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.