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13 Mitral Valve Infective Endocarditis
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Fig. 13.3 (a) Perforation of the anterior mitral valve leaet caused by the presence of a vegetation and infective destruction of the native tissue, and (b) repair with bovine pericardium patch augmentation of the anterior leaet and ring annuloplasty
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Fig. 13.4 Operative images illustrating (a) 0.7cm vegetation lying on the atrial surface A3 scallop of the anterior leaet, (b) resected vegeta­tion and surrounding infected tissue, (c) closure of the defect in the A3
segment of the leaet with a bovine pericardial patch, and (d) implanta­tion of an annuloplasty ring to support the repair
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Fig. 13.5 (a) Perforation of the posterior leaet caused by the presence of a vegetation and infective destruction of the native tissue, and (b) repair with bovine pericardium patch augmentation of the posterior leaet and ring annuloplasty
Fig. 13.6 (a) Prolapse of the posteromedial commissure caused by the presence of a vegetation and infective destruction of the underlying native tissue, (b) debridement of the infected tissue, (c) repair with sliding plasty advancement of the medial half of the posterior leaet and commissuroplasty, and (d) ring annuloplasty to support the repair
tion may also be required to support the commissural reconstruction.
The vegetation and any resected tissue should be sent for microbiological analysis. Any underlying mitral valve pathology, which may have contributed to the development of the infective endocarditis, should also be treated during the repair procedure using standard techniques. Degenerative mitral valve prolapse is the most common underlying cardiac
lesion that predisposes to mitral valve infective endocarditis.
Once the repair procedure has been completed, it is important to stabilise the mitral valve annulus with an annu­loplasty band or ring, thereby relieving the tension on the leaets by optimising the coaptation zone. Although some advocate avoidance of using prosthetic material in these patients, there is no evidence that using an annuloplasty ring
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13 Mitral Valve Infective Endocarditis
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101
or band increases the risk of recurrent endocarditis but it does increase the longevity of the repair.
Following implantation of the annuloplasty ring or band, injecting cold saline allows the mitral valve to be assessed for competency, adequate depth of coaptation (>8mm) and that the coaptation line runs parallel to the posterior annulus.
annulus and the abscess cavity, followed by reconstruction of the posterior annulus and atrioventricular groove (Fig.13.7). An oversized fresh autologous or bovine pericardial patch is used to cover the defect in the atrioventricular groove and attached to the adjacent posterior walls of the left ventricle and left atrium using a continuous 4/0 prolene suture. It is important to place the sutures in the ventricle distant from the edges of the resected material to ensure a strong suture
Annular Reconstruction
line. Left atrial and ventricular pressures help to maintain
apposition of the patch against the posterior wall of the heart. In patients with infective endocarditis of the mitral valve, it is important to explore the surrounding tissues to assess for the presence of any peri-annular abscess or spread onto the aorto-mitral curtain. If present, extension of the infective process into the posterior annulus with resulting peri-annular abscess formation will require extensive debridement of the
Fig. 13.7 (a) Abscess of the posterior mitral valve annulus, (b) debridement of infected tissue extending into the atrioventricular groove, (c) bovine pericardium patch reconstruction of the atrioventricular groove, extending onto the posterior wall of the left ventricle and left atrium, (d) bovine pericardium patch reconstruction of the posterior leaet, and (e) ring annuloplasty to support the repair
The reconstructed posterior annulus with pericardial patch
can then be used to receive the interrupted valve annulo-
plasty or replacement sutures, which will additionally help to
secure the patch in situ.
If repair is not possible and replacement is necessary, the
choice between a mechanical or biological valve should be
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N. Moorjani
made with the usual considerations, as there is no difference in recurrent endocarditis rates between the two valve choices.
Following all surgery for mitral valve endocarditis (repair or replacement), organism-specic intravenous antibiotics should be continued as dictated by current international rec­ommendations, usually for 4–6 weeks. If organisms are grown from the resected material, it is the authors recom­mendation that antibiotic treatment should continue for 6 weeks with a full endocarditis screen 2 weeks after the completion of the treatment.
Surgical Tips
1. Complete debridement of the vegetation and adja­cent infected and inamed tissue is necessary to reduce the risk of recurrence.
2. Assess that there is enough residual tissue after resection to allow for repair.
3. Augment any defects in the leaet tissue or annulus with bovine or autologous pericardium.
4. Support the leaet repair procedure with an annulo­plasty ring or band.
Comment
For endocarditis patients who have limited valve destruction, the results of mitral valve repair have shown excellent out­comes, with an in-hospital mortality of 3% and a low peri­operative complication rate. In general, however, patients with acute mitral valve endocarditis have an operative mor­tality of 10–20%. Long-term outcome measures at 10years of patients who have undergone repair have also demon­strated excellent freedom from recurrent mitral regurgitation (91% with no or 1+ MR), freedom from reoperation (91%), and survival (80%). Meta-analyses and large series compar­ing repair versus replacement in patients with mitral valve infective endocarditis have shown better short- and long­term outcome measures, with a lower operative mortality, increased long-term survival, reduced risk of recurrent endo-
carditis, and reduced need for a reoperation in patients undergoing repair. The increased incidence of reoperation in patients undergoing replacement for mitral valve endocardi­tis is related to paravalvular leaks, structural valve deteriora­tion, and prosthetic valve endocarditis.
Suggested Reading
AATS Surgical Treatment of Infective Endocarditis Consensus
Guidelines Writing Committee Chairs, Pettersson GB, Coselli JS, Writing Committee, Pettersson GB, Coselli JS, Hussain ST, Grifn B, Blackstone EH, Gordon SM, LeMaire SA, Woc-Colburn LE.The 2016 the American Association for Thoracic Surgery (AATS) con­sensus guidelines: surgical treatment of infective endocarditis. J Thorac Cardiovasc Surg. 2017;153(6):1241–58.
de Kerchove L, Price J, Tamer S, Glineur D, Momeni M, Noirhomme
P, ElKhoury G.Extending the scope of mitral valve repair in active endocarditis. J Thorac Cardiovasc Surg. 2012;123(4 Suppl):S91–5.
Evans CF, Gammie JS.Surgical management of mitral valve infective
endocarditis. Semin Thorac Cardiovasc Surg. 2011;23(3):232–40.
Harky A, Hof A, Garner M, Froghi S, Bashir M. Mitral valve repair
or replacement in native valve endocarditis? Systematic review and meta-analysis. J Card Surg. 2018;33(7):364–71.
Kitai T, Masumoto A, Okada T, Koyama T, Furukawa Y.Optimal timing
of surgery for patients with active infective endocarditis. Cardiol Clin. 2021;39(2):197–209.
Okada Y, Nakai T, Kitai T.Role of mitral valve repair for mitral infec-
tive endocarditis. Cardiol Clin. 2021;39(2):189–96.
Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd,
Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, O'Gara PT, Rigolin VH, Sundt TM 3rd, Thompson A, Toly C. 2020 ACC/ AHA guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143(5):e35–71.
Sareyyupoglu B, Schaff HV, Suri RM, Connolly HM, Daly RC, Orszulak
TA.Safety and durability of mitral valve repair for anterior leaet perforation. J Thorac Cardiovasc Surg. 2010;139(6):1288–93.
Shimokawa T, Kasegawa H, Matsuyama S, Seki H, Manabe S, Fukui T,
Morita S, Takanashi S.Long-term outcome of mitral valve repair for infective endocarditis. Ann Thorac Surg. 2009;88(3):733–9.
Toyoda N, Itagaki S, Egorova NN, Tannous H, Anyanwu AC,
El-Eshmawi A, Adams DH, Chikwe J.Real-world outcomes of sur­gery for native mitral valve endocarditis. J Thorac Cardiovasc Surg. 2017;154(6):1906–12.
Zegdi R, Debièche M, Latrémouille C, Lebied D, Chardigny C, Grinda
JM, Chauvaud S, Deloche A, Carpentier A, Fabiani JN.Long-term results of mitral valve repair in active endocarditis. Circulation. 2005;111(19):2532–6.
Part IV
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Valve Surgery: Tricuspid Valve Surgery
Tricuspid Valve Disease Techniques
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NarainMoorjani, FrancisC.Wells, andSamerA.M.Nashef
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As the name suggests the right-sided atrioventricular valve has three primary leaets, the anterior, septal, and inferior leaets. Other than that, the same basic components of papil­lary muscles and tendinous cords are present. The overall shape is more a rounded triangle than the oval mitral valve orice.
This shape required the development of the third, inferior, leaet which may represent an enlarged commissural leaet. The largest leaet is the anterior leaet, the third being the septal leaet (Fig.14.1).
The relationships of the leaets to the supporting cardiac chamber muscle are as follows and shown in Fig.14.1. The origin of the anterior leaet is at the septal junction with the aortic root and extends along the majority of the right ven­tricular muscular free wall. This is an important point as it is this portion of the atrioventricular junction that stretches giv­ing rise to type 1 annular dilatation and is the cause of sec­ondary tricuspid regurgitation. As the right ventricle dilates progressively with volume and pressure overload, this dilata­tion causes distraction of the tricuspid valve leaets from their natural coaptation lines. Correction of the valve incom­petence is achieved by reducing this part of the circumfer­ence of the orice.
The inferior leaet is associated with the remainder of the right ventricular wall and its junction with the septum, and is of variable length.
As in functional (secondary) mitral regurgitation, in tri­cuspid regurgitation there is no visible stretching of the sep­tal portion nor of the aortic outow area.
N. Moorjani Department of Cardiothoracic Surgery, Royal Papworth Hospital, Cambridge, UK
F. C. Wells (*) Royal Papworth Hospital, Cambridge University Group of Hospitals, Cambridge, UK e-mail: francis.wells@nhs.net
S. A. M. Nashef Department of Surgery, Royal Papworth Hospital, Cambridge, UK e-mail: sam.nashef@nhs.net
In the normal tricuspid valve, the plane of the valve in relation to the atrioventricular junction is complicated with more deviation from the neutral plane than is found in the mitral valve (see Fig.14.1). Of how much this is of impor­tance to the normal function of the valve is debatable. Although some of the industry offer rigid annuloplasty rings that pay homage to this differential planar, it is no more than a gesture as they only adjust in one direction. The only annu­loplasty support that more closely allows approximation to the natural shape is one that is exible for the whole of the right ventricular line of attachment. Whilst some would argue that the draw string approach of the De Vega procedure will allow for this, the suture is usually pulled so tight, to reduce the orice size, as to become relatively stiff. The role of any annuloplasty ring is to reduce the orice size to bring the leaets back into coaptation and to stabilize the base of the right ventricle. Allowing motion of the annulus through­out the cardiac cycle may be an added benet though none has been shown. The most common cause of tricuspid regur­gitation is atrial and ventricular dilatation, usually as a result of chronic atrial brillation.
Whilst this statement is true, it is always important to look out for loss of sub-valvar integrity through cordal or papil­lary muscle elongation, rupture, or congenital absence. In Barlow’s disease, the changes that are seen in the mitral valve are frequently found in the tricuspid valve.
Although as a result of the lower pressures on the right side, the excess tissue seen in this condition prevents early regurgitation, it can be seen in patients that present late with raised pulmonary artery pressures and RV dilatation. In this situation, an annuloplasty ring will usually sufce.
Causes of cordal and papillary muscle rupture include endocarditis (particularly with Staphylococcus), trauma (both blunt and sharp forms), and occasionally catheter trauma from malpositioned Swan-Gantz catheters and pac­ing wires. Sudden and massive deceleration against the closed valve in systole can cause rupture as in road trafc accidents or falls from a height. Knife wounds are another cause and should be thought of in penetrating chest injury.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 F. C. Wells (ed.), Atlas of Cardiac Surgery, Springer Surgery Atlas Series, https://doi.org/10.1007/978-3-031-43195-1_14
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Low RV apex
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Anteroseptal
commissure
N. Moorjani et al.
Anterior leaflet
Posterior
leaflet
Septal leafleft
Membranous
septum
AV
node
Coronary
sinus
Posteroseptal commissure
c
Control
RA high
P
Fig. 14.1 (a) The functional anatomy of the tricuspid valve. (b) The site of annular dilatation of the valve orice. (c) The planar shape of the tri- cuspid annulus in the normal and the dilated state
Much greater attention has been given to both primary and secondary Tricuspid regurgitation (TR) of late, and the morbidity and mortality from untreated TR have been reported more widely in recent years [1]. The traditional acceptance of the lesion as a bystander lesion, not needing attention, has been consigned to the dustbin of cardiac surgi­cal history.
Something less spoken of however is the production of tricuspid stenosis from too great a reduction of orice cir­cumference and hence orice area brought about by an assumption that the greater the degree of coaptation the lon­ger lasting the result. In choosing the appropriate ring size, it should at least approximate to the size of the fully developed
Ao
valve
A
P
The ‘de Vega’ technique of suture annuloplasty has been shown to have inferior results in most hands and is rarely used in the modern era [2].
The development of worsening TR post left-sided valve surgery is accompanied by worse long-term results. There is a higher morbidity and mortality when tricuspid regurgita­tion is corrected at a second operation, hence restoration of competency at the rst operation for mitral valve disease is to be recommended if the orice is dilated signicantly, with an orice diameter in the diagonal plane of greater than
4.0cm and there is more than mild regurgitation.
A tabular schema for the management of tricuspid regur­gitation is shown in Fig.14.2 [3].
Functional TR
RA High
Low RV apex
anterior leaet.
A
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FTR disease processes
Left-sided
heart
disease
Right
ventricular
(RV) afterload
increase
(with or without
pulmonary
hypertension)
RV
remodeling
Tr icuspid annular dilation.
(In some instances leaflet
tethering occurs with the
same triggering factors)
Abnormalities of tricuspid
anatomy and function
lead to functional
tricuspid regurgitation
Atrial
fibrillation
Altered
RV function
(FTR)
FTR assessments Diagnosis and treatment
Tricuspid regurgitation (TR)
TR is the leakage of blood backwards through the tricuspid valve each time the right ventricle contracts
Color flow jet visualization is used to evaluate PISA radius and effective regurgitant orifice or regurgitant volume
Annular dilation
The annular ring is attached to the tricuspid valve leaflets. Dilation can result in poor leaflet apposition
2D-echocardiography coupled with 3D imaging is used to accurately measure annular diameter
Leaflet coaptation mode
Coaptation is the surface where the leaflets meet. If decreased, contact is made at the leaflet edge (edge-to­edge), leaflet tethering can restrict leaflet closure
3D echocardiography is recommended to measure tenting volume (TV) the area within the tricuspid leaflets
Stage 1
TR severity:
None or mild
Annular
diameter:
<40 mm
Coaptation
mode: Normal
(body-to-body),
with no leaflet
tethering
Medical
treatment.
No surgical
Intervention
is indicated
Stage 2
TR severity:
Mild or moderate
Annular
diameter:
>40 mm
Coaptation
mode:
Abnormal
(edge-to-edge),
with or without
tethering of
<8 mm below
the annular
plane
Concomitant
tricuspid valve
annuloplasty is
recommended
the annular plane
Stage 3
TR severity:
Severe
Annular
diameter:
>40 mm
Coaptation
mode:
No coaptation,
with or without
tethering of
>8 mm below
Concomitant
tricuspid valve
annuloplasty
and leaflet augmentation (if tethering is
present)
Fig. 14.2 Tabular classication of tricuspid regurgitation. (From Dreyfus etal. [4]; with permission)
Insertion ofAnnuloplasty Band
may cause problems. In the A-V nodal area, that of heart block and in the region of the right coronary artery, coronary
In placing the annuloplasty ring, suture care must be taken at two sites in particular. The rst is in the region of the atrio­ventricular node and bundle and the second in the region of the right coronary artery. Too deep placement in both areas
distortion and occlusion can occur to devastating effect [4]. It is most important the needle is directed down into ven­tricular muscle and not tangentially into the surrounding atrial tissues (Fig.14.3).
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Through hinge
Backhand
Forehand
Forehand
Backhand
Fig. 14.3 Suture techniques for tricuspid annuloplasty
Aortic segment
De Vega Technique
2mm from hinge
2mm
from hinge
Through hinge
The de Vega annuloplasty is a simple suture technique with which to narrow down the annulus of the tricuspid valve. Although it was the most common procedure to correct TR, it has largely fallen out of favour because of evidence of higher rates of recurrent tricuspid regurgita­tion, largely due to sutures cutting out of the imsy tricus­pid ‘annulus’, resulting in the return of annular enlargement and the ‘guitar string sign’ of sutures cross­ing the orice. This can be avoided by a slight modica­tion of the technique: the rst suture is taken inferiorly at the septal-posterior leaet commissure, with the second suture going back on itself to start at the midpoint of the rst suture (Figs.14.4 and 14.5). This is continued until the point where conduction tissue begins (X in the gure), then the course of the suture is reversed to anticlockwise and the suture line is completed in the same way back to the starting point. This results in a double line of cinching sutures that simply cannot cut out. In the overwhelming majority of cases, the annulus can be reduced to the desired diameter with two sutures lines as above. Where the annulus is enlarged to an exceptional degree, a third or even a fourth suture line may be needed.
As mentioned earlier this was the mainstay of manage-
ment of tricuspid annular dilatation. Several recent papers
Fig. 14.4 Classical de Vega suture technique
have shown the relative inferiority of this technique over ring annuloplasty, but the double row of suturing technique as shown here seems to be more stable over long follow-up periods. The important points to stress with this modication are as follows. First the suture line must start and nish at the same end points as they would for an annuloplasty ring, and secondly, a two-layer approach as shown should be used rather than the single traditional layer.
a
b
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c
Fig. 14.5 Modied de Vega technique
The Clover Leaf Stitch
In this technique, the central coaptation point of each leaet is sewn together giving a central point of xation, analogous to the Aleri edge-to-edge technique in the mitral valve (Fig.14.6).
Fig. 14.6 (a–c) Clover stitch