Our cover story this month, which outlines the issues surrounding tricuspid valve (TV) dysfunction, is worth a careful read. The story highlights the etiology, diagnosis and recent evolution of treatment strategies for TV dysfunction – medical, surgical and interventional.

Yet despite the careful reporting and words of advice from experts, the overall message is that the TV is still rather enigmatic but should not be overlooked. Readers will come to understand that much has been learned. For example, note that careful imaging has revealed only slightly more than half of tricuspid valves are truly "tricuspid"!

Yet, TV stenosis is easiest to understand. Rheumatic heart disease, and rarely carcinoid, lupus and congenital stenosis, cover that base. If TV leaflets are fused, transcatheter balloon valvotomy can even be considered.

However, tricuspid regurgitation (TR) is a more complex story and the pathophysiology surrounding TR still can baffle us. Who is the real culprit for TR – the TV itself? The right atrium or right ventricle (RV)? The pulmonary pressure? The left ventricle (LV)? The mitral valve? The pulmonic or aortic valve? Making that judgment is a good first step toward defining a therapeutic strategy. But it isn't always easy!

Here are my of takeaways from this month's cover story:

Color Doppler and transesophageal echo, so successful in defining mitral regurgitation, may not be helpful in evaluating TR. Transthoracic echo puts the transducer close to the TV, and must be used. However, defining TR severity on the basis of color area can often underestimate TR. Right-sided cardiac pressures are lower than pressures on the left. Severe TR jets may look like mild or moderate MR jets, be misread, and encourage clinical "watchful waiting." Beware.

The level of evidence for the recommendations for medical therapy of TR is classified as IIa in both the U.S. and European guidelines because of the lack of better data. The obvious use of diuretics and treating nonvalvar causes round out the list of useful medical therapies. Initially diuretics may help but may also lose efficacy over time as TR continues.

Remember that TR raises venous pressure and thus intestinal absorption of medications, liver function and renal function can be insidiously affected. TR also reduces forward cardiac output. Subsequent symptoms of fatigue and "losing pep" are often disregarded, and ascites may masquerade as "weight gain."

It makes sense that improvement in LV dysfunction can improve TR. Unloading the LV and decreasing LV end-diastolic pressure and mitral regurgitation decreases left atrial, and subsequently, pulmonary and RV pressures. Cardiac resynchronization therapy (CRT) can also help improve LV pressures enough to reduce TR. Remember that many patients in need of CRT have previously had RV leads placed – another cause of TR that is human-made and often forgotten.

Regurgitant valve lesions all can lead to ventricular overload/dilatation and failure. Waiting for ejection fraction to decrease or fixed atrial fibrillation to appear is a strategy that has been superseded by early intervention. Early mitral or aortic valve interventions increase the likelihood of LV recovery, and the same is true for TR and the RV.

Invasive therapies have until lately been the purview of cardiac surgeons. Tricuspid annuloplasty after left-sided surgery has long been used and is effective for patients with associated TR. For tricuspid valves with intrinsic pathology or severe annular dilatation for which annuloplasty cannot be effective, tricuspid replacement may be needed. Both procedures increase the length of the pump run but improved RV dynamics postoperatively hopefully offset that.

In any case, cardiac surgeons are increasingly aware that associated TR during cardiac surgery complicates recovery and TR should be addressed intra-operatively if needed.

More recently, transcatheter therapies for TR have been developed. The Tri-Clip, a TV transcatheter valve procedure similar with the MitraClip has been approved by the U.S. Food and Drug Administration (FDA) for selected patients with TR and is now in routine use in centers that have expertise in transcatheter valve therapies.

The Edwards EVOQUE TV replacement system, which replaces the TV, was also approved by the FDA, early in 2024, and similarly is in use for selected patients approved by the Heart Team. As experience with such devices increases and as new devices emerge, the transcatheter treatment of TR will certainly gain traction.

Finally, as mentioned at the beginning, we need more information. There is much still to be learned about how, when and which treatments of TR are best chosen to improve morbidity, mortality and quality of life in patients with TR.

 

Peter C. Block
MD, FACC

 

Clinical Topics: Heart Failure and Cardiomyopathies, Valvular Heart Disease, Mitral Regurgitation

Keywords: Cardiology Magazine, ACC Publications, Tricuspid Valve, Rheumatic Heart Disease, Mitral Valve Insufficiency, Heart Atria, Cardiac Output