Mechanism Of Tricuspid Regurgitation Research Articles

Insights of tricuspid regurgitation mechanisms in patients with right ventricular apical pacing by three-dimensional echocardiography.

Device lead-induced tricuspid regurgitation (LITR) mechanisms are well-defined by 3D transthoracic echocardiography (3D-TTE). There is a lack of data on the Latin-American population. The objective of this study was to describe the prevalence of several mechanisms and insights in patients with permanent right ventricular (RV) implanted devices by 3D-TTE examination. We performed a cross-sectional analysis of 101 patients with permanent cardiac devices such as pacemakers or defibrillators. 3D-TTE was obtained on all patients in RV-focused apical views to perform a complete tricuspid valve (TV) evaluation: leaflets, subvalvular apparatus, precise lead location, and functional assessment to evaluate possible mechanisms of tricuspid regurgitation (TR). In a total of 101 patients, the leads did not interfere with TV function in 53 p. (59%), while LITR was observed in 38 (41%) patients. Adherent, impinging, entangled, and mixed lead-induced mechanisms were observed. Time in years since device implantation was significantly higher in patients with LITR. LITR was present in a high proportion of our population. LITR is the result of damage to the TV as well as its subvalvular apparatus due to the fibrotic and inflammatory response over time when leads are situated in unfavorable locations.

3D-Echocardiography in the assessment of lead-induced tricuspid regurgitation

Abstract Background Lead-induced tricuspid regurgitation (LITR) is caused by several mechanisms that can be assessed by 3D-Echocardiography (3DE). Its prevalence was not studied to date in the Latin-American series. Purpose To determine prevalence and mechanisms of LITR in a series of patients with permanent cardiac devices by 3DE. Methods We perform a cross-sectional analysis of 101 patients with permanent cardiac devices as pacemakers or defibrillators. Transthoracic 3DE was obtained on all patients in RV-focused apical views to perform a complete tricuspid valve leaflets, subvalvular apparatus, lead placement and functional assessment to evaluate possible mechanisms of tricuspid regurgitation. Results Of a total of 101 patients, lead visualization was possible in 88%. In 59% lead was in commissural position and did not interfere with tricuspid leaflet mobility. Nevertheless, in 41% LITR was observed by several mechanisms. Leaflet impingement was the most prevalent cause in 30,7% causing valve leaflet interference and organic damage. Catheter adherence and/or entrapment to the leaflet or the tricuspid subvalvular apparatus was present in 10.3%. Two patients seem to have leaflet perforation by the catheter as the main mechanism; however, a further assessment was not possible. Patients with LITR had higher time since catheter implantation, lower left ventricular ejection fraction, more severity of tricuspid regurgitation, and right ventricular dilatation. Conclusions 3DE enables to the identification of 41% of patients with LITR and leaflet impingement was the most prevalent mechanism. LITR patients had more time since cardiac device implantation. Some unfavorable catheter locations on the tricuspid valve can have some influence on the development of LITR over time. Funding Acknowledgement Type of funding sources: None.

Influence of Shunt Type on Survival and Right Heart Function after the Norwood Procedure for Aortic Atresia

The study objective was to compare the results after Norwood procedure between modified Blalock-Taussig shunt (MBTS) and right ventricle-to-pulmonary artery conduit (RVPAC) according to Sano in patients with hypoplastic left heart syndrome (HLHS) and aortic atresia (AA). A total of 146 neonates with HLHS and AA who underwent the Norwood procedure at our institution between 2001 and 2020 were divided into 2 groups according to shunt type (MBTS or RVPAC). Survival after the Norwood procedure was compared between the groups. Longitudinal right ventricular and tricuspid valve function in each group were evaluated using cubic splines method. RVPAC was performed in 103 patients and MBTS in 43 according to surgeon preference. There were no differences in the 30-day mortality rates (16.5% vs 16.3%, P =0.973). Survival at 0.5, 1 and 3 years was 79.6%, 74.6%, and 68.9% in RVPAC and 66.8%, 64.3%, and 58.5% in MBTS (P = 0.293). Among 23 patients undergoing tricuspid valve procedure, different mechanisms of tricuspid regurgitation were observed between the groups. Longitudinal analysis revealed greater prevalence of late right ventricular dysfunction in RVPAC patients. In 77 patients who completed Fontan procedure, the postoperative N-terminal pro B-type natriuretic peptide value was significantly higher in RVPAC vs MBTS (554 vs 276 ng/L, P = 0.007). No survival advantage of RVPAC over MBTS was observed in neonates with HLHS and AA undergoing the Norwood procedure. Longitudinal analysis demonstrated a greater prevalence of right ventricular dysfunction and higher N-terminal pro B-type natriuretic peptide values during late follow-up in patients with RVPAC.

TRI-SCORE: a new risk score for in-hospital mortality prediction after isolated tricuspid valve surgery.

Aims Isolated tricuspid valve surgery (ITVS) is considered to be a high-risk procedure, but in-hospital mortality is markedly variable. This study sought to develop a dedicated risk score model to predict the outcome of patients after ITVS for severe tricuspid regurgitation (TR).Methods and results All consecutive adult patients who underwent ITVS for severe non-congenital TR at 12 French centres between 2007 and 2017 were included. We identified 466 patients (60 ± 16 years, 49% female, functional TR in 49%). In-hospital mortality rate was 10%. We derived and internally validated a scoring system to predict in-hospital mortality using multivariable logistic regression and bootstrapping with 1000 re-samples. The final risk score ranged from 0 to 12 points and included eight parameters: age ≥70 years, New York Heart Association Class III–IV, right-sided heart failure signs, daily dose of furosemide ≥125 mg, glomerular filtration rate <30 mL/min, elevated bilirubin, left ventricular ejection fraction <60%, and moderate/severe right ventricular dysfunction. Tricuspid regurgitation mechanism was not an independent predictor of outcome. Observed and predicted in-hospital mortality rates increased from 0% to 60% and from 1% to 65%, respectively, as the score increased from 0 up to ≥9 points. Apparent and bias-corrected areas under the receiver operating characteristic curves were 0.81 and 0.75, respectively, much higher than the logistic EuroSCORE (0.67) or EuroSCORE II (0.63).Conclusion We propose TRI-SCORE as a dedicated risk score model based on eight easy to ascertain parameters to inform patients and physicians regarding the risk of ITVS and guide the clinical decision-making process of patients with severe TR, especially as transcatheter therapies are emerging (www.tri-score.com).

Imaging for transcatheter native tricuspid valve intervention: patient selection, procedural planning and interventional guidance.

There are an increasing number of transcatheter tricuspid valve interventions being performed worldwide using commercially available and investigational devices. Imaging in the pre-procedural and periprocedural period is essential for procedural and clinical success. Echocardiographic-based techniques are particularly important in these procedures, especially for interventional guidance. This review summarizes the current devices in use and how imaging is used for patient selection, procedural planning, and interventional guidance. The most commonly used method of transcatheter tricuspid intervention is edge-to-edge repair using the MitraClip or TriClip devices (Abbott, Santa Clara, CA, USA). Randomized controlled data is pending but observational studies have demonstrated success, especially in the setting of smaller coaptation gaps and adequate transesophageal imaging windows. Direct annuloplasty with the Cardioband (Edwards Lifesciences, Irvine, CA, USA) has also been used in many centers and has demonstrated success when the anatomy and mechanism of tricuspid regurgitation are appropriate for annuloplasty based on imaging evaluation. Lastly, transcatheter valve replacement is becoming more common using several investigational devices and relies heavily on imaging methods to achieve procedural success.

Tricuspid valve repair in children with hypoplastic left heart syndrome: impact of timing and mechanism on outcome.

Our aim was to evaluate the results of tricuspid valve repair (TVr) in patients with hypoplastic left heart syndrome during staged reconstruction, focussing on the timing of the repair and the mechanisms of tricuspid regurgitation (TR). Records of 44 children with hypoplastic left heart syndrome who underwent a total of 62 tricuspid valve (TV) procedures during staged reconstruction were retrospectively analysed. TVr was performed before stage II in 4 (9%) patients, at stage II in 23 (52%) patients, between stages II and III in 3 (7%) patients and at stage III in 14 (32%) patients. The median age at the first TV procedure was 5 months. At surgery, TR emanated commonly from the anteroseptal commissure in 21 (48%) patients. Anterior leaflet prolapse was observed most frequently (n = 23; 52%), followed by septal leaflet restriction (n = 22; 50%), dilated annulus (n = 21; 48%) and cleft anterior leaflet (n = 9; 21%). Surgical techniques included commissuroplasty in 27 (61.4%) patients, leaflet adaptation in 20 (44%) patients, partial annuloplasty in 11 (25%) patients, chordal reconstruction in 10 (23%) patients and cleft closure in 10 (23%) patients. Among all 44 patients, 27 (61%) patients had preoperative grade III TR and 17 (39%) patients had grade IV; postoperatively, there were no patients with grade IV, 25 patients with grade III (57%), 10 patients with grade II (23%) and 6 patients with grade I (14%). Fifteen patients required redo TV surgeries. Reoperation-free survival was 52% at 5 years. Lower weight at initial TVr predicted mortality [hazard ratio (HR) 0.7, P = 0.044] and reoperation (HR 0.8, P = 0.015). TVr before stage II was a risk for both reoperation (HR 5.5, P = 0.042) and TV replacement (HR 36.9, P = 0.013). Among morphological factors, septal leaflet restriction was a risk for reoperation (HR 4.7, P = 0.017) and anterior (HR 4.7, P = 0.037) and posterior (HR 7.3, P = 0.015) leaflet chordal anomaly for TV replacement. Anterior leaflet prolapse and septal leaflet restriction are the main mechanisms of TR in hypoplastic left heart syndrome. Early-onset TR before stage II predicts worse outcome. Refinements to repair techniques in early infancy, especially for septal leaflet restrictions and chordal anomalies, are mandatory to improve outcomes.

Reoperation for isolated rheumatic tricuspid regurgitation

BackgroundThe reoperation for isolated tricuspid regurgitation in rheumatic population is rare and still unclear and controversial because of the rarity of publications. The aim of this study was to analyze short and long-term results and outcome of tricuspid valve surgery after left-sided valve surgery in rheumatic patients.MethodsTwenty six consecutive rheumatic patients who underwent isolated tricuspid valve surgery after left-sided valve surgery between January 2000 and January2017 were retrospectively registered in the study. The mean age was 48.2 ± 8.6 years with 8.3% as sex-ratio (M/F). EuroSCORE was 6.1 ± 5 (range 2.5 to 24.1). The mechanism of tricuspid regurgitation was functional and organic in respectively 14 (53.8%) and 12 cases (46.2%). Ten patients (38.5%) had previous tricuspid valve repair. Surgery consisted of 15 ring annuloplasty and 11 tricuspid valve replacement (5 bioprostheses and 6 mechanical prostheses). Follow-up was 96.1% complete, with a mean follow-up of 55.6 ± 38.8 months (range 1 to 165).ResultsThe operative mortality rate was 15.4% (n = 4) and the cumulative survival at 1, 5 and 10 years was respectively 80% ± 8%, 75.6% ± 8.7% and 67.2% ± 11.1% with no significant difference at 8 years between tricuspid valve replacement (80% ± 12.6%) and repair (57.6% ± 16.1%) (p = 0.5). Multivariable Cox regression analysis revealed that ascites (HR, 5.8; p = 0.01), and right ventricular dysfunction (HR, 0.94; p = 0.001) were predictors of major adverse cardiac events. There were no recurrence of tricuspid regurgitation and no structural or non-structural deterioration of valvular prostheses.ConclusionThe reoperation of rheumatic tricuspid regurgitation should be considered before the installation of complications such as right ventricular dysfunction and major signs of right heart failure. Despite the superiority of repair techniques, tricuspid valve replacement should not be banished.

The tricuspid valve and the right heart: anatomical, pathological and imaging specifications.

Transcatheter tricuspid valve repair/replacement is an emerging therapy for patients with symptomatic severe tricuspid regurgitation who are deemed inoperable. Accurate knowledge of the anatomy of the tricuspid valve and right ventricle is key to developing transcatheter techniques. In addition, it is important to understand the mechanistic concept of transcatheter tricuspid valve repair/replacement in order to select the patients who may benefit from it. The severity and mechanism of tricuspid regurgitation, right ventricular function, dimensions of the caval veins and the course of the right coronary artery in relation to the atrioventricular groove are important aspects to be evaluated before embarking on these procedures. The present article reviews current advances in transcatheter approaches for significant tricuspid regurgitation and the role of imaging modalities to characterise the anatomy of the tricuspid valve and right ventricle as well as the underlying pathophysiology of tricuspid regurgitation.

The various mechanisms of tricuspid regurgitation in patients with right ventricular leads: a case series.

The various mechanisms of tricuspid regurgitation in patients with right ventricular leads: a case series.

Incomplete leaflet coaptation and tricuspid regurgitation mechanism in right ventricular Tako-Tsubo cardiomyopathy

Tako-Tsubo cardiomyopathy (TTC) is a well-known form of acuteand reversible heart failure due to either an emotional or a physicalstressor,whichinvolvesmainlytheleftventriclewithatypicalechocar-diographic pattern (apical ballooningand basal hyperkinesis) [1].Rightventricular(RV)involvementhasaprevalenceof25%[2].Aclinicalcase,a short literature review and possible explaining mechanism areprovided.An86-yearoldwoman,withoutcardiovascularriskfactorsandwithhistory of bipolardisorder [3] cameto the emergency department afteran episode of syncope. At admission blood pressure was 70/50 mm Hg,ECG showed atrial fibrillation and ST-elevation in anterior and lateralleads (V2–V4, DI, aVL) (Fig. 1). Troponin I levels were increased(4.54 ng/ml, n.v. b 0.10). Trans-thoracic echocardiogram showed leftventricular (LV) systolic dysfunction (ejection fraction of 25%),akinesisofLVmidventricularsegments,dyskinesisofRVapicalsegmentsandin-complete coaptation of tricuspid leaflets (Video 1). At color-Dopplermild mitral regurgitation and severe tricuspid regurgitation werefound (Figs. 2 and 3, Video 2). Coronary angiography showed diffuseatherosclerosis not needing coronary intervention. Echocardiographyanomalies gradually recovered and the patient was discharged after acouple of weeks (Figs. 4 and 5) (Video 3). Discharge electrocardiogramshowed negative T-waves in anterior leads previously interested byST-elevation and diffuse decrease in QRS amplitude [4].Despite TTC affects mainly left ventricle, RV involvement is presentinoneoutoffourpatientsaffectedbyTTC.Severalechocardiographicstudies described acute mitral regurgitation and its clinical impor-tance in TTC[5], but, to the best of our knowledge, possible mecha-nism of tricuspid regurgitationduring RV TTC was never describedbefore.We report a case of RV apical dyskinesis causing traction of thepostero-lateral papillary muscle and consequent compromised coapta-tion of thetricuspid valve leaflets (Fig. 2);that could have led to severetricuspid regurgitation completely reversible after RV recovery.The mechanism of RV regurgitation seems to be different from thatwe have previously described in the left ventricle. LV basal hyperkinesis, consequent mitral valve area reduction and mitral leafletsredundancy may lead to LV outflow tract obstruction, increased intraventricular pressure and mitral regurgitation [6,7]. Systolic anteriormotion and tethering have been shown as independent predictors ofacute mitral regurgitation in patients with TTC [8].In thecaseof mid-LVballooning, rightward movement of midseptalsegmentsmayhaveincreasedRVpressure,thusimpairingRVgeometryand kinesis, and precipitating RV ballooning.Tricuspid regurgitation has not yet been evaluated as a marker ofprognosisinTTC;however,inacutemyocardialinfarctionoftheinferiorwall, moderate tricuspid regurgitation, affecting about one third ofpatients, is a predictor of rehospitalization at one-year follow-up [9].Although no in-hospital complication was present in our case, RVsystolic dysfunction represents an independent predictor of worseprognosis and is associated with a higher rate of in-hospital complica-tion both in inferior myocardial infarction [10] and TTC [2].Haghiet al. found in 34 patients with TTC that RV involvement is associatedwith a severe impairment in LV systolic function and a higher rate ofbilateral pleural effusion [2]. Elesber et al. showed in a population of30patientswithTTCthatRVinvolvementcarriesahigherriskofseverecongestive heart failure and longer in-hospital stay [11].We therefore believe that a systematic evaluation of RV function byechocardiogram is recommended for an optimal management of pa-tients with TTC. When an impaired LVEF is associated with abnormalRV function, there is a higher risk of hemodynamic complications.Therefore a strict monitoring is required and an early therapeuticstrategy including diuretics, levosimendan infusion and intra-aorticballoon pump counterpulsation should be considered [12–14].In conclusion, RV involvement in TTC may lead to severe tricuspidregurgitationduetoincompletecoaptationofvalveleaflets.This finding

Mechanisms of tricuspid regurgitation in patients with hypoplastic left heart syndrome undergoing tricuspid valvuloplasty

Tricuspid regurgitation (TR) remains a risk factor for morbidity and mortality through staged palliation in patients with hypoplastic left heart syndrome (HLHS). Reports on the mechanisms associated with TR in patients with HLHS are limited. Thus, we sought to describe our experience with tricuspid valve (TV) repair in these patients, focusing on the mechanisms of TR and corresponding surgical techniques. We performed a retrospective single-center review (January 2000 to December 2012) of patients with HLHS undergoing TV repair and completing Fontan circulation. We evaluated the pre- and postoperative echocardiograms, intraoperative findings, and surgical techniques used. A total of 53 TV repairs were performed in 35 patients with HLHS completing staged palliation. TV repairs were performed at stage II in 15, between stage II and III in 4, at stage III in 27, and after stage III in 7. The surgical techniques for valvuloplasty included annuloplasty (38%), anteroseptal (AS) commissuroplasty (66%), anterior papillary muscle repositioning (11%), multiple commissuroplasties (9%), septal-posterior commissuroplasty (9%), and fenestration closure (4%). The predominant jet of TR emanated along the AS commissure in 68% of the cases. All patients survived the procedure and were discharged. Preoperative echocardiography showed a dilated TV annulus on the lateral dimension, anteroposterior dimension, and area that was significantly reduced after TV repair (P < .0001). The preoperative mean TR, as assessed by lateral (P = .002) and anteroposterior (P = .005) vena contracta, was also significantly reduced after TV repair. TV repair did not significantly affect right ventricular systolic function immediately after surgery (P = .17) or at the most recent follow-up visit (P = .52). Patients with anterior leaflet prolapse were at increased risk of worse outcomes, including moderate or greater right ventricular dysfunction (P = .02). Patients requiring reoperation for TV repair were younger (6.3 vs 28.1 months, P < .0001) at the initial operation. One patient died of heart failure. Freedom from TV replacement and transplant-free survival were both 97% at the most recent follow-up point. TR in patients with HLHS commonly emanates from the AS commissure. The associated mechanisms are often annular dilatation and anterior leaflet prolapse. Preoperative anterior leaflet prolapse was associated with worse outcomes. Annuloplasty, closure of the AS commissure, and repositioning of the anterior papillary muscle are effective in addressing TR in the short- and mid-term in this challenging population.

Mechanism of tricuspid regurgitation in corrected transposition of great arteries.

The morphologic tricuspid valve in congenitally corrected transposition (C-TGA) exhibits some abnormality in the majority of cases [1]. Clinically significant tricuspid regurgitation has been reported to occur in 20–50% of patients with C-TGA and was found to be the single most important factor associated with poor outcome [2]. The most common and important underlying pathology is dysplasia of the valve with or without displacement of the septal or posterior leaflet of the tricuspid valve [1]. The tricuspid valve function is dependent on the loading condition of both the ventricles and on septal geometry [3]. The septal shift makes a significant contribution to the development of tricuspid regurgitation in these hearts. Conversely, efforts to modify this septal shift can produce profound improvements in the degree of tricuspid incompetence. Reduction of tricuspid regurgitation and a remarkable change in left atrial size can occur as a consequence of pulmonary artery banding [4]. Case

Optimal Surgical Management of Severe Tricuspid Regurgitation in Cardiac Transplant Patients

Severe tricuspid regurgitation (TR) with signs of right-sided heart failure is rare after orthotopic heart transplantation (OHT). In some instances, this condition will require surgical correction using reconstructive surgery or prosthetic valve replacement. Repair techniques of atrioventricular valves are now well described. However, the results of the different surgical procedures in this setting have not been widely reported and may depend on the type of valvular dysfunction and lesions present. Herein we report our experience in a group of patients requiring surgical correction of symptomatic severe TR after OHT. We reviewed our transplant experience during the period from July 1992 to July 1999 (n = 138 cardiac transplants). Eight patients (5.8%) developed symptomatic severe TR requiring surgical correction after a mean duration of 21 months after OHT. Patients were divided into 2 groups based on the mechanism of regurgitation using Carpentier's functional classification. In Group 1 (n = 4), the mechanism of tricuspid regurgitation was Carpentier's Type I, secondary to annular dilation. In Group 2 (n = 4) the mechanism of TR was leaflet prolapse (Type II), due to chordal rupture after biopsy injury. Initially, tricuspid valve integrity was surgically restored in all 8 patients with either valve repair (n = 6) or replacement (n = 2). In Group 1, 2 patients underwent valve repair using a ring annuloplasty and 2 patients underwent valve replacement with a bioprosthetic valve (n = 1) or pulmonary allograft (n = 1). In Group 2, all patients underwent valve repair using a variety of techniques in combination with tricuspid annuloplasty. During the follow-up period, 3 of the 6 (50%) primary repairs (1 patient in Group 1 and 2 in Group 2) failed and required replacement with a bioprosthesis at 8 days, 14 days and 4 years, respectively. The pulmonary allograft failed secondary to valvular stenosis and was replaced with a bioprosthesis after 10 months. Overall, no failures occurred in any of the 5 bioprosthetic valves placed at the primary operation (n = 1) or after failed tricuspid repair/pulmonary allograft (n = 4), after a mean follow-up of 55 months. TR requiring surgical correction after OHT is a rare condition and requires a tailored surgical strategy. This strategy should take into account the mechanism of valve dysfunction and specific valvular lesions. In patients with Type I dysfunction secondary to annular dilation, valve repair with a remodeling annuloplasty should be performed; however, in the presence of any residual TR on transesophageal echocardiography (TEE) at the completion of cardiopulmonary bypass (CPB), a valve replacement with a bioprosthesis is warranted during the same procedure. In patients with Type II dysfunction with leaflet prolapse and biopsy-induced chordal injury, a bioprosthetic valve replacement seems a reliable surgical option.

The “clover technique” as a novel approach for correction of post-traumatic tricuspid regurgitation

Objective To describe a novel technique, named “clover,” to correct complex post-traumatic tricuspid valve lesions. Methods Five patients with severe post-traumatic tricuspid insufficiency underwent valve reconstruction with the clover technique, a new surgical approach that consists of stitching together the middle point of the free edges of the tricuspid leaflets, producing a clover-shaped valve. The mechanism of tricuspid regurgitation was complex in all patients, and right ventricular function was always moderately to severely depressed. An echocardiographic study was performed after cardiopulmonary bypass, at discharge, and at follow-up. Results Cardiopulmonary bypass time was 32 ± 6.3 minutes and crossclamp time was 23 ± 7.4. There was no hospital mortality or morbidity. Intraoperative transesophageal and predischarge transthoracic echocardiography showed perfect results in all patients. No late deaths occurred. At the latest follow-up, extending to 14.2 months (mean 11.3; median 12.4), all patients were asymptomatic (New York Heart Association class I) with trivial (2 patients) or no residual regurgitation (3 patients) on 2-dimensional echocardiogram. No transvalvular gradient was revealed in any patient. A significant reduction of the right ventricular end-diastolic dimensions was noted as well (from 54 ± 7.1 mm to 40 ± 7.5 mm, P < .001). Conclusions In this preliminary experience, the clover technique increased the feasibility of tricuspid valve repair in case of severe traumatic tricuspid valve insufficiency, leading to very satisfactory mid-term results even in the presence of complex lesions or dilatation and deterioration of the right ventricle.