Risk factors for postoperative recurrent tricuspid regurgitation after concomitant tricuspid annuloplasty during left heart surgery and the association between tricuspid annular circumference and secondary tricuspid regurgitation

Background To identify the association between tricuspid annular circumference and secondary tricuspid regurgitation and analyze the risk factors of recurrent tricuspid regurgitation after concomitant tricuspid annuloplasty during left heart surgery. Methods From October 2018 to June 2019, a total of 117 patients receiving concomitant tricuspid annuloplasty within left heart surgery were enrolled. Severity of tricuspid regurgitation was classified as 4 subtypes: normal, mild, moderate and severe. Perioperative data and mid-term outcome were collected. Tricuspid annular circumference (TAC) was measured under cardiac arrest during surgery procedure by cardioplegia. Optimal TAC and TAC index (TAC/body surface area, BSA) cutoffs of significant tricuspid annulus dilatation (moderate and severe) were obtained. Univariable and multivariable logistic regression analyses were performed to identify the risk factors of postoperative recurrent tricuspid regurgitation. The follow up period is 13–19 months (mean 15.5 ± 3.2 months). Results There was 1 patient was excluded who died after surgery. A total of 116 patients receiving tricuspid annuloplasty were included. Optimal cutoffs of significant tricuspid annulus dilatation were recommended (TAC 11.45 cm, Sensitivity 82.89%, Specificity 73.68%, AUC 0.915; TAC index 7.09 cm/m2, Sensitivity 73.68%, Specificity 85%, AUC 0.825, respectively). Based on findings of multivariable logistic regression, it has been showed that TAC index and postoperative atrial fibrillation were the independent risk factors of recurrent regurgitation after surgery. Optimal TAC index cutoff to predict recurrent tricuspid regurgitation was 7.86 cm/m2 Conclusions The severity of secondary tricuspid regurgitation is associated with the tricuspid annular circumference. The cut-offs of significant tricuspid regurgitation (more than moderate) were TAC 11.45 cm and TAC index 7.09 cm/m2, respectively. Clinically, concomitant tricuspid annuloplasty is relative safe and effective. TAC index ≥ 7.86 cm/m2 and postoperative atrial fibrillation are the risk factors of recurrent significant tricuspid regurgitation after concomitant tricuspid annuloplasty during left heart surgery.

Total root remodelling by the Sleeve technique for aortic regurgitation in patients with repaired tetralogy of Fallot

We report the case of a 15-year-old male patient who had developed aortic regurgitation primarily because of aortic annulus dilatation late after definitive repair of tetralogy of Fallot. Valsalva sinus dilatation was not remarkable enough for root replacement. For the purpose of total root remodelling, the Sleeve procedure was employed. This procedure not only reduced the root diameters but also augmented commissure heights. With concomitant non-coronary cusp plication, aortic regurgitation was effectively controlled. Thus, the Sleeve technique may be a preferable option for patients who develop aortic regurgitation, due to dilatation of the annulus or sinotubular junction without significant dilatation of the sinus of Valsalva, after congenital heart surgery.

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction

Progressive superior shift of the mitral valve (MV) during systole is associated with abnormal papillary muscle (PM) superior shift in late systolic MV prolapse (MVP). The causal relation of these superior shifts remains unclarified. We hypothesized that the MV superior shift is related to augmented MV superiorly pushing force by systolic left ventricular pressure due to MV annular dilatation, which can be corrected by surgical MV plasty, leading to postoperative disappearance of these superior shifts. In 35 controls, 28 patients with holosystolic MVP, and 28 patients with late systolic MVP, the MV coaptation depth from the MV annulus was measured at early and late systole by two-dimensional echocardiography. The PM tip superior shift was monitored by echocardiographic speckle tracking. MV superiorly pushing force was obtained as MV annular area × (systolic blood pressure − 10). Measurements were repeated after MV plasty in 14 patients with late systolic MVP. Compared with controls and patients with holosystolic MVP, MV and PM superior shifts and MV superiorly pushing force were greater in patients with late systolic MVP [1.3 (0.5) vs. 0.9 (0.6) vs. 3.9 (1.0) mm/m2, 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m2, and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm2·m−2, respectively, means (SD), P < 0.001]. MV superior shift was correlated with PM superior shift ( P < 0.001), which was further related to augmented MV superiorly pushing force ( P < 0.001). MV and PM superior shift disappeared after surgical MV plasty for late systolic MVP. These data suggest that MV annulus dilatation augmenting MV superiorly pushing force may promote secondary superior shift of the MV (equal to late systolic MVP) that causes subvalvular PM traction in patients with late systolic MVP. NEW & NOTEWORTHY Late systolic mitral valve prolapse (MVP) is associated with mitral valve (MV) and papillary muscle (PM) abnormal superior shifts during systole, but the causal relation remains unclarified. MV and PM superior shifts were correlated with augmented MV superiorly pushing force by annular dilatation and disappeared after surgical MV plasty with annulus size and MV superiorly pushing force reduction. This suggests that MV annulus dilatation may promote secondary superior shifts of the MV (late systolic MVP) that cause subvalvular PM traction.

Tricuspid Valve Annulus Tension

Functional tricuspid regurgitation is a direct outcome of right ventricular dilatation and tricuspid annulus dilatation. The mechanism underlying functional tricuspid regurgitation is believed to be multifactorial and related to abnormalities in right ventricular volume, function and shape. Changes in the right ventricle geometry may lead to alterations in the positions of the papillary muscles (PM) of the tricuspid valve (TV). PM displacement happens in right ventricular dilatation but its correlation with tricuspid annulus dilatation is still unknown. The unique structure and orientation of tricuspid PM has role to play in TV annulus mechanics and right ventricular mechanics (Fig.1). It has been already shown that annulus tension (AT) is a parameter to evaluate left ventricular function that, previously, was evaluated via the left ventricular geometry and pressure [1–3].

Mitral Valve Annulus Tension

The mitral valve annulus is an anatomical structure joining the leaflets and left ventricle wall. It is divided into the fibrous annulus in the anteromedial section and the myocardium annulus in the posterolateral section, according to annulus histology. Two trigones are in the fibrous annulus. Mitral annulus supports leaflets in the valve coaptation and controls inflow hemodynamics during a cardiac cycle. When the mitral valve is fully open during diastole, inflow drag force on the leaflets and chordae pulls the leaflets approximately apically. As mitral valve leaflets coaptate during systole, trans-mitral pressure acts on the leaflets and induces leaflet tension which is transferred to the annulus and chordae. The leaflet tension at the annulus per unit length is defined as annulus tension (AT). Annulus dilatation is a mitral valve pathology that is related to AT and its interaction with the myocardium. Little is known about the detailed mechanism of annulus dilatation. But from mechanics standpoint, there are two possible mechanisms that change annulus size. AT pulls annulus towards the center of mitral valve orifice and is balanced by myocardium force on the annulus that pulls the annulus outward. Annulus size depends upon which force is predominant in annulus mechanics. It is hypothesized that the AT is one of the important mechanism to control annulus size. This hypothesis suggests that annulus size can be controlled by the AT and its interaction with the myocardium. We aim to understand annulus dilatation by the AT. The objective of the current study was to understand the tension transferred to the mitral annulus by the leaflets during the valve coaptation.

Aberrant tendinous chords with tethering of the tricuspid leaflets: a congenital anomaly causing severe tricuspid regurgitation

Objective: To define the entity of tricuspid regurgitation caused by tethering of the tricuspid valve leaflets by aberrant tendinous chords.Design: Retrospective study.Setting: Tertiary care centre (university teaching hospital).Patients: 10 patients with unexplained severe tricuspid regurgitation.Methods: The last 13 500 echocardiographic studies from our facility were reviewed to identify patients with severe unexplained tricuspid regurgitation. Tethering was defined by the presence of aberrant tendinous chords to the tricuspid valve leaflets limiting the mobility of the tricuspid leaflet and resulting in incomplete coaptation and apical displacement of the regurgitant jet origin. Aberrant tendinous chords were defined as those inserting at the clear zone of the tricuspid leaflet and not originating from the papillary muscle. Patients fulfilling the diagnostic criteria for Ebstein’s anomaly were excluded.Results: 10 patients with aberrant tendinous chords tethering one or more tricuspid valve leaflets were identified. There were short non-aberrant tendinous chords in seven patients, five of whom also had right ventricular or tricuspid annulus dilatation.Conclusions: Tethering of the tricuspid valve leaflets by aberrant tendinous chords can be the sole mechanism of congenital tricuspid regurgitation. It is often associated with short non-aberrant tendinous chords, which may develop secondary to right ventricular or tricuspid annulus dilatation. Awareness of tethering as a cause of tricuspid regurgitation may be important in planning reconstructive surgery.