Worldwide incidence of tricuspid regurgitation is 1 %. Prevalence of moderate to severe FTR is 0.8 %, affecting approximately 1.6 million individuals in the United States, and increases with advancing age. Tricuspid regurgitation is frequently present in patients with a clinical history of mitral valve disease, and more than 30 % of patients with mitral stenosis have at least moderate TR. Severe TR has been reported in 23–37 % of patients after mitral valve replacement for rheumatic valve disease, in most cases being diagnosed as late as 10 years, on average, following the procedure. Furthermore, up to 14 % of patients undergoing surgery for functional mitral regurgitation secondary to dilated cardiomyopathy reported grade 3 or higher TR.

Prevalence of significant TR is reported to be 4.3 times greater in women than in men, especially in redo cardiac surgery series [3]. Further assessing possible clinical characteristics, gender, together with age and BMI, plays an important role as determinant of TR; more than a moderate degree of TR correlates with increasing age and with female sex, while an inverse association is generally seen between TR severity and BMI. All such associations require further investigations [4].

Tricuspid insufficiency is the most common pathology affecting the tricuspid valve. Secondary TR or FTR is the major etiology of tricuspid insufficiency in Western countries, accounting for 75 % of cases.

FTR is not related to primary leaflet pathology but secondary to other disease processes causing RV dilation, distortion of the subvalvular apparatus, tricuspid annular dilation, or a combination of these factors. Among the most relevant secondary causes are left-sided heart diseases (left ventricular dysfunction or mitral valve disease), any primary cause of pulmonary hypertension (chronic lung disease or pulmonary thromboembolism), and any cause of right ventricular (RV) dysfunction (myocardial disease or RV ischemia).

On the contrary, less common causes of tricuspid valve pathology (8–10 % of cases), affecting the valvular complex directly, include rheumatic disease, myxomatous degeneration, congenital anomalies (Ebstein’s anomaly, ASD), endocarditis, carcinoid disease, and iatrogenic causes (pacemaker leads, defibrillators, drugs) [5].

In order for the three leaflets to correctly coapt during ventricular systole, all of the valvular complex components need to be functioning correctly.

The main mechanisms underlining FTR and preventing normal leaflet coaptation are two: annular dilation and leaflet tethering. The tricuspid annulus (TA) is a component of both the valvular complex and the right ventricle; therefore, upon ventricular or annular dilation, there will be leakage of the tricuspid valve. Assessing pathologically dilated annuli shows a dilation occurring mainly in the septal-lateral direction, involving the free wall of the right ventricle, at the anterior and posterior annular portion (Fig. 11.2). This results in a more circular shape, as compared to a more elliptical shape of healthy subjects. Patients with FTR have a peculiar asymmetric reduction in TA contraction, possibly related to a circular dilated TA, contributing to the extent of TR [6]. Flattening of the valvular annulus and progressive RV dilation cause consequent stretching and displacement of the papillary muscles, leading to an increased tethering effect on the valvular leaflets.

The European guidelines (2012 ESC/EACTS) define the most recent indications for surgical therapy of TR.

Current European and US guidelines (AHA/ACC) are reported in Table 11.1 [7].

Both guidelines pose surgical indication in patients with severe TR undergoing concomitant left-sided valve surgery. European guidelines are more aggressive in posing sufficient level of evidence for surgical treatments of patients with moderate TR and annular dilation (always in a setting of left-sided valve surgery) or cases of reoperations. Elseways, the AHA/ACC guidelines do not consider there is enough evidence to recommend correction of isolated FTR. Intervention is considered feasible in patients with less than severe TR with concomitant left heart surgery and initial signs of RV dysfunction or annular dilation, or in severe cases of primary TR nonresponsive to medical therapy. An even lower recommendation (IIb) is for cases of moderate TR or of reinterventions. The main underlining reason for this conservative approach and for late intervention is the certainty that simply treating left-heart valves is sufficient to improve tricuspid valve function. Reported evidence that TR does not simply regress suggests that a more aggressive approach on the tricuspid valve may help in early postoperative course and may prevent residual or progressive TR.

All studies conducted analyzing the proper timing for FTR surgical treatment took into consideration the importance of assessing preoperatively the annulus dimension (dilation) rather than simply the entity of the regurgitant jet, based on the dependence of the latter on many variables (preload, afterload, and ventricular function) which may interfere with adequate TR severity grading. Dilation of the tricuspid annulus >40 mm or, more importantly in women with small BMI, indexed tricuspid annular dimension (>21 mm/m²), is used as a marker for the choice of surgical treatment, with good clinical efficacy and late functional results.

Patients suffering from TR can result completely asymptomatic for the disease or can present with varying degrees of heart failure. Presenting symptoms of fatigue and weakness are related to a decreased cardiac output, while right-sided heart failure leads to ascites, congestive hepatosplenomegaly, pleural effusions, and peripheral edema. Further findings are atrial fibrillation and jugular venous distension.

Even if severe, tricuspid insufficiency can be tolerated functionally for many years. The importance of tricuspid regurgitation, regardless of the etiology, as a pathology that impacts on long-term survival is reported: more than moderate TR is to be considered a predictor of mortality, with a relevant difference in survival between severe TR (63.9 %) and no TR (91.7 %) [8].

Conservative treatment has always been considered the gold standard for TR, with pharmacological therapy being the first available choice, based on diuretics with fluid and sodium restriction. Although this approach improves peripheral edema and heart failure symptomatology, the decrease in cardiac output may further exacerbate fatigue and dyspnea. Another category of drugs useful in reducing right ventricular overload and ventricular remodeling are angiotensin converting enzyme (ACE-I) inhibitors but an excessive reduction in central venous pressure may result in worsening of TR severity. These findings suggest surgery as the most effective treatment for symptomatic TR.