Tricuspid regurgitation (TR) is a common condition most commonly associated with degenerative and left-sided heart disease (1, 2). Right-sided cardiac chambers and TR have been historically overlooked and mostly become relevant during the surgical evaluation of left valvular heart disease.

TR can lead to dysfunction of the right ventricle (RV) due to increased preload and progressive remodeling. This consequently results in signs and symptoms of heart failure (HF) and subsequently contributes to a spectrum of liver and kidney impairment (3–5) primarily attributable to persistent right-sided congestion. The interplay between the cardiovascular and renal systems becomes evident in the context of cardiorenal syndrome, wherein chronic abnormalities in heart function leads to kidney dysfunction (6).

TR has long been considered a relatively benign entity resulting in the underutilization of diagnostic and therapeutic resources. The underestimation of the clinical impact of TR has led to a pattern of care delaying intervention until very advanced stages of disease where the risks of treatment become excessively elevated (7). While surgical treatment of TR, even in early stages, has been associated with poor outcomes, innovative percutaneous techniques have emerged as a potential alternative. These percutaneous techniques have expanded their scope beyond the conventional surgical indications, encompassing high-risk patients previously excluded from surgical studies (8). In addition to mechanical treatments decongestion management in TR is of paramount importance, so the cardiorenal interaction is a key factor. Hemodynamic profiling of patients and the assessment of right ventricular function and systemic congestion are crucial to determine optimal timing and indications for percutaneous interventions along with identifying who would not derive any benefit from further interventions.

TR is frequently encountered in the echocardiography laboratory. While mild TR may not have significant consequences, advanced degrees of TR are associated with factors such as advanced age, female sex, and left sided heart disease. Moderate to severe TR is present in 4%–6.6% of patients older than 75 years and is associated with increased mortality and morbidity independent of RV dysfunction and pulmonary hypertension (1, 2).

Primary TR is the least prevalent etiology, representing only 8%–10% of all TR cases and is mainly related to pathologies affecting the tricuspid apparatus (papillary muscles, chordae and annulus) and tricuspid valve (TV) leaflets. Causes of primary TR include carcinoid syndrome, rheumatic heart disease, congenital abnormality of TV, iatrogenic valve damage and endocarditis. Lead impingements from cardiac implantable electronic devices are a leading cause of primary TR, as it has been reported to occur in up to 38% of patients following implant (9–11).

Secondary TR can arise as a consequence of various factors, including RV dilatation due to volume overload or increased pulmonary pressures. It may also result from dilatation of the right atrium or tricuspid annulus as occurs in atrial fibrillation. Additionally left heart or valvular diseases can contribute to the development of secondary TR. Interestingly, 8% of cases of secondary TR can occur in isolation (1). In the setting of left-sided heart pathology, TR is a late event indicating a more advanced disease, higher pulmonary pressures, extensive ventricular remodeling, and worse prognosis (12). Without appropriate intervention, TR perpetuates a vicious pathophysiological cycle that leads to further adverse remodeling of the ventricles, atria, tricuspid annulus, with increasing TR severity and subsequent irreversible RV dysfunction leading to unfavorable outcomes (7, 13).

Transthoracic echocardiography (TTE) is the preferred diagnostic method for TR, allowing TV visualization as well as RV function (10). Despite its widespread use, TTE has limitations in TV assessment, since only two leaflets can be visualized simultaneously. 3D echocardiography, an extension of TTE, provides simultaneous visualization of the three leaflets and surrounding structures including a complete visualization of the annulus, providing a better characterization of TV. The addition of color flow Doppler allows to quantify the severity of TR by analyzing the effective regurgitant orifice size, regurgitant volume, the TR jet, and the vena contracta width. Of note, transesophageal echocardiography (TEE) is no more effective in providing optimal views of the TV than TTE (10, 14).

The impact of TR on the RV varies on a number of factors including the underlying cause, degree of anatomical alteration, presence of pulmonary hypertension, left valvular heart disease or presence of atrial fibrillation (AF) (15, 16). Several phenotypical classifications have been used to predict outcomes. Deitz et al. describe four RV remodeling patterns based on RV dilatation and dysfunction in patients with secondary moderate to severe TR: (1) normal RV size with normal function, (2) dilated RV with normal function, (3) normal RV size with reduced function, and (4) dilated RV with reduced function. The 4th pattern is common in patients with severe TR, accounting for 43%. Any degree of RV dysfunction (patterns 3 and 4) is associated with decreased survival when compared to patients with normal RV function (17). Two additional phenotypes of functional TR have been described: atrial functional TR (A-FTR) and ventricular functional TR (V-FTR). A-FTR refers to TR associated with AF leading to a progressive dilatation and enlargement of the tricuspid annulus associated with right atrial enlargement (18, 19). In this group, the RV changes its shape into a conical remodeling pattern with annular enlargement and dilatation of the RV basal segments despite a normal RV length (20). In contrast, in V-FTR [as seen in left-sided heart disease, RV dysfunction or pulmonary hypertension (PH)], the RV takes on a spherical or elliptical pattern as a consequence of a longitudinal remodeling with valvular tethering, while tricuspid annulus enlargement is only mild (18, 19, 21, 22). Patients with V-FTR have worse survival compared with patients with A-FTR, especially in the PH subgroup (23). RV function is the main prognostic factor in HF and in TR. Therefore, its evaluation is essential for risk stratification (7, 24).

As in the case of TR, TTE remains the primary imaging modality for RV assessment, for practical reasons. Conventional TTE parameters such as tricuspid annular systolic excursion (TAPSE), tissue Doppler velocity at the lateral tricuspid annulus and fractional area change rely on geometric assumptions and are load and angle-dependent leading to an overestimation of RV function in severe TR (25). Other parameters, such as free wall longitudinal strain, can provide a more accurate assessment of RV function (26). TAPSE/SPAP (systolic pulmonary arterial pressure), a parameter of ventricular arterial coupling, which assesses the relationship between RV contractility and afterload, has proven to be a valuable prognostic parameter in this context (27, 28). In general, multimodality imaging would be the preferred approach for RV assessment in the context of severe TR, with cardiac magnetic resonance as the gold standard for evaluating RV volumes and function (29–31).

TR causes an elevation of RV preload leading to a decrease in cardiac output, and an increase in venous congestion. Consequently, signs and symptoms of right heart failure (RHF) include an elevated jugular venous pressure, edema, ascites, hepatomegaly and, in advanced stages, renal and hepatic failure with malnutrition (32). Congestion is one of the main manifestations of RV dysfunction and it is associated with worse quality of life, frequent admissions, and increased mortality. As the disease progresses, a shift in the clinical phenotype can be seen: with a low cardiac output state can advance towards a high cardiac output state secondary to hepatic failure and portal hypertension. Decreased splanchnic wash-out of vasoactive substances often leads to vasoplegia and high and a hyperdynamic state resulting in hepatorenal failure. End stage RV failure is associated with a poor response to percutaneous treatment of TR (33).

When evaluating congestion in TR, it is crucial to employ diverse diagnostic methods. These may encompass clinical scoring systems, imaging techniques, bioimpedance measurements, hemodynamic tests, and analysis of circulating biomarkers.

TR is highly prevalent, particularly when associated with left heart disease and among vulnerable populations such as women and the elderly. Although it has been historically overlooked, TR is associated with a 65% increase in hospitalizations and death, a risk that is even higher in patients with RV dysfunction. Diagnosis is made by TTE (2D and 3D). RV assessment by TTE is more challenging in the presence of severe TR.

Clinical manifestations of TR revolve around signs of abdominal congestion, which bear prognostic implications even when mild (72). A comprehensive approach to diagnose and manage congestion includes abdominal ultrasound and biomarkers in addition to clinical evaluation. Renal, hepatic, and intestinal involvement are key findings that may perpetuate a cycle of refractory congestion and hemodynamic abnormalities. Treatment strategies are based on combination of diuretics and renal replacement techniques in refractory patients. RV failure often coexists with severe TR and represents a significant prognostic factor although there is no evidence-based medical treatment available (Figure 1).

In the recent years, several percutaneous treatment techniques have emerged, with different mechanistic approaches, showing promising safety profiles. However, there remains limited evidence regarding their clinical and prognostic impact, and more importantly their appropriate indications. More advanced patients may benefit less from the therapy, therefore identifying optimal timing for these interventions becomes a crucial element (73). Further refinement of clinical, laboratory and echocardiographic assessment are needed to establish ideal timing and preferred technique for percutaneous TR interventions. Additionally, understanding how these procedures can improve RV function combined with medical therapy to enhance decongestive effects and protect against end-organ failure is an important area for future research. This is an exciting time as emerging TR innovations hold promise to improve outcomes and quality of life in patients facing this challenging yet common condition.