Discussion
This retrospective study confirms that TA besides left-sided valve surgery has still suboptimal results, with residual TR of 13%, within the range reported in the literature (9-39%)10-14. In our series, 20% of cases experienced TR recurrence at mid-term, lower than others (31-45%)10,14,15. However, the rate of late TA failure increased significantly in patients discharged with residual TR. Kuwaki et al11 reported an hazard ratio of even 15.1% TV reoperation in patients with residual TR.
In patients without residual TR at the discharge, preoperative severity of TR and TV remodeling, preoperative RV remodeling, functional MR and systolic pulmonary pressure were identified as risk factors for moderate-or-more late TR.
As expected11,14-16, preoperative severe TR was found to be an important predictor for TR recurrence. Although TA can effectively reduce annular dimension, it further increases chordal tethering with aggravation of leaflet tenting as a consequence of increased interpapillary muscle distance and incomplete leaflet closure due to inward annulus displacement after TA, ultimately leading to TA failure.
Nowadays surgery is indicated in patients with severe TR and should be considered in patients with mild-or-moderate TR with a TA≥40m17. However, besides TA dilatation, tethering severity plays a key-role for TA durability. Fukuda et al15 proposed a tenting height of 5.1 mm and a tenting area>0.8 cm2 as predictors for TV recurrence. In our study, a CD≥6.5mm, tenting area≥0.85cm2 and a tricuspid annulus≥35mm were predictive for recurrent TR even in presence of moderate-or-less TR. This result supports the rationale for performing prophylactic TA in low-graded TR with TV remodeling, since TA does not increase operative risk18. Shiran et al19 suggested to perform TA for low-graded TR and tricuspid annulus≥35mm. We believe that TA size alone cannot be used to identify patients who should receive prophylactic TA, but tethering severity should also be considered.
The purpose of surgery should be to interfere with the mechanisms leading to irreversible RV damage by correcting both left-sided lesions (to reduce pulmonary pressure) and TR (to eliminate volume overload)20,21.
The main finding of this study is the strict correlation between the evolution of TA and RV remodeling. Risk factors impairing late result of TA are the same impairing late RV remodeling, demonstrating a synergistic relationship between these two entities. Failure of TA causes increased volume overload with possible RV dilatation and dysfunction, which in turn begets TR. The patients with preoperative severe-or-less TR with TA dilatation can show positive RV remodeling after TA21. However, in some cases, RV remodeling after TA12 is not so positive as expected, likely due to irreversible maladaptive RV hypertrophy/enlargement with reduced RV contractility. RV enlargement can result in disproportionate dilatation along the free wall to the septum minor axis and a more spherical RV shape, which implies a greater displacement of the papillary muscles22. Yu and coworkers22demonstrated that patients undergoing TA who had a larger RV mid-cavity diameter along with larger TV tethering area, developed adverse events at 1-year follow up. So, TA may not be able to approximate displaced papillary muscle to achieve an effective TV closure.
Moreover, both late significant TR and RV remodeling were found to be risk factors for lower survival. In a recent echocardiographic analysis23, 5-year survival was significantly worse in patients presenting RV dilatation or dysfunction than normal RV.
How much preoperative pulmonary pressure can be improved by TA is still debated. Chickwe et al24 analyzed results of 419 patients receiving TA along with MV repair, showing sPAP improved significantly at discharge and follow-up. Conversely, Chen et al25 demonstrated that 43% of patients undergoing TA had residual PH; De Bonis et al26 reported 26% of patients has still higher sPAP at follow up. In patients having MV surgery, residual PH is likely due to irreversible pulmonary vascular remodeling, and this barrage can produce both RV remodeling and TR recurrence over time27.
In our experience, patients with FMR undergoing MV/ TV surgery showed more dilated and dysfunctioning LV than no-FMR, with higher sPAP. The underlying disease of FMR is both valvular and ventricular, so, despite surgical correction of MV, LV remodeling may not improve. Higher intraventricular end-diastolic pressure may persist after surgery, with consequent high post-capillary pulmonary pressure.26Moreover, most of the effects of LV contraction on the RV are mediated by the interventricular septum. In presence of cardiomyopathy, septal twisting is reduced due to septal damage, especially when pulmonary vascular resistances are increased.
The natural consequence is that RV remodeling may not improve, with increasing of tethering forces on TV leaflets and the inability to coapt despite TA.
Whether the surgical technique could influence TR recurrence remains debated27-30 . In our experience, no difference was observed according to the surgical strategy.
Patients with severe TR and dilated RV represent a challenging subgroup where TA id not a reasonable treatment option. The clover technique31 or anterior leaflet patch augmentation32, may be valuable alternatives. We recently reported a strategy where the anterior and posterior leaflets are almost entirely detached (50% of the annulus) and a patch as large as the full tricuspid orifice is inserted without TA33. It is however evident that there is no definite solution yet to this problem, and perhaps it is time to think to a prospective randomized study to find the best treatment option.