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Functional tricuspid regurgitation: a more complex entity than it appears
  1. Gilles D Dreyfus1,2,
  2. K M John Chan1,2
  1. 1
    Department of Cardiac & Transplant Surgery, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Harefield, UK
  2. 2
    Department of Cardiovascular Sciences, National Heart and Lung Institute, Imperial College London, London, UK
  1. Professor Gilles D Dreyfus, Department of Cardiac & Transplant Surgery, Harefield Hospital, Hill End Road, Harefield UB9 6JH, UK; g.dreyfus{at}rbht.nhs.uk

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The optimal management of patients with functional tricuspid regurgitation (TR) at the time of left-sided heart-valve surgery continues to cause controversy. It is well recognised that patients with severe functional TR should have concomitant tricuspid-valve repair, but the management of mild or moderate TR at the time of left-sided heart-valve surgery continues to be debated.1

In this issue of the journal, Song et al (see article on page 931) address the very important question of whether mild TR should be surgically addressed during left-sided heart-valve surgery.2 In a retrospective study of 638 patients who underwent left-sided heart-valve surgery without tricuspid valve surgery, 548 patients had none or trace TR (grade 0–1/4), and 90 patients had mild TR (grade 2/4). At a mean follow-up of 64 months, moderate or severe TR developed in 7.3% in those who had none or trace TR, and in 20% in those who had mild TR. Compared with patients who did not develop significant late TR, patients who developed significant late TR had a higher late mortality (16.3% vs 4.9%, p = 0.004) and a lower event-free survival (76% vs 91%, p<0.001).

Limitations to this study include:

  1. It is a retrospective study and measurements of TR grade and tricuspid annulus size were done retrospectively. It is well recognised that retrospective assessment of such parameters is not as accurate as real-time assessment, as adequate imaging views may not have been obtained. Moreover, a single preoperative echo measurement of TR severity done at rest may not reflect the true severity of TR, as this is dependent on right ventricular (RV) preload, afterload and contractility.

  2. The aetiology of the left-sided heart-valve lesion included a high proportion of patients with rheumatic valve disease (45%). Although the authors report that there was no rheumatic involvement of the tricuspid valve by echocardiographic assessment, this cannot be fully excluded, and it is likely that some of these patients have organic rheumatic TR and not functional TR.

  3. The left-sided heart-valve lesion included patients with aortic stenosis, aortic regurgitation, mitral regurgitation, mitral stenosis, and mixed aortic and mitral valve disease. The physiological impact of these conditions on pulmonary artery pressures, and left and right ventricle remodelling are very different, and this may have influenced the progression of TR.

Two important messages emerge from this study:

  1. Following left-sided heart-valve surgery, significant TR develops at late follow-up in a proportion of patients with none or trace TR at the time of the initial surgery, and in a significant proportion of patients with mild TR.

  2. In those patients who develop significant late TR following left-sided heart-valve surgery, both long-term survival and event-free survival are reduced.

These two messages are consistent with the current published literature on the subject. We have previously reported an increase in TR severity of more than two grades in 45% of patients 6 years after mitral valve repair for mitral regurgitation, most of whom had none or trace TR at the time of the initial surgery, and the majority of whom had degenerative mitral valve disease.3 Similarly, Matsunaga and Duran reported an incidence of moderate or severe TR in 75% of patients 3 years after mitral valve repair for functional ischaemic mitral regurgitation.4

However, the presence of mild TR alone should not be a criterion to indicate the need for concomitant tricuspid valve repair at the time of left-sided heart-valve surgery. The grading of TR is highly subjective, and there is considerable variation in the severity of TR depending on RV preload, afterload and contractility. Rather, a decision to perform concomitant tricuspid valve surgery at the time of left-sided heart-valve surgery in patients with less than severe TR should be based on other parameters as well such as the tricuspid annular diameter.1 3 It is unlikely that patients with none or trace TR will develop significant TR late after left-sided heart-valve surgery if the tricuspid annulus is not dilated at the time of the initial surgery. Conversely, it is very likely that significant TR will develop in these patients if significant tricuspid annular dilatation is present and is not corrected at the time of left-sided heart-valve surgery.1 3

We directly measure the size of the tricuspid annulus at the time of mitral valve surgery and repair the tricuspid valve concomitantly if the tricuspid annulus is dilated beyond 70 mm, that is twice its normal size. In our series of 311 patients, we found that 48% of our patients had such tricuspid annular dilatation, even though the majority had no more than trace TR.3 Functional class at late follow-up was significantly improved in those patients who had a concomitant tricuspid valve repair as compared with those who did not. Such intraoperative measurement of the tricuspid annulus size is highly reliable and reproducible, and measures the maximum tricuspid annulus in the fully relaxed heart from the anteroseptal commissure to the anteroposterior commissure. It should be noted that this differs from echocardiographic measurement of the tricuspid annular diameter. A typical four-chamber echocardiographic view would measure the tricuspid annulus from the middle of the septal annulus to the middle of the anterior annulus. It has been suggested that using echocardiographic measurements, a tricuspid annulus diameter of greater than 40 mm or 21 mm/m2 measured in the four-chamber view should indicate the need for concomitant tricuspid valve repair.5 We therefore recommend that in patients with less than severe functional TR, the tricuspid annular diameter should be measured, and if this is dilated beyond 70 mm as measured directly in the operating theatre (from the anteroseptal to the anteroposterior commissure) or greater than 40 mm in the four-chamber echocardiogram (from the middle of the septal annulus to the middle of the anterior annulus), then concomitant tricuspid valve repair should be performed.1 3

The results of concomitant tricuspid valve annuloplasty in these patients are excellent. In our series, the hospital mortality was 0.7%, and at a mean follow-up of 6 years, 97% of patients had no more than trace TR, and the mean NYHA functional class was 1.1.3 However, it must be recognised that a significant recurrence rate of TR of up to 20% following tricuspid annuloplasty has been reported in some series, mostly in patients with severe TR at the time of the initial surgery.6 Such a high recurrence rate has been attributed to several factors including surgical technique, when a rigid anuuloplasty ring is not used, and to severe tethering of the tricuspid leaflets.6

It must be appreciated that functional TR is a result of progressive dysfunction and dilatation of the RV and can be divided into three phases:

  1. In the first phase, dilatation of the RV results in dilatation of the tricuspid annulus. TR may or may not be present, depending on the degree of annular dilatation and resulting lack of leaflet coaptation.3

  2. In the second phase, with progressive dilatation of the RV and tricuspid annulus, significant TR will occur due to failure of leaflet coaptation.7

  3. Finally, in the third phase, with progressive RV dilatation and eccentricity, tethering of the tricuspid leaflets also occurs, in addition to annular dilatation, due to the attachment of the papillary muscles of the tricuspid leaflets to the free wall of the RV.8 A tethering height of 8 mm or more, measured from the plane of the tricuspid annulus to the theoretical point of coaptation of the tricuspid valve leaflets at end-systole, has been reported to be predictive of greater than moderate functional TR.9

Surgical repair of the tricuspid valve for functional TR may therefore need to be tailored to the stage of the disease. In the first two phases, where the problem is that of tricuspid annular dilatation without leaflet tethering, tricuspid annuloplasty alone gives excellent results.3 However, in the third phase where both significant annular dilatation and leaflet tethering are present, annuloplasty alone is unlikely to be successful in correcting the TR, and some additional procedure to overcome the tethering effects is likely to be necessary.6 Our recently proposed technique of anterior tricuspid leaflet augmentation to increase the surface area of the anterior tricuspid leaflet, and by doing so increasing its surface of coaptation with the septal and posterior leaflets, has shown promising early results, and long term follow-up is awaited.10

Functional TR is therefore a complex entity. As our knowledge of its pathophysiology increases, so too does our understanding of the indications for concomitant tricuspid valve repair at the time of left-sided heart-valve surgery, and the type of repair we should be performing. There is no question that patients with severe functional TR should have this corrected at the time of left-sided heart-valve surgery. For those with less than severe TR, the tricuspid annulus should be measured either by echocardiography or directly during left-sided heart-valve surgery, and concomitant tricuspid-valve annuloplasty should be performed if the tricuspid annulus is significantly dilated. If severe tricuspid leaflet tethering is also present, then anterior tricuspid leaflet augmentation should also be considered in addition to tricuspid annuloplasty to prevent residual or recurrent TR.

REFERENCES

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Footnotes

  • Competing interests: None.

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