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Management and prognosis of tricuspid regurgitation

Management and prognosis of tricuspid regurgitation
Literature review current through: Jan 2024.
This topic last updated: Apr 11, 2023.

INTRODUCTION — Tricuspid regurgitation (TR) is a relatively common abnormality. Since this lesion is frequently asymptomatic and may not be detected on physical examination, it is often diagnosed solely by echocardiography. This topic will review the prognosis and management of TR.

Etiology, clinical features, and evaluation of TR are discussed separately. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation".)

APPROACH TO MANAGEMENT — Management of TR is based upon the cause of TR, the presence and extent of symptoms and signs of heart failure (HF), the severity of TR, and the presence and extent of associated abnormalities, including pulmonary hypertension, tricuspid annular dilation, and other valve disease.

The severity of TR is generally assessed by Doppler echocardiography as discussed separately [1], in selected cases may be quantitated with cardiovascular magnetic resonance imaging [2], and is categorized in disease stages as defined by the 2020 American College of Cardiology/American Heart Association guidelines (table 1). Trace TR is present in approximately 80 percent of normal individuals [3], so a Stage A is not included in these definitions. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Diagnosis'.)

The causes of TR are categorized as primary or secondary. Primary TR is due to disease of the valve apparatus (leaflets and chordae) including rheumatic, congenital, endocarditis, and carcinoid heart disease. Secondary TR is due pulmonary hypertension with right ventricular (RV) dilation and systolic dysfunction due to either left sided heart disease, primary pulmonary hypertension, pulmonic stenosis, or other causes of pulmonary hypertension. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Etiology'.)

Management of severe TR includes medical therapy, counseling regarding pregnancy and physical activity, and consideration of tricuspid valve surgery. Management also includes evaluation and treatment of the underlying cause(s), which often includes other cardiovascular disorders, particularly mitral valve disease and/or HF. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Etiology'.)

Specific considerations apply to Ebstein anomaly of the tricuspid valve and carcinoid heart disease; management of these conditions is discussed separately. (See "Ebstein anomaly: Clinical manifestations and diagnosis" and "Carcinoid heart disease".)

GENERAL MANAGEMENT

Follow-up — Given the adverse prognosis associated with significant TR (see 'Prognosis' below), evaluation of the cause and routine clinical and echocardiographic follow-up is recommended in patients with increasing severity of TR (table 1). (See "Etiology, clinical features, and evaluation of tricuspid regurgitation".)

We suggest the following frequencies of serial transthoracic echocardiography (TTE) for asymptomatic TR (including evaluation of the tricuspid valve structure and function, RV size and function, and left heart disease) (see "Echocardiographic evaluation of the tricuspid valve"):

Mild TR – For patients with isolated mild TR with a normal tricuspid valve, no routine follow-up is required. For mild TR with concomitant RV dilation/dysfunction or pulmonary hypertension, we suggest follow-up every three to five years.

Moderate TR – Every one to two years.

Severe TR – Every year (more frequently if the RV is dilating).

In addition, TTE should be performed in patients with a significant change in symptoms or signs that might be due to increasing severity of TR.

Treatment of heart failure — In patients with severe TR and right-sided HF, diuretics are suggested to treat volume overload, including peripheral edema and ascites [4]. Loop diuretics are typically used. Aldosterone antagonists may provide additional benefit, particularly in those with hepatic congestion with secondary hyperaldosteronism.

Most adults with TR have significant left-sided heart disease and treatment should be directed at the primary disease process. If HF with reduced ejection fraction is present, standard therapy is recommended [4]. (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction" and "Secondary pharmacologic therapy for heart failure with reduced ejection fraction".)

Medical therapy remains the primary approach to management of severe TR in most patients. In a series of 87 patients with severe TR referred for intervention, the mean age was 80 years (56 percent female), 93 percent were in atrial fibrillation, and 64 percent had Stage 3a or higher chronic kidney disease [5]. Most were treated with loop diuretics and about one-third received mineralocorticoid receptor antagonists. Overall, 75 percent were treated with medications alone with a 30-day and 1-year survival of 100 percent and 76 percent, respectively.

In a retrospective analysis of 3276 adults identified from an echocardiography database with isolated severe TR, only 5 percent underwent tricuspid valve surgery (mostly repair not replacement) with 95 percent managed on medical therapy. Using a propensity matched sample with surgery as a time-dependent covariate, there was no difference in overall survival between medical and surgery therapy (hazard ratio 1.34, 95% CI 0.78-2.30) [6].

Treatment of causes of pulmonary hypertension — Reduction of high pulmonary artery pressures may help reduce secondary TR (ie, due to pulmonary hypertension without intrinsic tricuspid valvular disease) [4]. Treatment of pulmonary hypertension likely contributes to improvement in TR during medical treatment of systolic HF [7].

Treatment of the cause of pulmonary hypertension is recommended, including treatment of HF if present. Pulmonary vasodilators to reduce elevated pulmonary pressures also may be helpful in secondary or primary pulmonary hypertension [8]. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults" and "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)" and "Treatment of pulmonary arterial hypertension (group 1) in adults: Pulmonary hypertension-specific therapy".)

Improvement in TR has been demonstrated in at least two other settings with correction of reversible pulmonary hypertension: mitral stenosis and chronic thromboembolic pulmonary hypertension.

A number of observational studies have documented improvement in TR (particularly functional TR) after percutaneous balloon valvotomy for mitral stenosis [9-11] (see "Percutaneous mitral balloon commissurotomy in adults"). In a series of 71 patients with mitral stenosis and moderate to severe functional TR, percutaneous mitral balloon valvotomy led to resolution of TR on follow-up echocardiography in 23 (32 percent) [9]. In a report of 53 patients with mitral stenosis and significant TR who underwent balloon valvotomy, 27 (51 percent) had an improvement in the severity of TR that paralleled the decrease in pulmonary artery systolic pressures [10]. The patients with an improvement in TR had a much higher prevalence of functional TR (85 versus 8 percent in those in whom TR did not improve).

The effect of pulmonary thromboendarterectomy on severe TR was evaluated in an analysis of 27 patients with chronic thromboembolic pulmonary hypertension [12]. The severity of TR diminished in 19 (70 percent) without tricuspid valve annuloplasty. Compared with the eight patients with persistent severe TR, those with diminished TR were more likely to have had a reduction in pulmonary artery systolic pressure below 40 mmHg. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy".)

Treatment of atrial fibrillation — There is an emerging concept that some patients have TR related to atrial dilation and atrial fibrillation without RV dilation or primary leaflet disease [13-17]. Rhythm control of atrial fibrillation may be helpful in these patients, although further studies are needed.

Management of pacemaker therapy — Strategies to avoid endocardial lead interference with native, repaired, or prosthetic valves include securing the leads in a commissure, securing them in a position outside the valve annulus, or replacement with epicardial leads [4,18].

Lead removal after development of moderate to severe TR and tricuspid annulus dilation may not reduce TR because the leaflet damage often is not reversible [19]. Also, in some patients the TR is secondary to RV pacing (possibly related to RV and/or LV dyssynchrony) rather than the pacer lead [20,21].

Pregnancy — Management of patients with valve disease (including TR) during pregnancy is discussed separately. (See "Pregnancy and valve disease".)

Physical activity and exercise — We agree with the 36th Bethesda Conference task force recommendation (published in 2005) that patients with primary TR with normal RV function, a right atrial pressure less than 20 mmHg, and normal RV systolic pressure can participate in all competitive sports, regardless of TR severity [22]. The 2015 task force statement does not discuss isolated tricuspid valve disease [23].

Separate recommendations in a 2015 task force statement apply to patients mitral and aortic valve lesions (who may have concurrent TR) [23]. Since multiple lesions of moderate severity may have additive effects, the 36th Bethesda Conference task force recommended that athletes with significant multiple valvular disease should generally not participate in any competitive sports.

Exercise in patients with functional TR may be limited by the underlying cause. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Secondary TR'.)

TRICUSPID VALVE SURGERY — Tricuspid valve surgery usually is performed at the time of surgery for left sided heart disease. Isolated tricuspid valve surgery is rarely performed with only 5005 procedures over a 10-year period (2004 to 2013) nationally in the United States [24]. Operative mortality for isolated tricuspid valve surgery in the United States is 8.8 percent with a higher adjusted in-hospital mortality for tricuspid replacement compared with repair (odds ratio [OR]: 1.91; 95% CI 1.18-3.09) [24].

Indications — Indications for tricuspid valve surgery depend upon whether surgery for left-sided (mitral or aortic) valve disease is indicated.

For patients undergoing left-sided valve surgery:

For patients with severe TR who are undergoing left-sided valve surgery, tricuspid valve surgery is recommended [4,25]. Primary or functional severe TR does not consistently improve after treatment of a left-sided valve lesion (with reduction of RV afterload) [26,27].

For patients with mild, moderate, or greater functional TR who are undergoing left-sided valve surgery, concomitant tricuspid valve repair is suggested if there is either tricuspid annular dilation (diameter on TTE >40 mm) or prior evidence of right HF [4,25].

Isolated tricuspid surgery – The optimum timing of isolated tricuspid valve surgery is not well established [6,24,28,29], as reflected by some differences between AHA/ACC and European Society of Cardiology (ESC) guideline recommendations [4,25].

Tricuspid valve surgery is suggested (weak recommendation) for patients with severe primary TR with symptoms unresponsive to medical therapy to reduce symptoms and prevent recurrent hospitalization, preferably before the onset of significant RV dysfunction [4,30].

The 2021 ESC valvular guidelines include a strong recommendation for tricuspid valve surgery in patients with symptomatic severe isolated primary TR without severe RV dysfunction [25].

Tricuspid valve surgery can be beneficial to reduce symptoms and recurrent hospitalizations in patients with signs and symptoms of right-sided HF and severe isolated secondary TR attributable to annular dilation who are poorly responsive to medical therapy (in the absence of pulmonary hypertension or left-sided disease).

The role of tricuspid valve surgery in patients with severe TR with no or minimal symptoms is uncertain. The 2020 AHA/ACC valvular guidelines note this uncertainty and include a very weak recommendation that tricuspid valve surgery may be considered for asymptomatic or minimally symptomatic patients with severe primary TR and progressive moderate or greater RV dilation and/or systolic dysfunction [4]. The ESC guidelines view surgery in this setting slightly more favorably and indicate that surgery should be considered in patients with severe primary or secondary TR with no symptoms and RV dilation [25].

Tricuspid valve surgery may be considered in patients with signs and symptoms of right-sided HF and severe TR (Stage D) who have undergone previous left-sided valve surgery in the absence of severe pulmonary hypertension or severe RV systolic dysfunction [4].

Indications for surgery for TR in patients with Ebstein anomaly are discussed separately. (See "Ebstein anomaly: Clinical manifestations and diagnosis".)

Settings

At the time of left-sided valve surgery — Significant TR is common at the time of and following left heart valve (particularly mitral) surgery [31-34]. The rationale for tricuspid valve repair in patients with TR at the time of left-sided valve surgery is to prevent progressive TR, to prevent or improve HF symptoms, and to reduce the risk of requiring later tricuspid valve surgery, although an impact on survival has not been established [31,33]. Concomitant tricuspid valve repair does not add appreciably to the mortality risk of mitral valve surgery. Reoperation for severe TR after left-sided valve surgery is associated with a 10 to 25 percent risk of perioperative mortality [4].

Tricuspid valve surgery at the time of left-sided valve surgery is suggested in patients at greatest risk for progressive TR (ie, those with functional TR with dilated tricuspid annulus or evidence of right HF), given the risk of tricuspid valve surgery at a later date. Mild or moderate TR is expected to progress in approximately 25 percent of patients who have undergone left-sided valve surgery [4].

Observational studies indicate that the presence of significant pre-operative TR is a predictor of increased postoperative mortality [33] and development of significant TR late post-operatively is also associated with increased mortality rate [34]. Risk factors for persistence or progression of TR include tricuspid annulus dilation (diameter on TTE >40 mm or 21 mm/m2 diameter indexed to body surface area; or >70 mm diameter on direct operative measurement), RV dysfunction/remodeling, leaflet tethering height, pulmonary artery hypertension, atrial fibrillation, nonmyxomatous etiology of MR, and a pacemaker or implantable cardioverter-defibrillator lead across the tricuspid annulus [4].

A meta-analysis included 10 studies of 2488 patients found to have mild to moderate functional TR during mitral valve operations [35]. The duration of postoperative follow-up ranged from 3 to over 100 months (at least 12 months in all studies except one). Patients who underwent concurrent tricuspid annuloplasty had a lower likelihood (odds ratio 0.29; 95% CI 0.19-0.44) of progressing to moderate to severe TR. However, concurrent tricuspid annuloplasty was not associated with any significant difference in mortality rate or in the need for subsequent tricuspid valve surgery.

A randomized trial in patients undergoing mitral valve surgery for primary mitral regurgitation found that concomitant tricuspid valve repair reduced the risk of progression of TR but resulted in more frequent permanent pacemaker implantation [36]. The 401 trial participants had either moderate TR or less than moderate TR with annular dilation of ≥40 mm (≥21 mm/m2) and were randomly assigned to undergo mitral valve surgery with or without tricuspid valve repair. The two-year mortality rate was similar in the two groups (3.2 versus 4.5 percent; relative risk [RR] 0.69, 95% CI 0.25-1.88). Progression of TR at two years was less frequent in the patients who received tricuspid valve repair (0.6 versus 6.1 percent; RR 0.09, 95% CI 0.01-0.69). However, the incidence of permanent pacemaker implantation was higher in these patients (14.1 versus 2.5 percent; rate ratio 5.75, 95% CI 2.27-14.60).

For isolated tricuspid valve surgery — Tricuspid valve repair or replacement is performed to control regurgitation and thus improve or prevent symptoms. Medical therapy generally has limited efficacy in reducing regurgitant flow in patients with symptomatic TR, particularly if caused by intrinsic tricuspid valve disease. Severe TR causes progressive RV dilatation, which may worsen TR and lead to RV dysfunction.

Observational data suggest that tricuspid valve surgery can improve functional capacity [37-40]. As an example, among 926 consecutive patients who underwent tricuspid valve surgery (792 repairs, 134 replacements) at a single center who were followed for a median of 4.3 years, either repair or replacement was associated with significant improvement in functional status, as measured by New York Heart Association (NYHA) class (34 percent with NYHA class III or IV postoperatively, compared with 85 percent preoperatively) [40].

However, scant evidence is available on the impact of tricuspid valve surgery on survival. In a propensity-score matched analysis of patients with isolated significant TR comparing 57 patients who underwent tricuspid valve surgery with 813 who did not, survival was not significantly different between the groups [41].

Timing and risk stratification — The timing of isolated tricuspid valve surgery is controversial. One study suggested that tricuspid valve surgery should be performed in patients with symptomatic TR before the development of RV end-systolic area ≥20 cm2 or anemia with hemoglobin ≤11.3 g/dL [37]. In a series of 61 patients undergoing isolated tricuspid valve surgery for severe TR, preoperative hemoglobin level and RV end-systolic area were independent determinants of clinical outcomes (death or readmission) at a mean of 32 months. An RV end-systolic area <20 cm2 predicted event-free survival with a sensitivity of 73 percent and a specificity of 67 percent; a hemoglobin level >11.3 g/dL predicted event-free survival with a sensitivity of 73 percent and a specificity of 83 percent.

Risk stratification models are generally helpful in estimating operative risk for patients undergoing valve surgery. A risk score (TRI-SCORE, www.tri-score.com) has been proposed to predict in-hospital mortality after isolated tricuspid valve surgery [42], as commonly used cardiac surgery risk scores do not directly address tricuspid surgery. The TRI-SCORE was derived from a study of 466 patients at 12 French centers. The risk score ranges from 0 to 12 points and is based on eight clinical parameters; observed and predicted in-hospital rates ranged from 0 to 60 percent and from 1 to 65 percent. The apparent area under the receiver operating curve was 0.81, higher than for the logistic Euroscore (0.67) and EuroSCORE II (0.63).

The EuroSCORE II risk model incorporates patient characteristics but does not provide procedure-specific risk estimates (http://euroscore.org/) [43,44]. The 2018 Society of Thoracic Surgeons model does not include risk estimates for tricuspid valve surgery (https://riskcalc.sts.org/stswebriskcalc/calculate) [45]. (See "Estimating the risk of valvular procedures".)

Surgical repair versus replacement — Although comparative data are limited, tricuspid valve repair is generally preferred to tricuspid valve replacement, with valve replacement performed only when repair is not feasible. Advantages of tricuspid valve repair include technical ease and speed of operation. On the other hand, the rate of recurrent TR following tricuspid repair is substantial and the mortality risk of tricuspid valve reoperation is high. (See 'Surgical valve repair' below.)

In observational series, operative mortality rates for tricuspid replacement are generally higher than those for tricuspid repair [46]. However, patients undergoing tricuspid replacement may have greater risk factors for mortality. A study using propensity-matched cohorts found that operative mortality was similar for tricuspid valve repair (18 percent) and replacement (13 percent) [47]. Survival rates at 1, 5, and 10 years were similar for repair (80, 72, and 66 percent) and replacement (85, 79, and 49 percent).

Surgical valve repair — Tricuspid repair procedures include placement of a prosthetic annular ring, a biologic annuloplasty repair, or more complex repair procedures [48,49]. Recurrence rates and mortality after valve repair are different for primary versus secondary TR.

In a series of 178 adults with primary TR (largely rheumatic or congenital tricuspid disease undergoing tricuspid repair) a relatively low operative mortality (4 percent) and relatively high mid-term survival rates were observed (90 percent at five years and 76 percent at 10 years) [50]. In a retrospective study of 74 rheumatic heart disease patients undergoing tricuspid valve repair at the time of mitral and/or aortic valve replacement, use of an annular ring (versus repair without a ring) was associated with decreased recurrence of TR, a higher quality of life, and improved survival [51]. At one week post repair, moderate to severe TR was observed in 2.5 percent with ring annuloplasty (versus 2.9 percent without a ring) and at one year was observed in 2.5 percent with ring annuloplasty (versus 17.6 percent without a ring).

Tricuspid repair is frequently performed for secondary TR, most often at the time of left-sided valve surgery and in the setting of other risk factors, such as impaired LV and/or RV function; outcomes reflect these associated risks:

In adults with secondary TR operative mortality rates for tricuspid valve repair have ranged from 6 to 14 percent in series in which most patients underwent concomitant surgery on another valve [46,52-54]. Mid- to long-term survival rates are limited with five-year survival of 64 to 72 percent and 10-year survival of 44 to 47 percent [46,53,54].

Risk factors associated with worse postoperative TR have included worse preoperative TR, impaired LV systolic function, presence of a permanent pacemaker [53], and higher pulmonary artery pressure [52]. Despite high rates of TR recurrence, reoperation after tricuspid annuloplasty is rarely performed. Hospital mortality after repeat tricuspid surgery is high (eg, 37 percent in one series [53]).

The choice of procedure to minimize recurrence of TR following tricuspid valve repair is controversial. Residual TR following ring annuloplasty is seen in approximately 10 percent of patients five years after repair [4]. Some observational series have suggested that the risk of postoperative TR is lower with a prosthetic ring than with suture repair procedures [53,54]. As an example, in a series of 790 patients, the rate of at least moderate to severe (3+ to 4+) TR five years postoperatively was 16 to 18 percent in those with rings versus 28 to 32 percent in those without annular support [53].

On the other hand, some investigators have found similar rates of significant postoperative TR with ring and suture repairs. For example, in a series of 237 patients, the rate of at least moderate to severe (3+ to 4+) TR three years postoperatively was 14 percent for suture bicuspidization (plication of the posterior tricuspid leaflet) as compared with 17 percent for ring annuloplasty [52]. Tricuspid valve tethering is a risk factor for postoperative TR [55]. Measurement of tricuspid annulus diameter and tethering distances may be helpful in choosing repair procedures with a goal of improving outcomes [56]. In a long-term (14-year) outcome study of 96 patients who underwent a complex valve repair with placement of an annuloplasty ring, 96 percent of patients had no TR at hospital discharge with a 12-year survival of 72 percent and with a rate of recurrent moderate to severe TR of 28 percent [57].

In a meta-analysis of 87 studies published between 2005 and 2017 of 13,184 patients undergoing tricuspid valve surgery for secondary TR, 92 percent of patients had a concurrent mitral valve procedure. The risk of moderate-severe TR at hospital discharge was 9.4 percent with late reintervention rates of 0.3 percent per year. Mortality and rates of recurrent TR were similar for suture versus ring annuloplasty but overall TR rate was higher after flexible versus rigid ring annuloplasty [58].

Valve replacement — Tricuspid valve replacement may be required if leaflet anatomy is not amenable to repair.

Operative mortality rates for tricuspid valve replacement in adults have generally been high (10 to 33 percent; 10 to 22 percent for series beginning after 1985) [37,38,46,59-62]. In these series, the majority of patients had concomitant surgery on another valve and/or prior valve surgery. Mid- to long-term survival following tricuspid valve replacement has been limited with five-year survival rates of 60 to 74 percent and 10-year survival rates of 37 to 58 percent [46,59-61,63]. The etiology of tricuspid valve dysfunction was not specified in most of these series.

Disparate mortality rates were observed in two studies of patients with primary (organic) tricuspid valve disease. In a series of 72 patients with primary tricuspid valve disease (largely rheumatic and congenital) undergoing valve replacement from 1979 to 2003, operative mortality was 22 percent, five-year survival was 63 percent, and 10-year survival was 55 percent [50]. In contrast, a study of patients with primary tricuspid disease (rheumatic, congenital, endocarditis, degenerative) undergoing valve replacement from 1994 to 2007 reported a much lower operative mortality rate (1.4 percent) and high five-year survival (95 percent) [62]. Possible explanations for the lower mortality in the later study include fewer comorbidities and improved perioperative care, which included routine ultrafiltration.

If valve replacement is necessary, bioprosthetic valves are preferred due to a high rate of valve thrombosis with mechanical prosthetic valves in the tricuspid position, despite the risk of bioprosthetic valve deterioration [64].

TRANSCATHETER TRICUSPID VALVE REPAIR — Devices for transcatheter tricuspid edge-to-edge repair (TEER; Triclip and PASCAL) are approved for use in Europe [65,66] but are investigational in the United States. Studies have investigated the efficacy of treating TR with transcatheter approaches similar to those used for mitral valve disease with either a clip on the valve leaflets or an annular remodeling device [57,67-69]. These approaches require advanced imaging modalities for patient selection and procedural guidance [70-72].

An open-label trial randomly assigned 350 symptomatic patients (mean age 78 years) with severe TR to TEER or continued medical management [73]. A mean of 2.2 clips were implanted per patient. At 30 days, the percentage of patients with moderate or less TR was higher in the TEER group compared with the control group (87.0 versus 4.8 percent). At one year, quality of life as measured by the Kansas City Cardiomyopathy Questionnaire increased by 12.3 points in the TEER group versus 0.6 points in the control group, and the percentage of patients in New York Heart Association functional class I or II was higher in the TEER group than in the control group (83.9 versus 59.5 percent). Mortality rates of tricuspid valve surgery (1.8 versus 3.6 percent) and the rate of hospitalization for HF (0.21 versus 0.17 events per patient-year) were similar in the two groups.

PROGNOSIS

Impact of severity on prognosis — While the clinical setting (particularly concomitant cardiovascular disease) influences survival in patients with TR, increasing grades of TR are independent predictors of mortality in populations of individuals with and without left-heart disease [41,74-78], as illustrated by the following studies:

In a study of 439,558 adults (mean age 62) undergoing evaluation for heart disease from 2000 to 2019 by 25 centers contributing to the National Echocardiography Database of Australia, 29.1 percent of the patients had at least mild TR [78]. After adjustment for age, sex, RV systolic pressure, atrial fibrillation, and significant left-heart disease, the risk of mortality was independently associated with mild TR (hazard ratio [HR] 1.24, 95% CI 1.23-1.26), moderate TR (HR 1.72, 95% CI 1.68-1.75), or severe TR (HR 2.65, 95% CI 2.57-2.73) compared with those with no or trivial TR. Increasing grades of TR were also independently associated with increasing risk of cardiovascular mortality.

In a study of 5223 patients (mean age 67 years) at three Veterans Affairs medical centers, one-year survival rates were 92, 90, 79, and 64 percent in patient groups with no, mild, moderate, or severe TR, respectively [74]. Moderate or greater TR was associated with increased mortality regardless of pulmonary artery systolic pressure or left ventricular ejection fraction (LVEF). Severe TR, older age, lower LVEF, inferior vena cava dilation, and moderate or greater RV enlargement were associated with impaired survival.

Similarly, in a study of 296 patients with TR, those with the highest tertile of quantitative TR measurements (vena contracta >6 mm, effective regurgitant orifice area (EROA) >0.3 cm2, regurgitant volume >30 mL, and regurgitant fraction >45 percent) had higher rates of adverse events (death and HF) [75]. Event-free survival rates were 93, 48, and 14 percent in patients with mild, moderate, and severe TR.

Prognosis of severe TR — Even among patients with severe TR, patients with greater TR may have worse outcomes, as illustrated by a study of 284 patients with severe TR in which those with a vena contracta >0.92 cm (termed massive TR) had higher mortality rates [77].

Patients with severe TR commonly have left-sided valve disease, which impacts prognosis. Patients with severe TR without significant left-sided valve disease also have an adverse prognosis, as illustrated by a study of 613 patients with isolated severe TR (mean age 74 years) [79]. During 26.5 months median follow-up, 141 (23.3 percent) died and 62 (10.2 percent) were hospitalized for HF. Adverse prognostic factors included pulmonary hypertension, elevated blood urea nitrogen levels, decreased albumin levels, and left atrial enlargement.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Tricuspid regurgitation (The Basics)")

SUMMARY AND RECOMMENDATIONS

Severe tricuspid regurgitation (TR) is an independent predictor of mortality even in patients with other cardiovascular conditions. (See 'Prognosis' above.)

In symptomatic patients with severe TR, management includes evaluation and treatment of the underlying cause(s), which often includes other cardiovascular disorders, particularly mitral valve disease and/or left ventricular systolic dysfunction (heart failure [HF] with reduced ejection fraction). (See 'Approach to management' above.)

In symptomatic patients with severe TR, diuretics are indicated to treat volume overload and congestion. However, many patients with severe TR have refractory peripheral edema unresponsive to medical management. (See 'Treatment of heart failure' above.)

Treatment of the causes of pulmonary hypertension (such as HF, mitral stenosis, and chronic thromboembolic pulmonary disease) can result in improvement in secondary TR. (See 'Treatment of causes of pulmonary hypertension' above.)

Patients with primary TR who have normal right ventricular (RV) systolic function, a right atrial pressure less than 20 mmHg, and normal RV systolic pressure can participate in all competitive sports, regardless of TR severity. (See 'Physical activity and exercise' above.)

Management of symptomatic TR associated with a pacer lead is problematic; TR often persists after lead removal.

For patients with severe primary TR undergoing surgery for left-sided (eg, mitral) valve disease, tricuspid surgery is recommended (Grade 1C).

For patients with mild, moderate, or greater secondary TR who are undergoing left-sided valve surgery, we suggest concomitant tricuspid valve repair if there is either tricuspid annular dilation (diameter on transthoracic echocardiogram [TTE] >40 mm) or prior evidence of right HF (Grade 2C).

Tricuspid valve surgery is suggested for symptomatic patients with severe primary TR despite medical therapy without severe RV systolic dysfunction (Grade 2C).

When feasible, tricuspid valve repair is generally preferred to tricuspid valve replacement. However, repair is associated with significant risk of recurrent TR. (See 'Surgical repair versus replacement' above and 'Surgical valve repair' above.)

A bioprosthetic valve is preferred over a mechanical prosthetic in the tricuspid position due to the high risk of right-sided mechanical valve thrombosis. Transcatheter approaches to treatment of TR are investigational. (See 'Valve replacement' above.)

An association between TR and prognosis was evaluated in a study of adults undergoing echocardiography for evaluation of heart disease. Grades of TR from mild to severe were associated with increasing risk of all-cause mortality and cardiovascular mortality; even mild TR was an independent predictor of increased mortality. (See 'Prognosis' above.)

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