The criteria established by the Valve Academic Research Consortium (VARC) — whether we like them or not — represent the rules of engagement for studies addressing structural heart disease treatment. These guidelines define the criteria for a successful procedure and provide a framework for grading the severity of developed complications. This is critical because it establishes a benchmark for determining which “suboptimal” outcomes might be acceptable and which are not. Additionally, these criteria enable quality and outcome comparisons across different procedures by following a common and objective standard. While VARC guidelines have traditionally been more intervention-focused, they also allow for comparisons between surgical techniques and transcatheter procedures. Initially, these criteria were introduced for aortic stenosis treatment, with three updates solidifying their role. Criteria for mitral insufficiency have since been published, and in this analysis, we focus on tricuspid regurgitation (TR).

As with previous editions, this publication includes contributions from both cardiologists and surgeons from renowned international institutions. The article is organized into two sections, which we will summarize to outline the essentials needed to critically assess the controversy surrounding the interventional versus surgical management of TR — at both the individual patient level and in anticipation of the wave of studies soon to flood the literature.

1. Characterization of Tricuspid Regurgitation

The first aspect to address is the characterization of tricuspid regurgitation (TR). This involves multiple concepts, many of which are essential when considering the treatment of TR. We will outline each below with a brief description of key knowledge points:

1.a) New Etiological Classification of TR

The relationship of this new classification with Carpentier’s classification has been previously introduced in the blog. Carpentier’s classification was functional; however, given that over 80% of TR cases stem from secondary causes (predominantly mechanisms I and IIIB), a reformulation was warranted. Primary etiology (5-10% of cases) involves intrinsic leaflet pathology due to degenerative, congenital, or acquired causes (e.g., tumors, trauma, carcinoid syndrome, rheumatic disease, radiotherapy). Secondary etiology includes two subclassifications: “ventricular,” which encompasses left ventricular dysfunction affecting the right side, precapillary/parenchymal pulmonary hypertension, and right ventricular dysfunction itself, with coexisting Carpentier type I and IIIB mechanisms to varying degrees. The second subclassification, “atrial,” considers atrial dilation due to atrial fibrillation (AF) and annular dysfunction, as well as atrial enlargement resulting from hypertensive cardiopathy, age, or heart failure with preserved ventricular function (Carpentier type I). Lastly, a third classification involves transvalvular device leads, which can be subdivided into type A if the lead directly contributes to TR or type B if the lead simply passes through the valve without affecting function.

The core of this new classification lies in distinguishing the prevalence of the “ventricular” versus “atrial” phenotypes in secondary TR, or, more specifically, how much annular dilation (type I) or systolic restriction in leaflet movement (Carpentier type IIIB) predominate. This distinction, with prognostic implications for edge-to-edge therapy, is equally applicable in surgical technique and should be required in preoperative studies. Relevant parameters include tenting analysis, with cut-off points of 9 mm for tenting height, 2.1 cm² for tenting area, and 2.5 cc for tenting volume. Furthermore, right ventricular dilation with an indexed end-diastolic volume cut-off at 80 cc/m² and end-systolic volume at 21 cc/m² differentiates between an “atrial” versus “ventricular” phenotype, with values below and above these thresholds, respectively. Lastly, a simple yet highly intuitive parameter is the right atrium-to-ventricle area ratio with a cut-off of 1.5. Values at or above this ratio indicate an “atrial” phenotype, whereas those below suggest a “ventricular” phenotype.

1.b) New Morphological Characterization

The tricuspid valve could more aptly be renamed the “right atrioventricular valve,” as seen in the congenital heart disease field. This is due to the fact that, in many cases, we cannot accurately describe the valve as having three cusps. The most common morphology (54%) is type I, featuring the traditionally described three leaflets. Type II (5%) involves fusion of the anterior and posterior leaflets, creating a bicuspid valve. Type III, subdivided into three subtypes, features an indentation dividing one of the leaflets. In type IIIA (3%), the anterior leaflet divides into A1 and A2; type IIIB, the second most common (32%), involves the posterior leaflet dividing into P1 and P2; and type IIIC (4%) involves the septal leaflet dividing into S1 and S2. By convention, the closest scallop to the atrioventricular node is labeled as A1, P1, or S1, with the most anterior scallop designated for the posterior leaflet. Lastly, type IV (2%) involves two indentations, with divisions in the anterior (A1 and A2) and posterior leaflets (P1 and P2), leaving the septal leaflet intact.

1.c) New Severity Classification of TR

Like mitral regurgitation, TR was initially graded into three categories: mild, moderate, and severe. This classification primarily uses semiquantitative parameters, such as the PISA radius (<5.4 mm², 5.5-8.9 mm², and ≥9 mm², respectively) and vena contracta width (<3 mm², 3-6.9 mm², and ≥7 mm², respectively). Given the significance of severe TR, three additional gradations were created, forming a five-level scale. Although initially controversial, this extended scale gained support due to the unique nature of the right heart. Right-sided regurgitant volumes that cause systemic venous congestion are manageable in the right heart but would be unmanageable in the left heart due to pulmonary edema and postcapillary pulmonary hypertension incompatible with sustained circulation. This extended grading scale has demonstrated prognostic implications, with worsened survival correlating with each step up in severity. The selected parameters for classifying severe, massive, and torrential TR include quantitative metrics such as PISA-derived regurgitant orifice area (40-59 mm², 60-79 mm², and ≥80 mm², respectively) and 3D vena contracta area (75-94.9 mm², 95-114.9 mm², and ≥115 mm², respectively), although vena contracta width remains a useful semiquantitative parameter (7-13.9 mm², 14-20.9 mm², and ≥21 mm², respectively). This classification also has technical implications: one main limitation for edge-to-edge or isolated annuloplasty techniques is the presence of a significant leaflet gap (>1 cm). Given the strong dependency of right heart hemodynamics on preload, afterload, and respiratory dynamics, these parameters should be measured at end-expiration in spontaneously breathing patients and in a state of euvolemia, stable diuretic therapy, and normalized blood pressure.

1.d) Assessment of Right Ventricular Function and Right Ventricular-Pulmonary Artery Coupling

One primary concern in addressing TR is assessing whether the right ventricle (RV) can sustain cardiac output after residual TR is minimized or eliminated. Evaluating RV function pre-procedure is challenging, as it may be masked by regurgitation, which acts as a relief valve. RV function assessment should encompass multiple parameters since a single definitive measure remains elusive. The evaluation should include traditional measurements, such as tissue Doppler wave S (mild dysfunction, 9-11 cm/s; moderate, 6-8 cm/s; and severe, <6 cm/s), TAPSE (mild dysfunction, 14-17 mm; moderate, 10-13 mm; and severe, <10 mm), global strain (mild dysfunction, 18-21%; moderate, 14-17%; and severe, <14%), and free wall strain (mild dysfunction, 20-23%; moderate, 15-19%; and severe, <15%), with the more precise but complex three-dimensional ejection fraction (mild dysfunction, 45-50%; moderate, 35-45%; and severe, <35%). This RV functional assessment should also consider pulmonary afterload using the right ventricular-pulmonary artery coupling concept, which describes the hemodynamic conditions where the RV can maintain forward pulmonary flow. Suggested indices include TAPSE/pulmonary artery systolic pressure, though no definitive cut-off exists. Alternatively, the indexed RV stroke volume relative to end-systolic volume can be measured using 3D echocardiography, CT, or MRI. This measure does not depend on pulmonary artery pressure but, while intuitive, lacks standardization.

1.e) Characterizing the Risk of Invasive Procedures

This aspect will be discussed in future blog entries, though it is worth noting that the effects of systemic venous congestion warrant a multimodal assessment across organs and systems, rather than focusing solely on cardiac disease and related morbidities, as is typical in conventional risk-scoring systems. This unique profile has led to the development of tricuspid valve-specific risk scores, such as TRI-SCORE, among others.

2. Characterization of Outcomes in Invasive Procedures

The VARC panel’s guidelines on outcomes criteria for future studies and grading the impact of complications or suboptimal results are notably less biased than those used for aortic and mitral valves. There are no significant biases that would disadvantage surgical outcomes relative to interventional ones. In fact, some points are particularly striking, including:

• 2.a) “Technical success” requires proper device implantation, with reduction of TR to mild or lower (optimal outcome) or moderate or lower (acceptable outcome), absence of tricuspid stenosis, and absence of major complications. A cut-off for tricuspid stenosis is set at a valve area >1.5 cm² or indexed >0.9 cm²/m² (>0.75 cm² if BMI >30 kg/m²) with a mean gradient <5 mmHg. Tricuspid stenosis is less common with edge-to-edge tricuspid repair than with mitral, as the tricuspid valve is physiologically 20% larger. However, prosthetic replacement, particularly percutaneous, may carry this risk.
• 2.b) A “clinical success” criterion is added, requiring no adverse events (e.g., bleeding, AKIN stage II or III renal dysfunction, heart failure, embolism) from 30 days post-procedure to one year, with no re-hospitalizations, improvement in dyspnea class, improved functional capacity (6-minute walk test increase by 50 meters), and/or improved quality of life as measured by at least a 5-point increase on the KCCQ scale.
• 2.c) Follow-up for different devices must be sufficient to confirm effectiveness, with a minimum threshold of five years, especially for newly introduced devices.
• 2.d) Device-related complications are categorized and graded, including phenomena like thrombosis (HALT) or leaflet mobility impairments.
• 2.e) Results on all-cause mortality and re-hospitalization are required. Only secondary outcomes categorize cause-specific mortality or re-hospitalization, with heart failure-related readmissions as especially relevant.
• 2.f) Post-procedure hemodynamic studies should be conducted in a stable medical treatment context. Increased diuretic therapy in control groups, as seen in the Triluminate study, or pre-transcatheter therapy to reduce leaflet gap could skew results. Reporting medical therapy is essential, as it may serve as a major confounding factor.

COMMENTARY:

Surgery pioneered valve treatment, and percutaneous intervention, currently expanding, attempts to replicate surgical concepts with transcatheter devices and techniques. As surgeons, we must ensure this exchange of knowledge flows both ways. The cardiology community’s interest in TR and valvular diseases has spurred innovation in the past two decades. Surgeons should embrace and integrate this knowledge, holding it to the same standard in our procedures. Although VARC’s tricuspid criteria seem intervention-focused, they present a neutral scenario for the surgical alternative without any biases. By doing things right and knowing what we’re doing, we can compete effectively in this emerging arena of debate.

REFERENCE:

Hahn RT, Lawlor MK, Davidson CJ, Badhwar V, Sannino A, Spitzer E, et al.; TVARC Steering Committee. Tricuspid Valve Academic Research Consortium Definitions for Tricuspid Regurgitation and Trial Endpoints. Ann Thorac Surg. 2023 Nov;116(5):908-932. doi: 10.1016/j.athoracsur.2023.09.018.