The multitude of chordal attachments of the TV, described in Chapter 1 , may impair proper leaflet coaptation and promote tricuspid regurgitation (TR) in the presence of right ventricular (RV) dysfunction and dilation. The tricuspid anulus shortens during systole when the TV is competent. ^, When RV dilation develops, usually as a consequence of important disease of the left-sided heart valves in association with pulmonary arterial hypertension, the tricuspid anulus also dilates (lengthens) and fails to shorten during systole. The leaflets and chordae remain normal in appearance. The septal leaflet portion of the anulus lengthens least in this process because it is fixed between the right and left trigones and the atrial and ventricular septa. As the RV free wall dilates, the remaining two-thirds of the anulus lengthens, particularly that part giving origin to the posterior leaflet ( Fig. 13.1 ). ^{, ,} The anular dilation results in failure of leaflet coaptation, which is contributed to in some patients by chordal shortening secondary to the RV dilation. Thus, a strong correlation exists between tricuspid anular diameter measured echocardiographically and presence and severity of TR ( Fig. 13.2 ). As the tricuspid anulus dilates, it assumes a more circular shape in a flat plane. The reported threshold for TR based on anular dilation is 27 mm · m2 or about 34 mm in the average adult.

Dilation of the TV anulus, indicated by a sequence of overlaid annuli. Tricuspid anular dilation due to increased RV and pulmonary artery pressures secondary to left-sided heart valve disease occurs predominantly in the septal-lateral direction, as indicated by arrows.

Correlation between tricuspid anulus diameter (TAD) and tricuspid regurgitant volume (V _TR ) in patients with valvular heart disease ( open circles ) and those with atrial septal defect ( closed circles ). Correlation with the former is 0.87 and with the latter, 0.88. Correlation lines cross the horizontal axis at a TAD of 33 to 34 mm, which is the threshold for TR in adult patients. ASD, Atrial septal defect; VHD, valvular heart disease.

The degree of TR is also importantly influenced by RV preload, afterload, and systolic function because the tricuspid anulus is very dynamic, with a 15% to 20% reduction in circumference during atrial systole. ^{, ,}

Early experimental work by Tsakiris and colleagues showed that perfect systolic tricuspid leaflet closure depends on proper systolic shortening in the circumference of the tricuspid anulus. ^, In support of this finding, Simon and colleagues demonstrated a considerable increase in systolic shortening postoperatively in patients whose TR lessens after mitral valve surgery and no change in those in whom it persists or worsens. In addition, increased diastolic diameter of the tricuspid anulus results in TR; diastolic diameter is increased by pulmonary artery hypertension, RV myocardial failure, and increased diastolic volume secondary to left-sided heart pathology.

The pathogenesis of functional TR in mitral valve disease is summarized in Fig. 13.3 . The final common pathway is RV dysfunction and dilation and tricuspid anular dilation. The process becomes self-propagating because worsening TR exacerbates RV volume overload with further RV dysfunction and enlargement. In addition, because of ventricular interdependence, worsening RV dysfunction increases interventricular shift toward the left, causing restricted left ventricular filling, further elevation of left atrial pressure, pulmonary hypertension, and greater RV afterload, which further affects the right ventricle.

Pathogenesis of TR in mitral valve disease. DCM, dilated cardiomyopathy; RHD, rheumatic heart disease; RV, right ventricle; TV, tricuspid valve.

(Redrawn from Shiran A, Sagie A. Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. J Am Coll Cardiol . 2009;53:401-408.)

It is these mechanisms that may produce TR late after isolated mitral valve operations or after combined aortic and mitral valve operations (see Chapters 11 and 12 ).

Rheumatic TV disease occurs in association with rheumatic involvement of the mitral valve, the mitral and aortic valves combined, or rarely, the aortic valve alone. It is not seen as an isolated lesion.

Rheumatic tricuspid disease usually results in a regurgitant valve with variable amounts of stenosis, but in rare cases, there may be pure stenosis. In tricuspid stenosis, the orifice is larger than in mitral stenosis, even when hemodynamically there is severe obstruction. Therefore, the hemodynamic effects of anatomically moderate tricuspid stenosis are the equivalent of tight mitral stenosis. A mean diastolic gradient of even 4 to 5 mmHg across the TV indicates important stenosis. Borders of the stenotic tricuspid orifice are usually fibrous and thickened, although peripheral portions of the leaflets remain thin.

The hallmark of organic tricuspid stenosis is commissural fusion. All commissures are usually equally fused, but occasionally, fusion is limited to the anteroseptal commissure. Chordal thickening and fusion are usually mild, and calcification is usually absent.

Acute TV endocarditis is rapidly increasing in frequency and is usually associated with intravenous drug use or long-term indwelling catheters. The most common etiologic organism is Staphylococcus aureus in drug-use patients, with coagulase-negative Staphylococcus being more common in patients with indwelling catheters. A variety of gram-negative bacilli or Candida albicans can rarely be the infective organism. The organisms may form masses on the valve leaflets or erode and destroy large portions of leaflets and chordae (see Chapter 14 ).

TR is an uncommon result of severe, nonpenetrating chest injury and, in this setting, is due to rupture of one or more papillary muscles or chordae (see “ Atrioventricular Valve Rupture ” in Section II of Chapter 16 ). Usually, it is the anterior tricuspid leaflet that becomes flail. Rarely, the ventricular septum may rupture.

Injury of the TV due to a transvenous ventricular lead of a cardiac implantable electronic device (CIED) or its removal is occasionally associated with important TR. This may be due to perforation, laceration, or scarring for indwelling leads or avulsion in the case of lead removal. Rarely, CIED leads can cause tricuspid stenosis secondary to leaflet scarring and adhesions. Similar scarring of the septal and posterior leaflets following cryothermic or radiofrequency ablative procedures rarely can produce severe TR. Following cardiac transplantation, many years of repeated transvenous endomyocardial biopsies may induce severe TR secondary to inadvertent severing of chordae during biopsy.

Carcinoid tumors originate from Kulchitsky cells in the gastrointestinal tract, which produce serotonin (5-hydroxytryptamine), a substance inactivated in the liver. However, carcinoid tumors that metastasize to the liver produce serotonin there, and this powerful substance passes into the pulmonary and, to a lesser extent, systemic circulation. Thereby, carcinoid syndrome may be produced with bronchospasm, diarrhea, nausea, malabsorption, flushing, and telangiectasia. In some of these patients, cicatricial deformity of the tricuspid and pulmonary valves also develops.

Typical carcinoid symptoms are considerably more common in carcinoid patients with valvar involvement than in noncardiac carcinoid patients. Tricuspid commissures are fused, chordae tendineae thickened and fused, and leaflets thickened and shortened, resulting in regurgitation and in some patients a mild degree of stenosis. Microscopically, a deposition of loose or compact fibrous tissue is present on both surfaces of the tricuspid leaflets. The white fibrous plaques, if present on the ventricular side of the leaflets, promote adherence of the leaflet to the underlying ventricular myocardium, preventing appropriate leaflet coaptation.

TR is the most common cardiac manifestation of carcinoid syndrome and is managed surgically by TV replacement, usually with a bioprosthesis. Concomitant pulmonary valve replacement is necessary in approximately 85% of patients. Perioperative mortality of valve replacement for carcinoid heart disease is acceptably low in the current era (5%), but early and late mortality is closely related to the degree of preoperative disability and right heart failure as reflected by New York Heart Association (NYHA) functional class. Furthermore, patients should be monitored closely postoperatively because of a high incidence of bioprosthetic valve degeneration.

Moderate degrees of tricuspid stenosis may be overlooked, particularly if the patient is in atrial fibrillation. If sinus rhythm is present, there is a dominant a wave in the jugular venous pulse (immediately preceding the carotid pulse). Other signs include a mid-diastolic, often high-pitched murmur maximal over the lower left sternal edge, which increases on inspiration; there may be a tricuspid opening snap. The murmur can be confused with an aortic early diastolic murmur (because its timing may be relatively early) or with a conducted mitral diastolic murmur. The liver is usually enlarged but not pulsatile (unless from forceful atrial contraction that produces a presystolic pulse).

The chest x-ray shows right atrial enlargement, and in the presence of sinus rhythm, the electrocardiogram shows a prominent P wave. Two-dimensional (2D) echocardiography is helpful in establishing the presence of leaflet thickening and mobility. Doppler echocardiography helps quantify the valve area and transvalvular gradient. There is no general consensus on the grading of tricuspid stenosis severity, but a TV area <1.0 cm ² and a mean transvalvular gradient >5 mmHg at normal heart rate are indicative of significant tricuspid stenosis.

History and physical signs are often highly suggestive of significant TR. The jugular venous pulse shows dominant fused c and v waves, followed by a sharp, deep y descent. The murmur, maximal over the lower left sternal edge, is pansystolic, often high pitched, and increases on inspiration. However, when TR is severe, a murmur may be absent. The enlarged liver shows systolic pulsation. In advanced cases, there are other signs of right heart failure, including peripheral edema and ascites. Concomitant mitral or aortic valve disease occurs frequently, and severe right heart failure may occur under such conditions without TR.

Severe TR is generally manifested by progressive fatigue and weakness related to reduction in cardiac output and the unpleasant sensation of ascites, congestive hepatosplenomegaly, and peripheral edema. These symptoms are related to heart failure and volume overload and can be palliated with aggressive diuretic therapy. In the chronic stages, however, symptoms become refractory, and cachexia and jaundice may be present.

Quantification of the degree of TR is important when interventional treatment is being considered, but preoperative assessment is often difficult because of the confounding effect of severe cardiac failure. In this regard, 2D echocardiography and cardiac magnetic resonance (CMR) are particularly useful.

Echocardiography is the preferred method to evaluate TR. In the more uncommon primary TR, specific abnormalities of the leaflets or the subvalvular apparatus can be identified. In secondary TR, anular dilation along with increased RV and right atrial dimensions are typically observed. RV function should be assessed, given its prognostic relevance. RV strain and three-dimensional (3D) measurements of RV volumes are helpful in overcoming the limitations of conventional RV function indexes.

Echocardiographic evaluation of TR severity is based on multiple parameters, including (1) qualitative: color flow regurgitant jet and valve morphology; (2) semiquantitative: vena contracta and proximal isovelocity surface area (PISA) radius; and (3) quantitative: effective regurgitant orifice area (EROA), regurgitant volume, and size of the right cardiac chambers/vena cava. In addition, pulmonary pressures can be estimated using Doppler gradients. However, this may not be possible or might underestimate the severity of pulmonary hypertension in the presence of severe TR. Hence, in the presence of severe TR and suspected pulmonary hypertension, right cardiac catheterization is the method of choice to evaluate pulmonary vascular resistance.

In addition to echocardiography, CMR is a highly accurate and reproducible method to assess RV function, dimensions, and morphology, but its availability may be limited. CMR is also a helpful tool to calculate the tricuspid regurgitant volume by means of RV volumetry. ^,

The classical quantification of TR included mild, moderate, and severe degrees. Recently, a new grading scheme including two additional degrees (“massive” and “torrential”) has been proposed and implemented in clinical studies on transcatheter interventions. ^, Including the two additional grades of TR has shown an improved predictive value in terms of mortality and rehospitalization for heart failure, especially in patients with advanced disease. ^, Assessment of TR may be dynamic, and the decision for intervention is best made based on preoperative assessment. Moderate and severe TR grades have a fair agreement between preoperative transthoracic echocardiography (TTE) and intraoperative transesophageal echocardiography (TEE) assessment, but mild TR on preoperative TTE is often downgraded to minimal TR on intraoperative assessment. In contrast, there is reasonably good correlation between anulus diameter measurements from preoperative TTE and intraoperative TEE images.

In the special setting of TV endocarditis in intravenous drug users, the valve is usually rapidly destroyed, and classic signs and symptoms of severe TR may develop very precipitously. The illness is usually only a few weeks in duration before the patient presents for medical care. Frequently, pulmonary symptoms and signs secondary to septic pulmonary emboli are marked. The diagnosis can be strongly suspected from a history of drug abuse, evidence of pulmonary infection, elevated jugular venous pressure, pulsatile neck veins, and pulsatile liver. These features, combined with positive blood cultures and echocardiography, are usually sufficient to establish the diagnosis.

Diagnosis of traumatic TR is usually easily established by signs of severe TR and a history of chest trauma. Occasionally, however, the relationship of these signs to a history of injury is not obvious. In patients with traumatic TR, right-to-left shunting may occur across a patent foramen ovale.

Several techniques can be used to address TR due to tricuspid anular dilation. All of them aim to provide long-term anular stabilization and preserve leaflet mobility and coaptation. Because isolated TV disease is rare, the following operative technique describes tricuspid repair with accompanying left-sided valve disease. Bicaval venous cannulation is routinely used. After the mitral procedure is completed, the right atrium is opened with the usual oblique incision ( Fig. 13.5 ). The tricuspid procedure can be performed with or without cardioplegic arrest. Once a possible intracardiac shunt (e.g., patent foramen ovale) has been ruled out or repaired, the tricuspid procedure may be performed on the beating, perfused heart during rewarming of the patient after the left-sided procedure, with suction on the aortic vent needle after the left heart has been carefully de-aired. To improve visualization and facilitate the beating-heart tricuspid procedure, a flexible cardiotomy suction device is inserted to remove blood that drains from the coronary sinus. Once the valve procedure has been performed, a water test is used to assess valve competency. However, water may quickly drain out of the right ventricle before achieving closure of the valve leaflets; therefore, interpretation of this test may be challenging, and after discontinuing cardiopulmonary bypass but prior to decannulation, TEE is used to assess valve competency and RV function. The presence of residual moderate or severe TR is an indication for a second repair attempt or valve replacement. New signs of RV dysfunction, particularly with inferior segmental wall motion abnormalities, may signify compromise of the right coronary artery, a rare but well-described complication of TV surgery.

Tricuspid ring anuloplasty. (A) Exposure is through usual oblique right atriotomy. Venous cannulas are inserted directly into superior and inferior venae cava (for alternatives, see Chapter 2 ). (B) Stay sutures provide excellent exposure (alternatively, an atrial retractor may be used). The surgeon identifies anteroseptal TV commissure, membranous part of AV septum, and coronary sinus orifice and can then mentally visualize location of the AV node and penetrating portion of the bundle of His. Using appropriate sizers, notched at points corresponding to anteroseptal and posteroseptal commissures at both ends of the septal tricuspid leaflet, a proper-sized tricuspid anuloplasty ring is selected. (C) The first stitch, of No. 2-0 or 3-0 polyester, is positioned exactly at the midpoint of the septal leaflet anulus, and only two more mattress stitches are needed for the septal portion of the ring. Small pledgets may be used on these mattress sutures. These and all other sutures are passed first through host tissue and then through the cloth of the undersurface of the ring, just as in suturing the ring for mitral anuloplasty (see Chapter 11 ). (D) Five or six mattress stitches are needed in the portion of the anulus to be plicated, which is adjacent to the posterior leaflet, and these are passed through the cloth of the ring close together (marking stitches are present on the ring cloth to guide the surgeon). The remainder of the ring, corresponding to about half its circumference, is attached to the anulus at the base of the anterior cusp with, at most, four fairly widely spaced mattress sutures. The ring is lowered into position along the sutures and the sutures tied, with great care taken not to pull upward strongly on them, lest they tear out. In some cases, the anuloplasty ring can be secured in place with three or four interrupted mattress sutures along the septal leaflet and then with continuous sutures for the remainder.

De vega technique.

The De Vega technique has the advantages of simplicity and low cost. In this technique, a 0 polypropylene suture is passed in a clockwise direction as a running stitch into the junction of the anulus and RV wall, from the commissure between the septal and anterior leaflet to a point opposite the os of the coronary sinus ( Fig. 13.6 ). The same suture is then reversed and passed in a counterclockwise direction slightly peripherally to the first stitch back to the starting point. Separate pledgets of polyester felt are incorporated in the suture at each end to prevent its pulling through the tissues. The suture is tightened until the orifice will admit an appropriate sizer (24 to 28 mm) and is then tied. When properly performed, the De Vega suture anuloplasty is as effective and durable as the ring technique.

De Vega anuloplasty. (A) The classic De Vega anuloplasty is accomplished using a double-armed No. 2-0 braided polyester suture or a 0 polypropylene suture. It is designed to narrow the tricuspid anulus at the base of the anterior and posterior leaflets, avoiding the area of the penetrating bundle of His and AV membranous septum. One arm and then the other arm of the suture pass into the tricuspid anulus, taking 8 to 10 fairly deep bites. (B) Suture is tied over a felt pledget, producing a purse-string effect and narrowing the orifice to admit a 24- to 28-mm sizer. (C) Often a sufficient repair can be done by narrowing the anulus only in the lateral half of the anterior leaflet and the base of the posterior leaflet.

When TV replacement is required, the leaflets are excised, and a 3- to 5-mm fringe of leaflet tissue is left on the anulus ( Fig. 13.7 ). Alternatively, the septal leaflet may be left in situ. Interrupted pledgeted mattress sutures are placed in the remaining skirt of leaflet tissue along the area occupied by the septal leaflet to avoid damaging the AV node and the bundle of His. Either a continuous polypropylene suture or interrupted pledgeted mattress sutures may be used for the remainder of the insertion. Alternatively, simple interrupted sutures may be used throughout.

TV replacement. (A) Exposure is as for repair. All three leaflets of the TV are excised, leaving a cuff at the base of the septal leaflet 5 to 8 mm wide. Alternatively, the septal leaflet may be left in situ. (B) Starting at the midpoint of the septal leaflet cuff, interrupted horizontal mattress sutures buttressed with felt pledgets are placed first into remaining valve tissue and then through the sewing ring of the replacement device. (C) After placing four to five interrupted mattress sutures, remainder of the insertion might be completed using a continuous suture technique. Interrupted sutures can also be used circumferentially. Bites may be through the anulus, mindful that the right coronary artery lies deep to the anulus anteriorly. AV, Atrioventricular.

In intravenous drug users or patients with multiple recurrent episodes of TV endocarditis, the three leaflets and their chordae tendineae can be excised to avoid implantation of prosthetic material and reduce the risk of recurrent infection. However, postoperative recovery and late cardiac performance are compromised by the resulting torrential TR. In addition, later valve replacement is more difficult.

Partial replacement of the TV with a cryopreserved allograft is an attractive option for severe TR caused by endocarditis, because allografts are thought to result in a lower risk of recurrent infection. Shrestha and colleagues from Brisbane, Australia, reported favorable outcomes in 13 patients (three late reoperations) using TV allografts for tricuspid endocarditis.