Yes, functional TR is worth repairing (David H. Adams, MD)
Functional tricuspid regurgitation is a common finding in patients undergoing degenerative mitral valve repair. Severe tricuspid regurgitation is unusual, and clearly there is little debate on the merits of concomitant tricuspid repair for these patients. Moderate tricuspid regurgitation is identified preoperatively in around 15% of patients undergoing degenerative mitral repair (), and concomitant tricuspid repair in these patients is certainly supported by both the American and European guidelines (J Am Coll Cardiol. 2017. ; ).
What experience and evidence has led us to a more aggressive approach? One of the most important influences on our early adoption of tricuspid repair at the time of mitral surgery was linked to observations that tricuspid regurgitation (TR) sometimes progressed after isolated mitral valve repair (MVR), with some patients developing moderate or worse insufficiency. Certainly, the impact of significant tricuspid regurgitation on the quality and length of patients’ lives and the challenges of reoperation for isolated tricuspid regurgitation are well known to all surgeons.
However, the first objective data supporting a more aggressive approach to abnormal tricuspid valve function was provided by Gilles Dreyfus, MD, and his team at Harefield Hospital in London, who reported significantly better symptomatic and echocardiographic outcomes after concomitant tricuspid repair for tricuspid annular dilatation (irrespective of the degree of tricuspid regurgitation), compared with patients who did not undergo tricuspid repair ().
Consequently, the importance of treating significant annular dilatation, even without significant tricuspid regurgitation, is supported by the guidelines. Our own experience with an aggressive approach to functional tricuspid regurgitation (FTR) at the time of mitral surgery put an exclamation point on this (). We found that concomitant tricuspid repair in patients who were worse off before surgery with more TR and higher rates of atrial fibrillation and right-sided dysfunction, actually did better during 5 years of follow-up than the isolated mitral repair patients who started with completely normal tricuspid valve anatomy and ventricular function.
Benign neglect is always an option (), but we agree with Roberto Dion, MD – despite our friends’ opinions in Toronto and Rochester – we would much prefer to have minimal TR and a normal sized tricuspid valve after MVR. Ask yourself: would you rather have no TR and a normal sized tricuspid valve after you undergo a mitral operation, or a very dilated annulus and perhaps moderate FTR? I am pretty sure I know the answer, but if you are not sure, read our paper.
Dr. Adams is cardiac surgeon-in-chief, Mount Sinai Health System, and Marie-Josée and Henry R. Kravis Professor and Chairman, department of cardiovascular surgery, Icahn School of Medicine at Mount Sinai and The Mount Sinai Hospital, and president-elect of the American Association for Thoracic Surgery. He disclosed he is the national co-principal investigator for the Medtronic NeoChord trial, and receives royalties from Medtronic and Edwards Lifesciences. The Icahn School of Medicine at Mount Sinai receives royalty payments from Edwards Lifesciences and Medtronic for intellectual property related to Dr. Adams’ involvement in the development of 2 mitral valve repair rings and 1 tricuspid valve repair ring.
No, a patient with FTR does not necessarily need repair (Tirone David, MD)
In our clinic, a patient who undergoes MVR and has FTR generally goes home without an annuloplasty. We now have 12 years or more of follow-up in these patients, and they do not develop TR if their MVR is competent. We have reported that preoperative TR in patients who had MVR is associated with mitral valve disease and often improves after the operation (). New postoperative TR is uncommon.
Ninety percent of my mitral valve repair patients today have no symptoms. Of those patients, a small proportion have moderate TR.
Predicting severe FTR is difficult in these patients. For reasons that we don’t know, when you perform mitral valve repair in a patient with ejection fraction less than 40%, ultimately the tricuspid valve begins to leak 10 or 15 years later. Longstanding atrial fibrillation also causes TR. The data published to date on tricuspid annuloplasty show that at 10 years, 30% had recurrent TR regardless of whether or not they’ve had mitral valve repair ().
Dr. David is a professor of surgery at Toronto General Hospital. He reported no financial relationships.
Yes, but repair of FTR requires caution (Gilles Dreyfus, MD)
The controversy surrounding the legitimacy of concomitant tricuspid annuloplasty for functional TR during MVR begs for a clinical trial, but before we can conduct a clinical trial, we must define the primary and secondary endpoints. We’ve seen recent prospective, randomized trials that have reported faulty conclusions because the primary endpoints were wrong.
We need a strong debate to agree on those endpoints. Mortality as an endpoint will probably take a very long time to arrive at.
We’re mixing up many different factors. We’re mixing up TR grading, and we know that grading is unreliable. We have all seen patients with full-fledged TR, and after we put them on Lasix (furosemide, Sanofi), 3 days later they have mild TR. So the same patient with no treatment becomes let’s say a “Dreyfus indication,” and then suddenly in 3 days the patient doesn’t need surgery. At any further stage of his life this patient can experience severe TR again; tricuspid annuloplasty will prevent that from happening.
It is a big mistake to rely only on grading to determine the need for surgery to treat FTR. We are superimposing the assessment of the right ventricle (RV) to the left one, but that is mixing apples and pears. The left ventricle (LV) is working against resistances and its volume does not change; the RV supplies only the pulmonary system and is volume-dependent. You can double the size of the RV without changing its function whatsoever, and that’s when TR may appear if all the features are present: annular dilatation and RV dilatation. Any changes in preload such as severe renal failure, as well as any changes in afterload such as moderate LV impairment or mild/moderate MR after MVR, may modify RV size and TR grading.
Moderate TR according to the common definition does not exist. If you look at the reports in echocardiography and if you ask any cardiologist, everything between no TR and severe TR is considered moderate. We have proposed a new staging system for evaluating FTR that uses three factors: TR severity; annular dilatation; and extent of tethering, or mode of leaflet coaptation ().
Dr. Dreyfus is director of the medical and surgical team at the Cardiothoracic Centre of Monaco in Monte Carlo and professor of cardiothoracic surgery at Paris V University and the Imperial College of London. He disclosed receiving speaker fees from Edwards Lifesciences, LivaNova, and Medtronic.
No, few FTR patients at risk after MVR (Hartzell Schaff, MD)
Echocardiography can provide a great deal of information about when concomitant repair for TR is indicated during MVR. We’ve found that if the patient has no right-sided signs, has normal right atrial pressure, and has mild or mild/moderate TR at the time of repair to the journey mitral valve, the chance of him returning for a tricuspid valve procedure is near zero.
A few patients do return after MVR. They develop atrial fibrillation and may need a pacemaker, but we see very few patients return for tricuspid surgery.
There is a hierarchy of valves: the tricuspid valve; the pulmonary; the aortic valve; and the mitral valve. You can do without the pulmonary valve and live. In fact you can do without a tricuspid valve and live; there was a surgeon that used to do tricuspid valvectomies for endocarditis. You don’t live well; you’ll eventually have to have the tricuspid valve replaced. But you cannot live without a mitral valve and you cannot live without an aortic valve.
It’s fair to say we cannot demonstrate any benefit of correcting functional mitral regurgitation. Why would we think there’s a benefit of correcting FTR? We can say we’re going to look at grade of TR down the road, or we could look at some other endpoint, but think about it this way: If we cannot prove that correcting functional mitral regurgitation is helpful, why is correcting FTR going to help?
Dr. Schaff is a cardiothoracic surgeon at Mayo Clinic Foundation, Rochester, Minn. He reported no financial relationships.