Jennie H. Kwon and Marc R. Katz
This chapter is a revision and update of that included in previous editions of the TSRA Review written by Brian Solomon (2nd edition) and Lucas M. Duvall (1st edition).
Functional TR
In up to 80% of cases, tricuspid regurgitation (TR) occurs secondary to other cardiopulmonary pathologies. This is called functional TR and refers to the absence of any primary valve abnormalities (i.e., isolated leaflet, chordae or annular structural issues). Secondary causes of TR include chronic left heart disease (either valvular or ventricular dysfunction) resulting in pulmonary hypertension or other drivers of pulmonary hypertension such as chronic pulmonary disease, pulmonary thromboembolism, or left-to-right shunt. TR may also occur secondary to right ventricular dysfunction due to myocardial disease or infarction.
Functional TR develops progressively as morphologic changes of a failing right ventricle distort the tricuspid valve apparatus. As right ventricular pressure or volume overload leads to cavitary dilation, the tricuspid annulus dilates, and chordae tendineae are increasingly tethered. This results in eventual loss of tricuspid leaflet coaptation and valve incompetence. The septal intratrigonal portion of the annulus is relatively fixed; thus, annular dilation predominantly involves the anterior and posterior annulus corresponding to the right ventricular free wall.
Primary TR
Primary, or organic TR occurs as a result of leaflet pathology and is most frequently due to bacterial endocarditis, which is more prevalent with rising intravenous drug abuse. In the developing world, rheumatic fever remains the most frequent cause of primary tricuspid valve disease, including TR. Other primary causes of TR include myxomatous degeneration, Ebstein’s anomaly, and carcinoid syndrome. TR may also be iatrogenic and is frequently seen in patients receiving trans-tricuspid valve leads for permanent pacemakers or implantable cardiac defibrillators. Serial endomyocardial biopsies in patients after heart transplantation may also result in valvular injury or chordal rupture with subsequent TR.
Epidemiology
The prevalence of moderate to severe TR is 1.6 million in the United States, but only 8,000 undergo tricuspid valve surgery each year. About one-third of patients with degenerative mitral regurgitation have moderate or severe TR at the time of mitral valve surgery. Similarly, a third of patients with severe mitral stenosis have moderate to severe TR. Patients who require reoperation for isolated TR after left-sided valve surgery have demonstrated high rates of perioperative mortality of 10 to 25%.
Clinical Presentation
Many patients with TR have few or no symptoms. Patients may present with fatigue due to reduced cardiac output and signs of systemic venous congestion, including peripheral edema, ascites, congestive hepatosplenomegaly, and jugular venous distension. Physical examination may reveal an S3 heart sound, a systolic murmur at the left lower sternal border, and a pulsatile liver. Atrial fibrillation frequently occurs with TR due to atrial dilation. At late stages, cardiac cachexia and hepatic cirrhosis may occur.
Diagnosis
Echocardiography is the preferred diagnostic modality for characterizing TR. Transthoracic echocardiogram (TTE) is usually sufficient to visualize the tricuspid valve and should evaluate TR severity, etiology, ventricular function, and pulmonary artery systolic pressure. Severe TR is defined by a central jet area of >10 cm2, vena contracta width >0.7 cm, continuous wave doppler with a dense and triangular early peaking jet, and hepatic vein systolic flow reversal. Right heart catheterization may be useful for measurement of pulmonary artery pressures as severe TR often compromises estimation by TTE. Additionally, the diagnosis of pulmonary hypertension serves an important part in understanding the etiology of TR and planning treatment.
In infective endocarditis, the location, size, and mobility of vegetations should be noted on TTE. Infectious workup is imperative to identify an infectious source, and optimally, cultures are negative prior to operation. CT imaging may be helpful to identify septic pulmonary emboli.
Treatment Algorithm
Medical therapies for severe TR are limited but may delay or replace surgery for a high-risk surgical patient. Diuretics can be used to relieve systemic congestion, and ACE inhibitors or ARBs may slow ventricular remodeling. In patients with medically responsive pulmonary hypertension, pulmonary vasodilators may reduce RV afterload and functional TR.
Surgical intervention for TR is most often performed in the setting of concomitant mitral or aortic valve surgery. Recommended surgical indications from the 2020 AHA/ACC Valvular Heart Disease Guidelines are summarized below:
Class I recommendations:
- Whether symptomatic or asymptomatic, severe functional TR should be addressed with repair or replacement at the time of left-sided valve surgery.
Class IIa recommendations:
- Mild to moderate TR that is functional in nature should be repaired at the time of left-sided valve surgery if tricuspid annular dilation is present, defined by >40 mm on TTE (indexed to >21 mm/m2) or >70 mm on direct intraoperative measurement, or with a history of right heart failure.
- Symptomatic severe primary TR may benefit from surgical correction if refractory to medical therapy. This is preferentially performed before onset of significant RV dysfunction.
- Symptomatic severe isolated secondary TR may benefit from isolated tricuspid valve surgery if attributable to annular dilation (in the absence of pulmonary hypertension or left-sided disease) and poorly responsive to medical therapy.
Class IIb recommendations:
- Surgery may be considered for asymptomatic severe primary TR when progressive RV dilation or dysfunction is present, but in the absence of severe RV dysfunction or severe pulmonary hypertension.
- Reoperation for isolated tricuspid valve repair or replacement may be considered for symptomatic severe TR in patients who have previously undergone left-sided valve surgery in the absence of severe RV dysfunction or severe pulmonary hypertension.
Infective endocarditis involving the tricuspid valve is better tolerated than left-sided valve involvement. Because many patients with tricuspid endocarditis develop infection as a result of intravenous drug use, the general approach is to pursue medical therapy and avoid placement of valve prostheses due to risk of device infection with continued drug abuse. By 2015 AHA Endocarditis Guidelines, surgical intervention is reasonable for such patients with right heart failure refractory to medical therapy, sustained infection due to difficult organisms (fungi or multidrug resistant bacteria), lack of response to appropriate antimicrobial therapy, tricuspid vegetation >20 mm in diameter, and recurrent pulmonary embolism despite antimicrobial therapy.
Surgical Approach
The surgical approach for tricuspid valve intervention typically involves median sternotomy, right anterior thoracotomy, or a robotic approach. Cardiopulmonary bypass is commenced with bicaval and aortic cannulation with caval snaring for right atrial isolation. Tricuspid repair or replacement can be completed under cardioplegic arrest, cold fibrillatory arrest, or on a warm beating heart, though concomitant cardiac procedures may require complete arrest. If a left-sided valve intervention is required, this is performed prior to the tricuspid valve intervention, which may then be performed during rewarming and cardiac reperfusion. Performing tricuspid valve surgery on a beating heart may alert the surgeon immediately to any disruption to the AV nodal conduction system.
The tricuspid valve is exposed with a right atriotomy oriented obliquely from adjacent to the right atrial appendage down to the posterior aspect of the atrium adjacent to the IVC. For concomitant mitral valve surgery, a transeptal approach may be taken from the right atrial incision.
Tricuspid valve repair is preferred over replacement and is performed using several techniques. Annuloplasty is well-suited for functional TR to restore annular geometry. This is accomplished with suture annuloplasty using the De Vega technique or Kay bicuspidization or with ring annuloplasty. The De Vega annuloplasty is a plication of the posterior and anterior annulus using a double continuous suture. The suture is run in two rows in intercalated fashion from the antero-septal commissure to the postero-septal commissure and back. The degree of plication may be controlled over a Hegar dilator or valve sizer as the suture is tied down over a felt pledget. In the modified De Vega technique, a felt pledget is interposed in each bite of the suture in the annulus to permit a more uniform distribution of tension. Alternatively, Kay bicuspidization is accomplished by plicating the posterior leaflet with mattress sutures from the antero-posterior to the postero-septal commissures along the posterior annulus. The sutures are tied down, obliterating the posterior leaflet and creating a bicuspid valve.
Ring annuloplasty of the tricuspid valve is accomplished using only a few commercially available prosthetic rings, which are limited by the complex 3-dimensional saddle shape of the tricuspid annulus. The Carpentier-Edwards semi-rigid ring is an oval 2-dimensional ring that is incomplete at the anteroseptal commissure, allowing surgeons to avoid injury to AV nodal tissue. The Edwards MC3 flexible ring is a newer 3-dimensional saddle-shaped partial ring that has achieved similar results to the Carpentier-Edwards ring. Ring prostheses are sized according to the intratrigonal length of the septal leaflet, as this length is spared in annular dilation. Assessment of tricuspid valve repair is performed with a beating heart by filling the RV with saline and occluding the pulmonary artery to generate sufficient intracavitary pressure. In the case of an inadequate result, ring downsizing or valve replacement should be performed. Reoperative tricuspid valve surgery is associated with significant in-hospital mortality of 37%.
In primary TR, complex leaflet repair may require application of Carpentier techniques of mitral valve repair, including chordal resuspension, neo-chordae, leaflet resections, and leaflet patching. Tricuspid valve replacement may be necessary for primary TR with uncorrectable defects. Available prosthetics include mechanical valves, stented porcine or pericardial valves, or homografts. The choice of prosthesis is guided by the trade-off between the risks of valve thrombosis and anticoagulation with mechanical valves and the risk of degeneration with biologic valves. Right-sided tissue valves are thought to have superior durability compared to left-sided valves due to low valvular pressure gradients. As in mitral valve replacement, the native valve is left in place if possible, to preserve the subvalvular apparatus.
Tricuspid valve endocarditis associated with intravenous drug abuse may be treated surgically in a staged approach, first with tricuspid valvectomy if the patient does not have severely elevated pulmonary artery pressures or pulmonary vascular resistance. The second stage insertion of a tricuspid prosthetic valve should be performed after drug dependence is controlled. Late survival and valve reinfection are directly correlated with continued drug use.
Outcomes
Concomitant TV repair at the time of mitral valve surgery results in resolution of TR in 85% of patients at 6 years. However, tricuspid valve repair may fail at a rate of 10%-15% even less than one year after surgery. Risk factors for failure include pulmonary arterial hypertension, ring annuloplasty with a larger ring size, suture rather than ring annuloplasty, LV dysfunction, and retention of trans-tricuspid valve ICD or pacemaker leads. Notably, patients with retained trans-tricuspid leads after tricuspid valve repair have been found to have a high incidence of late repair failure of 42% at 5 years. Complete heart block occurs in up to 25% of patients receiving mitral and tricuspid valve prostheses at 10 years and is best addressed with epicardial lead placement for ventricular pacing.
Impaired RV systolic function is a risk factor for reduced survival after tricuspid valve surgery, and late mortality after tricuspid valve repair is most commonly attributable to advanced right ventricular failure or arrhythmia. Meta-analysis has found no difference in survival after tricuspid valve replacement between patients receiving mechanical and tissue valves.
Suggested Readings
- Shemin, R.J., & Benharash, P. (2017). Tricuspid Valve Disease. In Cohn, L. H. (Author). Cardiac surgery in the adult. New York, McGraw Hill Education.
- Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O. The growing clinical importance of secondary tricuspid regurgitation. J Am Coll Cardiol. 2012;59(8):703-10.
