Chapter 46. Tricuspid Valve Disease

The tricuspid valve consists of three leaflets (anterior, posterior, and septal), the chordae tendinea, two discrete papillary muscles, the fibrous tricuspid annulus, and the right atrial and right ventricular myocardium (Fig. 46-1A). Valve function depends on coordination of all these components. The anterior leaflet is the largest. The septal leaflet is the smallest and arises medially directly from the tricuspid annulus above the interventricular septum. Because the small septal wall leaflet is fixed and is relatively spared from annular dilation, tricuspid annular sizing has been based on the dimension of the base of the septal leaflet.1,2 The posterior leaflet often has multiple scallops. The anterior papillary muscle provides chordae to the anterior and posterior leaflets, and the medial papillary muscle provides chordae to the posterior and septal leaflets. The septal wall gives chordae to the anterior and septal leaflets. There may be accessory chordal attachments to the right ventricular free wall and the moderator band.

Right ventricular dysfunction and dilation lead to chordal tethering contributing to loss of leaflet apposition.2 In addition, dilation of the free wall of the right ventricle results in tricuspid annular enlargement, primarily in its anterior/posterior (mural) aspect, resulting in significant functional TR (fTR) as a result of leaflet malcoaptation3 (Fig. 46-1B).

The tricuspid annulus has a complex three-dimensional structure, which differs from the more symmetric "saddle-shaped" mitral annulus. The tricuspid annulus is dynamic and can change markedly with loading conditions. During the cardiac cycle, there is a ∼20% reduction in annular circumference (∼30% reduction in annular area) with atrial systole.4,5 This distinct shape has implications for the design and application of currently available annuloplasty rings in the tricuspid position. Most commercially available rings or bands are essentially planar except for the Edwards MC3 annuloplasty system.

Fukuda et al.4 studied the shape and movement of the healthy and diseased tricuspid annulus performing a real-time three-dimensional transthoracic echocardiographic study. Healthy subjects had a nonplanar, elliptical-shaped tricuspid annulus, with the posteroseptal portion being "lowest" (toward the right ventricular apex) and the anteroseptal portion the "highest" (Fig. 46-2). Patients with functional TR generally had a more planar annulus, which was dilated primarily in the septal-lateral direction, resulting in a more circular shape as compared with the elliptical shape in healthy subjects.

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. 46-1B). With progressive annular and ventricular dilatation, the chordal papillary muscle complex becomes functionally shortened, causing leaflet tethering. This combination prevents leaflet apposition, resulting in valvular incompetence.6–9

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. This prevents normal leaflet apposition by a tethering effect on the leaflets. Marfan's 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.10–13 Infectious endocarditis can destroy leaflet tissue, mostly in drug addicts with staphylococcal infection.14–16

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.17–19 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 regurgitation20 (Table 46-1).

A unique cause of TR is the result of pacemaker or defibrillator leads, which cross from the right atrium into the right ventricle and may directly interfere with leaflet coaptation. This entity has been reported in case reports and small series but is likely more significant and prevalent than currently perceived. In a recent report by Kim et al., the effect of transtricuspid permanent pacemaker or implantable cardiac defibrillator leads on 248 subjects with echocardiograms before and after device placement was studied TR worsened by one grade or more after implant in 24.2% of subjects and that TR worsening was more common with implantable cardiac defibrillators than permanent pacemakers.21,22

The current guidelines do not recommend lead extraction for patients with existing TR and transtricuspid pacing leads, because the risks of lead extraction are significant and there is potential for injury to the tricuspid valve if the lead is adherent to the valve apparatus.23

It has also been shown at 5 years after successful tricuspid valve repair, 42% of patients with a pacemaker had severe TR, almost double the incidence of those without pacemaker implantation.24 This suggests removing a transtricuspid lead and replacing it with an epicardial lead at the time of tricuspid valve surgery may reduce late repair failure.

Tricuspid Regurgitation

Patients with TR have the presenting symptoms of fatigue and weakness related to a reduction in cardiac output. Atrial fibrillation is common. Jugular vein distention is found, especially during inspiration, when a physiologic increase in venous return is accentuated. 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. Hepatic cardiac cirrhosis can develop in neglected cases.

Echocardiography is routinely used to assess the severity of TR in clinical practice. The exam is performed in an integrative manner using color Doppler flow mapping of the direction and size of the TR jet. In addition, the morphology of continuous wave Doppler recordings across the valve and pulsed wave Doppler of the hepatic veins can be used.25

Serial assessments of TR must be interpreted within the clinical context, because functional mitral regurgitation severity can be affected by multiple factors, such as volume status (preload) and afterload. Right ventricular shape is complex as compared with the left ventricle, appearing crescent shaped in cross-section and triangular when viewed en face.26 Right ventricular function can be assessed quantitatively in the four-chamber view by measuring the end-diastolic and end-systolic area to calculate the fractional area change of the right ventricle.27 Although right ventricular chamber dimensions may be obtained during echocardiography, magnetic resonance imaging is emerging as an improved technique for assessing right ventricular diastolic and systolic volumes.28

Other echocardiographic findings include a shift in the atrial septum to the left and paradoxical septal motion, 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. Endocarditis vegetations are clearly visible on echocardiography. 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 semi-open position throughout the cardiac cycle.29–34

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.35–37 Mitral valve disease coexists with occasional involvement of the aortic valve. The third still have a significant prevalence of rheumatic mitral and tricuspid valvular disease. The anatomical 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.

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.

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.

Functional Tricuspid Regurgitation (fTR)

Without treatment, fTR may become worse over time, leading to severe symptoms, biventricular heart failure, and death.24 In a large retrospective echocardiographic analysis of 5223 Veterans Administration patients by Nath et al.38 showed that independent of echo-derived pulmonary artery systolic pressure, left ventricular ejection fraction, inferior vena cava size, and right ventricular size and function, survival is worse for patients with moderate and severe TR than for those with no TR.

Pulmonary artery hypertension from any cause is known to be associated with the development of secondary tricuspid regurgitation. However, not all patients with pulmonary hypertension develop significant tricuspid regurgitation, and the mechanisms of secondary TR are multifactorial.

Mutlak et al.39 studied 2139 subjects with mild (<50), moderate (50 to 69), or severe (≥70) elevations in pulmonary artery systolic pressure. In their analysis, increasing PASP was independently associated with greater degrees of TR (odds ratio, 2.26 per 10 mm Hg increase). However, many patients with high PASP had only mild TR (mild TR in 65.4% of patients with PASP 50 to 69 mm Hg and in 45.6% of patients with PASP ≥70 mm Hg). Other factors, such as atrial fibrillation, pacemaker leads, and right heart enlargement, were also importantly associated with TR severity. The authors concluded that the cause of TR in patients with pulmonary hypertension is only partially related to an increase in transtricuspid pressure gradient. It remains unproved if surgical annuloplasty, in the setting of pulmonary hypertension, alters the natural course of right ventricular dilation and recurrent TR.

Thus, functional tricuspid incompetence is progressive. Surgical treatment of left-sided valvular lesions are not always adequate to resolve or prevent progressive TR. This is particularly true when pulmonary hypertension persists.

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 (ie, thrombosis and thromboembolism). The surgical literature can be misleading because of 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.

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 with mitral valve procedures. 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. 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 cardioplegia arrest with antegrade and/or retrograde administration, moderate systemic hypothermia, and optional 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. 46-3). The transseptal incision is particularly useful when there is an aortic valve prosthesis or in a reoperation.

After completing the mitral valve procedure and the de-airing maneuvers, the aorta is unclamped and caval snares are tightened around the venous drainage cannula. Attention can be turned to the tricuspid valve while 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. Femoral vein and internal jugular vein cannula are positioned outside the right atrium and confirmed by echo. Caval snares below the cannula tips ensure venous drainage. Coronary sinus return is controlled by a sucker in the coronary sinus.

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 can be added to the technical maneuvers.

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 (Fig. 46-4). Preoperative and intraoperative echocardiograms are valuable assessment tools to help the surgeon understand the structure and function of the valve.30–34

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 pursestring suture, into the right atrium to palpate the tricuspid valve and withdrawing the fingertip 2 to 3 cm from the valve orifice, so as to access the force of the regurgitant jet is of historical importance in the current era of cardiac surgery. The intraoperative transesophageal echocardiogram (TEE) allows the surgeon to access the degree of tricuspid regurgitation and look for reversal of flow in the inferior cava. The TEE assessment after the repair and under the appropriate loading conditions ensures leaving the operating room with confidence that the repair is functioning satisfactorily.

Classic surgical teaching has been that patients with minimal right atrial enlargement and +1 to +2 regurgitation do well and resolve the TR after successful 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 (fTR) requires an understanding that the tricuspid annulus is a component of both the tricuspid valve and the right ventricular myocardium. For the tricuspid valve to leak, the tricuspid annulus; therefore, 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 (see Fig. 46-1B) 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, afterload, and right ventricular function. Thus, TR is difficult to assess accurately because these factors can interfere with the observed severity of TR under different conditions. Significant TR may not be detected echocardiographically despite considerable annular dilatation in the tricuspid valve annulus.

An understanding of these important fundamental concepts 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 (ie, 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 explains why some patients require a second operation for TR years after the initial mitral valve surgery. The reoperative risks are very high.

Tricuspid annular dilatation is the primary mechanism in the development of functional TR. Dreyfus and colleagues postulated that annular size may be a more reliable indicator of late outcomes than the degree of TR. Moreover, successful treatment of functional (secondary) tricuspid valve pathology may necessitate the correction of tricuspid annular dilatation in addition to mitral valve surgery even when TR is mild.

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 prospectively studied more than 300 patients 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 remodeling 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.40

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 residual TR that increases over time. The annular size may become the objective criteria, regardless of the degree of TR, to determine the need for a tricuspid annuloplasty.41

Special note should be taken in assessing the foramen ovale for patency. If patent the foramen should always be sutured closed, reducing the possibility of arterial desaturation from right-to-left shunting or paradoxic embolization.

Surgical Repair of the TV

The main surgical approaches to rectify functional TR (occurring in the presence of a dilated annulus with normal leaflets and chordal structures) involve rigid or flexible annular bands (open or closed), which are used to reduce annular size and achieve leaflet coaptation, as with mitral valve disease. Another less commonly used technique involves posterior annular bicuspidalization. This surgical technique places a pledget-supported mattress suture from the anteroposterior commissure to the posteroseptal commissure along the posterior annulus. This is based on prior studies by Deloche et al.42 that showed posterior annulus dilation occurs in functional TR and that a focal posterior tricuspid annuloplasty can be effective in selected cases. Other approaches include edge-to-edge (Alfieri-type) repairs as described by Castedo et al.43,44 and partial purse-string suture techniques to reduce the anterior and posterior portions of the annulus (DeVega-style techniques; see Fig. 46-4). DeVega and flexible annuloplasty bands appear to have a lower freedom from recurrent TR than rigid annuloplasty rings.24,45–47

In the absence of simultaneous tricuspid valve repair, the prevalence of TR in the postoperative period after mitral valve surgery depends to some degree on the mechanism of MR. Matsuyama et al.48 reported in a study of 174 patients that only 16% of patients who underwent nonischemic (ie, degenerative) mitral valve surgery without tricuspid valve surgery developed 3 to 4+ TR at 8-year follow-up. Conversely, TR appears to be far more prevalent in patients undergoing mitral valve repair for functional ischemic mitral regurgitation. In the series by Matsunaga et al.49 of 70 patients undergoing mitral valve repair for functional ischemic mitral regurgitation, 30% of patients (21/70) had at least moderate TR before surgery. In the postoperative period, the prevalence of at least moderate TR increased over time, from 25% at less than 1 year, 53% at 1 to 3 years, and 74% at greater than 3 years of follow-up.

Significant residual tricuspid valve insufficiency contributes to a poor postoperative result, even after successful mitral valve repair. King et al.50 studied patients requiring subsequent tricuspid valve surgery after mitral valve surgery. They had high early and late mortality. The authors encouraged a policy of liberal use of tricuspid annuloplasty at initial mitral valve surgery. Surgical series have shown that successful tricuspid valve repair (primarily when combined with other valve surgeries) resulted in a significant improvement in recurrent TR, survival, and event-free survival. Accordingly, 50 to 67% of patients undergoing surgery for mitral valve disease have been reported to undergo concomitant surgical tricuspid valve repair or replacement (although this may approach 80% in some dedicated centers).45,51,52

Specific Techniques

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 before 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. 46-5).

DeVega Technique

The DeVega technique also can be employed for mild to moderate annular dilatation.53 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 pursestring effect and reducing the length of the anterior and posterior annulus to provide adequate leaflet coaptation and orifice of flow (Fig. 46-6).

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 pursestring 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 (ie, 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.54–56

Rings and Bands

Significant degrees of annular reduction requiring durability are best accomplished with rigid rings (eg, Carpentier-Edwards and MC3), flexible rings (eg, Duran), or flexible bands (eg, Cosgrove annuloplasty system). The length of the base of the septal leaflet (ie, 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 annular tissue57,58 (Fig. 46-7).

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 Peri-Guard (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 annuloplasty. Therefore, these repair techniques should be abandoned, and transtricuspid pacing leads should be replaced with epicardial leads.59

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 occluded 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.

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 a bioprosthesis. The tricuspid valve leaflets are left in place, preserving the subvalvular structures and helping to avoid injury to the conduction system (Fig. 46-8). 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.

Tricuspid valve replacement with a homograft is more complicated. The homograft tissue is a mitral valve.60–62 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 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 commissural posts.63 Low profile AV bioprosthesis should be chosen.

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, chordal transfer, artificial Gore-Tex chordae, Alfieri suture and ring annuloplasty are standard techniques used to produce competent valves and avoid replacement.64–66

Tricuspid valve excision is possible if pulmonary pressures and the pulmonary vascular resistance are not elevated and the degree of infection is extensive.66–68 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 owing 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.69,70 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.63,64

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 caused by valve thrombosis. Most of these reports were during the era of cage-ball and tilting-disk prostheses.71 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.72–78

This strategy will avoid the not uncommon situation in the past in which patients received a bioprosthetic 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.79–82 The data demonstrate a longer duration of freedom from structural valve dysfunction or re-replacement for a bioprosthetic valve in the tricuspid compared with the mitral valve position.83

Table 46-2 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 bioprosthesis, 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 and pannus formation (interpreted as organized thrombotic material) were observed more frequently in the tricuspid position.83

Nakano's review of the Carpentier-Edwards bovine pericardial valve 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 anatomical finding in patients with at least 5 years of follow-up.81

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.84

Nakano's 2001 report of bioprosthetic tricuspid valves reported an 18-year freedom from reoperation of 63%.80 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. 46-9). 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.

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 bioprosthesis over a mechanical valve85–87 (Fig. 46-10). 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 unrepaired, reassessment of the tricuspid valve by TEE after weaning from cardiopulmonary bypass is essential.

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 must 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.

Temporary right ventricular dysfunction caused by 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, elevated blood pressure, and reassessment of the TR and cardiac function.

Historical 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 have guided the approach to tricuspid valve surgery, ultimately leading to variability in reported clinical data. The accuracy of these judgments can have been guided by assessment of the risk factors for persistent or progressive tricuspid valve regurgitation. Recent studies have taught us that our ability to make these judgments is flawed and unpredictable. We have learned about the dilated tricuspid valve annulus, the progression of TR in spite of successful left-sided surgery, and the unpredictable resolution of pulmonary hypertension. Failure to improve can have adverse impacts on late morbidity, mortality, and residual or progressive TR. Therefore, the current recommendation is to aggressively pursue tricuspid annuloplasty with remodeling rings or bands.

Older studies showed 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 (NYHA 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. In the current era adding an annuloplasty can have minimal adverse impact in the perioperative period and seems to confer long-term benefit.

The durability of simple annuloplasty techniques such as bicuspidization and the DeVega technique has been satisfactory 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, and MC3 rings or bands have 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.

The American College of Cardiology/American Heart Association 2006 Practice Guidelines for the surgical management of patients with TR (Table 46-3)88 are driven by the individual patient's clinical status and the cause of their tricuspid valve abnormality. The guidelines state that the timing of surgical intervention for TR remains controversial, as do the surgical techniques. At present, surgery on the tricuspid valve for significant TR should occur at the time of mitral valve surgery, as TR does not reliably resolve after mitral valve surgery. TR associated with dilatation of the tricuspid annulus should be repaired, to prevent tricuspid annular dilation progressing and producing severe TR.89–96

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. 46-10 A,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.

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. The presence of two rigid prosthetic sewing rings can produce ongoing trauma and lead to AV node dysfunction over time. Late development of heart block rarely occurs after mitral valve replacement and tricuspid annuloplasty.

The surgical treatment of tricuspid valve disease presents the surgeon with challenges requiring clinical and intraoperative judgment. Following the principles presented in this chapter, appropriate decisions should lead to optimal clinical outcomes. The data support the safe use of mechanical bileaflet prostheses in select patients. 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.