Most tricuspid regurgitation (TR) is secondary to overload caused by left-sided heart disease or by lung disease. Causes of primary TR include blunt trauma such as might occur in a motor vehicle accident, direct trauma from errant myocardial biopsies, carcinoid syndrome (or use of drugs with serotonin similarities), rheumatic heart disease, infective endocarditis, and interference from transvalvular pacing electrodes.
The general rule for treating secondary TR is to optimize therapy for the primary cause. Thus, if left-sided heart failure has resulted in pulmonary hypertension with adverse effects on the right ventricle, treatment of heart failure will reduce pulmonary pressure and improve secondary TR. Or, if lung disease has created cor pulmonale, therapy to improve pulmonary function is apt. However, this rule may be inappropriate when secondary TR is caused by left-sided valve lesions. Although it has long been hoped that correction of the hemodynamic overload produced by mitral or aortic valve disease would improve secondary TR, the results are unpredictable, with TR sometimes improving, sometimes worsening, and sometimes even arising de novo following left-sided valve surgery.3,4,5,6,7,8 Although there is general agreement that severe TR, irrespective of its cause, should be addressed during surgery for left-sided disease, the approach to less than severe secondary TR is the subject of intense controversy. If leaving moderate TR uncorrected results in worsening rather than improvement in TR following successful left-sided surgery, the patient is then consigned either to the consequences of right-sided heart failure, despite the correction of the primary valve lesion, or to a second operation to address the residual TR, which has had an unusually variable and sometimes high mortality in reports of small series.3,9,10 The variable response of TR to correction of left-sided valve disease is in part related to the causes and effects of the left-sided disease and its correction. As noted in other chapters, if the left-sided disease is secondary mitral regurgitation, left ventricular (LV) dysfunction is almost surely present and is not addressed by mitral surgery, serving as a cause for persistently elevated left- and right-sided chamber pressures, perpetuating TR. Even if pulmonary pressure is reduced by left-sided surgery, left sided cardiac output may be improved in turn increasing right ventricular (RV) volume load.
As shown in Fig. 54–1, the severity of TR (90% of which was secondary) impacted survival in one study. This was true even in the absence of pulmonary hypertension and even when LV ejection fraction was normal.11 Thus, it would seem logical that preventing TR following left-sided surgery would improve mortality; however, this contention is unproven.
Survival according to the severity of tricuspid regurgitation (TR). Reproduced with permission from Nath J, Foster E, Heidenreich PA: Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004 Feb 4;43(3):405-409.
Outcomes of TR Correction During Left-Sided Surgery
It seems clear that tricuspid intervention during left-sided surgery reduces postoperative TR and RV dilatation. However, it has been difficult to show that TR surgery reduces mortality (Table 54–1),7,12,13,14,15,16,17,18,19 although lack of mortality benefit might be predicated on surgery that was performed for secondary MR that inherently has a poor prognosis, or from retrospective series that were not designed to detect a mortality difference.
TABLE 54–1.Comparison of Surgery vs No Surgery for Secondary Tricuspid Regurgitation ||Download (.pdf) TABLE 54–1. Comparison of Surgery vs No Surgery for Secondary Tricuspid Regurgitation
|Author ||Study Type ||Left Op ||Indication for TR Op ||No. TR Op ||No. TR Op ||Results |
|Dreyfus7 ||R, NR ||MV Repair ||Annular size >70 mm ||148 ||163 || |
TR annuloplasty group lower NYHA 1.59 to 1.11.
TR increased by 2 grades in 48% of No TR Op group vs 2% in the Op group.
|Chan12 || |
|≥ +2 TR ||125 ||106 || |
Similar survival: Less HF in the repair group.
8% of pts with repair had worsened TR vs 17% who had no repair.
|Calafiore13 ||R NR ||2° MR ||≥ +2 TR ||51 ||59 ||Adjusted 5-year survival 75% in the treated group vs 45% in the untreated group, although crude survival similar. Progression of TR 5% in the treated group vs 40% in the untreated group. |
|Navia14 ||R, PM ||Multiple ||+2 TR ||91 ||91 ||7% 3-4 + TR in repair group vs 15% in the untreated group. |
|Kim15 ||R, NR ||236 ||≤ +2 ||123 ||113 ||No diff in mortality or HF at 5 years; freedom of severe TR 93% repair vs 61% no repair. |
|Chikwe16 ||R, NR ||645 primary MR ||Annular enlargement vs no indication ||413 ||232 ||No diff in mortality or pacemaker, less late moderate TR in the treatment group and faster return to normal RV function. |
|Benedetto17 ||RCT ||44 mitral surgery ||≤ +2 TR ||22 ||22 ||Moderate to severe TR 28% in untreated vs 0% treated group at 1 year! Greater improvement in 6-minute walk in treated group. |
|Yilmaz18 ||R, NR || |
|None ||0 ||699 ||TR progression post-op very rare and only 1 patient required re-op but 1/3 had at least moderate post-op TR. |
|Kusajima19 ||R, NR ||96 || |
|47 ||96 ||TR decreased early but increased late in patients without TVS. At 10 years, no patients with TVS had ≥ +3 TR vs 53.3% without TVS. |
Although tricuspid repair reduces postoperative heart failure and TR, it has increased the risk of postoperative conduction abnormalities, requiring permanent pacemaker implantation in some but not all reports.16,20
In summary, severe primary and secondary TR is usually corrected during left-sided valve surgery. Most,7,12,13,14,15,16,17 but not all,18 data support addressing less than severe TR during left-sided valve surgery. TR is corrected because of unpredictable changes in TR after successful correction of mitral and aortic lesions and for the fear of residual postoperative right-sided heart failure. It is most probably this concern that is driving an increased rate of tricuspid surgery in the United States today.21