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Treatment Options for Severe Functional Tricuspid Regurgitation

Updated: May 7

Indications, Techniques and Current Challenges



Christian Besler, MD; Joerg Seeburger, MD; Holger Thiele, MD; Philipp Lurz, MD, PhD

Topics: Interventional Cardiology and Cardiovascular Surgery, Valvular Heart Disease

Pulmonary hypertension, right ventricle, transcatheter therapy, tricuspid regurgitation, tricuspid valve


Severe functional tricuspid regurgitation represents an important unmet need in clinical cardiology given its prevalence, adverse prognostic impact and symptom burden. Surgical tricuspid valve annuloplasty remains the treatment of choice for the majority of patients, especially if the operative risk is acceptable and preserved right ventricular function is present. However, several transcatheter techniques are currently in bench and early clinical testing to provide alternative treatment options for patients with a very high surgical risk. Future trials are needed to address the question as to whether transcatheter treatment of tricuspid regurgitation improves long-term prognosis and is superior to medical treatment alone in these patients.

FIGURE 1 Causes of Organic and Functional TR. AS: aortic stenosis; DCM: dilated cardiomyopathy; EMB: endomyocardial biopsy; ICM: ischaemic cardiomyopathy; LA: left atrial; LV: left ventricular; MR: mitral regurgitation; MS: mitral stenosis; RV: right ventricular; TV: tricuspid valve.



Introduction

Tricuspid regurgitation (TR) is an important, yet often underappreciated, disease in cardiology practice. In up to 90% of patients in Western countries, moderate-to-severe TR is secondary or functional, most often due to left-sided heart disease and other causes of pulmonary hypertension.[1] In these cases, functional TR results from tricuspid annular dilatation in the setting of right ventricular remodeling, mainly due to pressure or volume overload (Figure 1). Up to 50% of patients undergoing mitral valve surgery for functional ischaemic mitral regurgitation have moderate or severe TR, and a substantial proportion of patients develop TR late after previous left-heart surgery.[2] Given the overall increase in life expectancy, improved treatment options for patients with ischaemic or non-ischaemic cardiomyopathy and expanding transcatheter interventions for mitral valve pathologies in patients at increased surgical risk, the number of patients presenting with relevant TR may increase in the coming decades. Importantly, recent publications have challenged the long-held misperception that functional moderate-to-severe TR will resolve once successful treatment of mitral regurgitation has been carried out. About 70% of patients with a more than moderate TR before mitral valve edge-to-edge repair still had moderate-to-severe TR after two years of follow-up.[3] The prevalence of coexisting moderate-to-severe TR is between 11% and 26% in patients undergoing Transcatheter Aortic Valve Replacement (TAVR) for native aortic valve stenosis, and a reduction in echocardiographic TR grade has been observed in 15% to 50% following TAVR in these patients.[4] Conflicting results have been reported regarding the prognostic impact of TR following TAVR and surgical aortic valve replacement. Interestingly, a recent analysis in patients at high surgical risk undergoing valve-in-valve TAVR for degenerated surgical aortic bio-prosthesis suggested a significant reduction in TR severity and lack of prognostic impact of preprocedural TR at short- and long-term follow-up.[4]


Medical Treatment Options for Functional TR

Frequently, patients with moderate-to-severe TR present late in the natural history of the disease with exercise limitation and other symptoms of right heart failure difficult to treat by medical therapy. In the diagnostic and treatment process, the underlying cause of functional TR needs to be identified and treated, if possible. Patients with ischaemic or non-ischaemic cardiomyopathy are managed according to current heart failure guidelines.[5] If there is clinical suspicion of pulmonary hypertension, further differential diagnosis, including right heart catheterisation, is mandatory to classify pulmonary hypertension and identify patients who might benefit from specific drug therapy (e.g., calcium channel blockers, endothelin receptor antagonists, phosphodiesterase type five inhibitors and guanylate cyclase stimulators, prostacyclin analogues and prostacyclin receptor agonists). Oral anticoagulation should be initiated in patients with right heart chamber dilatation due to (repeated) pulmonary embolism. Nevertheless, in a considerable number of patients, medical treatment options of TR are limited for the following reason: often, an impairment of kidney function in patients with advanced TR limits further escalations of the diuretic dose to improve symptoms of volume overload. If kidney function is preserved, adding an aldosterone antagonist represents a possible treatment option, in particular for patients with hepatic congestion and secondary hyperaldosteronism. However, the benefit either of aldosterone antagonists or of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers on right ventricular remodeling or functional improvement in patients with severe functional TR has not been validated in clinical studies.



To read the full article, please go to the April 2019 Issue of CCT.

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