The document discusses mitral regurgitation (MR), including its natural history, pathophysiology, classification, causes, symptoms, signs, quantification via echocardiography, and indications for mitral valve surgery. It notes that asymptomatic patients with MR can have a long latent period before symptoms develop. Severe MR is classified based on criteria such as jet area, regurgitant volume, and effective regurgitant orifice area. Etiologies include myxomatous degeneration, rheumatic fever, and ischemic cardiomyopathy. Evaluation involves assessing left atrial and ventricular size and function along with MR severity. Surgery is indicated for severe, symptomatic MR or asymptomatic patients with good ventricular function and a high likelihood of
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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¢ CARPENTIERāS 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¢ CARPENTIERāS 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 BARLOWāS 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¢ PATIENTāS 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 (
ORTNERāS 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¢ - WATERSTONāS 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 %