA WITH OR
WITHOUT MR
ā€¢ CAN BE FAMILIAL OR NON-FAMILIAL AND
MAY BE ASSOCIATED WITH MARFAN
SYNDROME
ā€¢ HISTOLOGICAL ANALYSIS: MARKED
MYXOMATOUS PROLIFERATION OF ACID
MUCOPOLYSACCHARIDES IN ZONA
SPONGIOSA OF MV LEAFLETS, RESULTING
IN THINNING AND ELONGATION OF
CHORDAE TENDINEAE
ā€¢ PATIENTS WITH BARLOWā€™S DISEASE CAN BE
ASYMPTOMATIC OR PRESENT WITH SEVERE
MR OR ARRHYTHMIAS ( AFIB OR
VENTRICULAR TACHICARDIA )
ā€¢ SURGERY INDICATED AS PER AHA
GUIDELINES FOR NON-ISCHAEMIC MR
M I T R A L S T E N O S I S
N A T U R A L H I S T O R Y
ā€¢ PATIENTS USUALLY BECOME SYMPTOMATIC ON EXERTION WHEN MITRAL VALVE AREA (
MVA ) BECOMES < 2,5 CM2 AND SYMPTOMATIC AT REST WHEN MVA BECOMES <1,5 CM2
ā€¢ NATURAL PROGRESSION OF MS CAUSES MITRAL VALVE AREA TO TEDUCE BY 0,1-0,3 CM2
PER YEAR
ā€¢ PROGRESSION FROM ONSET OF RHEUMATIC FEVER TO ONSET OF SIGNS OF MS TAKES
AROUND 10-20 YEARS
ā€¢ PROGRESSION FROM SIGNS OF MS TO MILD SYMPTOMS OF MS TAKES 10-20 YEARS
ā€¢ PROGRESSION FROM MILD SYMPTOMS OF MS TO DECOMPENSATION ( OFTEN
PRECIPITATED BY AFIB ) TAKES 10-20 YEARS
ā€¢ - 10 YEAR SURVIVAL IN PATIENTS WITH NYHA I/II CLASS SYMPTOMS - 80%
ā€¢ - 10 YEAR SURVIVAL IN PATIENTS WITH NYHA III/IV CLASS SYMPTOMS - 10-15%
ā€¢ - AROUND 3 YEAR SURVIVAL IN PATIENTS WITH PULMONARY HYPERTENSION ( >50 MMHG
)
M I T R A L S T E N O S I S
P A T H O P H Y S I O L O G Y
ā€¢ RESTRICTED LV INFLOW RESULTS IN INCREASED
LV PRESSURE
ā€¢ BACK PRESSURE ON PULMONARY CIRCULATION
CAUSES:
ā€¢ - DYSPNOEA AND PULMONARY HYPERTENSION;
ā€¢ - RIGHT VENTRICULAR FAILURE;
ā€¢ - SUBSEQUENTLY LEFT VENTRICULAR FAILURE
M I T R A L S T E N O S I S
P A T H O P H Y S I O L O G Y
ā€¢ PULMONARY HYPERTENSION OCCURS
SECONDARY TO COMPENSATORY
VASOCONSTRICTION AND HYPERTROPHY OF
PULMONARY ARTERIOLES
ā€¢ PATIENTā€™S HAEMODYNAMIC STATE IS WORSENED
BY TACHYCARDIA OR AFIB WHICH REDUCES
DIASTOLIC FILLING PERIOD
W H A T A R E T H E C A U S E S O F
M I T R A L S T E N O S I S ?
ā€¢ MAJORITY OF CASES ARE CAUSED BY
RHEUMATIC FEVER (
LANCEFIELD GROUP A beta-HAEMOLYTIC
STREPTOCOCCUS)
ā€¢ VERY RARE CAUSES INCLUDE:
ā€¢ - CONGENITAL PARACHUTE MITRAL
VALVE;
ā€¢ - ENDOCARDIAL FIBROELASTOSIS;
ā€¢ - CARCINOID SYNDROME
ā€¢ PATHOPHYSIOLOGY OF MS CAN ALSO
BE CAUSED BY:
ā€¢ - COR TRIATRIATUM;
ā€¢ - LA MYXOMA;
ā€¢ - PULMONARY VEIN STENOSIS
R H E U M A T I C
F E V E R
T Y P E I I I A R E S T R I C T E D
L E A F L E T O P E N I N G
( D I A S T O L I C )
S Y M P T O M S
M I T R A L S T E N O S I S
ā€¢ MS HAS LONG LATENT PERIOD AND CAN BE ASYMPTOMATIC FOR MANY YEARS
ā€¢ FATIGUE
ā€¢ DYSPNOEA, ORTHOPNOEA AND PAROXYSMAL NOCTURNAL DYSPNOEA
ā€¢ LEFT ATRIAL DISTENTION RESULTING IN:
ā€¢ - AFIB AND SUBSEQUENT THROMBO-EMBOLIC EVENTS;
ā€¢ - LEFT RECURRENT LARYNGEAL NERVE COMPRESSION PRESENTING WITH HOARSENESS (
ORTNERā€™S SYNDROME );
ā€¢ - OESOPHAGEAL COMPRESSION PRODUCING DYSPHAGIA;
ā€¢ - RARELY, LEFT MAIN BRONCHUS COMPRESSION CAUSING LEFT LUNG COLLAPSE
ā€¢ PULMONARY HYPERTENSION AND RIGHT HEART FAILURE WHICH PRESENT IN:
ā€¢ - PERIPHERAL OEDEMA AND ASCITES;
ā€¢ HAEMOPTYSIS DUE TO DISTENSION AND RUPTURE OF BRONCHIAL VEINS
S I G N S
M I T R A L S T E N O S I S
ā€¢ LOW VOLUME PULSE
ā€¢ IRREGULAR PULSE
ā€¢ TAPPING NON-DISPLACED APEX BEAT
ā€¢ OPENING SNAP
ā€¢ LOUD S1 HEART SOUND
ā€¢ MID-DIASTOLIC RUMBLING MURMUR LOUDEST AT APEX
ā€¢ PULMONARY HYPERTENSION:
ā€¢ - MITRAL FACIES;
ā€¢ - CENTRAL CYANOSIS;
ā€¢ - LOUD P2 HEART SOUND;
ā€¢ - TRICUSPID REGURGITATION - PAN-SYSTOLIC MURMUR AT RIGHT STERNAL EDGE;
ā€¢ - PULMONARY REGURGITATION - GRAHAM STEEL EARLY DIASTOLIC MURMUR ON INSPIRATION
H O W I S M S Q U A N T I F I E D
E C H O C A R D I O G R A P H I C A L L Y
ā€¢ ACCORDING TO AMERICAN HEART ASSOCIATION
( AHA ) THERE ARE 3 MAIN CRITERIA
A H A G U I D E L I N E S F O R S E V E R I T Y O F M S
M I L D M O D E R A T E S E V E R E
M I T R A L V A L V E A R E A (
C M 2 ) > 1 , 5 1 , 0 - 1 , 5 < 1 , 0
M E A N P R E S S U R E
G R A D I E N T ( M M H G ) < 5 5 - 1 0 > 1 0
P U L M O N A R Y A R T E R Y
S Y S T O L I C P R E S S U R E (
M M H G )
< 3 0 3 0 - 5 0 > 5 0
H O W I S M S Q U A N T I F I E D
E C H O C A R D I O G R A P H I C A L L Y
ā€¢ INFORMATION REGARDING:
ā€¢ - LEFT ATRIAL SIZE;
ā€¢ - VALVE MORPHOLOGY;
ā€¢ - PRESENCE OF LA THROMBUS;
ā€¢ - UNDERLYING ETIOLOGY OF MS;
ā€¢ - CHANGES OF LV FUNCTION AND SIZE
ā€¢ ALSO IMPORTANT WHEN ASSESSING SEVERITY OF
MS
I N D I C A T I O N S F O R M I T R A L V A L V E
S U R G E R Y I N P A T I E N T S W I T H M S
ā€¢ AHA GUIDELINES
G U I G E L I N E S
C L A S S I
M O D E R A T E - S E V E R E M S W I T H S Y M P T O M S ( N Y H A I I I - I V
) W H E R E P E R C U T A N E O U S M I T R A L B A L L O O N
V A L V U L O P L A S T Y ( P M B V ) I S N O T S U I T A B L E
C L A S S I I A
S E V E R E M S W I T H S E V E R E P U L M O N A R Y
H Y P E R T E N S I O N ( > 5 0 M M H G ) O R S Y M P T O M S ( N Y H A
I - I I ) W H E R E P M B V I S N O T S U I T A B L E
C L A S S I I B
M O D E R A T E - S E V E R E M S W I T H R E C U R R E N T E M B O L I C
E V E N T S O N A N T I C O A G U L A T I O N
W H A T A R E D E T E R M I N A N T S O F
W I L K I N S M I T R A L S T E N O S I S S C O R E
W I L K I N S S C O R E
L E A F L E T
M O B I L I T Y 0 1 2 3 4
L E A F L E T
T H I C K E N I N G 0 1 2 3 4
L E A F L E T
C A L C I F I C A T I O
N
0 1 2 3 4
S U B V A L V U L A R
T H I C K E N I N G 0 1 2 3 4
EACH SCORES BETWEEN 0-4, WITH MAX. SCORE OF 16
WILKINS SCORE > 9 SUGGESTS LESION IS UNLIKELY TO BE AMENABLE
TO PMBV
I N D I C A T I O N S F O R P E R C U T A N E O U S M I T R A L
B A L L O O N V A L V U L O P L A S T Y ( P M B V ) I N P A T I E N T S
W I T H M S
ā€¢ AHA GUIDELINES
G U I G E L I N E S
C L A S S I
M O D E R A T E - S E V E R E M S W I T H E I T H E R S Y M P T O M S (
N Y H A I I - I V ) O R P U L M O N A R Y H Y P E R T E N S I O N ( > 5 0
M M H G A T R E S T O R 6 0 M M H G 0 N E X E R C I S E )
C L A S S I I A
M O D E R A T E - S E V E R E M S W I T H S Y M P T O M S ( N Y H A I I I - I V
) I N P A T I E N T S W I T H N O N - P L I A B L E V A L V E O R
P A T I E N T S W H O A R E A T H I G H S U R G I C A L R I S K O F
D E A T H
PMBV SHOULD BE ONLY PERFORMED IN PATIENTS
WITH FAVOURABLE VALVE MORPHOLOGY (
WILKINS SCORE OF AT LEAST 8 OR LESS ) AND
NO CONTRAINDICATIONS: LEFT ATRIAL THROMBUS,
MODERATE SEVERE MR
H O W I S P E R C U T A N E O U S M I T R A L
B A L L O O N V A L V U L O P L A S T Y ( P M B V )
P E R F O R M E D ?
ā€¢ LOCAL ANAESTHESIA AND SEDATION
ā€¢ VALVULOPLASTY BALLOON IS PASSED:
ā€¢ - VIA FEMORAL VEIN;
ā€¢ - INTO RIGHT ATRIUM;
ā€¢ - ACROSS INTRA-ATRIAL SEPTUM;
ā€¢ - INTO LEFT ATRIUM;
ā€¢ - ACROSS MITRAL VALVE
ā€¢ AND INFLATED
ā€¢ RESULTS ARE BEST WHEN LEAFLETS ARE: THIN, MOBILE, NOT CALCIFIED, IN YOUNGER AGE GROUP AND WHERE
SUBVALVULAR CHORDAE HAVE NOT FUSED/CALCIFIED
ā€¢ PMBV TYPICALLY INCREASE MITRALVALVE AREA FROM 1-2 CM2
ā€¢ COMPLICATIONS:
M O R T A L I T Y
C A R D I A C
P E R F O R A T I O N
S T R O K E S E V E R E M R
1 % 1 % 2 % 3 %
H O W I S C L O S E D M I T R A L
V A L V U L O T O M Y P E R F O R M E D ?
ā€¢ LEFT POSTEROLATERAL
THORACOTOMY
ā€¢ PERICARDIUM OPENED ANTERIOR TO
PHRENIC NERVE
ā€¢ INDEX FINGER IS INSERTED INTO LEFT
ATRIUM
ā€¢ TUBBS DILATOR IS PASSED VIA APEX
THROUG LV, USING PURSE STRING
SUTURES TO REDUCE BLOOD LOSS
AND AIR EMBOLISM
ā€¢ DILATOR IS THEN GUIDED MANUALLY
THROUGH MITRAL VALVE ORIFICE AND
OPENED ALONG NATURAL INTER-
COMMISSURAL LINE
ā€¢ RESULTING DILATATION IS ASSESSED
MANUALLY AND BY TRANSESOPHAGEAL
ECHOCARDIOGRAPHY
M I T R A L V A L V E S U R G I C A L
T E C H N I Q U E S
M I T R A L V A L V E R E P A I R & M I T R A L V A L V E R E P L A C E M E N T
S U R G I C A L A P P R O A C H E S
T O M I T R A L V A L V E
ā€¢ STANDARD LEFT
ATRIOTOMY:
ā€¢ - PERICARDIAL REFLECTIONS
AROUND INFERIOR AND
SUPERIOR PULMONARY VEINS
ARE MOBILISED;
ā€¢ - WATERSTONā€™S INTERATRIAL
GROOVE IS DEVELOPED
THEREBY REFLECTING RA
BACK OVER LA;
ā€¢ INCISION IS MADE IN LA
ANTERIOR AND MEDIAL TO
RIGHT SUPERIOR PULMONARY
VEIN AND CONTINUED
INFERIORLY AND SUPERIORLY
S U R G I C A L A P P R O A C H E S
T O M I T R A L V A L V E
ā€¢ OTHER SURGICAL
APPROACHES TO
MITRAL VALVE:
ā€¢ - BI-ATRIAL TRAS-
SEPTAL INCISION;
ā€¢ - SUPERIOR ROOF
INCISION;
ā€¢ - BI-ATRIAL ( DUBOST )
INCISION;
S U R G I C A L A P P R O A C H E S
T O M I T R A L V A L V E
ā€¢ OTHER SURGICAL APPROACHES TO MITRAL
VALVE:
S U R G I C A L A P P R O A C H E S
T O M I T R A L V A L V E
ā€¢ OTHER SURGICAL APPROACHES TO MITRAL VALVE:
ā€¢ - RIGHT ANTEROLATERAL THORACOTOMY;
ā€¢ - RIGHT ANTEROLATERAL MINI-THORACOTOMY
S U R G I C A L A P P R O A C H E S
T O M I T R A L V A L V E
ā€¢ OTHER SURGICAL APPROACHES TO MITRAL
VALVE:
H O W I S M I T R A L V A L V E A S S E S S E D
I N T R A - O P E R A T I V E L Y ?
ā€¢ MV IS INSPECTED USING NERVE HOOKS TO MEASURE
DEGREE OF MOTION OF EACH SCALLOP ( P1, P2, P3, A1, A2, A3
) OF BOTH LEAFLETS COMPARED AGAINST REFERENCE POINT
( USUALLY P1 OR ANTEROLATERAL COMMISSURE )
H O W I S M I T R A L V A L V E A S S E S S E D
I N T R A - O P E R A T I V E L Y ?
ā€¢ VALVE COMPETENCY CAN BE CHECKED BEFORE REPAIR BY DISTENDING LV WITH
COLD SALINE AND IDENTIFYING AETIOLOGY AND LOCATION OF REGURGITATION JET
ā€¢ COMPETENCE OF MV FOLLOWING REPAIR IS ASSESSED BY:
ā€¢ - STATIC TESTING UNDER DIRECT VISION BY DISTENDING LV WITH COLD SALINE;
ā€¢ - TEE WITH APPROPRIATELY FILLED LV OFF CPB SUPPORT
W H A T S T R U C T U R E S A R E A T R I S K
D U R I N G M I T R A L V A L V E S U R G E R Y ?
ā€¢ CIRCUMFLEX
CORONARY ARTERY
ā€¢ CORONARY SINUS
ā€¢ AORTIC VALVE
( LEFT & NON-
CORONARY CUSPS )
ā€¢ ATRIOVENTRICULAR
NODE AND BUNDLE
OF HIS
W H A T I S S Y S T O L I C A N T E R I O R M O T I O N
( S A M ) O F M I T R A L V A L V E ?
ā€¢ SYSTOLIC ANTERIOR MOTION ( SAM )
OCCURS WHEN THE TIPS OF MV
LEAFLETS ARE DISPLACED ANTERIORLY
INTO LVOT
ā€¢ THIS RESULTS IN VENTURI EFFECT
PULLING ON MITRAL VALVE LEAFLETS
CAUSING MR AND LVOT OBSTRUCTION
ā€¢ IN COMPARISON, DURING DIASTOLE LVOT
DIAMETER IS NORMAL
ā€¢ SAM IS MORE COMMON IN PATIENTS
WITH:
ā€¢ - HYPERTROPHIC OBSTRUCTIVE
CARDIOMYOPATHY ( HOCM );
ā€¢ - SMALL ELDERLY WOMEN WITH
ASYMMETRIC SEPTAL HYPERTROPHY
W H A T A R E S U R G I C A L T R E A T M E N T
O P T I O N S F O R M I T R A L V A L V E
D I S E A S E
L E S I O N D Y S F U N C T I O N T Y P E O P T I O N
A N N U L A R D I L A T A T I O N N O R M A L L E A F L E T M O T I O N I C O MP L E TE F L E XI B L E A N N U L O P L A S TY R I N G ( P H YS I O
)
L E A F L E T P E R F O R A T I O N N O R M A L L E A F L E T M O T I O N I B O V I N E P E R I C A R D I A L P A TC H
P O S T E R I O R M I T R A L V A L V E
L E A F L E T P R O L A P S E
E X C E S S L E A F L E T M O T I O N I I
- Q U A D R A N G U L A R R E S E C TI O N
- TR I A N G U L A R R E S E C TI O N
- S L I D I N G A N N U L O P L A S TY
- A R TI F I C I A L C H O R D I MP L A N TA TI O N
A N T E R I O R M I T R A L V A L V E
L E A F L E T P R O L A P S E
E X C E S S L E A F L E T M O T I O N I I - TR I A N G U L A R R E S E C TI O N
- A R TI F I C I A L C H O R D I MP L A N TA TI O N
B I L E A F L E T M I T R A L V A L V E
P R O L A P S E
E X C E S S L E A F L E T M O T I O N I I
- L E A F L E T R E S E C TI O N
- A R TI F I C I A L C H O R D I MP L A N TA TI O N
- A L F I E R I S TI TC H
- MI TR A L V A L V E R E P L A C E ME N T
P A R T I A L P A P I L L A R Y M U S C L E
R U P T U R E
E X C E S S L E A F L E T M O T I O N I I R E I MP L A N TA TI O N O F P A P I L L A R Y MU S C L E
C O M P L E T E P A P I L L A R Y
M U S C L E R U P T U R E
E X C E S S L E A F L E T M O T I O N I I MI TR A L V A L V E R E P L A C E ME N T
I S C H A E M I C M R
R E S T R I C T E D L E A F L E T
C L O S U R E I I I B
- MC C A R TH Y - A D A MS I MR R I N G
- D O W N S I Z I N G A N N U L O P L A S TY
- MI TR A L V A L V E R E P L A C E ME T
R H E U M A T I C M R
R E S T R I C T E D L E A F L E T
O P E N I N G I I I A MI TR A L V A L V E R E P L A C E ME N T
T E C H N I Q U E S
M I T R A L V A L V E R E P A I R
B E N E F I T S O F
M I T R A L A N N U L O P L A S T Y R I N G S
ā€¢ CORRECTS ANNULAR
DILATATION
ā€¢ PREVENTS FURTHER
ANNULAR DILATATION
ā€¢ INCREASES LEAFLET
COAPTATION
ā€¢ REINFORCES ANNULAR
SUTURE LINES
P R O S T H E T I C R I N G S &
B A N D S
M I T R A L V A L V E R E P A I R
F E A T U R E S O F D I F F E R E N T M I T R A L
V A L V E R I N G P R O S T H E S I S
ā€¢ CARPENTIER-EDWARDS
PHYSIO ANNULOPLASTY
RING:
ā€¢ - COMPLETE, SEMI-FLEXIBLE;
ā€¢ - FREQUENTLY USED
ANNULOPLASTY RING
ā€¢ CARPENTIER RING
ā€¢ - RIGID, COMPLETE
ā€¢ - ANTERIOR-POSTERIOR
DIAMETER CAN BE ADJUSTED
FOR A BESPOKE RING SHAPE
F E A T U R E S O F D I F F E R E N T M I T R A L
V A L V E R I N G P R O S T H E S I S
ā€¢ COSGROVE-
EDWARDS
ANNULOPLASTY
SYSTEM ( BAND)
ā€¢ - INCOMPLETE, FLEXIBLE
ā€¢ CARPENTIER-
MACCARTHY-ADAMS
IMR ETILOGIX
ANNULOPLASTY RING
ā€¢ - FOR ISCHAEMIC MR
P R O S T H E T I C R I N G
S T A N D A R D I M P L A N T A T I O N T E C H N I Q U E
M I T R A L V A L V E R E P A I R
3
2
1
4
5
D I L A T E D
C A R D O P M Y O P A T H Y
T Y P E I I I B R E S T R I C T E D L E A F L E T C L O S U R E ( S Y S T O L I C )
T R I A N G U L A R / Q U A D R A N G U L A R R E S E C T I O N & S L I D I N G
R E P A I R
M I T R A L V A L V E R E P A I R
1 2
3
Q U A D R A N G U L A R R E S E C T I O N O F P 2 P M L
M I T R A L V A L V E R E P A I R
4
1
2 3
T R I A N G U L A R R E S E C T I O N O F A 3 A M L
M I T R A L V A L V E R E P A I R
1 2
R H E U M A T I C F E V E R ( T Y P E I I I A ) - C O M M I S S U R O T O M Y
M I T R A L V A L V E R E P A I R
1
2
C H O R D A L R U P T U R E ( T Y P E I I ) - A R T I F I C I A L C H O R D S
M I T R A L V A L V E R E P A I R
C H O R D A L R U P T U R E ( T Y P E I I ) - A R T I F I C I A L C H O R D S
M I T R A L V A L V E R E P A I R
I S C H A E M I C M I T R A L R I N G I M P L A N T A T I O N
M I T R A L V A L V E R E P A I R
T E C H N I Q U E S
M I T R A L V A L V E R E P L A C E M E N T
T Y P E S O F P R O S T H E T I C
V A L V E S
M I T R A L V A L V E R E P L A C E M E N T
A D V A N T A G E S O F R E P A I R I N G R A T H E R
T H A N R E P L A C I N G M I T R A L V A L V E
ā€¢ AS COMPARED WITH MITRAL VALVE REPLACEMENT, MITRAL VALVE REPAIR IS
ASSOCIATED WITH GREATER FREEDOM FROM:
ā€¢ - MORTALITY ( OPERATIVE AND LONG-TERM );
ā€¢ - STRUCTURAL VALVE DETERIORATION;
ā€¢ - RE-OPERATION;
ā€¢ - INFECTIVE ENDOCARDITIS;
ā€¢ - THROMBO-EMBOLISM
ā€¢ - HAEMORRHAGE
ā€¢ AS MORE OF SUBVALVULAR APPARATUS IS PRESERVED, MITRAL VALVE REPAIR IS
BETTER AT MAINTAINIG LV GEOMETRY AND HENCE IS ASSOCIATED WITH LESS LV
DYSFUNCTION COMPARED WITH MITRAL VALVE REPLACEMENT
F R E E D O M F R O M R E - I N T E R V E N T I O N F O R P A T I E N T S
O L D E R T H A N 7 0 Y E A R S F O R D I F F E R E N T M I T R A L V A L V E
P R O S T H E S E S A N D R E P A I R T E C H N I Q U E S A V A I L A B L E
F R E E D O M F R O M R E - I N T E R V E N T I O N A T 1 0 Y E A R S
M E C H A N I C A L V A L V E P R O S T H E S I S 9 8 %
B O V I N E P E R I C A R D I A L B I O P R O S T H E S I S 8 0 %
P O R C I N E B I O P R O S T H E S I S 7 5 %
P M B V 8 0 %
O P E N M V C O M M I S S U R O T O M Y 8 0 %
C L O S E D M V C O M M I S S U R O T O M Y 7 0 %
R E P A I R O F A N T E R I O R M I T R A L
L E A F L E T
7 8 %
R E P A I R O F P O S T E R I O R M I T R A L
L E A F L E T
9 8 %

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Mitral valve disease

  • 1. M I T R A L V A L V E D I S E A S E D E P A R T M E N T O F C A R D I A C A N D V A S C U L A R S U R G E R Y M E D I C A L U N I V E R S I T Y P L O V D I V H R I S T O R A H M A N
  • 2. M I T R A L R E G U R G I T A T I O N N A T U R A L H I S T O R Y ā€¢ ASYMPTOMATIC PATIENTS HAVE LONG LATENT PERIOD BEFORE ONSET OF SYMPTOMS ā€¢ CHRONIC MR - WELL TOLERATED IF LV FUNCTION IS WELL PRESERVED
  • 3. M I T R A L R E G U R G I T A T I O N N A T U R A L H I S T O R Y ā€¢ POOR PROGNOSTIC FEATURES OF MR: ā€¢ - SYMPTOMS >1 YEAR; ā€¢ - ATRIAL FIBRILLATION; ā€¢ - AGE >60 YEARS; ā€¢ - EF <50% ā€¢ - LVEDV >100 mL/m2; LVESV >60 mL/m2; ā€¢ - LVESD >5 cm; LVEDD >7cm
  • 4. M I T R A L R E G U R G I T A T I O N P A T H O P H Y S I O L O G Y ā€¢ CHRONIC LV VOLUME OVERLOAD ASSOCIATED WITH MR LEADS TO LV HYPERTROPHY ā€¢ STROKE VOLUME INITIALLY MAINTAINED BY THE FRANK- STARLING MECHANISM ā€¢ EVENTUALLY LV CONTRACTILE FUNCTION DECLINES PRODUCING: ā€¢ - INCREASED LVESV; ā€¢ - RAISED LV FILLING PRESSURES; ā€¢ - RAISED LA AND PULMONARY FILLING PRESSURES; R E S U L T I N R E S U L T P U L M O N A R Y O E D E M A & C H F
  • 5. M I T R A L R E G U R G I T A T I O N P A T H O P H Y S I O L O G Y ā€¢ ONCE LV EJECTION FRACTION FALLS BELOW APPROX. 60%, LV SYSTOLIC DYSFUNCTION IS ALMOST CERTAINLY PRESENT AS SOME OF THE EJECTED VOLUME FLOWS BACK INTO LA ( AFTERLOAD-REDUCING EFFECT OF MR)
  • 6. M I T R A L R E G U R G I T A T I O N C L A S S I F I C A T I O N ā€¢ CARPENTIERā€™S FUNCTIONAL CLASSIFICATION D Y S F U N C T I O N L E S I O N T Y P E I N O R M A L L E A F L E T M O T I O N A N N U L A R D I L A T A T I O N , L E A F L E T P E R F O R A T I O N T Y P E I I E X C E S S L E A F L E T M O T I O N M YX O M A T O U S D E G E N E R A T I O N , C H O R D A L R U P T U R E T Y P E I I I R E S T R I C T E D L E A F L E T M O T I O N I I I A R E S T R I C T E D O P E N I N G R H E U M A T I C F E V E R I I I B R E S T R I C T E D C L O S U R E I S C H A E M I C C A R D I O M YO P A T H Y
  • 7. M I T R A L R E G U R G I T A T I O N C L A S S I F I C A T I O N ā€¢ CARPENTIERā€™S FUNCTIONAL CLASSIFICATION
  • 8. T Y P E I N O R M A L L E A F L E T M O T I O N C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
  • 9. T Y P E I I E X C E S S L E A F L E T M O T I O N C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
  • 10. T Y P E I I E X C E S S L E A F L E T M O T I O N C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
  • 11. T Y P E I I I A ( D I A S T O L I C ) R E S T R I C T E D L E A F L E T O P E N I N G C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
  • 12. T Y P E I I I B ( S Y S T O L I C ) R E S T R I C T E D L E A F L E T C L O S U R E C A R P E N T I E R ā€™ S C L A S S I F I C A T I O N
  • 13. W H A T A R E T H E C A U S E S O F C H R O N I C M I T R A L R E G U R G I T A T I O N ? ā€¢ 1. MYXOMATOUS DEGENERATION ( TYPE II ) ā€¢ 2. RHEUMATIC FEVER ( TYPE IIIA ) ā€¢ 3. ISCHAEMIC CARDIOMYOPATHY ( TYPE IIIB & TYPE I ) 1 2 3 +
  • 14. W H A T A R E T H E C A U S E S O F A C U T E M I T R A L R E G U R G I T A T I O N ? ā€¢ 1. CHORDAL RUPTURE ( TYPE II ) ā€¢ 2. INFECTIVE ENDOCARDITIS ( TYPE I ) ā€¢ 3. PAPILLARY MUSCLE RUPTURE AFTER MI ( TYPE II ) 1 & 3 2
  • 15. I N F E C T I V E E N D O C A R D I T I S T Y P E I N O R M A L L E A F L E T M O T I O N
  • 16. E T I O L O G Y I S C H A E M I C M I T R A L R E G U R G I T A T I O N ā€¢ ACUTE ISCHAEMIC MR IS USUALLY CAUSED BY: ā€¢ - INFARCTED; ā€¢ - RUPTURED; ā€¢ - NON-RUPTURED PAPILLARY MUSCLE T Y P E I I E X C E S S L E A F L E T M O T I O N
  • 17. E T I O L O G Y I S C H A E M I C M I T R A L R E G U R G I T A T I O N ā€¢ CHRONIC ISCHAEMIC MR IS CAUSED BY: ā€¢ COMBINATION OF: ā€¢ - RESTRICTED MOVEMENT OF P2 & P3 SCALLOPS OF POSTERIOR MITRAL VALVE LEAFLET (PML) DUE TO VENTRICULAR DILATATION DISPLACING PAPILLARY MUSCLES; ā€¢ - FUNCTIONAL DILATATION OF MITRAL VALVE ANNULUS C O M B I N A T I O N O F : T Y P E I I I B + T Y P E I R E S T R I C T E D C L O S U R E + N O R M A L L E A F L E T M O T I O N
  • 18. E T I O L O G Y I S C H A E M I C M I T R A L R E G U R G I T A T I O N ā€¢ REDUCED CONTRACTION OF MV ANNULUS ā€¢ + ā€¢ REDUCED VENTRICULAR CLOSING FORCES ON MV DUE TO POOR LV FUNCTION ā€¢ = CONTRIBUTE TO ISCHAEMIC MR
  • 19. S Y M P T O M S M I T R A L R E G U R G I T A T I O N ā€¢ MR IS PROGRESSIVE DISEASE AND PATIENTS CAN BE ASYMPTOMATIC FOR MANY YEARS ā€¢ FATIGUE AND WEAKNESS RELATED TO LOW CARDIAC OUTPUT ā€¢ DYSPNOEA, ORTHOPNOEA AND PAROXYSMAL NOCTURNAL DYSPNOEA ā€¢ EVENTUALLY PATIENTS MAY DEVELOP PULMONARY HYPERTENSION AND RIGHT HEART FAILURE
  • 20. S I G N S M I T R A L R E G U R G I T A T I O N ā€¢ DISPLACES VOLUME-LOADED APEX BEAT ā€¢ APICAL THRILL ā€¢ 3RD HEART SOUND ā€¢ APICAL PANSYSTOLIC MURMUR - RADIATING TO THE AXILLA ( INTENSITY OF MURMUR DOES NOT NECESSARILY CORRELATE WITH SEVERITY OF MR ) ā€¢ APICAL DIASTOLIC MURMUR ( DUE TO INCREASED FLOW ACROSS MV IN DIASTOLE ) ā€¢ RIGHT VENTRICULAR HEAVE AND INCREASED PULMONARY COMPONENT OF 2ND HEART SOUND ( IF PULMONARY HYPERTENSION IS PRESENT )
  • 21. H O W I S M R Q U A N T I F I E D E C H O C A R D I O G R A P H I C A L L Y ā€¢ ACCORDING TO AMERICAN HEART ASSOCIATION ( AHA ) THERE ARE 5 MAIN CRITERIA A H A G U I D E L I N E S F O R S E V E R I T Y O F M R M I L D M O D E R A T E S E V E R E J E T A R E A ( % L A A R E A ) < 2 0 % 2 0 - 4 0 % > 4 0 % V E N A C O N T R A C T A ( C M . ) < 0 , 3 0 , 3 - 0 , 7 > 0 , 7 R E G U R G I T A N T V O L U M E ( M L . ) < 3 0 3 0 - 6 0 > 6 0 R E G U R G I T A N T F R A C T I O N ( % ) < 3 0 3 0 - 5 0 > 5 0 E F F E C T I V E R E G U R G I T A N T O R I F I C E A R E A ( C M 2 ) < 0 , 2 0 , 2 - 0 , 4 > 0 , 4
  • 22. H O W I S M R Q U A N T I F I E D E C H O C A R D I O G R A P H I C A L L Y ā€¢ INFORMATION REGARDING: ā€¢ - LEFT ATRIAL SIZE; ā€¢ - VALVE MORPHOLOGY; ā€¢ - FLOW REVERSAL IN PULMONARY VEINS; ā€¢ - UNDERLYING ETIOLOGY OF MR; ā€¢ - CHANGES OF LV FUNCTION AND SIZE ā€¢ ALSO IMPORTANT WHEN ASSESSING SEVERITY OF MR
  • 23. H O W I S M R Q U A N T I F I E D E C H O C A R D I O G R A P H I C A L L Y ā€¢ FOR ISCHAEMIC MR: ā€¢ - REGURGITANT VOLUME >30 ML; ā€¢ - EFFECTIVE REGURG. ORIFICE AREA >0,2 CM2 S E V E R E VENA CONTRACTA REFERS TO NARROWEST PART OF REGURG. JET JUST AFTER VALVE ORIFICE
  • 24. I N D I C A T I O N S F O R M I T R A L V A L V E S U R G E R Y I N P A T I E N T S W I T H M R ā€¢ AHA GUIDELINES G U I G E L I N E S C L A S S I S E V E R E M R W I T H S Y M P T O M S ( N Y H A I I - I V ) O R L V C H A N G E S ( L V E S D > 4 0 M M O R E F < 6 0 % ) C L A S S I I A S E V E R E M R I N A S Y M P T O M A T I C P A T I E N T S W I T H G O O D L V F U N C T I O N A N D S I Z E , W H E R E L I K E L I H O OD O F R E P A I R I N O P E R A T I N G C E N T R E I S > 9 0 % C L A S S I I A S E V E R E M R W I T H A F I B . O R P U L M O N A R Y H Y P E R T E N S I O N ( > 5 0 M M H G A T R E S T O R 6 0 M M H G W I T H E X E R C I S E ) C L A S S I I B S E V E R E M R , P O O R L V E F < 3 0 % A N D S Y M P T O M S ( N Y H A I I I - I V ) D E S P I T E M A X . A N T I - F A I L U R E M E D I C A L T H E R A P Y A N D B I V E N T R I C U L A R P A C I N G )
  • 25. S H O U L D T R A N S O E S O P H A G E A L E C H O C A R D I O G R A P H Y ( T E E ) B E P E R F O R M E D I N P A T I E N T S W I T H S E V E R E M R ? ā€¢ CLASS I : INTRAOPERATIVE TEE, PRE-CPB TO ASSESS FEASIBILITY OF REPAIR AND POST-CPB TO ASSESS SUCCESS OF REPAIR; ā€¢ CLASS IIA: PRE-OPERATIVE TO GUIDE WHETHER ASYMPTOMATIC PATIENTS HAVE >90% CHANCE OF REPAIR
  • 26. M I T R A L V A L V E P R O L A P S E D U E T O B A R L O W ā€™ S D I S E A S E ā€¢ MITRAL VALVE PROLAPSE IS DEFINED AS >2 MM BILLOWING OF AML OR PML BEYOND ANNULAR PLANE INTO LA WITH OR WITHOUT MR ā€¢ CAN BE FAMILIAL OR NON-FAMILIAL AND MAY BE ASSOCIATED WITH MARFAN SYNDROME ā€¢ HISTOLOGICAL ANALYSIS: MARKED MYXOMATOUS PROLIFERATION OF ACID MUCOPOLYSACCHARIDES IN ZONA SPONGIOSA OF MV LEAFLETS, RESULTING IN THINNING AND ELONGATION OF CHORDAE TENDINEAE ā€¢ PATIENTS WITH BARLOWā€™S DISEASE CAN BE ASYMPTOMATIC OR PRESENT WITH SEVERE MR OR ARRHYTHMIAS ( AFIB OR VENTRICULAR TACHICARDIA ) ā€¢ SURGERY INDICATED AS PER AHA GUIDELINES FOR NON-ISCHAEMIC MR
  • 27.
  • 28. M I T R A L S T E N O S I S N A T U R A L H I S T O R Y ā€¢ PATIENTS USUALLY BECOME SYMPTOMATIC ON EXERTION WHEN MITRAL VALVE AREA ( MVA ) BECOMES < 2,5 CM2 AND SYMPTOMATIC AT REST WHEN MVA BECOMES <1,5 CM2 ā€¢ NATURAL PROGRESSION OF MS CAUSES MITRAL VALVE AREA TO TEDUCE BY 0,1-0,3 CM2 PER YEAR ā€¢ PROGRESSION FROM ONSET OF RHEUMATIC FEVER TO ONSET OF SIGNS OF MS TAKES AROUND 10-20 YEARS ā€¢ PROGRESSION FROM SIGNS OF MS TO MILD SYMPTOMS OF MS TAKES 10-20 YEARS ā€¢ PROGRESSION FROM MILD SYMPTOMS OF MS TO DECOMPENSATION ( OFTEN PRECIPITATED BY AFIB ) TAKES 10-20 YEARS ā€¢ - 10 YEAR SURVIVAL IN PATIENTS WITH NYHA I/II CLASS SYMPTOMS - 80% ā€¢ - 10 YEAR SURVIVAL IN PATIENTS WITH NYHA III/IV CLASS SYMPTOMS - 10-15% ā€¢ - AROUND 3 YEAR SURVIVAL IN PATIENTS WITH PULMONARY HYPERTENSION ( >50 MMHG )
  • 29. M I T R A L S T E N O S I S P A T H O P H Y S I O L O G Y ā€¢ RESTRICTED LV INFLOW RESULTS IN INCREASED LV PRESSURE ā€¢ BACK PRESSURE ON PULMONARY CIRCULATION CAUSES: ā€¢ - DYSPNOEA AND PULMONARY HYPERTENSION; ā€¢ - RIGHT VENTRICULAR FAILURE; ā€¢ - SUBSEQUENTLY LEFT VENTRICULAR FAILURE
  • 30. M I T R A L S T E N O S I S P A T H O P H Y S I O L O G Y ā€¢ PULMONARY HYPERTENSION OCCURS SECONDARY TO COMPENSATORY VASOCONSTRICTION AND HYPERTROPHY OF PULMONARY ARTERIOLES ā€¢ PATIENTā€™S HAEMODYNAMIC STATE IS WORSENED BY TACHYCARDIA OR AFIB WHICH REDUCES DIASTOLIC FILLING PERIOD
  • 31. W H A T A R E T H E C A U S E S O F M I T R A L S T E N O S I S ? ā€¢ MAJORITY OF CASES ARE CAUSED BY RHEUMATIC FEVER ( LANCEFIELD GROUP A beta-HAEMOLYTIC STREPTOCOCCUS) ā€¢ VERY RARE CAUSES INCLUDE: ā€¢ - CONGENITAL PARACHUTE MITRAL VALVE; ā€¢ - ENDOCARDIAL FIBROELASTOSIS; ā€¢ - CARCINOID SYNDROME ā€¢ PATHOPHYSIOLOGY OF MS CAN ALSO BE CAUSED BY: ā€¢ - COR TRIATRIATUM; ā€¢ - LA MYXOMA; ā€¢ - PULMONARY VEIN STENOSIS
  • 32. R H E U M A T I C F E V E R T Y P E I I I A R E S T R I C T E D L E A F L E T O P E N I N G ( D I A S T O L I C )
  • 33. S Y M P T O M S M I T R A L S T E N O S I S ā€¢ MS HAS LONG LATENT PERIOD AND CAN BE ASYMPTOMATIC FOR MANY YEARS ā€¢ FATIGUE ā€¢ DYSPNOEA, ORTHOPNOEA AND PAROXYSMAL NOCTURNAL DYSPNOEA ā€¢ LEFT ATRIAL DISTENTION RESULTING IN: ā€¢ - AFIB AND SUBSEQUENT THROMBO-EMBOLIC EVENTS; ā€¢ - LEFT RECURRENT LARYNGEAL NERVE COMPRESSION PRESENTING WITH HOARSENESS ( ORTNERā€™S SYNDROME ); ā€¢ - OESOPHAGEAL COMPRESSION PRODUCING DYSPHAGIA; ā€¢ - RARELY, LEFT MAIN BRONCHUS COMPRESSION CAUSING LEFT LUNG COLLAPSE ā€¢ PULMONARY HYPERTENSION AND RIGHT HEART FAILURE WHICH PRESENT IN: ā€¢ - PERIPHERAL OEDEMA AND ASCITES; ā€¢ HAEMOPTYSIS DUE TO DISTENSION AND RUPTURE OF BRONCHIAL VEINS
  • 34. S I G N S M I T R A L S T E N O S I S ā€¢ LOW VOLUME PULSE ā€¢ IRREGULAR PULSE ā€¢ TAPPING NON-DISPLACED APEX BEAT ā€¢ OPENING SNAP ā€¢ LOUD S1 HEART SOUND ā€¢ MID-DIASTOLIC RUMBLING MURMUR LOUDEST AT APEX ā€¢ PULMONARY HYPERTENSION: ā€¢ - MITRAL FACIES; ā€¢ - CENTRAL CYANOSIS; ā€¢ - LOUD P2 HEART SOUND; ā€¢ - TRICUSPID REGURGITATION - PAN-SYSTOLIC MURMUR AT RIGHT STERNAL EDGE; ā€¢ - PULMONARY REGURGITATION - GRAHAM STEEL EARLY DIASTOLIC MURMUR ON INSPIRATION
  • 35. H O W I S M S Q U A N T I F I E D E C H O C A R D I O G R A P H I C A L L Y ā€¢ ACCORDING TO AMERICAN HEART ASSOCIATION ( AHA ) THERE ARE 3 MAIN CRITERIA A H A G U I D E L I N E S F O R S E V E R I T Y O F M S M I L D M O D E R A T E S E V E R E M I T R A L V A L V E A R E A ( C M 2 ) > 1 , 5 1 , 0 - 1 , 5 < 1 , 0 M E A N P R E S S U R E G R A D I E N T ( M M H G ) < 5 5 - 1 0 > 1 0 P U L M O N A R Y A R T E R Y S Y S T O L I C P R E S S U R E ( M M H G ) < 3 0 3 0 - 5 0 > 5 0
  • 36. H O W I S M S Q U A N T I F I E D E C H O C A R D I O G R A P H I C A L L Y ā€¢ INFORMATION REGARDING: ā€¢ - LEFT ATRIAL SIZE; ā€¢ - VALVE MORPHOLOGY; ā€¢ - PRESENCE OF LA THROMBUS; ā€¢ - UNDERLYING ETIOLOGY OF MS; ā€¢ - CHANGES OF LV FUNCTION AND SIZE ā€¢ ALSO IMPORTANT WHEN ASSESSING SEVERITY OF MS
  • 37. I N D I C A T I O N S F O R M I T R A L V A L V E S U R G E R Y I N P A T I E N T S W I T H M S ā€¢ AHA GUIDELINES G U I G E L I N E S C L A S S I M O D E R A T E - S E V E R E M S W I T H S Y M P T O M S ( N Y H A I I I - I V ) W H E R E P E R C U T A N E O U S M I T R A L B A L L O O N V A L V U L O P L A S T Y ( P M B V ) I S N O T S U I T A B L E C L A S S I I A S E V E R E M S W I T H S E V E R E P U L M O N A R Y H Y P E R T E N S I O N ( > 5 0 M M H G ) O R S Y M P T O M S ( N Y H A I - I I ) W H E R E P M B V I S N O T S U I T A B L E C L A S S I I B M O D E R A T E - S E V E R E M S W I T H R E C U R R E N T E M B O L I C E V E N T S O N A N T I C O A G U L A T I O N
  • 38. W H A T A R E D E T E R M I N A N T S O F W I L K I N S M I T R A L S T E N O S I S S C O R E W I L K I N S S C O R E L E A F L E T M O B I L I T Y 0 1 2 3 4 L E A F L E T T H I C K E N I N G 0 1 2 3 4 L E A F L E T C A L C I F I C A T I O N 0 1 2 3 4 S U B V A L V U L A R T H I C K E N I N G 0 1 2 3 4 EACH SCORES BETWEEN 0-4, WITH MAX. SCORE OF 16 WILKINS SCORE > 9 SUGGESTS LESION IS UNLIKELY TO BE AMENABLE TO PMBV
  • 39.
  • 40. I N D I C A T I O N S F O R P E R C U T A N E O U S M I T R A L B A L L O O N V A L V U L O P L A S T Y ( P M B V ) I N P A T I E N T S W I T H M S ā€¢ AHA GUIDELINES G U I G E L I N E S C L A S S I M O D E R A T E - S E V E R E M S W I T H E I T H E R S Y M P T O M S ( N Y H A I I - I V ) O R P U L M O N A R Y H Y P E R T E N S I O N ( > 5 0 M M H G A T R E S T O R 6 0 M M H G 0 N E X E R C I S E ) C L A S S I I A M O D E R A T E - S E V E R E M S W I T H S Y M P T O M S ( N Y H A I I I - I V ) I N P A T I E N T S W I T H N O N - P L I A B L E V A L V E O R P A T I E N T S W H O A R E A T H I G H S U R G I C A L R I S K O F D E A T H PMBV SHOULD BE ONLY PERFORMED IN PATIENTS WITH FAVOURABLE VALVE MORPHOLOGY ( WILKINS SCORE OF AT LEAST 8 OR LESS ) AND NO CONTRAINDICATIONS: LEFT ATRIAL THROMBUS, MODERATE SEVERE MR
  • 41. H O W I S P E R C U T A N E O U S M I T R A L B A L L O O N V A L V U L O P L A S T Y ( P M B V ) P E R F O R M E D ? ā€¢ LOCAL ANAESTHESIA AND SEDATION ā€¢ VALVULOPLASTY BALLOON IS PASSED: ā€¢ - VIA FEMORAL VEIN; ā€¢ - INTO RIGHT ATRIUM; ā€¢ - ACROSS INTRA-ATRIAL SEPTUM; ā€¢ - INTO LEFT ATRIUM; ā€¢ - ACROSS MITRAL VALVE ā€¢ AND INFLATED ā€¢ RESULTS ARE BEST WHEN LEAFLETS ARE: THIN, MOBILE, NOT CALCIFIED, IN YOUNGER AGE GROUP AND WHERE SUBVALVULAR CHORDAE HAVE NOT FUSED/CALCIFIED ā€¢ PMBV TYPICALLY INCREASE MITRALVALVE AREA FROM 1-2 CM2 ā€¢ COMPLICATIONS: M O R T A L I T Y C A R D I A C P E R F O R A T I O N S T R O K E S E V E R E M R 1 % 1 % 2 % 3 %
  • 42. H O W I S C L O S E D M I T R A L V A L V U L O T O M Y P E R F O R M E D ? ā€¢ LEFT POSTEROLATERAL THORACOTOMY ā€¢ PERICARDIUM OPENED ANTERIOR TO PHRENIC NERVE ā€¢ INDEX FINGER IS INSERTED INTO LEFT ATRIUM ā€¢ TUBBS DILATOR IS PASSED VIA APEX THROUG LV, USING PURSE STRING SUTURES TO REDUCE BLOOD LOSS AND AIR EMBOLISM ā€¢ DILATOR IS THEN GUIDED MANUALLY THROUGH MITRAL VALVE ORIFICE AND OPENED ALONG NATURAL INTER- COMMISSURAL LINE ā€¢ RESULTING DILATATION IS ASSESSED MANUALLY AND BY TRANSESOPHAGEAL ECHOCARDIOGRAPHY
  • 43. M I T R A L V A L V E S U R G I C A L T E C H N I Q U E S M I T R A L V A L V E R E P A I R & M I T R A L V A L V E R E P L A C E M E N T
  • 44. S U R G I C A L A P P R O A C H E S T O M I T R A L V A L V E ā€¢ STANDARD LEFT ATRIOTOMY: ā€¢ - PERICARDIAL REFLECTIONS AROUND INFERIOR AND SUPERIOR PULMONARY VEINS ARE MOBILISED; ā€¢ - WATERSTONā€™S INTERATRIAL GROOVE IS DEVELOPED THEREBY REFLECTING RA BACK OVER LA; ā€¢ INCISION IS MADE IN LA ANTERIOR AND MEDIAL TO RIGHT SUPERIOR PULMONARY VEIN AND CONTINUED INFERIORLY AND SUPERIORLY
  • 45. S U R G I C A L A P P R O A C H E S T O M I T R A L V A L V E ā€¢ OTHER SURGICAL APPROACHES TO MITRAL VALVE: ā€¢ - BI-ATRIAL TRAS- SEPTAL INCISION; ā€¢ - SUPERIOR ROOF INCISION; ā€¢ - BI-ATRIAL ( DUBOST ) INCISION;
  • 46. S U R G I C A L A P P R O A C H E S T O M I T R A L V A L V E ā€¢ OTHER SURGICAL APPROACHES TO MITRAL VALVE:
  • 47. S U R G I C A L A P P R O A C H E S T O M I T R A L V A L V E ā€¢ OTHER SURGICAL APPROACHES TO MITRAL VALVE: ā€¢ - RIGHT ANTEROLATERAL THORACOTOMY; ā€¢ - RIGHT ANTEROLATERAL MINI-THORACOTOMY
  • 48. S U R G I C A L A P P R O A C H E S T O M I T R A L V A L V E ā€¢ OTHER SURGICAL APPROACHES TO MITRAL VALVE:
  • 49. H O W I S M I T R A L V A L V E A S S E S S E D I N T R A - O P E R A T I V E L Y ? ā€¢ MV IS INSPECTED USING NERVE HOOKS TO MEASURE DEGREE OF MOTION OF EACH SCALLOP ( P1, P2, P3, A1, A2, A3 ) OF BOTH LEAFLETS COMPARED AGAINST REFERENCE POINT ( USUALLY P1 OR ANTEROLATERAL COMMISSURE )
  • 50. H O W I S M I T R A L V A L V E A S S E S S E D I N T R A - O P E R A T I V E L Y ? ā€¢ VALVE COMPETENCY CAN BE CHECKED BEFORE REPAIR BY DISTENDING LV WITH COLD SALINE AND IDENTIFYING AETIOLOGY AND LOCATION OF REGURGITATION JET ā€¢ COMPETENCE OF MV FOLLOWING REPAIR IS ASSESSED BY: ā€¢ - STATIC TESTING UNDER DIRECT VISION BY DISTENDING LV WITH COLD SALINE; ā€¢ - TEE WITH APPROPRIATELY FILLED LV OFF CPB SUPPORT
  • 51. W H A T S T R U C T U R E S A R E A T R I S K D U R I N G M I T R A L V A L V E S U R G E R Y ? ā€¢ CIRCUMFLEX CORONARY ARTERY ā€¢ CORONARY SINUS ā€¢ AORTIC VALVE ( LEFT & NON- CORONARY CUSPS ) ā€¢ ATRIOVENTRICULAR NODE AND BUNDLE OF HIS
  • 52.
  • 53. W H A T I S S Y S T O L I C A N T E R I O R M O T I O N ( S A M ) O F M I T R A L V A L V E ? ā€¢ SYSTOLIC ANTERIOR MOTION ( SAM ) OCCURS WHEN THE TIPS OF MV LEAFLETS ARE DISPLACED ANTERIORLY INTO LVOT ā€¢ THIS RESULTS IN VENTURI EFFECT PULLING ON MITRAL VALVE LEAFLETS CAUSING MR AND LVOT OBSTRUCTION ā€¢ IN COMPARISON, DURING DIASTOLE LVOT DIAMETER IS NORMAL ā€¢ SAM IS MORE COMMON IN PATIENTS WITH: ā€¢ - HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY ( HOCM ); ā€¢ - SMALL ELDERLY WOMEN WITH ASYMMETRIC SEPTAL HYPERTROPHY
  • 54. W H A T A R E S U R G I C A L T R E A T M E N T O P T I O N S F O R M I T R A L V A L V E D I S E A S E L E S I O N D Y S F U N C T I O N T Y P E O P T I O N A N N U L A R D I L A T A T I O N N O R M A L L E A F L E T M O T I O N I C O MP L E TE F L E XI B L E A N N U L O P L A S TY R I N G ( P H YS I O ) L E A F L E T P E R F O R A T I O N N O R M A L L E A F L E T M O T I O N I B O V I N E P E R I C A R D I A L P A TC H P O S T E R I O R M I T R A L V A L V E L E A F L E T P R O L A P S E E X C E S S L E A F L E T M O T I O N I I - Q U A D R A N G U L A R R E S E C TI O N - TR I A N G U L A R R E S E C TI O N - S L I D I N G A N N U L O P L A S TY - A R TI F I C I A L C H O R D I MP L A N TA TI O N A N T E R I O R M I T R A L V A L V E L E A F L E T P R O L A P S E E X C E S S L E A F L E T M O T I O N I I - TR I A N G U L A R R E S E C TI O N - A R TI F I C I A L C H O R D I MP L A N TA TI O N B I L E A F L E T M I T R A L V A L V E P R O L A P S E E X C E S S L E A F L E T M O T I O N I I - L E A F L E T R E S E C TI O N - A R TI F I C I A L C H O R D I MP L A N TA TI O N - A L F I E R I S TI TC H - MI TR A L V A L V E R E P L A C E ME N T P A R T I A L P A P I L L A R Y M U S C L E R U P T U R E E X C E S S L E A F L E T M O T I O N I I R E I MP L A N TA TI O N O F P A P I L L A R Y MU S C L E C O M P L E T E P A P I L L A R Y M U S C L E R U P T U R E E X C E S S L E A F L E T M O T I O N I I MI TR A L V A L V E R E P L A C E ME N T I S C H A E M I C M R R E S T R I C T E D L E A F L E T C L O S U R E I I I B - MC C A R TH Y - A D A MS I MR R I N G - D O W N S I Z I N G A N N U L O P L A S TY - MI TR A L V A L V E R E P L A C E ME T R H E U M A T I C M R R E S T R I C T E D L E A F L E T O P E N I N G I I I A MI TR A L V A L V E R E P L A C E ME N T
  • 55. T E C H N I Q U E S M I T R A L V A L V E R E P A I R
  • 56. B E N E F I T S O F M I T R A L A N N U L O P L A S T Y R I N G S ā€¢ CORRECTS ANNULAR DILATATION ā€¢ PREVENTS FURTHER ANNULAR DILATATION ā€¢ INCREASES LEAFLET COAPTATION ā€¢ REINFORCES ANNULAR SUTURE LINES
  • 57. P R O S T H E T I C R I N G S & B A N D S M I T R A L V A L V E R E P A I R
  • 58. F E A T U R E S O F D I F F E R E N T M I T R A L V A L V E R I N G P R O S T H E S I S ā€¢ CARPENTIER-EDWARDS PHYSIO ANNULOPLASTY RING: ā€¢ - COMPLETE, SEMI-FLEXIBLE; ā€¢ - FREQUENTLY USED ANNULOPLASTY RING ā€¢ CARPENTIER RING ā€¢ - RIGID, COMPLETE ā€¢ - ANTERIOR-POSTERIOR DIAMETER CAN BE ADJUSTED FOR A BESPOKE RING SHAPE
  • 59. F E A T U R E S O F D I F F E R E N T M I T R A L V A L V E R I N G P R O S T H E S I S ā€¢ COSGROVE- EDWARDS ANNULOPLASTY SYSTEM ( BAND) ā€¢ - INCOMPLETE, FLEXIBLE ā€¢ CARPENTIER- MACCARTHY-ADAMS IMR ETILOGIX ANNULOPLASTY RING ā€¢ - FOR ISCHAEMIC MR
  • 60. P R O S T H E T I C R I N G S T A N D A R D I M P L A N T A T I O N T E C H N I Q U E M I T R A L V A L V E R E P A I R 3 2 1 4 5
  • 61. D I L A T E D C A R D O P M Y O P A T H Y T Y P E I I I B R E S T R I C T E D L E A F L E T C L O S U R E ( S Y S T O L I C )
  • 62. T R I A N G U L A R / Q U A D R A N G U L A R R E S E C T I O N & S L I D I N G R E P A I R M I T R A L V A L V E R E P A I R 1 2 3
  • 63. Q U A D R A N G U L A R R E S E C T I O N O F P 2 P M L M I T R A L V A L V E R E P A I R 4 1 2 3
  • 64. T R I A N G U L A R R E S E C T I O N O F A 3 A M L M I T R A L V A L V E R E P A I R 1 2
  • 65. R H E U M A T I C F E V E R ( T Y P E I I I A ) - C O M M I S S U R O T O M Y M I T R A L V A L V E R E P A I R 1 2
  • 66. C H O R D A L R U P T U R E ( T Y P E I I ) - A R T I F I C I A L C H O R D S M I T R A L V A L V E R E P A I R
  • 67. C H O R D A L R U P T U R E ( T Y P E I I ) - A R T I F I C I A L C H O R D S M I T R A L V A L V E R E P A I R
  • 68. I S C H A E M I C M I T R A L R I N G I M P L A N T A T I O N M I T R A L V A L V E R E P A I R
  • 69. T E C H N I Q U E S M I T R A L V A L V E R E P L A C E M E N T
  • 70. T Y P E S O F P R O S T H E T I C V A L V E S M I T R A L V A L V E R E P L A C E M E N T
  • 71. A D V A N T A G E S O F R E P A I R I N G R A T H E R T H A N R E P L A C I N G M I T R A L V A L V E ā€¢ AS COMPARED WITH MITRAL VALVE REPLACEMENT, MITRAL VALVE REPAIR IS ASSOCIATED WITH GREATER FREEDOM FROM: ā€¢ - MORTALITY ( OPERATIVE AND LONG-TERM ); ā€¢ - STRUCTURAL VALVE DETERIORATION; ā€¢ - RE-OPERATION; ā€¢ - INFECTIVE ENDOCARDITIS; ā€¢ - THROMBO-EMBOLISM ā€¢ - HAEMORRHAGE ā€¢ AS MORE OF SUBVALVULAR APPARATUS IS PRESERVED, MITRAL VALVE REPAIR IS BETTER AT MAINTAINIG LV GEOMETRY AND HENCE IS ASSOCIATED WITH LESS LV DYSFUNCTION COMPARED WITH MITRAL VALVE REPLACEMENT
  • 72. F R E E D O M F R O M R E - I N T E R V E N T I O N F O R P A T I E N T S O L D E R T H A N 7 0 Y E A R S F O R D I F F E R E N T M I T R A L V A L V E P R O S T H E S E S A N D R E P A I R T E C H N I Q U E S A V A I L A B L E F R E E D O M F R O M R E - I N T E R V E N T I O N A T 1 0 Y E A R S M E C H A N I C A L V A L V E P R O S T H E S I S 9 8 % B O V I N E P E R I C A R D I A L B I O P R O S T H E S I S 8 0 % P O R C I N E B I O P R O S T H E S I S 7 5 % P M B V 8 0 % O P E N M V C O M M I S S U R O T O M Y 8 0 % C L O S E D M V C O M M I S S U R O T O M Y 7 0 % R E P A I R O F A N T E R I O R M I T R A L L E A F L E T 7 8 % R E P A I R O F P O S T E R I O R M I T R A L L E A F L E T 9 8 %