Tricuspid Valve Disease

Functional (Secondary) Tricuspid Regurgitation

The multitude of chordal attachments of the tricuspid valve, described in Chapter 1 , may impair proper leaflet coaptation and promote tricuspid regurgitation (TR) in the presence of right ventricular (RV) dysfunction and dilatation. The tricuspid anulus shortens during systole when the tricuspid valve is competent. When right ventricular (RV) dilatation 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. 14-1 ). The anular dilatation results in failure of leaflet coaptation, contributed to in some patients by chordal shortening secondary to the RV dilatation. Thus, a strong correlation exists between tricuspid anular diameter measured echocardiographically and presence and severity of TR ( Fig. 14-2 ). As the tricuspid anulus dilates, it assumes a more circular shape in a flat plane. The reported threshold for TR based on anular dilatation is 27 mm · m ⁻² or about 34 mm in the average adult.

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.

Experimental work by Tsakiris and colleagues has shown 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 have 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, an 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. 14-3 . The final common pathway is RV dysfunction and dilatation 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 RV.

It is these mechanisms that may produce TR late after isolated mitral valve operations or after combined aortic and mitral valve operations (see Chapter 11, Chapter 13 ).

Rheumatic Tricuspid Stenosis and Regurgitation

Rheumatic tricuspid valve 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 tricuspid valve 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.

Tricuspid Valve Endocarditis

Acute tricuspid valve endocarditis is rare and usually associated with habitual intravenous self-administration of drugs. The most common etiologic organism is Pseudomonas aeruginosa, followed by Staphylococcus aureus . A variety of gram-negative bacilli may be involved. Rarely, Candida albicans is the infective organism. The organisms may form masses on the valve leaflets, or simply erode and destroy large portions of leaflets and chordae (see Chapter 15 ).

Traumatic Injury of Tricuspid Valve

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 17 ). Usually it is the anterior tricuspid leaflet that becomes flailed. Rarely, the ventricular septum may rupture. Occasionally a transvenous ventricular pacing lead is associated with important TR. This may be due to perforation, laceration, or scarring. Apical electric activation may also contribute. Rarely, pacemaker 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 tricuspid regurgitation. Following cardiac transplantation, many years of repeated transvenous endomyocardial biopsies may induce severe TR secondary to inadvertent severing of chordae during biopsy.

Carcinoid Tricuspid Valve Disease

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 (because a good deal of it is inactivated in the lungs). Thereby, the 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 (see “Carcinoid Heart Disease” in Chapter 18 ).

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 combined stenosis and regurgitation. 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 the carcinoid syndrome. Tricuspid valve replacement may be required, but operative mortality is high as a result of comorbidity, particularly in patients above the age of 60.

Tricuspid Stenosis

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 enlarged but not pulsatile (unless from forceful atrial contraction that produces a presystolic pulse).

The chest radiograph shows right atrial enlargement, and the electrocardiogram shows a prominent P wave unless atrial fibrillation is present. Two-dimensional (2D) echocardiography is helpful in establishing the presence of leaflet thickening. Cardiac catheterization with simultaneous measurement of right atrial and RV pressures identifies a diastolic gradient (>4 mmHg) across the valve.

Tricuspid Regurgitation

History and physical signs are sufficient to suggest diagnosis of important TR. The jugular venous pulse shows a dominant fused c and v wave, followed by a sharp, deep y descent. The murmur, maximal over the lower left sternal edge, is pansystolic, is often high pitched, and increases on inspiration. The enlarged liver shows systolic pulsation. However, when TR is severe, such as after excision of the tricuspid valve, a murmur may be absent. In advanced cases, there are other signs of right heart failure, including peripheral edema and ascites. Mitral or aortic valve disease signs can dominate the findings, and severe right heart failure may occur under such conditions without TR.

The symptomatic state of 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. The symptomatic state of right heart failure and volume overload can be palliated with aggressive diuretic therapy, but in the chronic stages, symptoms become refractory. In late stages, cachexia and jaundice may complicate the clinical complex.

Quantification of the degree of TR is important when surgical treatment of valvar heart disease is being considered, but preoperative assessment is often difficult because of the confounding effect of severe cardiac failure. In this regard, 2D echocardiography is particularly useful, because presence of the cardiac catheter across the tricuspid valve interferes with angiographic assessment. Both contrast and Doppler echocardiography have been useful, but the increasing precision of color flow mapping and Doppler color flow map-guided interrogation have made them the favored methods for estimating tricuspid regurgitant flow. The vena contracta, as determined by color flow Doppler, indirectly reflects effective regurgitant orifice area, which if greater than 0.7 cm indicates severe TR. Quantitative assessment of TR can also be accomplished with the proximal isovelocity surface area (PISA) method. Dilatation of the inferior vena cava and flow reversal in the inferior vena caval and hepatic veins provide supporting evidence. Echocardiography can also detect paradoxical ventricular septal motion and shift of the atrial septum toward the left atrium in isolated TR. Maximum circumference of the tricuspid anulus is larger in patients with TR than in normal adults (14 ± 0.7 cm and 11.9 ± 0.9 cm, respectively), and its reduction during systole is less (10% ± 2% vs. 19% ± 4%).

Despite these refinements in diagnosis, the presence and severity of TR need to be assessed in the operating room. The patient's hemodynamic state must be optimized by the anesthesiologist for any form of assessment to have validity. The surgeon's finger, inserted through the right atrial appendage, can appreciate a TR jet. Severe TR correlates reasonably well with a jet of greater intensity, greater width, and increased propagation from the valve orifice. If TR is severe, however, there may not be a jet with sufficient velocity to be identified in this manner. In the current era, rigorous assessment of TR and tricuspid anular circumference by transesophageal echocardiography in the operating room has largely supplanted finger palpation.

In the special setting of tricuspid valve endocarditis in drug addicts, the valve is usually rapidly destroyed, and classic signs and symptoms of severe TR develop. The illness is usually only 1 to 3 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 (in samples withdrawn from the RV or pulmonary artery) 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 a blow to the chest (see Chapter 17 ). 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, which can lead to the mistaken diagnosis of Ebstein anomaly.

Tricuspid Valve Anuloplasty

Anuloplasty Ring Technique

Because isolated tricuspid valve disease is rare, the technique of operation is given for TR accompanying left-sided valve disease. When evaluation before cardiopulmonary bypass (CPB) indicates important TR, two venous cannulae are used. The tricuspid procedure may be performed in the beating, perfused heart during rewarming of the patient, with suction on the aortic vent needle after the left heart has been carefully de-aired, or during continuing antegrade/retrograde cold cardioplegia with addition of external cardiac cooling.

After the mitral procedure is completed, the right atrium is opened with the usual oblique incision ( Fig. 14-5 ). When an anuloplasty is performed using a ring, length of the base of the tricuspid septal leaflet is measured with calipers, or area of the anterior leaflet with a sizer, and on this basis the proper-sized ring is selected. The Carpentier-Edwards anuloplasty ring, for example, is a modified oval corresponding to configuration of the tricuspid anulus, with a gap in the portion designed to overlie the atrioventricular (AV) node so that the conduction tissue is not compromised. Rings correct TR by returning the anulus to slightly less than its normal size by plicating that portion at the base of the posterior (posteroinferior) leaflet and at the commissure between that and the anterior leaflet. Thus, the ring effectively “bicuspidizes” the tricuspid valve. The anulus is not plicated at either the attachment of the septal leaflet or along the major part of the attachment of the large anterior leaflet. A flexible “half ring” (Cosgrove) accomplishes a similar function, leaving the base of the septal leaflet untouched but plicating the anulus at the attachment of the anterior and posterior leaflets. The size of the ring is determined by length of the septal leaflet (intertrigonal distance). It is unwise to select too small a ring in the belief that it will be more effective, because it distorts and narrows the orifice and may subsequently detach. Because tissues around the tricuspid valve are usually tenuous, sutures must take adequate bites, beginning in the atrial wall and passing into the deeper part of the anulus itself, carefully avoiding leaflet tissue. The surgeon must also be cognizant of the location and course of the right coronary artery, as its inadvertent suture ligation has been reported.

After discontinuing CPB and before decannulation, competence of the valve is assessed by 2D echocardiography, using either a handheld or esophageal probe. Presence of moderate or severe TR is an indication for valve replacement or repair. If the heart is beating and normothermic, a reasonable assessment of competence of the repair is possible as soon as it is completed. With the atrium still open, the RV is allowed to fill with blood, and the tricuspid leaflet apposition is assessed. If apposition is obviously inadequate, the valve is replaced or repaired. If it appears adequate, the right atrium is closed, air is aspirated from the RV and pulmonary artery, and the operation is completed in the usual manner (see “Completing Operation” in Section III of Chapter 2 ).

De Vega Technique

The De Vega technique is used in patients with no more than moderate TR from anular dilatation, where it is anticipated that good long-term function is not dependent on integrity of the repair. This technique has the advantages of simplicity and low cost. A No. 2-0 polyester suture (not monofilament polypropylene) is passed in a counterclockwise direction as a circular stitch deeply into the junction of the anulus and right ventricular wall from 1 or 2 cm medial to the posteroseptal commissure to the base of the anterior leaflet 2 to 4 cm medial to the anteroseptal commissure ( Fig. 14-6 ). The same suture is then reversed and passed in clockwise 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 30 mm) and is then tied.

Tricuspid Valve Replacement

When tricuspid valve replacement is elected, the leaflets are excised, and a 2- to 3-mm fringe of leaflet tissue is left on the anulus ( Fig. 14-7 ). Alternatively, the septal leaflet may be left in situ. Interrupted pledgeted mattress sutures are placed in the fringe of leaflet tissue along the area occupied by the septal leaflet, to avoid damaging the AV node and 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. Infrequently, to avoid heart block, the suture line for valve insertion can be placed on the atrial aspect above the coronary sinus and base of the septal defect.

Tricuspid Valve Excision

In drug addicts with active tricuspid valve endocarditis, the three leaflets and their chordae tendineae can simply be excised, using the general techniques described earlier. However, postoperative convalescence and late cardiac performance are compromised by the resulting severe TR. In addition, later valve replacement is more difficult.

Stern and colleagues suggest that primary bioprosthetic valve replacement is preferable to valve excision and is not followed by recurrent endocarditis unless intravenous drug abuse continues.

Partial Tricuspid Valve Replacement with Cryopreserved Tricuspid Valve Allograft

Partial replacement of the tricuspid valve with a cryopreserved allograft is an attractive option for severe TR caused by endocarditis, because allografts are known to demonstrate greater freedom from reinfection compared with xenografts or mechanical valves in the aortic position (see Chapter 15 ). Shrestha and colleagues from Brisbane, Australia, reported favorable outcomes in 13 patients (three late reoperations) using tricuspid valve allografts for tricuspid endocarditis.

Tricuspid Valve Anuloplasty