Author + information
- aCollege of Medicine, School of Public Health, SUNY Downstate Medical Center, Brooklyn, New York
- bWeill Cornell Medicine, New York, New York
- ↵∗Address for correspondence:
Dr. Jeffrey S. Borer, The Howard Gilman Institute for Heart Valve Disease, SUNY Downstate Medical College and School of Public Health, 635 Madison Avenue, 3rd Floor, New York, New York 10022.
By 50 years ago, considerable discussion had developed concerning the appropriateness of repair or replacement of a regurgitant tricuspid valve (TV), both in the context of primary tricuspid regurgitation (TR) (the underlying cause of 20%) and of secondary TR, which underlies 80%, the latter most often related to mitral valve (MV) disease (1). At that time, pioneering studies at the then National Heart Institute (now the National Heart, Lung, and Blood Institute) of the National Institutes of Health revealed that successful surgical remediation of the MV pathology often was associated with reduction in the magnitude of TR and resolution of the consequent clinical debility (2). With these findings, it was widely accepted that TR, and particularly secondary TR, was a relatively benign condition and usually did not require specific surgical therapy if the responsible left-sided disease was remedied. This was fortuitous: the valve deformities of primary TR vary widely and limit the success of replacement and repair efforts. Secondary TR generally causes more predictable anatomic valve distortions and is more amenable to surgical repair than the primary variety, but even here, sustained success is not invariable. Moreover, because of the propinquity of the conduction system to the TV annulus, replacement and repair frequently require permanent pacemaker implantation (3).
In the years that have passed since the report of Braunwald and Ross et al. (2) in 1967, the volume of MV surgery has increased dramatically and with it, the volume of patients with secondary TR. As a result, databases from which current epidemiological information is derived are far larger than those available in 1967. From the current perspective, TR is prognostically very important, and the threshold for mechanical remediation, by open chest surgery or by catheter-based repair, is far lower than it was 50 years ago, and the results of TV surgery are far better. It may be worth considering, then, the basis for the assumption that TR generally is benign and can be controlled by surgical correction of left-sided lesions. First, the 1967 population included 100 consecutive patients who underwent MV replacement (21 for mitral regurgitation and 8 for mitral stenosis); of these, 28 had substantial TR without tricuspid stenosis. The mean right atrial pressure was abnormally high in every patient (average 11 mm Hg); 25 had severe pulmonary hypertension (average systolic pressure 75 mm Hg). At the time of MV replacement, 25 patients had no operative procedure on the TV, and 3 had a TV annuloplasty. Four patients (14%) died, a rate similar to that in the patients without TR. Twenty-four patients were reassessed at 1 to 4 years (average 30 months) post-procedure. These evidenced symptomatic and hemodynamic improvement, with mean right atrial pressures averaging 5 mm Hg and systolic pulmonary arterial pressures averaging 39 mm Hg.
The investigators concluded that many patients with advanced MV disease could be expected to develop functional TR and that in such patients, TR will improve or disappear after MV surgery, generally precluding the need for TV replacement. However, by current standards, the number of study subjects and the number of outcome events is quite small and may not be acceptable for conclusions about the current implications of post-procedure TR. A reassessment of this issue in the era of “big data” would be appropriate.
Furthermore, once the criteria for TV therapy are determined, a remedial technique must be selected. Many repair techniques currently exist. No consensus has been reached concerning valve ring selection, suture positioning, and so on, nor regarding prosthesis selection when repair cannot be achieved. Annuloplasty rings for repair of the TV were developed and ultimately were shown to minimize the rate of recurrent TR compared with suture annuloplasty alone (4), but valve prostheses specific for the TV were not developed; devices intended for the MV or aortic valve were applied to the TV. However, the TV and MV have some important structural differences, including that the TV is far larger than the MV, comprises 3 rather than 2 leaflets, each leaflet is tethered to a single papillary muscle (though multiple papillary muscles may be present), and the TV manifests a relatively large fibrous annulus that is fixed at the septal origin and can expand at the free wall, distorting the shape and orientation of the TV.
The development of catheter-based replacement and repair techniques for the MV soon led to assessment of parallel methods for the TV. Initial efforts involved placement of devices meant for transcutaneous aortic valve replacement (TAVR) into the 2 venae cavae, catheter-based plication of the TV annulus, and application of the MitraClip device (Abbott Vascular, Santa Clara, California). The first successful transcatheter TV repair (which included annuloplasty plication) was reported 6 years ago (5). However, as yet, none of the reported approaches has generated a consensus about the most appropriate method for TV repair or the settings in which specific approaches should predominate. To aid in these determinations, the TriValve registry was initiated, comprising catheter-based TV repair efforts in 312 patients collected across 18 centers in 6 countries, from which interim results were reported late in 2018 (6). For purposes of the registry, procedural success was defined as survival at the end of the procedure with the device successfully implanted and delivery system retrieved, associated with ≤2+ residual TR; follow-up data were collected 1-month post-procedure and at data lock for the interim analysis. Most patients had been severely symptomatic at TV repair (95% were in New York Heart Association [NYHA] functional class III or IV) and systolic pulmonary artery pressure was only moderately abnormal (mean 41 ± 14.8 mm Hg). Eight different devices were used but the MitraClip predominated, implanted >7-fold more frequently than any other device. Importantly, one-third of the TV repairs were performed in conjunction with another catheter-based structural heart procedure (most often MV repair). Survival at 30 days was significantly better if procedural success had been achieved than if it was not (98.1% vs. 93.1%) and clinical improvement generally was observed within 6 months, with slightly more than one-half of patients having achieved NYHA functional class I or II by this time, again with better survival among those who had achieved procedural success. The authors of the report concluded, reasonably, that catheter-based TV repair in severely ill patients with otherwise limited options is feasible with several different technologies. However, data were far too few to suggest a preferred approach; more information is needed. Another reasonable conclusion is that more devices would be preferable.
In this context, the paper by Nickenig et al. (6) in this issue of the Journal reporting the 6-month outcomes of 30 patients with TR undergoing Cardioband TR reconstruction as part of the TRI-REPAIR study is an important addition to current knowledge. In this experience with a very severely ill population, mortality was 10% at 6 months post-procedure despite 100% procedural success, significant reduction in annular size, and improvement in heart failure symptoms and exercise capacity. Clearly more information is needed. As TR becomes ever more prevalent, and its predictive value for late outcomes increases, a basis for selection of preventive countermeasures is more urgently required.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Dr. Borer has served as a consultant for Takeda, Novartis, AstraZeneca, BioMarin, GlaxoSmithKline, Servier, ECG, and CellAegis.
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