Tricuspid regurgitation is relatively common and can arise from a variety of causes. Primary TR is usually seen with congenital anomalies or anatomical-leaflet deformities. Secondary TR can exist with condition that leads to pulmonary hypertension or elevated right ventricular systolic pressure. Elevated left ventricular and/or left atrial pressures, from aortic or mitral disease, account for the majority of such cases. Left-sided congestive heart failure and primary pulmonary hypertension will also, eventually, result in secondary TR. It is well known that a right ventricular systolic pressure of greater than 55mmHg will lead to functional TR.[₁] Diseases of the right ventricle, such as pulmonary stenosis, right ventricular infarction, dilated cardiomyopathy, and pulmonary embolus can also lead to tricuspid regurgitation.

Regardless of the underlying etiology, ventricular dilatation exacerbates tricuspid insufficiency through annular dilatation. These changes in compliance are easily seen in tracings of the RA and RV end-diastolic pressures. In addition to an elevated baseline, the RA tracing becomes ventricularized with increasing degrees of insufficiency producing larger and larger “V” waves. Initially, the right heart compensates for these forces with its intrinsic compliance but, with time and increased severity, right atrial pressures overwhelm any compensatory compliance and signs of right-sided failure appear: jugular venous distension, hepatic congestion, ascites, and peripheral edema.

Tricuspid stenosis (TS) is a mechanical obstruction to the right ventricle that occurs throughout diastole.[₂] TS is due almost exclusively to rheumatic inflammation; it is found in combination with rheumatic mitral stenosis in up to 30% of patients. Rheumatic TS is usually accompanied by some degree of tricuspid regurgitation as well. Tricuspid stenosis may also be identified in the carcinoid syndrome, endocarditis, and intracardiac tumors. Clinically, TS is not well tolerated: impairment to RV filling (with mean diastolic gradients of as little as 5 mmHg) may produce impressive symptoms of right-sided failure[₃]. Given this, the importance of coexisting mitral disease may, at times, be overestimated.[₄]

Medical management of TS includes sodium restriction and diuretic therapy. However, the disease is progressive and surgical therapy is often required. The operative treatment of TS has involved closed commissurotomy[₅], open commissurotomy, and open valvuloplasty (balloon valvuloplasty has also been tried but with varying degrees of success[₆]36). All of these techniques have been associated with poor long-term results; the initial improvement in symptoms is accompanied by a technically-induced degree of regurgitation - which progresses over time and may lead to the restriction-dilation phenomenon. Therefore, to achieve long-lasting relief valve replacement is commonly required.

Tricuspid endocarditis is usually from intravenous seeding of the valve leaflets from recurrent episodes of bacteremia. The surgical options in addressing this disease provide unique insight into right-sided dynamics - specifically, in regards to atrioventricular compliance following valve excision. Surgical indications in tricuspid endocarditis include continued sepsis despite appropriate antibiotic coverage, heart failure due to tricuspid insufficiency, and multiple pulmonary emboli. Arbulu (37) was the first to advocate complete excision of the tricuspid valve (without subsequent replacement). Despite initial tolerance, this technique produces late-onset right-sided failure in the majority of patients.[₇,₈,₉] From an infectious disease standpoint, this approach has the distinct advantage of complete extirpation of tissue while avoiding placement of prosthetic material, but severe hepatic congestion, and the need for reoperative valve-replacement has made this approach untenable by some authors.[₁₀] In a 20-year follow-up of the originally reported series of 55 patients with intractable right-sided endocarditis who underwent tricuspid valvulectomy without replacement, two patients (4%) died in the post-operative period due to right-sided failure. In addition, six patients (11%) required prosthetic valve insertion 2 days to 13 years later for medically refractory right-sided heart failure. Of those who underwent re-operation (n = 6), four (66%) died. An alternative treatment option is to delay valve replacement for 3-9 months.. Reparative strategies, at time of the original operation, have also been successful in trying to treat this difficult sub-group of patients.[₁₁, ₁₂]

The most common cause of organic tricuspid disease worldwide is rheumatic fever. It usually affects the mitral valve and frequently, the aortic valve concomitantly. Resulting lesions almost uniformly produce a clinical picture of combined mitral stenosis with regurgitation. In rheumatic heart disease, annular deformity occurs from inherent weakening rather than from compensatory dilatation. As such, the “functional” TR reported in these patients is a misnomer; the rheumatically-diseased annulus is, by definition, organic. This type of annular pathology may be suspected when normal valve leaflets accompany the regurgitation in a patient with a history of rheumatic fever, a markedly dilated annulus, and severe TR. The regurgitant jet in these cases is frequently large in volume and low in velocity.

Distinguishing whether the dilated tricuspid annulus is due to secondary causes, or to primary rheumatic weakening, may be difficult but this distinction influences therapy. A number of authors have recognized the significance of rheumatic weakening of the tricuspid annulus and have noted that it may manifest after mitral valve repair.[₁₃, ₁₄]. In this complication, elevated atrial pressures lead to rapid and early right ventricular filling due to greater diastolic pressure gradients between the RA and RV. This early right ventricular filling and elevation in diastolic pressure, in conjunction with delayed left ventricular filling, displaces the IV septum toward the left in early diastole which compromises left ventricular function. In patients with these co-existing lesions, a vicious cycle is set into motion: further elevations in LAP, caused by left-sided valvular disease (MR/AI), further elevate pulmonary arterial resistance which increases tricuspid regurgitation and leads to a greater septal shift, higher LVEDP and LAP. While left ventricular function may be intrinsically normal under these conditions, the left end-diastolic pressures will be elevated. Post-operative adhesions will further exacerbate this cycle by precluding compensatory ventricular expansion which Barlow has described as the “restriction-dilation syndrome”[₁₅] The components of this syndrome include: myocardial dysfunction leading to ventricular dilation; left-sided valve lesions; tricuspid regurgitation; and pericardial constriction. This syndrome is possible after any left-sided surgery, but is most commonly seen in rheumatic heart disease.(58) In this phenomenon, the tricuspid valve leaflets are usually normal in the setting of overt annular dilatation. Correction of the tricuspid regurgitation as well as any hemodynamically-important left-sided valvular lesion will interrupt this cycle and provide symptomatic relief.

While early-onset TR following mitral valve surgery may reflect a variety of underlying causes (persistent pulmonary hypertension, mitral prosthetic dysfunction, progressive aortic valve disease or left ventricular failure), late-onset TR usually reflects intrinsic RV dysfunction and/or tricuspid annular abnormalities[₁₆]. Functional tricuspid insufficiency has been reported in up to 67% of those undergoing left heart surgery and is thought to be from the effects of transmitted afterload.[₁₇,₁₈,₁₉] While conservative management of TR was initially advocated[₂₀] due to expected improvements in functional regurgitation after left-sided surgery, it is now generally accepted that symptoms of right heart failure, and exercise intolerance, will persist in a significant number of patients.[₂₁] Groves[₂₂] compared the clinical and echocardiographic characteristics of 26 patients with and without late-onset TR after mitral valve surgery; between groups, doppler-estimated PAPs were similar and there was no evidence of prosthetic valve dysfunction nor significant aortic valve disease. In addition, intrinsic tricuspid disease could not be identified early on. In those patients that developed severe late-onset TR, both tricuspid annular diameter and RV diameter were noted to be much greater. He concluded that the development of late-onset TR was a marker of right heart failure. Similarly, Porter et al found late-onset TR in patients that had previously undergone MVR without tricuspid valve surgery for rheumatic heart disease[₁₉]. Echocardiography revealed that the pre- and post-operative PAP, the predominance of mitral lesions, the prosthetic valve gradient, and the degree of regurgitation were similar in patients with and without late-TR. These findings, taken together, suggest a mechanism similar to Barlow’s restriction-dilation syndrome. Whether TR is a causative factor following mitral valve repair - or a consequence thereof - is difficult to discern. In general, tricuspid regurgitation should be considered in those patients that do not clinically improve following left-sided heart surgery,. Of important note, those patients with moderate pre-operative TR, have a significant improvement in overall outcome when tricuspid valve annuloplasty (or valve replacement) is added during the initial aortic/mitral valve surgery.[₂₃,₂₄,₂₅]. The decision to operate on patients with late-onset symptomatic TR following remote left-sided valve surgery is a difficult one. Staab, et al. reviewed 34 patients who underwent isolated tricuspid valve operations for severe TR following prior left-sided valve surgery[₂₆]. While 85% of survivors improved symptomatically, the early mortality rate was 8.8%, and the five year event-free actuarial survival at five years only 41.6%. Predictors of poor outcome were increased age and previous cardiac surgery. Outcome did not vary depending on the degree of pulmonary hypertension, left ventricular EF, RV size/function, annular diameter, or the use of valve replacement versus repair. Similarly, King et al(2) reviewed their series of 16 tricuspid annuloplasties and 16 tricuspid valve replacements 4 months to 14 years after mitral valve surgery. While 53% of patients required concomitant mitral or aortic valve surgery at the time of reoperation, the hospital mortality was 25% and the 5-year actuarial survival was 44%. Moreover, nearly 54% of those surviving greater than thirty days had little or no improvement in tricuspid valve function following the procedure. They concluded that late-onset TR occurring after left-sided surgery was a signal of right ventricular failure and restoring valve competence was merely palliative: patient outcome was primarily determined by RV function. Given the high incidence of late mortality and poor long-term results, one should give serious consideration before embarking on re-operative tricuspid surgery which emphasizes the need for early diagnosis and treatment of TR when present at the initial operation.[₁₃, ₁₆, ₁₉, ₂₁]. Our general policy is to treat moderate or severe TR during the initial aortic or mitral valve operation. We share the opinion that late-reoperative tricuspid surgery following left-sided intervention should be approached with caution.

The pathophysiology of traumatic TR is thought to involve a severe and sudden elevation in right ventricular intracavitary pressure leading to disruption of the valve apparatus. This acute-onset regurgitation, if not diagnosed promptly, leads to volume loading of the right ventricle, ventricular enlargement, and subsequent annular dilatation. In a recent review of 13 patients of non-penetrating traumatic tricuspid insufficiency, Miller, et al(69) found that the majority of regurgitation resulted from a flail anterior leaflet. In over 90% of patients, this was due to ruptured chords, an avulsed anterior papillary muscle, or a tear in the leaflet proper. Patients with traumatic tricuspid regurgitation will present with signs of right heart failure (peripheral edema, hepatic congestion, ascites, etc.) and the diagnosis can be confirmed with bedside echocardiography.[₂₇, ₂₈] Severity of the valvular disease and associated injuries will then dictate the appropriateness of surgical repair.

Penetrating trauma of the heart leading to tricuspid disease is much less common (and much less survivable) than blunt injury. Associated bleeding into the pericardial cavity will frequently lead to tamponade. Penetration of the myocardial muscle mass may lead to associated valvular and/or septal damage. For this reason, a thorough evaluation - guided by intraoperative TEE - is warranted.[₂₉].

When feasible, tricuspid valve damage should be repaired electively unless tamponade or heart failure mandates immediate intervention. It should be noted that delayed presentation is in fact common, and in Miller’s series, the average time to presentation was nine years. With modern diagnostic techniques, early intervention may help to prevent irreparable heart damage. Though valve replacement has traditionally been performed, traumatic lesions are frequently amenable to repair thereby avoiding a mechanical prosthesis and systemic anticoagulation.[₂₇]