Abstract
Tricuspid valve surgery has evolved from an almost ignored valve in the past to an important valve that is critical to address at the time of left valve intervention. The incidence of tricuspid regurgitation associated with left valvular disease is quite significant and most common in conjunction with mitral valve disease; however, association with aortic valve pathology is not uncommon. Most commonly, tricuspid regurgitation is functional or secondary to dilation of the annulus, as a consequence of right ventricle dilation secondary to pulmonary hypertension. However, organic (rheumatic, endocarditis, or degenerative in origin) is not uncommon. The purposes of this chapter are to shed light on the anatomy of the tricuspid valve, and elucidate the etiology and pathogenesis of tricuspid valve disease, mainly tricuspid valve regurgitation, with a special focus on secondary tricuspid valve regurgitation. Indications for surgery as well as different surgical approaches (including different repair techniques and valve replacement) to correct tricuspid valve regurgitation are discussed in detail. A transcatheter approach for tricuspid valve repair or replacement is attractive, desirable, and beneficial to this high-risk population as an alternative to surgery.
Keywords
tricuspid valve, secondary tricuspid regurgitation, tricuspid valve repair, tricuspid valve replacement
Step 1
Surgical Anatomy
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The tricuspid valve is located between the right atrium (RA) and right ventricle and has a valve area of 4 to 6 cm. The tricuspid valve is composed of three leaflets—the anterior, posterior, and septal. The leaflets are supported by chordae tendineae and papillary muscles. Compared with the mitral valve, the leaflets and chordae tendineae of the tricuspid valve are thinner and the tricuspid orifice is larger and more triangular.
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The anterior leaflet is the largest of the three leaflets and extends through the anterior portion of the annulus. Its chordae attach to the anterior and septal papillary muscles. The posterior leaflet is the smallest leaflet and extends through the inferior and posterior edges of the annulus; its chordae originate from the posterior and anterior papillary muscles. The septal leaflet is the most medial and is attached directly to the interventricular septum; it is larger than the posterior leaflet, and its chordae attach to the posterior and septal papillary muscles. The septal leaflet is relatively immobile due to its attachment to the fibrous structure of the heart.
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The tricuspid valve is a continuous veil of thin fibrous tissue. Three commissures are delineated by fan-shaped chordae of the three leaflets:
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Anteroseptal commissure—where the basal attachment of the tricuspid valve reaches its highest level at the membranous interventricular septum and where the anterior and septal walls of the right ventricle join
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Anteroposterior commissure—forms a deep indentation in the leaflet tissue between the anterior and posterior leaflets
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Posteroseptal commissure—a deep indentation in the leaflet tissue at the junction of the posterior and septal walls of the right ventricle.
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1
Tricuspid Valve Annulus
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The tricuspid valve annulus is part of the fibrous skeleton of the heart. It consists of a ring of collagenous tissue that generally extends around the line of attachment of the leaflets of the tricuspid valve. It is very thin and difficult to identify. The tricuspid annulus is a complex three-dimensional (3D) structure; the normal tricuspid valve annulus is saddle-shaped, with the highest points located in an anteroposterior orientation and the lowest points at the area of the septal leaflet. With the development of functional tricuspid regurgitation (TR), changes in the 3D annular shape lead to loss of the saddle shape and more flattening of the annulus; that is, the tricuspid annulus becomes dilated and more planar and circular and hence, restoration of the 3D shape of the annulus may be an important therapeutic goal beyond that of annular reduction alone.
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Normal tricuspid valve annulus diameter in adults is 28 ± 5 mm in the four-chamber view. Significant tricuspid annular dilation is defined by a diastolic diameter of more than 21 mm/m 2 (> 35 mm).
2
Relation of the Tricuspid Valve to Other Structures
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Structures surrounding the tricuspid valve that are of major surgical significance include the coronary sinus, atrioventricular (AV) node, membranous septum, bundle of His, and right coronary artery ( Fig. 23.1 ).
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The conduction system is near the septal leaflet and its anterior septal commissure. The AV node lies in the atrial septum bordering the septal leaflet, superior and anterior to the coronary sinus. Its exact location can be approximated at the apex of the triangle of Koch, a triangle composed of the septal annulus and tendon of Todaro as its sides and the coronary sinus orifice as its base. Extending from the AV node is the bundle of His, which penetrates the right trigone under the interventricular component of the membranous septum (≈ 5 mm inferior to the anterior septal commissure) and runs along the crest of the muscular septum. The membranous septum usually lies beneath the septal leaflet inferior to the anterior septal commissure. The right coronary artery runs anterior to the anterior leaflet annulus and may be injured by deep sutures in the annulus.
Step 2
Preoperative Considerations
1
Causes of Tricuspid Valve Diseases
Tricuspid Stenosis
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This is usually rheumatic in origin. On rare occasions, infective endocarditis, congenital abnormalities, or carcinoid disease may be implicated. Rheumatic tricuspid involvement usually results in both tricuspid stenosis and regurgitation, and it typically coexists with mitral or aortic rheumatic disease. The hallmark features of rheumatic tricuspid stenosis are commissural fusion and leaflet thickening, but calcification is usually absent. Carcinoid syndrome leads to focal or diffuse deposits of fibrous tissue on the endocardium of the valve leaflets and cardiac chambers. The tricuspid valve in carcinoid syndrome is thickened, with retracted leaflets fixed in a semiopen position, resulting in both tricuspid stenosis and regurgitation, and usually not amenable for repair.
Tricuspid Valve Regurgitation
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TR can occur with abnormal or normal valve leaflets. Causes of TR associated with abnormalities of the tricuspid leaflets include rheumatic valve disease, endocarditis, carcinoid syndrome, radiation therapy, Marfan syndrome, papillary muscle dysfunction, and congenital disorders such as Ebstein anomaly. Penetrating and nonpenetrating trauma, iatrogenic damages during cardiac surgery, biopsies, catheter placement in right heart chambers, and placement or extraction of pacemakers and defibrillator leads are also rare causes of TR.
Degenerative Tricuspid Regurgitation
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Tricuspid prolapse is generally associated with mitral valve prolapse and is defined as a midsystole posterior leaflet displacement beyond the annular plane. The coaptation line is above the annular plane. Tricuspid prolapse usually involves more than one leaflet, and often the three leaflets are affected. The most common phenotype of tricuspid prolapse is diffuse myxomatous degeneration (Barlow disease). A flail tricuspid leaflet is observed when the free edge of a leaflet is completely reversed in the RA, usually as a consequence of ruptured chordae. It also is common in infective endocarditis in association with vegetations.
Secondary Tricuspid Regurgitation
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Approximately 80% of cases of significant TR are functional in nature. Regurgitation develops with normal tricuspid valve leaflets as a result of right ventricular (RV) dysfunction and tricuspid annular dilation (functional regurgitation), usually in the context of left-sided valvular disease. Pulmonary hypertension or RV dysfunction leads to elevations of RV systolic and diastolic pressures, RV cavity enlargement, and tricuspid annular dilation. The circumference of the tricuspid annulus lengthens primarily along the attachments of the anterior and posterior leaflets. The septal leaflet portion, on the other hand, is fixed between the right and left trigones and the atrial and ventricular septa, preventing its lengthening. As annular and ventricular dilation progress, the cordal–papillary muscle complex becomes functionally shortened, with tethering of the leaflets, although it remains normal in appearance. This combination of RV enlargement and tricuspid annular dilation prevents leaflet coaptation and leads to valvular incompetence ( Fig. 23.2 ).
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Previously, it was believed that functional TR decreased or even disappeared after surgical correction of left-sided valve disease. This concept influenced cardiac surgery practice for many years. More experience, however, has led to better appreciation of the potential for progression of functional TR and tricuspid annular dilation after left-sided surgery. This effect may occur in spite of the complete correction of the mitral and aortic disease and the resolution of pulmonary hypertension after surgery. Tricuspid annular dilation is the strongest and most consistent risk factor for the development of late TR after left-sided valve surgery.
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Severe TR and its resultant RV dysfunction and venous congestion contribute to an increase in early and late morbidity and mortality after left-sided valve surgery. Moreover, reoperation to correct worsening postoperative TR is associated with a high operative mortality rate and disappointing long-term results. Therefore, a proactive strategy of prophylactic repair of a dilated tricuspid annulus at the time of the initial left-sided valve surgery, regardless of the degree of TR, has been advocated as a strategy to help reduce the incidence of late TR and RV failure and the complexity and higher risk of redo surgery. Concomitant mitral and tricuspid valve repair is associated with significant RV reverse remodeling and improvement in functional class postoperatively.
2
Assessment of the Tricuspid Valve
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Imaging of the tricuspid valve is a challenging process. Functional TR is dynamic in nature, so the degree of severity of TR may change, especially under general anesthesia, and the decision for tricuspid valve intervention should be made before surgery based on preoperative echocardiography and careful clinical assessment of the patient.
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Tricuspid valve analysis can be achieved with two-dimensional (2D)–transthoracic echocardiography (TTE) imaging (the technique of choice). 3D-TTE can be used as an additive approach. Transesophageal echocardiography (TEE) is advised in case of suboptimal TTE images to evaluate the severity of TR. TTE helps determine cause, measures the size of right-sided chambers and the inferior vena cava (IVC), assesses RV systolic function, estimates pulmonary artery systolic pressure, and characterizes any associated left-sided heart disease. TEE describes the morphology and pathophysiology of the tricuspid valve and grades the severity of tricuspid valve regurgitation. It is of note that TEE usually underestimates the measurement of the tricuspid valve annulus. The evaluation of tricuspid valve annulus dilation is a matter of ongoing controversy and is less precise compared with mitral valve annulus assessment.
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Cardiovascular magnetic resonance (CMR) is another imaging modality for the tricuspid valve that allows visualization of the anatomy and function of the tricuspid valve. It also permits quantification of the regurgitant volume and regurgitant fraction.
3
Indications for Tricuspid Valve Intervention
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The 2014 American College of Cardiology/American Heart Association valve guidelines has indicated the following recommendations:
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Tricuspid valve repair for patients with severe functional TR who are undergoing concurrent surgery for mitral valve disease (Class I, level of evidence C).
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Tricuspid valve intervention for severe primary TR in symptomatic patients (Class IIa, level of evidence C). When the tricuspid valve leaflets are too diseased and not amenable to repair, tricuspid valve replacement is believed to be reasonable for patients with severe TR.
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Tricuspid valve repair may be considered for less than severe TR in patients undergoing mitral valve surgery in the presence of pulmonary hypertension or tricuspid annular dilation (Class IIa, level of evidence B).
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Tricuspid valve repair may be considered for patients with moderate functional TR and pulmonary artery hypertension at the time of left-sided valve surgery (Class IIa, level of evidence C).
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Tricuspid valve surgery may be considered for asymptomatic or minimally symptomatic patients with severe primary TR and progressive degree of moderate or greater RV dilation and/or systolic dysfunction (Class IIa, level of evidence C).
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Reoperation for isolated tricuspid valve repair or replacement may be considered for persistent symptoms due to severe TR in patients who have undergone previous left-sided valve surgery and who do not have severe pulmonary hypertension or significant RV systolic dysfunction (Class IIa, level of evidence C).
- 1.
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American College of Cardiology/American Heart Association practice guidelines have recommended against tricuspid surgery for patients with only mild primary TR. Tricuspid surgery is also not indicated for patients with some degree of TR who are asymptomatic, when there is no concurrent left-sided valve disease, or when severe pulmonary hypertension is absent.
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Several cardiac surgery centers currently advocate for the routine repair of the dilated tricuspid annulus at the time of left-sided heart surgery, regardless of the degree of TR. At our center, we consider valve repair even if there is no associated TR or only a mild degree of TR when the tricuspid annulus diameter is 40 mm or more with the presence of pulmonary hypertension (PH; defined as a mean pulmonary artery pressure ≥25 mm Hg at rest) or 45 mm or more in the absence of PH. Such repair could reduce the risk of RV dysfunction, both in the perioperative period and in the long term, as well as the need for a second operation ( Table 23.1 ).
Table 23.1
CLASS
TRICUSPID VALVE SURGERY
LEVEL OF EVIDENCE
TRICUSPID VALVE REGURGITATION
Tricuspid valve surgery is recommended for patients with severe tricuspid regurgitation (TR; symptomatic or nonsymptomatic) undergoing left-sided valve surgery. Tricuspid valve repair can be beneficial for patients with mild, moderate, or greater functional TR at the time of left-sided valve surgery with tricuspid annular dilation or prior evidence of right heart failure.
C
I
Tricuspid valve surgery can be beneficial for patients with symptoms due to severe primary TR that are unresponsive to medical therapy.
B
IIa
Tricuspid valve repair may be considered for patients with moderate functional TR and pulmonary artery hypertension at the time of left-sided valve surgery.
Tricuspid valve surgery may be considered for asymptomatic or minimally symptomatic patients with severe primary TR and progressive degrees of moderate or greater right ventricular (RV) dilation and/or systolic dysfunction.
C
IIb
Reoperation for isolated tricuspid valve repair or replacement may be considered for persistent symptoms due to severe TR in patients who have undergone previous left-sided valve surgery and who do not have severe pulmonary hypertension or significant RV systolic dysfunction.
C
TRICUSPID VALVE STENOSIS
I
Tricuspid valve surgery is recommended for patients with severe tricuspid stenosis (TS) at the time of operation for left-sided valve disease. Tricuspid valve surgery is recommended for patients with isolated, symptomatic, severe TS.
C
IIb
Percutaneous balloon tricuspid commissurotomy might be considered in patients with isolated tricuspid severe tenosis
C
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Functional TR in association with aortic stenosis may persist or even become progressive after aortic valve replacement alone; it is usually associated with left ventricular (LV) diastolic dysfunction. A concomitant tricuspid valve procedure should be considered in select patients with aortic stenosis at the time of aortic valve replacement.
4
Choice of Repair Technique
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Previously, it was believed that the type of tricuspid valve repair performed was of little importance as long as the size of the tricuspid annulus was secured to avoid progressive dilation. For patients with functional TR secondary to left-sided valve disease, the De Vega annuloplasty was thought to be the most appropriate procedure to reduce the size of the tricuspid annulus. However, recent data have demonstrated poor long-term results with the use of the De Vega technique. Although it is a safe and simple procedure, 30% or more of patients may develop recurrent moderate to severe TR after a De Vega repair, with progressive annular dilation and recurrence of symptoms.
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Long-term studies have also illustrated poor long-term durability and high rates of recurrent TR with the use of flexible rings and bands (Duran, Medtronic, Minneapolis, MN; Cosgrove-Edwards, Edwards Lifesciences, Irvine, CA; Peri-Guard, Synovis, MN). Only rigid rings have yielded good long-term results, with the bulk of evidence favoring the semirigid Carpentier-Edwards ring (Edwards Lifesciences) as the most durable after tricuspid valve repair.
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3D rings that aim to restore the annular geometry, such as contour 3D (Medtronic), GeoForm (Edwards Lifesciences), and 3D MC3 (Edwards Lifesciences) rings are being increasingly used for the treatment of functional tricuspid valve regurgitation with documented good results.
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At our center, we perform tricuspid valve repairs using 3D annuloplasty bands for all patients with a tricuspid annular dilation of greater than 40 mm, regardless of the presence of TR, at the time of concurrent left-sided valve surgery. The De Vega repair is reserved for older patients undergoing left-sided valve surgery who have 2+ TR or less and a tricuspid annular dimension of less than 40 mm. Also, in case of the presence of PH and concerns about postoperative RV dysfunction and the possibility of increasing TR, a quick De Vega repair helps those older patients pass the postoperative phase. In patients with a large annulus (> 50 mm) and severe TR, we perform annuloplasty and edge-to-edge techniques ( Fig. 23.3 ).
5
Choice of Prosthetic Valve Type
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Repair of the tricuspid valve is superior to valve replacement because it is associated with lower hospital mortality rates, better long-term survival, better preservation of ventricular function, fewer thromboembolic complications, and reduced risk of endocarditis. However, in the context of organic tricuspid disease with severe leaflet thickening and cordal retraction, tricuspid valve replacement is the preferred surgical intervention.
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The choice of prosthesis type in the tricuspid position has been debated in the cardiac surgery community for many years. A meta-analysis has summarized the published literature by comparing outcomes reported for contemporary mechanical and bioprosthetic tricuspid valves. A total of 11 studies, with 646 mechanical and 514 biologic tricuspid prostheses and 6046 follow-up years, were analyzed. Studies that reported prosthetic models from before 1970 were excluded. Overall, the pooled survival and reoperation data did not favor either prosthesis type. Furthermore, the incidence of mechanical valve thrombosis was comparable with the incidence of bioprosthetic valve deterioration. Therefore, the type of prosthetic valve is not a risk factor for adverse outcomes after tricuspid valve replacement, and there is no evidence favoring one prosthetic type or the other. In our experience, we almost never used a mechanical valve in the tricuspid position in the current era of the percutaneous valve; a bioprosthetic valve allows safe valve-in-valve implantation.
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As in other valve positions, there is no gold standard prosthetic valve available for tricuspid valve replacement. We believe that the choice between a mechanical and bioprosthetic valve in the tricuspid position should be individualized according to the surgeon’s clinical judgment, patient characteristics, anticoagulation considerations, likelihood of pregnancy, socioeconomic status, and lifestyle issues. A patient with drug addiction and a history of endocarditis, who may have difficulty with anticoagulation compliance, should have a bioprosthesis implanted.
6
Prosthesis and Ring Size
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Although not supported by good evidence, it is currently popular to implant undersized rings to improve coaptation during the repair of mitral regurgitation. This strategy may also apply to the repair of functional TR. However, there are no data to support the practice of implanting undersized rings in the tricuspid position. Long-term data from the Cleveland Clinic have demonstrated that the use of a small tricuspid ring for the repair of functional TR does not protect against the development of recurrent late TR. Use of the anterior leaflet for tricuspid valve sizing may be inaccurate to determine tricuspid annular size in functional TR because the tricuspid annulus is dynamic and may change in circumference during systole, with a reduction in annular dimension.
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We generally implant a tricuspid prosthesis (band or valve) identical or close in size to the mitral valve prosthesis used during concurrent mitral repair or replacement.
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When replacing the tricuspid valve, it is almost always possible to place a large bioprosthetic or mechanical valve. Prostheses with an internal diameter greater than 27 mm do not have clinically significant gradients, and thus hemodynamic performance is rarely an issue in tricuspid valve replacement; the patient prosthetic mismatch has not been reported in tricuspid valve replacement as a significant problem.