• tricuspid valve disease

The tricuspid valve is the largest orifice among the four cardiac valves. Secondary tricuspid regurgitation (TR) is not a disease of the leaflets but the consequence of loading conditions and of right chambers remodelling (figure 1). Prevalence of TR in the general population is equivalent to the one of aortic stenosis.1

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Figure 1

Vicious circle of the secondary tricuspid regurgitation.

The prevalence is high and the presence and severity sometimes unexpected. If age, gender, atrial arrhythmias or history of left heart surgery is associated with the risk of developing TR,2 not every single patient with atrial fibrillation and some degree of heart failure might one day have severe TR. The pathophysiology of secondary TR remains incompletely understood. The anatomy of the tricuspid valve apparatus is complicated to understand with many variabilities among patients. Secondary TR is highly load-dependent and diuretics might mask the TR for some time. Therefore, it sometimes remains challenging to understand why one patient develops TR and not others despite having the same aforementioned characteristics.1

Consistently and in different populations (online supplementary table 1), isolated TR (even after adjustment for age, sex, ejection fraction, atrial fibrillation and Charlson Comorbidity Index) independently predicted higher mortality.3 In a community study recently published, only 2.6% of patients with moderate to severe TR got surgery during follow-up despite the poor prognosis reported in online supplementary table 1.

Therefore, there is a clear need to underscore the importance of assessing TR and right heart chambers and valves in every single patient. If the understanding of the pathophysiology of secondary TR has improved in the past years, many issues still remain unresolved, as well as the impact of treatments on symptoms and prognosis. Strategies and treatments of patients with secondary TR will require studies to insure the best practices for now and for the future.

Isolated tricuspid valve  (TV) repair has been reported to be associated with high in-hospital mortality (8.1%) and significant rates of permanent pacemaker implantation (10.9%). Isolated TV replacement was associated with high in-hospital mortality (10.9%) and high rates of permanent pacemaker implantation (34.1%) but also of acute kidney injury requiring dialysis (5.5%).4

The manuscript proposed by Brenden et al 5 has to be highlighted because it shows management and treatment of moderate to severe TR at the Mayo Clinic, in real daily clinical practice. They are probably doing better than many. The Mayo Clinic experience shows that a significant proportion of patients remain free of intervention despite symptoms. These patients are often challenging, with a high surgical risk and many comorbidities. They might be weakly symptomatic because of their poor physical activity and are often reluctant to be ‘operated’.

Upcoming, new interventional treatments (percutaneous annuli, clips and so on) are being developed and will probably provide new opportunities for the management of secondary TR.6 7 These approaches will have to be tested in large randomised studies like it has been done before for clips. An exciting period is beginning for those acquiring a specialisation on the tricuspid valve. As a matter of fact, specific competences will be required because exploration of the tricuspid valve is much more complicated than the mitral or aortic valves. The consequences of TR on preload and afterload remain a challenge with significant interactions with renal and liver functions. In some patients, the overuse of diuretics is dangerous with risks for severe renal dysfunction, cardiogenic shock and death. Defining the correct timing for intervention is challenging. Most of the time, diuretics control the symptoms for some time. Nevertheless, diuretics alter renal function and favour the development of atrial fibrillation, without preventing the risk for rehospitalisation and death. Also, secondary TR progressively induces right heart remodelling. Waiting for diuretics to become inefficient at controlling symptoms, before suggesting an intervention, will probably lead to the demonstration of a lack of any beneficial effect of the intervention. Mitra-FR nicely showed how important it is to provide a timely intervention before the development of excessive heart dilatation, fibrosis and irreversible remodelling. We should not forget that secondary TR is a strong prognostic marker but is secondary to annular and right heart dilatation, and we should probably not wait for the right heart disease to be too advanced to consider correction of TR.8 As for other valvular disease, TR induces a vicious circle. It should probably be stopped as soon as the diagnosis of severe TR is made (figure 1).

Let us follow the upcoming evidence and let us appreciate the work made by Brenden et al.5