Tricuspid Valve
Gorav Ailawadi
INTRODUCTION
The tricuspid valve is arguably the least understood valve in the heart. Most often, the tricuspid valve is affected in the setting of left heart disease, specifically with mitral valvular disease. In this scenario, the pathophysiology of tricuspid valve insufficiency is a result of elevated left heart filling pressures with subsequent development of pulmonary hypertension leading to right ventricular (RV) hypertrophy or dysfunction, and ultimately tricuspid annular enlargement. This is often termed “functional tricuspid regurgitation” as it is due to a failure of coaptation of structurally normal leaflets. Although tricuspid repair, in general, is a simple technique, according to the Society for Thoracic Surgeons (STS) National database, the operative mortality in patients undergoing tricuspid valve surgery with or without concomitant operation is roughly 10%. Moreover, data from individual centers report an operative mortality for reoperations for recurrent TR in excess of 30%.
As such, many surgeons have trepidation in treating patients with tricuspid valve disease. In fact, the need for surgical repair of tricuspid regurgitation (TR) is unclear and often debated by the surgical and cardiology community. First, the usually low-pressure, right-sided circulation is tolerant to imperfect function of the tricuspid valve. Second, tricuspid valve regurgitation most often occurs in the setting of left-sided pathology, resulting in a longer and more complex procedure with additive risk. The argument against addressing the tricuspid valve also stems from the improvement in tricuspid valve function often seen after correction of left-sided pathology. However, accurate predictors of tricuspid valve improvement after sole correction of left-sided pathology have not been convincingly or prospectively studied.
Isolated tricuspid disease is much less common, especially in adults. Patients typically present with right-sided failure symptoms. Patients with fixed pulmonary hypertension, severe RV dysfunction, and severe TR with no left-sided pathology are often the most challenging and have the greatest risk. The prognosis in this especially high-risk group of patients can be poor due to RV dysfunction, and operative intervention is often associated with dismal outcomes. Primary leaflet abnormalities of the tricuspid valve are less common and are caused most commonly by infectious endocarditis and carcinoid heart disease. Finally, Ebstein’s anomaly, although most commonly treated in childhood, may also be first diagnosed in adulthood in its less severe forms.
The ACC/AHA has provided guidelines for operative intervention for tricuspid disease. Class I indications for surgical intervention include (1) patients with severe TR undergoing left-sided surgery, (2) primary severe TR without severe RV dysfunction, and (3) severe primary or secondary tricuspid stenosis. Class IIa indications include patients with moderate TR in the setting of left-sided surgery with or without tricuspid annular dilation (>40 mm by echocardiography). It should be noted that all guidelines are based on level C evidence indicating that this field has been largely guided based on retrospective series.
EVALUATION AND OPERATIVE INDICATIONS
Functional Tricuspid Regurgitation
Tricuspid annular dilation of the tricuspid valve due to left-sided pathology leads to functional TR. Generally, the annulus adjacent to the septal leaflet does not dilate, whereas the anterior and especially the posterior annulus dilates causing functional TR. Echocardiography is the most helpful modality in evaluating tricuspid valve regurgitation and distinguishes between annular problems and primary leaflet problems. Evidence of severe tricuspid insufficiency includes dilation of the right atrium, right ventricle, and inferior vena cava, along with a large color flow jet across the tricuspid valve. Hepatic vein flow reversal is likewise diagnostic. It is important to note that the degree of TR can be quite variable based on loading conditions and fluid status. Preoperative coronary artery catheterization is usually done given the typical patient age. Importantly, the assessment of right-sided hemodynamics should be done to evaluate RV function and pulmonary hypertension as these are significant predictors of outcomes in patients with TR. It should be noted that the degree of tricuspid regurgitation is poorly assessed by cardiac catheterization, while tricuspid stenosis can be diagnosed with this invasive test.
We often perform tricuspid annuloplasty in patients with more than moderate (>2+) TR in the setting of mitral valve disease. Selected patients with concomitant 2+ TR are also treated if there is any (1) evidence of RV dysfunction/significant pulmonary hypertension, (2) significant tricuspid annular dilation (annulus >40 mm), (3) elevated central venous pressure (>18 mmHg), or (4) in patients undergoing concomitant maze procedure as we believe even lesser degrees of TR may be contributing to AF.
In patients with isolated tricuspid insufficiency, surgical correction is warranted when symptoms are refractory to maximal medical therapy in selected patients. Often these patients will have difficult-to-treat right-sided congestive heart failure with significant peripheral edema and clinically significant passive congestion of the liver. Intensified diuretic administration often results in worsening renal function rather than improvement in the patient’s clinical status. Moreover, patients may
develop signs of liver dysfunction from passive congestion. Tricuspid operation should be cautioned in patients with severe liver dysfunction (MELD > 15) due to high operative mortality.
develop signs of liver dysfunction from passive congestion. Tricuspid operation should be cautioned in patients with severe liver dysfunction (MELD > 15) due to high operative mortality.
Endocarditis
Infectious endocarditis involving the tricuspid valve is the most frequent valve involved in cases of endocarditis secondary to intravenous (IV) drug abuse. Endocarditis in these patients involves the tricuspid valve in three-fourths of these patients, whereas involvement of the mitral and aortic valve occurs in one-fourth of cases. Pulmonic valve involvement is much less common, accounting for <1% of cases. The other common groups of patients who develop tricuspid endocarditis are those who develop infections of indwelling pacemakers and leads. Transthoracic echocardiography is typically sufficient in screening and evaluating for tricuspid endocarditis. Transesophageal echocardiography can be performed in cases where the tricuspid valve is not seen well by surface echocardiography.
Surgical intervention for IV drug abusers with isolated right-sided endocarditis should be performed with caution. First, imperfect tricuspid valve function is overall well tolerated in these patients as the right side is a low-pressure system. Second, the consequences of embolization from the tricuspid valve to the lungs are less catastrophic than those from embolization from the left-sided valves. Most importantly, the risk of ongoing IV drug abuse with ongoing risks including reinfection and overdose also may necessitate a conservative approach to surgery in these patients. Two important indications for surgery for tricuspid valve endocarditis are (1) endocarditis caused by microorganisms that are difficult to eradicate such as fungal organisms or bacteria resistant to antibiotic therapy and (2) patients with tricuspid valve vegetations >2 cm, a dilated right ventricle, and recurrent pulmonary emboli or right-sided heart failure. When surgery is necessary, debridement of infected tissue and preservation of the native valve is preferred when at all possible. Patients usually have significant degrees of valve regurgitation, and restoration of complete competence is neither possible nor necessary. Complete excision of the tricuspid valve will negate the risk of reinfection of an implanted prosthetic valve by continued IV drug use. This approach is not advocated by most surgeons since patients undergoing excision often have a challenging postoperative course and some eventually require prosthetic valve insertion secondary to poor cardiac output. Patients with pulmonary hypertension, sometimes related to multiple septic pulmonary emboli, will tolerate the absence of the tricuspid valve poorly.
In patients with infected pacemaker leads, the vegetations commonly involve the tricuspid valve. Diagnosis can be challenging in these patients as most patients with indwelling pacemaker leads have sterile vegetations on their leads without infection. Persistent positive blood cultures without other clear source or evidence of septic pulmonary emboli should prompt consideration for lead removal. While lead extraction alone may be sufficient therapy, in patients with large tricuspid valve vegetations (>2 cm) or significant TR, surgical removal and tricuspid repair should be considered. An alternative approach is the use of a hybrid approach with lead extraction by electrophysiologists and surgical tricuspid valve debridement and repair. Patients who require biventricular pacing may benefit from epicardial lead placement after tricuspid valve has been addressed and atrium closed. Great care must be taken to avoid cross-contamination of these new epicardial leads.
Carcinoid Heart Disease
Right-sided cardiac involvement is common in patients with carcinoid syndrome, although clinically significant lesions are much less frequent. Endocardial plaquing, the typical lesion seen in carcinoid heart disease, may involve either or both the pulmonic and tricuspid valves as well as the RV endocardial surface. Both tricuspid stenosis and regurgitation can occur in carcinoid disease. Evidence of tricuspid (and likely pulmonic) valve dysfunction and progressive right heart failure is the usual clinical presentation of patients considered for surgery. With current treatment of malignant carcinoid tumors, reasonable survival rates (>50% at 5 years) can be expected. Thus, patients with valvular dysfunction and progressive heart failure should be considered for valve replacement if their tumor is not imminently life-threatening.
Ebstein’s Anomaly
Ebstein’s anomaly causes varying degrees of TR and may be clinically silent or present at any time in children or adults. The lesion is characterized by downward displacement of the septal and often posterior leaflets of the valve into the right ventricle (Fig. 46.1). This gives the characteristic “atrialized” appearance of the right ventricle. The annular circumference is often quite large, and the right atrium is quite enlarged. The quality of the anterior leaflet is critical to the success of any attempted valve repair for Ebstein’s anomaly. The anterior leaflet is generally large, sail-like, and relatively thin. A thickened, muscularized anterior leaflet makes a poor substrate for repair. Ebstein’s anomaly valve may present along a spectrum of severity and may become clinically significant at any time during life and require surgical intervention.
Adults with less severe forms of Ebstein’s may become symptomatic and require surgical intervention. In adults presenting with Ebstein’s anomaly, symptoms may include arrhythmias, fatigability, dyspnea, and cyanosis. In addition, patients with Ebstein’s anomaly may have an associated atrial septal defect. Echocardiography is useful for characterizing the degree of valvular insufficiency and the quality of the leaflets, specifically the quality of the anterior leaflet when contemplating valve repair. Repair of the valve is obviously favored when possible. Replacement is necessary in some cases, however. In the neonatal period, transplantation or single-ventricle palliation (Starne’s procedure) may be required.
Anatomy of the Tricuspid Valve