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. 43-1A). 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 (RV) results in tricuspid annular enlargement, primarily in its anterior/posterior (mural) aspect, resulting in significant functional tricuspid regurgitation (fTR) as a result of leaflet malcoaptation³ (Fig. 43-1B).

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. 43-2). Patients with fTR generally had a more planar annulus, which was dilated primarily in the septal-lateral direction, resulting in a more circular and flat shape as compared with the elliptical shape in healthy subjects.⁵

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. 43-1B). 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 43-1).

A unique cause of TR is the result of pacemaker or defibrillator leads, which cross from the right atrium into the RV 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 (MR) 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 RV.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 More recently, the tricuspid annular peak systolic excursion, or apical movement of the annulus as measured on echocardiography, as been validated as a sensitive measure of RV function.²⁹ 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 semiopen position throughout the cardiac cycle.^29-34

Tricuspid Stenosis

Tricuspid stenosis (TS) is most commonly rheumatic. It is extremely rare to have isolated TS 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 is in young women.

The diastolic gradient between the right atrium and RV 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. Over time, 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

Secondary tricuspid regurgitation, also called fTR, may become worse over time, leading to severe symptoms, biventricular heart failure, and death.²⁴ IA large retrospective echocardiographic analysis of 5223 Veterans Administration patients by Nath et al. 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 was worse for patients with moderate and severe TR than for those with no TR.³⁸

Pulmonary arterial 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 and colleagues³⁹ studied 2139 subjects with mild (<50), moderate (50-69), 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 50-69 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 is not always adequate to resolve or prevent progressive TR. This is particularly true when pulmonary hypertension persists.

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 minithoracotomy 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 cardioplegic 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 intraatrial septum or through a right atrial and transseptal incision (Fig. 43-3). The transseptal incision is particularly useful when there is an aortic valve prosthesis, when a mitral and tricuspid valve procedure is required or in a reoperation.

After completing the mitral valve procedure and deairing maneuvers, the aorta is vented and unclamped. Attention can be turned to the tricuspid valve during rewarming and cardiac reperfusion. Using the beating heart technique, the caval snares are tightened around the venous drainage cannula and a right atriotomy is performed to expose the tricuspid valve. Misplacement of a suture potentially adversely affecting the cardiac conduction system can be assessed immediately and corrected.

In the reoperative setting, with a dilated RV adherent or close to the sternum, It is prudent to expose of the femoral artery and vein for rapid cannulation in the case of injury to the RA or RV during sternal reentry. It is also recommended to establish fem-fem bypass prior to sternotomy to decompress the RA and RV allowing a safer sternotomy to be performed.

Approaching the tricuspid valve through a right minithoracotomy has the advantage of avoiding adhesions and possible injury to the RV during sternotomy. Femoral vein and internal jugular vein cannulae 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 its ostium.

If the operation includes 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. 43-4). 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 process. 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, 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. Assessment of the repair with TEE under appropriate loading conditions ensures leaving the operating room with confidence that the repair is functioning satisfactorily.

Classic surgical teaching has been that in patients with minimal right atrial enlargement and +1 to +2 regurgitation, TR will resolve once left-sided valve lesions are addressed. Recent literature, however, has documented the variability in the resolution of TR after dealing effectively with the left-sided valvular lesions.

The pathologic process of 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 and therefore the RV must be dilated. Without dilation of these structures, there is little chance that TR can occur.

Dilation of the tricuspid annulus occurs in the anterior and posterior directions (see Fig. 43-1B) corresponding to the free wall of the RV. 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 dynamic factors can interfere with the observed severity of regurgitation. Therefore, significant TR may not be detected echocardiographically despite considerable dilatation of 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 reduces the RV afterload, but does not correct tricuspid annular dilatation, RV preload, and 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 in this setting are very high owing to poor myocardial function and difficulty with sternal reentry with a dilated RV.

Tricuspid annular dilatation is the primary mechanism in the development of fTR. 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 for secondary tricuspid valve dilatation irrespective of the severity of TR because secondary tricuspid dilatation may or not be accompanied by TR. Tricuspid annular 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.⁴⁰ 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 MR and TR coexist. Matsunaga and Duran analyzed TR in a group of patients who underwent successful revascularization and MVR for functional ischemic MR. They concluded that fTR 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. A patent foramen should always be sutured closed, reducing the possibility of paradoxical embolism or arterial desaturation from right-to-left shunting.

Surgical Repair of the TV

The main surgical approaches to rectify fTR (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 fTR 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. 43-4). 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 MVR for functional ischemic MR. In the series by Matsunaga et al.⁴⁹ 30% of patients undergoing MVR for functional ischemic MR 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.