Shemin
R
Ji
. Tricuspid Valve Disease.
Cohn Lh, ed. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2008:1111-1128.
Tricuspid Valve Disease
Richard J. Shemin
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INTRODUCTION
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The tricuspid valve is composed of three leaflets (i.e., anterior, posterior, and septal) attached to a fibrous annulus. The leaflets usually attach via chordae tendineae to three papillary muscles that are an integral part of the right ventricular wall. Surrounding structures of surgical importance are the coronary sinus, the atrioventricular node, and the right coronary artery (RCA) (Fig. 47-1A).
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Figure 47-1 (A) View of the tricuspid valve and labeled structures of surgical importance. (B) Direction of progressive tricuspid valve annular dilatation.
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The tricuspid valve may malfunction due to structural malformation secondary to other cardiac pathology or due to hardware through the valve [e.g., pacemaker or automatic internal cardiac defibrillation (AICD) wires]. Congenital abnormalities such as atrial septal defect (ASD), ventricular septal defect (VSD), and Ebstein disease lead to malfunction and tricuspid regurgitation (TR). Cases of isolated tricuspid disease associated with systemic lupus erythematosus, cor pulmonale, inferior myocardial infarction, scleroderma, or methysergide intake are noteworthy but rarely encountered in surgical practice.1–12
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ETIOLOGY
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The most common presentation of TR is secondary to cardiac valvular pathology (mostly mitral valve disease) on the left side of the heart. As pulmonary hypertension develops, leading to right ventricular dilatation, the tricuspid valve annulus will dilate. The circumference of the annulus lengthens primarily along the attachments of the anterior and posterior leaflets. The septal leaflet is fixed between the fibrous trigones, preventing lengthening (Fig. 47-1B). As the annular and ventricular dilatation progresses, the chordal papillary muscle complex becomes functionally shortened. This combination prevents leaflet apposition, resulting in valvular incompetence.13–18
Eisenmenger syndrome and primary pulmonary hypertension lead to the same pathophysiology of progressive right ventricular dilatation, tricuspid annular enlargement, and valvular incompetence. A right ventricular infarction produces either disruption of the papillary muscle or a severe regional wall motion abnormality that prevents normal leaflet apposition by a tethering effect on the leaflets, leading to regurgitation. Marfan syndrome and other variations of myxomatous disease affecting the mitral and tricuspid valves can lead to prolapsing leaflets, elongation of chordae, or chordal rupture, producing valvular incompetence. Blunt or penetrating chest trauma may disrupt the structural components of the tricuspid valve. Dilated cardiomyopathy in the late stages of biventricular failure and pulmonary hypertension produces TR.19–22 Infectious endocarditis can destroy leaflet tissue, mostly in drug addicts with staphylococcal infection.23–26
The carcinoid syndrome leads to either focal or diffuse deposits of fibrous tissue on the endocardium of valve cusps, cardiac chambers, intima of the great vessels, and coronary sinus. The white fibrous carcinoid plaques, if present on the ventricular side of the tricuspid valve cusps, adhere the leaflet tissue to the right ventricular wall, preventing leaflet coaptation.27–29 Rheumatic disease of the tricuspid valve is always associated with mitral valve involvement, and the deformity of the tricuspid tissue results in a tricuspid valve stenosis as well as regurgitation.30
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CLINICAL PRESENTATION AND PATHOPHYSIOLOGY
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Tricuspid Regurgitation
Patients with TR have the presenting symptoms of fatigue and weakness related to a reduction in cardiac output. Right-sided heart failure leads to ascites, congestive hepatosplenomegaly, pulsatile liver, pleural effusions, and peripheral edema. In the late stages, these patients are wasted with cachexia, cyanosis, and jaundice. Atrial fibrillation is common. Impressive jugular venous distention with an s wave or fused c and v waves, followed by a prominent y descent, is present. During inspiration, this finding is accentuated because of the physiologic increase in venous return. The cardiac oscillatory examination is notable for an S3 that increases with inspiration and decreases with a Valsalva maneuver, increased P2 if pulmonary hypertension has developed, and a parasternal pansystolic murmur increasing with inspiration.
The chest x-ray demonstrates cardiomegaly, increased right atrial and ventricular size, a prominent azygous vein, possible pleural effusion, and upward diaphragmatic displacement owing to ascites. Echocardiography best assesses the degree of regurgitation, structural abnormalities of the valve, pulmonary artery pressures (PAPs), and right ventricular function both preoperatively and intraoperatively. A shift in the atrial septum to the left and paradoxical septal motion are consistent with right ventricular diastolic overload. Pulsed Doppler and color-flow studies help to identify systolic right ventricular to right atrial flow with inferior vena cava and hepatic vein flow reversal. Contrast-enhanced echocardiography can be useful, with a rapid saline bolus injection producing microcavities that are visible on echo, demonstrating to-and-fro motion across the valve orifice and reversal into the inferior vena cava and hepatic veins. Possible ASD or patent foramen ovale should be sought. Endocarditic lesions and vegetations are clearly visible on echo; the valve may be destroyed, and septic pulmonary emboli are a common feature. The tricuspid valve in carcinoid syndrome is thickened with retracted leaflets fixed in a semiopen position throughout the cardiac cycle.31–42
Cardiac catheterization will document increased right atrial and right ventricular end-diastolic pressure.43 The right atrial pressure tracing has an absent x descent, prominent v wave, and "ventricularization" of the right atrial tracing, and the degree of pulmonary artery hypertension is documented. Pulmonary artery pressures of over 60 mm Hg usually are due to left-sided lesions leading to secondary TR. A right ventriculogram has been used but is unnecessary with current echocardiographic evaluation.
Tricuspid Stenosis
Tricuspid stenosis (TS) is most commonly rheumatic. It is extremely rare to have isolated tricuspid stenosis because some degree of TR will be present.44–47 Mitral valve disease coexists with occasional involvement of the aortic valve. The third world and especially the Indian subcontinent still have a significant prevalence of rheumatic tricuspid valvular disease. The anatomic features are similar to those of mitral stenosis, with fusion and shortening of the chordae and leaflet thickening. Fusion along the free edges and calcific deposits on the valve are found late in the disease. The preponderance of cases are in young women.
The diastolic gradient between the right atrium and right ventricle is significantly elevated even at 2 to 5 mm Hg mean pressure. As the right atrial pressure increases, venous congestion leads to distention of the jugular veins, ascites, pleural effusion, and peripheral edema. The right atrial wall thickens, and the atrial chamber dilates.
If the patient remains in normal sinus rhythm, the right atrial tracing and jugular venous pulse have prominent a waves that accentuate with inspiration. The cardiac murmur is mid-diastolic, increases with inspiration, is heard maximally along the left sternoid border, and may have an opening snap.
Clinical features are consistent with reduced cardiac output producing the symptoms of fatigue and malaise. Significant liver engorgement produces right upper quadrant tenderness with a palpable liver with a presystolic pulse. Ascites produces increased abdominal girth. Significant peripheral edema or anasarca can develop. Severe TS may mask or reduce the pulmonary congestion of mitral stenosis owing to reduced blood flow to the left side of the heart. The low output state of the patient is prominent.
The chest x-ray demonstrates cardiomegaly with an increase in the right atria and pulmonary artery size. The electrocardiogram (ECG) will demonstrate increased P-wave amplitude if the patient is in normal sinus rhythm. Echocardiography reveals the diagnostic features of diastolic doming of the thickened tricuspid valve leaflets, reduced leaflet mobility, and a reduced orifice of flow. The Doppler flow pattern across the tricuspid valve has a prolonged slope of antegrade flow.
The patient’s ability to tolerate stenotic lesions of the tricuspid valve is dictated to a large degree by the natural history of the mitral or aortic valve disease. In patients with predominant TR, the negative consequences of right ventricular volume overload develop slowly. Acute TR due to traumatic rupture or complete excision of the tricuspid valve as the treatment for infective endocarditis can be well tolerated for years if the PAP is not elevated. Functional tricuspid incompetence is progressive. Surgical treatment of -left-sided valvular lesions is not always adequate to resolve or prevent progressive TR. This is particularly true when pulmonary hypertension persists.
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SURGICAL DECISIONS
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The cardiologist and the cardiac surgeon face the decision as to when to intervene and when to surgically repair or replace the tricuspid valve. The choice of reparative technique to use for a durable result must be evaluated, as well as which type of valve, mechanical or bioprosthesis, to employ to maximize durability and minimize complications (i.e., thrombosis and thromboembolism). The surgical literature can be misleading due to case-selection bias and the various time frames of retrospective reviews. This is particularly true during the era that cage-ball and single-disk mechanical valves were in use.
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SURGICAL EXPOSURE
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Tricuspid valve annuloplasty performed with either mitral and/or aortic valve operations is accomplished either through a full or partial lower sternotomy approach or less invasive right mini thoracotomy exposure. Bicaval venous cannulation with caval snares is essential to isolate the right atrium. The cannula can be placed conventionally via the right atrium or less invasively via the femoral vein, and a superior vena cava cannula can be inserted via the internal jugular vein.
Left-sided valve repair or replacement (mitral and/or aortic) is performed under blood cardioplegic arrest with antegrade and/or retrograde administration, moderate systemic hypothermia, and topical cold saline surface cooling. The mitral valve can be exposed through a left atrial incision posterior to the intra-atrial septum or through a transseptal incision (Fig. 47-2). The transseptal incision is particularly useful when a prior aortic valve prosthesis is in place or in reoperations. After unclamping the aorta and completing de-airing maneuvers, attention can be turned to the tricuspid valve during rewarming and return of a cardiac rhythm. During tricuspid valve suturing, misplacement of a suture adversely affecting the cardiac conduction system can be assessed immediately and corrected. In a reoperative setting, approaching the tricuspid valve through a right mini thoracotomy has the advantage of avoiding adhesions and possible injury to the right ventricle during repeat sternotomy. If the operation will include the mitral valve, exposure can be simplified by using a right atrial incision and transseptal approach. If atrial fibrillation is present, a Maze procedure using the Cox-Maze III technique or ablation of atrial tissue using an energy source can be added to the technical maneuvers.
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Figure 47-2 (A) The superior and inferior venae cavae are cannulated, an oblique atriotomy incision is made, and stay sutures are placed on the right atrial wall to aid exposure. For transatrial exposure of the mitral valve, an incision is placed in the fossa ovale and extended superiorly through the interatrial septum. The superior aspect of the septal incision is extended if necessary into the dome of the left atrium behind the aorta. (B) Stay sutures in the interatrial septum are used for retraction. Use of retractors is avoided to prevent injury to the AV node. The mitral prosthesis is implanted in an antianatomic orientation. (C) The interatrial septum is closed primarily or by using a pericardial patch with a continuous 4-0 Prolene suture.
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ANNULOPLASTY TECHNIQUES
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Techniques to deal with a dilated tricuspid valve annulus with normal leaflets and chordal structures include plication of the posterior leaflet’s annulus (bicuspidization), partial purse-string reduction of the anterior and posterior leaflet annulus (DeVega-style techniques), and rigid or flexible rings or bands placed to reduce the annular size and achieve leaflet coaptation. Preoperative and intraoperative echocardiograms are valuable assessment tools to help the surgeon understand the structure and function of the valve.34–42
The degree of pulmonary hypertension, right ventricular dilatation, and systolic function, coupled with the size of the right atrium, must be factored into the surgical decision making. The classical technique of inserting a finger via a purse-string suture into the right atrium to palpate the tricuspid valve and withdrawing the fingertip 2 to 3 cm from the valve orifice trying to access the force of the regurgitant jet is of less importance in the current era of cardiac surgery than previously. The intraoperative transesophageal echocardiogram (TEE) allows the surgeon to access the tricuspid regurgitation and look for reversal of flow in the inferior cava. The TEE assessment after the repair ensures leaving the operating room with confidence that the repair is functioning satisfactorily.48–63
Minimal right atrial enlargement and + 1 to + 2 regurgitation usually will resolve after surgery on left-sided valve lesions, especially if the pulmonary hypertension resolves. Recent literature has documented the variability in the resolution of TR after dealing effectively with the left-sided valvular lesions.
The pathologic process of functional TR requires an understanding that the tricuspid annulus is a component of both the tricuspid valve and the right ventricle. For the tricuspid valve to leak, the tricuspid annulus and hence, the right ventricle have to be dilated. If the tricuspid annulus and the right ventricle are not dilated, there is a very low probability that TR can occur. Dilation of the tricuspid annulus occurs in the anterior and posterior directions (Fig. 47-1B) corresponding to the free wall of the right ventricle. In addition to tricuspid dilatation, the degree of TR is also directly related to three important factors: the preload, the afterload, and right ventricular function. Thus, TR is difficult to assess accurately because these factors can interfere with the severity of TR under different conditions. Significant TR may not be detected echocardiographically despite considerable annular dilatation in the tricuspid valve. An understanding of these important fundamental concepts would seem to contradict current practice regarding the management of secondary TR, which focuses on assessment of the severity of TR and advocates treatment of the primary lesion alone (i.e., mitral valve disease). Treatment of the mitral valve lesion alone only decreases the afterload. It does not correct tricuspid dilatation, nor does it affect preload or right ventricular function. Once the tricuspid annulus is dilated, its size cannot return to normal spontaneously, and it may, in fact, continue to dilate further. This may explain why some patients require a second operation for TR years after the initial mitral valve surgery.
Since tricuspid annular dilatation seems to be the underlying mechanism regarding nonorganic TR, Dreyfus and colleagues postulated that it may be a more reliable indicator of tricuspid valve pathology than the degree of TR. Moreover, successful treatment of secondary tricuspid valve pathology may necessitate the correction of tricuspid annular dilatation in addition to mitral valve surgery. Over a 12-year period, these authors performed tricuspid valve repair (TVR) for secondary tricuspid valve dilatation irrespective of the severity of TR because secondary tricuspid dilatation may or not be accompanied by TR. Tricuspid dilatation can be measured objectively, whereas TR can vary according to the preload, afterload, and right ventricular function.
Dreyfus and colleagues performed a prospective study of over 300 patients designed to determine whether surgical repair of the tricuspid valve based on tricuspid dilatation alone rather than TR could lead to potential benefits. Tricuspid annuloplasty was performed only if the tricuspid annular diameter was greater than twice the normal size (
70 mm) regardless of the grade of regurgitation. Patients in group 1 (163 patients, 52.4%) received mitral valve repair (MVR) alone. Patients in group 2 (148 patients, 47.6%) received MVR plus tricuspid annuloplasty. Tricuspid regurgitation increased by more than two grades in 48% of the patients in group 1 and in only 2% of the patients in group 2 (p < .001).
The authors concluded that modeling annuloplasty of the tricuspid valve based on tricuspid dilatation improved functional status irrespective of the grade of regurgitation. Considerable tricuspid dilatation can be present even in the absence of substantial TR. Tricuspid dilatation is an ongoing disease process that will, with time, lead to severe TR.109
More aggressive use of tricuspid annuloplasty appears to help improve the early postoperative course and prevent residual or progressive TR. Increasingly functional mitral regurgitation (MR) and TR coexist. Matsunaga and Duran analyzed TR in a group of patients who underwent successful revascularization and MVR for functional ischemic mitral regurgitation. They concluded that functional TR is frequently associated with functional ischemic MR. After MVR, close to 50% of patients have TR. The incidence of postoperative TR increases with time. Preoperative tricuspid annulus dilatation might be a predictor of late TR.110
Special note should be taken in assessing the foramen ovale for patency. These lesions always should be sutured closed, reducing the possibility of arterial desaturation from right-to-left shunting or paradoxical embolization.
Bicuspidization
After the caval snares are tightened, the right atrium is opened via an oblique incision. Exposure and assessment of all aspects of the tricuspid valve structure should be performed prior to choosing the technique of annuloplasty. Suture plication to deal with mild dilatation of the annulus is accomplished by placing pledgeted mattress sutures from the center of the posterior leaflet to the commissure between the septal and posterior leaflets. A second suture often is necessary to further reduce the annulus, ensuring proper leaflet coaptation while providing an adequate orifice for flow. An annuloplasty ring can be inserted to further support the annular reduction (Fig. 47-3).
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Figure 47-3 (A) Tricuspid valve bicuspidization is accomplished by plicating the annulus along the posterior leaflet. Two concentric, pledgeted 2-0 Ethibond sutures are used. (B) The sutures are tied, obliterating the posterior leaflet, effectively creating a bicuspid AV valve. Saline is injected into the right ventricle to test the competency of the repair. (C) As an option to support the bicuspidization repair, a flexible ring may be placed. Prior to ring implantation, measuring the intertrigonal distance determines the annular size. As an option, the ring can be inserted using a continuous 4-0 Prolene suture. Care is taken to avoid the AV node. As another option, the ring can be implanted above the coronary sinus.
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DeVega Technique
The DeVega technique also can be employed for mild to moderate annular dilatation.52 The technique employs a 2-0 Prolene or Dacron polyester suture placed at the junction of the annulus and right ventricular free wall, running from the anteroseptal commissure to the posteroseptal commissure. The second limb of the suture is placed through a pledget and run parallel and close to the first suture line in the same clockwise direction, placing it through a second pledget at the posteroseptal commissure. The suture is tightened, producing a purse-string effect and reducing the length of the anterior and posterior annulus to provide adequate leaflet coaptation and orifice of flow (Fig. 47-4).
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Figure 47-4 (A) A modified DeVega annuloplasty technique is shown. A single pledgeted 2-0 Prolene suture is placed. Care is taken to avoid the area of the AV node. (B) The suture is tied, completing the annuloplasty. Injecting saline into the right ventricle using a bulb syringe tests valve competency.
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The judgment regarding the degree of annular reduction has varied from the guideline of being able to insert two and one-half to three fingerbreadths snugly through the valve orifice to using the ring annuloplasty sizers designed for the tricuspid valve. An annuloplasty sizer, chosen by measuring the intertrigonal distance, can be used as a template while tying the purse-string suture to achieve the proper degree of reduction. The DeVega and suture plication techniques should be reserved for mild annular reductions and situations in which the structural integrity of the annulus is not absolutely necessary for long-term success (i.e., functional TR expected to resolve over time). In these situations, the annuloplasty provides a competent tricuspid valve during the early postoperative course while the heart remodels after surgical treatment of the left-sided valvular lesions.63–65
Rings and Bands
Significant degrees of annular reduction requiring durability are best accomplished with rigid rings (e.g., Carpentier-Edwards and MC3), flexible rings (e.g., Duran), or flexible bands (e.g., Cosgrove annuloplasty system). The length of the base of the septal leaflet (i.e., the intertrigonal distance) determines the size of the ring or band. These devices avoid suture placement in the region of the atrioventricular (AV) node (apex of the triangle of Koch) to avoid postoperative conduction problems. The mattress sutures are placed circumferentially, with wider bites on the annulus and smaller corresponding bites through the fabric of the ring or band, producing the annular plication mostly along the length of the posterior leaflet. The result allows the tricuspid valve orifice to be occluded primarily by the leaflet tissue of the anterior and septal leaflets. Overly aggressive annular reduction can lead to ring dehiscence owing to excessive tension on the tenuous tricuspid valve tissue66–75 (Fig. 47-5).
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Figure 47-5 (A) The Carpentier-Edwards ring annuloplasty is shown. A sizer measuring the intertrigonal distance was used to determine the ring size. Multiple interrupted, pledgeted 2-0 Ethibond sutures are placed at the atrioannular junction. All sutures are inserted prior to seating the ring. (B) The valve is seated, and the sutures are tied.
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A recent review of a 790-patient series for the durability and risk factors for failure of a repair was reported by McCarthy and colleagues. The authors reported that TR 1 week after annuloplasty was 3+ or 4+ in 14% of patients. Regurgitation severity remained stable over time with the Carpentier-Edwards ring (P = .7), increased slowly with the Cosgrove-Edwards band (P = .05), and rose more rapidly with the DeVega (P = .002) and PeriGuard (P = .0009) procedures. Risk factors for worsening regurgitation included higher preoperative regurgitation grade, poor left ventricular function, permanent pacemaker, and repair type other than ring annuloplasty. Right ventricular systolic pressure, ring size, preoperative New York Heart Association (NYHA) functional class, and concomitant surgery were not risk factors. Tricuspid reoperation was rare (3% at 8 years), and hospital mortality after reoperation was 37%. The authors concluded that tricuspid valve annuloplasty did not consistently eliminate functional regurgitation, and over time, regurgitation increased importantly after Peri-Guard and DeVega annuloplasties. Therefore, these repair techniques should be abandoned, and transtricuspid pacing leads should be replaced with epicardial leads.111
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INTRAOPERATIVE ASSESSMENT OF THE REPAIR
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Assessment of tricuspid valve competence after the annuloplasty requires filling the right ventricle with saline and observing leaflet coaptation. This assessment is best performed with the heart beating and the pulmonary artery clamped to allow right ventricular volume to generate enough intracavitary pressure to close the tricuspid valve tightly. If the result appears inadequate, downsizing the ring or ring replacement should be performed. Final assessment is by TEE examination after completely weaning from cardiopulmonary bypass with appropriate volume and afterload adjustment.
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TRICUSPID VALVE REPLACEMENT
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The technique for secure fixation of a tricuspid valve is with pledgeted mattress sutures using an everting suture technique for mechanical valves and either a supra-annular or an intra-annular technique for bioprostheses. The tricuspid valve leaflets are left in place, preserving the subvalvular structures and helping to avoid injury to the conduction system (Fig. 47-6). If there is concern that the anterior leaflet could billow and obstruct the right ventricular outflow tract, the central portion of the leaflet can be excised and still preserve the chordal attachments.
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Figure 47-6 (A) Tricuspid valve replacement is performed with a St. Jude Medical valve. The native leaflets are left in situ, and the pledgeted 2-0 Ethibond sutures are passed through the annulus and the edges of the leaflets. (B) The valve is seated, and the sutures are tied. The subvalvular apparatus is visualized to ensure that there is no impingement of the prosthetic valve leaflets. The valve can be rotated if necessary to prevent leaflet contact with tissue.
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Tricuspid valve replacement with a homograft is more complicated. The homograft tissue is a mitral valve.76–79 Sizing is performed by measuring the intratrigonal distances. Fixation of the papillary muscles is either intracavity (right ventricle) or through the wall of the right ventricle. This requires judgment and experience to gauge proper chordal length. The annulus is run with a monofilament suture line. An annuloplasty ring is inserted to prevent dilatation and to ensure adequate leaflet coaptation. Special care is necessary in suture placement to avoid conduction disturbances. Suture placement and tying with the heart beating provide immediate detection of rhythm disturbances. Similar to mitral valve replacement, leaflet and chordal preservation should be performed, or Gore-Tex suture should used as artificial chordae to maintain annular papillary muscle continuity.
A recent report documented the use of a stentless porcine valve in endocarditis in which the commissural posts were anchored to the right ventricular septal, anterior, and posterior walls. Orientation is critical to be sure that the right ventricular outflow tract is straddled by two of the commisural posts.112
Carpentier techniques for MVR can be applied to the tricuspid valve. Traumatic disruptions, occasionally endocarditis with healed lesions and perforations, or the rare myxomatous valve can be repaired. Pericardial patching of perforations, partial leaflet resections of the anterior (limited) or posterior (extensive) leaflets, and ring annuloplasty are standard techniques to produce competent valves and avoid replacement.80–82
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ENDOCARDITIS
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Tricuspid valve excision is possible if pulmonary pressures are not elevated and the degree of infection is extensive.83–91 Blood flows passively through the right side of the heart to the lungs. After eradication of the infection, a second-stage procedure with valve replacement can be performed months to years later. In patients with tricuspid valve endocarditis due to drug addiction, the second-stage valve insertion should be performed preferably after controlling the drug dependence or hopefully curing the accompanying addiction. Late survival and reinfection are correlated directly with continued drug use. Patients with less severe endocarditis can have one-stage procedures with prosthetic replacement or localized leaflet excision and repair.92,93 Homograft tissue often is versatile for partial or total tricuspid valve repair or replacement but has the limitations of availability, technical difficulty, and limited follow-up. The stentless aortic porcine valve is a novel option.112
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PROSTHETIC VALVE CHOICE
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The choice of prosthesis follows an algorithm similar to that used for valve replacement in other cardiac valve positions. The patient’s age, anticoagulation considerations, whether the patient is a young woman during her childbearing years, and social issues must be considered. The previously reported poor results with mechanical valves in the tricuspid position were due to valve thrombosis. Most of these reports were during the era of cage-ball and tilting-disk prostheses.94 More recent reports with the St. Jude bileaflet valve have provided encouraging data, allowing the surgeon to recommend a mechanical valve with confidence to younger patients who do not have a contraindication to anticoagulation.95–101 This strategy will avoid the not uncommon situation in the past in which patients received a bioprothesis on the right side and a mechanical prosthesis on the left. Bioprostheses, both porcine and of pericardial tissue, have functioned well in the tricuspid position.102–105 The data demonstrate a longer duration of freedom from structural valve dysfunction or rereplacement for a bioprosthetic valve in the tricuspid compared with the mitral valve position.106
Table 47-1 summarizes multiple reports from the literature. The reports either compare bioprosthetic and mechanical valves in the tricuspid position or present follow-up of bioprosthetic valves alone. The bioprostheses, either porcine or pericardial valves, have excellent freedom from degeneration and re-replacement for structural valve degeneration. In 1984, Cohen and colleagues reported on six simultaneously implanted and then explanted valves from the mitral and tricuspid positions. Degenerative changes were less extensive for the bioprosthetic valves in the tricuspid position than in the mitral position. However, thrombus formation and pannus formation (interpreted as organized thrombotic material) were observed more frequently in the tricuspid position.106
Nakano’s review of the Carpentier-Edwards pericardial xenograft reported a freedom from structural degeneration of 100% at 9 years, but nonstructural dysfunction was 72.8%. The cause of nonstructural dysfunction was pannus formation on the ventricular side of the cusps. This finding is often subclinical. Echocardiographic follow-up revealed a 35% incidence of this anatomic finding in patients with at least 5 years of follow-up.104 Guerra reported similar changes in simultaneously explanted porcine valves. The tricuspid position had less structural tissue degeneration and calcification than the mitral position. The report described the presence of pannus formation on the ventricular side of the cusps in tricuspid porcine valves. The pannus interfered with cuspal pliability and function.107
Nakano’s 2001 report of bioprosthetic tricuspid valves reported an 18-year freedom from reoperation of 63%.103 The freedom from structural deterioration was 96%, and nonstructural dysfunction was 77%. Reoperation replacing previously placed bioprosthetic valves occurred in 12 of 58 survivors. In 6 of the 12 patients, the primary indication for reoperation was tricuspid dysfunction, and 7 of the 12 had pannus formation on the ventricular side of the cusps (Fig. 47-7). This rate of degeneration and the subclinically high incidence of pannus formation, often eventually leading to reoperation, are major concerns. Tricuspid bioprosthetic valves require echocardiographic follow-up. Possible anticoagulation of bioprosthetic valves in the tricuspid position can reduce the incidence of pannus formation. The reported data in the literature categorize this pannus formation as nonstructural degeneration; therefore, clinical surgeons should be aware of future reports following this potentially serious clinical problem.
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Figure 47-7 (A) Fibrous pannus observed 8 years after implantation of a Carpentier-Edwards pericardial valve. (B) Photomicrograph of a pericardial leaflet. The bottom of the leaflet has pannus, a dense fibrous tissue on the ventricular side. (Reprinted with permission from the Society of Thoracic Surgeons and Nakano K, Ishibashi-Ueda H, Kobayashi J, et al: Tricuspid valve replacement with bioprostheses: Long-term results and causes of valve dysfunction. Ann Thorac Surg 2001; 71:105.)
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In the tricuspid position it is always possible to place large bioprosthetic or mechanical valves. Prostheses with more than a 27 mm internal diameter do not have clinically significant gradients. Therefore, hemodynamic performance is rarely an issue for tricuspid valve replacement. The data demonstrate excellent results with modern bileaflet mechanical valves. Series comparing bioprosthetic and mechanical valves have been consistent in demonstrating equality during the period of follow-up. The development of thrombus on a bileaflet valve can be treated successfully with thrombolysis.
A recent review by Filsoufi and a meta-analysis of biologic or mechanical prostheses in the tricuspid position both conclude that there is no survival benefit of a bioprothesis over a mechanical valve113-115 (see Fig. 47-7A,B). Some patients with mitral valve disease and TR undergoing surgery do not require surgical treatment of the tricuspid valve. Guidelines to identify these patients are poorly developed. Experience has shown that careful observation of the patient preoperatively is quite valuable. Absence of tricuspid valve regurgitation during periods of good medical control, absence of TR by transesophageal echocardiography (TEE) at the time of operation, minimal elevation of pulmonary vascular resistance, and absence of right atrial enlargement are helpful findings that permit the surgeon to replace the mitral valve confidently without performing an annuloplasty or replacement of the tricuspid valve. If left unrepaired, reassessment of the tricuspid valve by TEE after weaning from cardiopulmonary bypass is essential.
Temporary right ventricular dysfunction due to RCA air embolism often requires a brief return to cardiopulmonary bypass, repeat of air maneuvers, elevation of the blood pressure, TEE evaluation for residual intracavity air, and a search for the characteristic echogenic brightness in the myocardial distribution of the RCA confirming the suspicion of air embolism. Treatment should include 10 to 15 minutes of cardiopulmonary bypass support and reweaning from cardiopulmonary bypass, with inotropic support for right ventricular dysfunction and reassessment of the TR and cardiac function. If TR persists and elevated right atrial pressures greater than left atrial pressures are encountered with an underfilled, well-contracting left ventricle, tricuspid repair should be performed. A patent foramen ovale with interatrial shunting needs to be identified and closed surgically. Hemodynamically, when right atrial pressure is greater than left atrial pressure, the foramen may open, leading to systemic desaturation from a right-to-left shunt.
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CONCLUSION
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Clinical experience has demonstrated that up to 20% of patients undergoing mitral valve replacement receive a tricuspid annuloplasty, but less than 2% require replacement. The surgeon’s clinical judgment and experience guide the approach to tricuspid valve surgery and ultimately lead to variability in reported clinical data. The accuracy of the judgments can be guided by assessment of the risk factors for persistent or progressive tricuspid valve regurgitation. They are related to unresolved or recurrent mitral valve pathology; the degree of preoperative tricuspid regurgitation or the misjudgment of its severity; failure of the pulmonary hypertension and pulmonary vascular resistance to resolve, resulting in persistent impairment in right ventricular function (often with right ventricular dilatation); and failure to recognize organic tricuspid valve disease.
Patients undergoing a tricuspid valve annuloplasty during a mitral valve replacement have more advanced disease than those having mitral valve replacement alone. This is evidenced by the elevation in operative mortality (approximately 12 versus 3%) and the progressive increased hazard of late death (5-year survival of 80 versus 70%) despite good valve function. However, these patients achieved good functional results (class 1–2). It is unknown what the survival and functional result would have been if tricuspid repair had not been performed in these patients, but one presumes that it would have been worse.
The durability of simple annuloplasty techniques such as bicuspidization and the DeVega technique has been good when employed only for mild to moderate degrees of functional TR with successful resolution of pulmonary hypertension after the mitral valve operation. Extensive experience with the tricuspid annuloplasty using the Duran, Carpentier-Edwards, or Cosgrove rings or bands resulted in an 85% freedom from moderate to severe TR at 6 years. The subsequent requirement for tricuspid reoperation is very low. Inadequate resolution of the mitral disease and persistent pulmonary hypertension with right ventricular dilatation and dysfunction are the major predictors of poor late results.
Patients requiring tricuspid and mitral valve replacement have operative mortalities from 5 to 10% by current standards. Actuarial survival rates are 55% at 10 years (Fig. 47-8A,B). Advanced right ventricular failure or arrhythmia causes late death. Patients who need valve replacement for endocarditis comprise a unique subgroup with the additional risk for death owing to sepsis, reinfection, and the complications related to drug addiction.
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Figure 47-8 Meta-analysis of bioprosthetic vs mechanical valves replacing the tricuspid valve. (A) Survival hazard. (B) Survival curve of hospital survivors.
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Complete heart block can occur immediately postoperatively owing to damage to the conduction system during mitral and tricuspid valve surgery. This complication can be minimized intraoperatively by performing the tricuspid valve procedure on the perfused beating heart, as described earlier. Late heart block remains a persistent risk with a 25% actuarial incidence at 10 years for patients with mitral and tricuspid prostheses.108 Late development of heart block rarely occurs after mitral valve replacement and tricuspid annuloplasty (Fig. 47-8A, B). The presence of two rigid prosthetic sewing rings can produce ongoing trauma and lead to AV node dysfunction over time.
The surgical treatment of tricuspid valve disease presents the surgeon with challenges requiring clinical and intraoperative judgment. Following the guidelines presented in this chapter for when to repair or replace the tricuspid valve should lead to optimal clinical outcome. The data support the safe use of mechanical bileaflet prostheses. A lingering concern is the pannus formation on the ventricular side of bioprosthetic cusps. This observation should be followed closely as future clinical series are reported.
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