Imaging Considerations for Percutaneous Tricuspid Intervention
A review of imaging options relevant to treating functional tricuspid regurgitation with transcatheter techniques.
Functional or secondary tricuspid regurgitation (TR) is the most common etiology of severe TR,1 which is progressive2,3 and affects patient mortality.4-7 The high prevalence of secondary TR with mitral valve disease,8,9 as well the association with pulmonary hypertension6,10,11 and right ventricular dilatation and dysfunction,11 point to the complexity of the disease. The only treatment for functional TR that has a class I indication is use of a diuretic,12 and once annular dilatation occurs, tricuspid repair and replacement may be needed to prevent disease progression and to improve outcomes.13-16 However, this algorithm fails to recognize the frequent comorbidities associated with or resulting in TR.
Trend analysis of the Society of Thoracic Surgeons database between 2000 and 2010 confirmed that, over that time span, patients who underwent surgery for TR in the United States increased in age, comorbidity burden, and proportion of emergency presentations.17 As a result, surgical mortality for isolated tricuspid valve interventions remains higher than for any other single valve surgery.17,18 This evidence has supported early prophylactic interventions (combined tricuspid repair for less severe TR at the time of the left-sided disease treatment); however, concomitant valve surgery for TR remains underutilized.19-21
Finally, as more left-sided valve disease is treated with transcatheter therapies,22-25 the negative impact of TR on survival in these patients26-28 has underscored the importance of developing transcatheter solutions for this disease. Numerous lessons should be learned from the high recurrence rate after surgical repair for TR.29 One such lesson is that imaging is key to understanding the pathoanatomy, predictors of recurrent or progressive disease, and appropriateness of transcatheter treatment. Therefore, appropriate imaging is essential for preprocedural, intraprocedural, and postprocedural assessment of transcatheter therapies.
RIGHT HEART ANATOMY WITH FUNCTIONAL TR
Echocardiography remains the primary imaging modality for assessment of right heart size,30 and a number of measurements can be used to describe tricuspid annular and right ventricular changes with functional TR. When functional dilatation occurs, the septal portion of the annulus, which is supported by attachment to the muscular septum, is typically spared, and so the annulus primarily dilates along the anterior and posterior leaflet attachments, causing the annulus to become more circular and planar.31 Greater degrees of TR are associated with larger annular areas, larger right and left atrial volumes, a more circular annular shape, and right ventricular (RV) dilatation.32 Animal models of TR have suggested that greater degrees of TR may not be related to a loss of the three-dimensional (3D) annular shape but rather are associated with (1) greater “stretch” of the posterior leaflet (as compared to the anterior or septal leaflets), (2) greater annular or RV dilatation, and/or (3) displacement of the papillary muscles.33
Recent studies, however, have also shown that significant anatomic differences in the RV, valve, and annular anatomy may occur based on the etiology of functional TR.11 With idiopathic TR, there was marked basal RV dilatation associated with annular dilatation in the absence of leaflet tethering, with relatively normal RV length (RV conical deformation). With functional TR associated with pulmonary hypertension, there was significant lengthening of the RV with less basal dilatation (and low basal:midventricular diameter ratios) but more midventricular dilatation, resulting in both increased tenting as well as elliptical/spherical RV deformation.11,34 The RV morphologic changes associated with pulmonary hypertension may, in part, be related to ventricular interdependence and the interventricular septal shape and dyssynchrony, which is evident on echocardiography as flattening of the interventricular septum.35
RV function is another important contributor to functional TR. Echocardiographic measurements of RV function include tricuspid annular plane systolic excursion, fractional area change, 3D ejection fraction, tissue Doppler for peak systolic annular velocity, and longitudinal strain.30 RV dysfunction is commonly associated with significant TR in the setting of left heart valvular disease20,36-38 and likely reflects a longer duration of severe TR.37 After tricuspid annuloplasty, RV function typically improves.20 At what point the right heart fails to improve, however, is unknown. Measures of RV function remain unclear determinants of outcome, with some studies suggesting no significant impact of reduced function on outcomes.39,40
ECHOCARDIOGRAPHIC PREDICTORS OF PROGRESSION OR PERSISTENT DISEASE AFTER LEFT HEART SURGERY
After isolated mitral valve repair, significant residual TR is observed in up to 40% of patients.41 In patients undergoing concomitant TR repair at the time of mitral surgery, persistent severe TR is still present in 11% at 3 months and in 17% at 5 years.29 Clinical predictors for residual regurgitation after surgical repair have been identified and include higher preoperative TR severity, higher pulmonary artery pressures, mitral replacement rather than repair, worse left ventricular dysfunction, and the presence of pacemaker leads through the valve.42
Echocardiographic predictors of recurrent or progressive disease have also been identified. Significant tricuspid annular dilatation, as measured by transthoracic echocardiography (TTE), may be a better predictor of severe late TR after mitral valve surgery than those previously mentioned.14,43,44 Because of the linear relationship between annular diameter and TR volume, the annular diameter criterion has been used as a surrogate for regurgitation volume. Significant annular dilatation is defined by a diastolic diameter ≥ 40 mm or > 21 mm/m2 in the four-chamber transthoracic view44,45 and is the main imaging criteria used to indicate severe TR in the current American Heart Association/American College of Cardiology guidelines.45 Severe TR (stages C and D) is associated with poor prognosis independent of age, left and right systolic function, and RV size.10,46
Other authors47 suggest that the cutoff for severe TR should be > 42 mm or 23 mm/m2, which is supported by other studies.48 Dreyfus et al44 studied intraoperative predictors of worsening TR and found that 48% of patients with a tricuspid annular dimension > 70 mm (septolateral dimension) had worsening TR over time if not repaired at the time of surgery (compared to only 2% with a concomitant repair). Recent studies, however, have called into question the appropriateness of this measurement.47 The complex 3D shape of the RV and the multiple apical imaging windows suggested by the recent echocardiographic guidelines30 make for low reproducibility of this single-dimension measurement.
Numerous authors have explored the relationship between tenting of the leaflets and severity of TR, with tenting areas and volumes correlating with TR severity and with recurrence and outcomes after surgical repair.42,49-52 A TTE tethering distance > 0.76 cm or tethering area > 1.63 cm predicted recurrent TR after surgery.42,53 Tethering has been associated with RV dilatation, and an RV end-systolic area ≥ 20 cm2, as determined by TTE, predicted worse event-free survival rates.39
GRADING THE SEVERITY OF TR
Grading of TR severity has been reviewed in the recently updated American Society of Echocardiography (ASE) guidelines,54 as well as the European Association of Echocardiography guidelines.55 The parameters include structural variables (tricuspid valve morphology, right atrial and RV size, and inferior vena caval diameter) as well as qualitative parameters (color jet parameters, including jet area and flow convergence, and continuous wave Doppler), semiquantitative parameters (color jet area, vena contracta width, proximal isovelocity surface area [PISA] radius, hepatic vein flow, and tricuspid inflow pattern), and quantitative parameters (effective regurgitant orifice area [EROA] and regurgitant volume). Importantly, many of the studies validating the use of various echocardiographic parameters, particularly quantitative measures, have significant limitations and lack of a “gold standard” for comparison or support from outcomes data.
As transcatheter devices are being developed and tested, it is becoming increasingly important that accurate methods of assessing TR severity be validated. Although the PISA method is simple and easy to perform,56 the complex relationship of the isovelocity shell to the often elliptical shape57,58 and large size of the TR EROA results in a significant underestimation of the true EROA.59 More recently, 3D PISA has been used to quantify TR.60 This method uses a vendor-specific software package to analyze the largest convergence zone. Three-dimensional PISA-derived EROA correlated well with 3D planimetered vena contracta area (r = 0.97) and may overcome the underestimation of two-dimensional (2D) methods.
Quantification of TR by relative stroke volumes has shown high correlation with catheterization-derived data56,61,62 but is underused and not currently advocated by the guidelines. The recently published early feasibility trial of a pledgeted suture annuloplasty device suggested methods for quantifying TR using quantitative Doppler.63 In this study, tricuspid diastolic stroke volume was calculated as the product of the tricuspid annular area and pulsed-wave Doppler annular velocity-time integral (VTI). Tricuspid annular area was calculated with the elliptical formula, using diameters obtained from the orthogonal plane (inflow and the four-chamber views) in early diastole (one frame after initial valve opening) to more accurately calculate annular area. Tricuspid annular area was then multiplied by the tricuspid annular VTI to obtain diastolic stroke volume. The regurgitant volume was calculated as tricuspid valve diastolic stroke volume minus forward stroke volume. The EROA was calculated as the regurgitant volume divided by the TR VTI.
In this study, 2D PISA underestimated quantitative EROA in all patients by up to twofold. The two measurements were nonetheless highly correlative, and a reduction in both PISA EROA and quantitative EROA after transcatheter suture annuloplasty was associated with an increase in left ventricular stroke volume. These echocardiographic improvements in valvular and ventricular hemodynamics were associated with significant improvements in 6-minute walk test, New York Heart Association class, and Minnesota Living With Heart Failure Questionnaire, which helps validate the feasibility of the method for quantification.
A number of studies have shown the utility of 3D color Doppler to quantify TR by planimetry of the vena contracta area.57,60,64,65 Velayudhan et al was one of the first to correlate standard Doppler methods of quantifying TR with planimetry of the 3D vena contracta area. Using the validated measure of regurgitant jet area/right atrial area > 34%66 and regurgitant jet area > 10 cm2 to define severe TR,67 a 3D TTE planimetered vena contracta area of > 0.75 cm2 was the most sensitive cutoff (sensitivity, 85.2%; specificity, 82.1%). This higher cutoff has also been demonstrated by Chen et al, with severe TR (as defined by 2D criteria) associated with a 3D vena contracta area of > 0.6 ± 0.4 cm2 and nonsevere TR (as defined by 2D methods) associated with a 3D vena contracta area of ≤ 0.3 ± 0.1 cm2. However, the receiver-operator curve demonstrated that a 3D vena contracta area of 0.36 cm2 was the best cutoff value for severe TR, with a sensitivity of 89% and a specificity of 84% in predicting severe TR as defined by 2D echocardiographic integrative criteria.
However, current devices under investigation serve an unusual population of patients. In the SCOUT trial,63 a quantitative EROA of ≤ 1.2 cm2 was used for inclusion in the trial, and numerous patients were excluded who had an EROA that exceeded this cutoff. Because this patient population has largely been neglected until now, they often present with symptoms late in the disease process with regurgitant orifices that are two- to threefold more severe than what qualifies as severe TR.
Thus, a new grading scheme has been proposed that extends the current ASE categories (mild, moderate, and severe) to include massive (also suggested by the European Association of Echocardiography), as well as torrential.68 In this proposal, the additional grades are generated using the ranges defined by the mild, moderate, and severe categories. Thus, massive is defined as an average (from two orthogonal planes) vena contracta diameter of 14 to 20 mm, an EROA (by PISA) of 60 to 79 mm2, and a 3D vena contracta area or quantitative EROA of 95 to 114 mm2. Torrential is defined as a vena contracta diameter ≥ 21 mm, an EROA (PISA) of ≥ 80 mm2, and a 3D vena contracta area or quantitative EROA of ≥ 115 mm2. Using the old grading scheme, the reduction of mean quantitative EROA from 0.85 ± 0.22 mm2 to 0.63 ± 0.29 mm2 in the SCOUT trial would not represent a change in severity; however, using the new grading scheme, there is a one-grade reduction that more accurately reflects the changes in TR associated with clinical benefit.
OTHER IMAGING MODALITIES FOR ASSESSING THE TRICUSPID VALVE
Given the complex, 3D anatomy of both the tricuspid annulus and right ventricle, it is likely that 3D imaging modalities such as 3D echocardiography, CT scanning (Figure 1), and cardiovascular MRI will replace current measurements, which primarily rely on 2D imaging.69-71 There are some challenges to imaging the right heart. Homogeneous enhancement of the structures around the tricuspid valve annulus may be difficult, with streak artifact arising from high-attenuation superior vena cava contrast enhancement mixing with unenhanced blood of the inferior vena cava. These artifacts may be reduced by a femoral vein injection of contrast or, ideally, simultaneous injections.69,72 Assessing the end-systolic tenting distance and tricuspid annular dimensions, as well as right ventricular volumes and function, is feasible by CT in patients with functional TR.70,73
Kabasawa et al73 showed that preoperative leaflet tenting angles correlated with TR severity, and a tenting distance of > 7.2 mm predicted recurrent TR ≥ 2+ after surgical annuloplasty. Furthermore, van Rosendael et al70 showed that patients with TR < 3+ have significantly smaller CT annular measurements (anteroposterior diameter; septal-lateral diameter, perimeter, and area) and lower ventricular volumes. Patients with TR ≥ 3+ had significantly larger tenting angles of the septal and anterior leaflets but not of the posterior leaflet. Significant predictors of TR included pulmonary artery systolic pressure, RV end-systolic volume, and anteroposterior tricuspid annular diameter.
Other studies have shown that CT-defined annulus area correlated strongly with right and left atrial volume, and the annulus shape changed from elliptical to circular in moderate/severe TR.32 Atrial enlargement occurs before right ventricular dilation, which occurs late, when TR is severe. Atrial volume and tricuspid annular dilation may be early and sensitive indicators of significant TR.
Cardiac MRI can be useful for assessing the tricuspid valve annulus size and shape changes associated with the cardiac cycle.74,75 Both real-time 3D echocardiography and cardiac MRI are accurate in measuring the tricuspid annular area throughout the cardiac cycle with changes in annular dimensions correlating to right ventricular size (volume) and function.75 In addition to dynamic information about the annulus and right ventricle, cardiac MRI can also assess the flow across the tricuspid valve. Similar to echocardiographic assessment, a vena contracta of > 7 mm correlates with severe TR.76 Regurgitant volumes can be derived by subtracting forward flow (assessed by pulmonary artery phase contrast assessment) from RV stroke volume (assessed by steady-state free precession); however, major limitations include irregular rhythms and concomitant valvular disease (ie, pulmonic regurgitation).77,78
Thus, the recurrence of TR with surgical annular repair is related to RV dilatation and marked tenting, as well as severe pulmonary hypertension with related septal shift. These caveats may be important for deciding which patients should be candidates for treatment with transcatheter annular fixation devices, as these devices may not be ideal in those with predictors of surgical annuloplasty recurrence.
ECHOCARDIOGRAPHIC IMAGING OF THE TRICUSPID VALVE FOR TRANSCATHETER INTERVENTIONS
The current ASE guidelines79 for performing a comprehensive examination by transesophageal echocardiography (TEE) include additional imaging views, many of which are intended to improve imaging of the tricuspid valve. Given the position of the heart in relation to the esophagus and stomach, midesophageal, distal esophageal, shallow transgastric, and deep transgastric views may bring the probe close enough to the tricuspid valve for both 2D and 3D imaging. Many imaging planes may be similar to TTE imaging, and therefore, the same anatomic caveats are worth noting.
First, the commissure between the anterior and septal leaflets is adjacent to the noncoronary cusp of the aortic valve; the right coronary cusp is adjacent to only the anterior leaflet. Second, although a small (anterior) portion of the septal leaflet may be seen if the aortic valve is in view, most of the septal leaflet is attached to the interventricular septum. Third, the coronary sinus enters the right atrium at the commissure between the septal and posterior leaflets. Finally, the right atrial appendage is directly superior to the anterior leaflet. Any two-chamber imaging plane of the RV will tend to image the anterior and posterior leaflets as long as the anterior (curved, right atrial appendage in view) and posterior (flat, on the diaphragm) walls of the RV are imaged.80
A comprehensive TEE examination of the TV should include imaging from several depths and multiplane angles. Multilevel imaging begins at the midesophageal depth. The four-chamber view permits visualization of the septal and anterior leaflets, particularly if the probe is slightly anteflexed (Figure 2A). If retroflexed (Figure 2B), the septal-posterior leaflet coaptation is imaged.
The midesophageal inflow-outflow view at approximately 60° images the anterior leaflet (adjacent to the aorta) and the opposing posterior leaflet (Figure 3). From this imaging plane, the septal leaflet is typically only imaged using simultaneous biplane views. An orthogonal imaging plane adjacent to the aorta (Figure 3A) will image septal-anterior coaptation. Moving the orthogonal image away from the aorta (Figure 3B) will image the septal-posterior coaptation. Because the lower right heart border is close to the diaphragm, slow insertion brings the TEE probe to the distal esophagus just proximal to the gastroesophageal junction; there may be no view of the left atrium proximal to the tricuspid valve in this imaging plane, only the right atrium and coronary sinus (Figure 4A). As this view of the tricuspid valve is unobstructed by left heart structures, it is ideal for performing a comprehensive evaluation of tricuspid valve function and for acquiring 3D volumes of the tricuspid valve (Figure 4B and Figure 4C).
Advancing the TEE probe into the stomach results in transgastric views (Figure 5). At 0°, rightward anterior flexion will result in the inflow-outflow view, again with imaging of the anterior (adjacent to the aorta) and posterior (adjacent to the diaphragm) leaflets. Rotating the multiangle probe to 60° to 90° results in the only 2D view that provides simultaneous visualization of all three tricuspid valve leaflets with the posterior leaflet in the near field, the anterior leaflet in far field, and the septal leaflet adjacent to the septum (Figure 5A). Advancing the TEE probe further into the stomach along with rightward anterior flexion produces a deep transgastric view of the tricuspid valve (Figure 5B), which also permits optimal color flow and spectral Doppler evaluation of TR jets.
Because of the variability of imaging planes, as well as individual anatomy, leaflet identification should always be confirmed using 3D echocardiography. Three-dimensional echocardiography obviates the need for mental reconstruction of multiple 2D planes.81 Lang et al82 have suggested a standardized imaging display for the en face view of the tricuspid valve, with the interatrial septum placed inferiorly (at the 6 o’clock position), regardless of the atrial or ventricular orientation (Figure 4B). Because of the anterior position of the right heart, 3D TTE images may be equal or sometimes better in quality compared to 3D TEE images.
Interest in the tricuspid valve has increased due to the evidence that functional TR affects patients’ morbidity and mortality. Disease severity may be determined by the multiple comorbidities and right ventricular anatomy that can be identified by various imaging modalities. Transcatheter solutions for functional TR continue to be developed and will rely on optimal imaging techniques for procedural success.
1. Cohen SR, Sell JE, McIntosh CL, Clark RE. Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. II. Nonoperative management, tricuspid valve annuloplasty, and tricuspid valve replacement. J Thorac Cardiovasc Surg. 1987;94:488-497.
2. Najib MQ, Vinales KL, Vittala SS, et al. Predictors for the development of severe tricuspid regurgitation with anatomically normal valve in patients with atrial fibrillation. Echocardiography. 2012;29:140-146.
3. Kwak JJ, Kim YJ, Kim MK, et al. Development of tricuspid regurgitation late after left-sided valve surgery: a single-center experience with long-term echocardiographic examinations. Am Heart J. 2008;155:732-737.
4. Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004;43:405-409.
5. Voelkel NF, Quaife RA, Leinwand LA, et al. Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure. Circulation. 2006;114:1883-1891.
6. Bustamante-Labarta M, Perrone S, De La Fuente RL, et al. Right atrial size and tricuspid regurgitation severity predict mortality or transplantation in primary pulmonary hypertension. J Am Soc Echocardiogr. 2002;15:1160-1164.
7. Hung J, Koelling T, Semigran MJ, et al. Usefulness of echocardiographic determined tricuspid regurgitation in predicting event-free survival in severe heart failure secondary to idiopathic-dilated cardiomyopathy or to ischemic cardiomyopathy. Am J Cardiol. 1998;82:1301-1303, A10.
8. Antunes MJ, Barlow JB. Management of tricuspid valve regurgitation. Heart. 2007;93:271-276.
9. Rogers JH, Bolling SF. The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. Circulation. 2009;119:2718-2725.
10. Lee JW, Song JM, Park JP, et al. Long-term prognosis of isolated significant tricuspid regurgitation. Circ J. 2010;74:375-380.
11. Topilsky Y, Khanna A, Le Tourneau T, et al. Clinical context and mechanism of functional tricuspid regurgitation in patients with and without pulmonary hypertension. Circ Cardiovasc Imaging. 2012;5:314-323.
12. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2017;70:252-289.
13. Benedetto U, Melina G, Angeloni E, et al. Prophylactic tricuspid annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery. J Thorac Cardiovasc Surg. 2012;143:632-638.
14. Van de Veire NR, Braun J, Delgado V, et al. Tricuspid annuloplasty prevents right ventricular dilatation and progression of tricuspid regurgitation in patients with tricuspid annular dilatation undergoing mitral valve repair. J Thorac Cardiovasc Surg. 2011;141:1431-1439.
15. Colombo T, Russo C, Ciliberto GR, et al. Tricuspid regurgitation secondary to mitral valve disease: tricuspid annulus function as guide to tricuspid valve repair. Cardiovasc Surg. 2001;9:369-377.
16. Lee JW, Song JM, Park JP, et al. Long-term prognosis of isolated significant tricuspid regurgitation. Circ J. 2010;74:375-380.
17. Kilic A, Saha-Chaudhuri P, Rankin JS, Conte JV. Trends and outcomes of tricuspid valve surgery in North America: an analysis of more than 50,000 patients from the Society of Thoracic Surgeons database. Ann Thorac Surg. 2013;96:1546-1552; discussion 1552.
18. Beckmann A, Funkat AK, Lewandowski J, et al. Cardiac surgery in Germany during 2012: a report on behalf of the German Society for Thoracic and Cardiovascular Surgery. Thorac Cardiovasc Surg. 2014;62:5-17.
19. Badhwar V, Rankin JS, He M, et al. Performing concomitant tricuspid valve repair at the time of mitral valve operations is not associated with increased operative mortality. Ann Thorac Surg. 2017;103:587-593.
20. Chikwe J, Itagaki S, Anyanwu A, Adams DH. Impact of concomitant tricuspid annuloplasty on tricuspid regurgitation, right ventricular function, and pulmonary artery hypertension after repair of mitral valve prolapse. J Am Coll Cardiol. 2015;65:1931-1938.
21. Goldstone AB, Howard JL, Cohen JE, et al. Natural history of coexistent tricuspid regurgitation in patients with degenerative mitral valve disease: implications for future guidelines. J Thorac Cardiovasc Surg. 2014;148:2802-2809.
22. Mack MJ, Brennan JM, Brindis R, et al. Outcomes following transcatheter aortic valve replacement in the United States. JAMA. 2013;310:2069-2077.
23. Thourani VH, Kodali S, Makkar RR, et al. Transcatheter aortic valve replacement versus surgical valve replacement in intermediate-risk patients: a propensity score analysis. Lancet. 2016;387:2218-2225.
24. Feldman T, Foster E, Glower DD, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med. 2011;364:1395-1406.
25. Maisano F, Franzen O, Baldus S, et al. Percutaneous mitral valve interventions in the real world: early and 1-year results from the ACCESS-EU, a prospective, multicenter, nonrandomized post-approval study of the MitraClip therapy in Europe. J Am Coll Cardiol. 2013;62:1052-1061.
26. Lindman BR, Maniar HS, Jaber WA, et al. The effect of tricuspid regurgitation and the right heart on survival after transcatheter aortic valve replacement: insights from the PARTNER II inoperable cohort. Circ Cardiovasc Interv. 2015;8:pii:e002073.
27. Ohno Y, Attizzani GF, Capodanno D, et al. Association of tricuspid regurgitation with clinical and echocardiographic outcomes after percutaneous mitral valve repair with the MitraClip System: 30-day and 12-month follow-up from the GRASP Registry. Euro Heart J Cardiovasc Imaging. 2014;15:1246-1255.
28. Frangieh AH, Gruner C, Mikulicic F, et al. Impact of percutaneous mitral valve repair using the MitraClip system on tricuspid regurgitation. EuroIntervention. 2016;11:E1680-1686.
29. Navia JL, Nowicki ER, Blackstone EH, et al. Surgical management of secondary tricuspid valve regurgitation: annulus, commissure, or leaflet procedure? J Thorac Cardiovasc Surg. 2010;139:1473-1482 e5.
30. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American society of echocardiography and the European association of cardiovascular imaging. J Am Soc Echocardiogr. 2015;28:1-39 e14.
31. Mahmood F, Kim H, Chaudary B, et al. Tricuspid annular geometry: a three-dimensional transesophageal echocardiographic study. J Cardiothorac Vasc Anesth. 2013;27:639-646.
32. Nemoto N, Lesser JR, Pedersen WR, et al. Pathogenic structural heart changes in early tricuspid regurgitation. J Thorac Cardiovasc Surg. 2015;150:323-330.
33. Spinner EM, Buice D, Yap CH, Yoganathan AP. The effects of a three-dimensional, saddle-shaped annulus on anterior and posterior leaflet stretch and regurgitation of the tricuspid valve. Ann Biomedical Engineer. 2012;40:996-1005.
34. Ryo K, Goda A, Onishi T, et al. Characterization of right ventricular remodeling in pulmonary hypertension associated with patient outcomes by 3-dimensional wall motion tracking echocardiography. Circ Cardiovasc Imaging. 2015;8:pii:e003176.
35. Palau-Caballero G, Walmsley J, Van Empel V, et al. Why septal motion is a marker of right ventricular failure in pulmonary arterial hypertension: mechanistic analysis using a computer model. Am J Physiol Heart Circulatory Physiol. 2017;312:H691-H700.
36. Praz F, Windecker S. Effect of right ventricular function and tricuspid regurgitation on outcomes after transcatheter aortic valve implantation: forgotten side of the heart. Circ Cardiovasc Interv. 2015;8:pii:3002577.
37. Vargas Abello LM, Klein AL, Marwick TH, et al. Understanding right ventricular dysfunction and functional tricuspid regurgitation accompanying mitral valve disease. J Thorac Cardiovasc Surg. 2013;145:1234-1241.e5.
38. Tamborini G, Fusini L, Muratori M, et al. Right heart chamber geometry and tricuspid annulus morphology in patients undergoing mitral valve repair with and without tricuspid valve annuloplasty. Int J Cardiovasc Imaging. 2016;32:885-894.
39. Kim YJ, Kwon DA, Kim HK, et al. Determinants of surgical outcome in patients with isolated tricuspid regurgitation. Circulation. 2009;120:1672-1678.
40. Staab ME, Nishimura RA, Dearani JA. Isolated tricuspid valve surgery for severe tricuspid regurgitation following prior left heart valve surgery: analysis of outcome in 34 patients. J Heart Valve Dis. 1999;8:567-574.
41. Matsunaga A, Duran CM. Progression of tricuspid regurgitation after repaired functional ischemic mitral regurgitation. Circulation. 2005;112:I453-457.
42. Fukuda S, Song JM, Gillinov AM, et al. Tricuspid valve tethering predicts residual tricuspid regurgitation after tricuspid annuloplasty. Circulation. 2005;111:975-979.
43. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): the Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur J Cardiothorac Surg. 2012;42:S1-44.
44. Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair? Ann Thorac Surg. 2005;79:127-132.
45. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:2438-2488.
46. Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004;43:405-409.
47. Dreyfus J, Durand-Viel G, Raffoul R, et al. Comparison of 2-dimensional, 3-dimensional, and surgical measurements of the tricuspid annulus size: clinical implications. Circ Cardiovasc Imaging. 2015;8:e003241.
48. Kim H-K, Kim Y-J, Park J-S, et al. Determinants of the severity of functional tricuspid regurgitation. Am J Cardiol. 2006;98:236-242.
49. Sagie A, Schwammenthal E, Padial LR, et al. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. J Am Coll Cardiol. 1994;24:446-453.
50. Sukmawan R, Watanabe N, Ogasawara Y, et al. Geometric changes of tricuspid valve tenting in tricuspid regurgitation secondary to pulmonary hypertension quantified by novel system with transthoracic real-time 3-dimensional echocardiography. J Am Soc Echocardiogr. 2007;20:470-476.
51. Park YH, Song JM, Lee EY, et al. Geometric and hemodynamic determinants of functional tricuspid regurgitation: a real-time three-dimensional echocardiography study. Int J Cardiol. 2008;124:160-165.
52. Min SY, Song JM, Kim JH, et al. Geometric changes after tricuspid annuloplasty and predictors of residual tricuspid regurgitation: a real-time three-dimensional echocardiography study. Eur Heart J. 2010;31:2871-2880.
53. Raja SG, Dreyfus GD. Basis for intervention on functional tricuspid regurgitation. Semin Thorac Cardiovasc Surg. 2010;22:79-83.
54. Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation: a report from the American Society of Echocardiography developed in collaboration with the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2017;30:303-371.
55. Lancellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010;11:307-332.
56. Rivera JM, Mele D, Vandervoort PM, et al. Effective regurgitant orifice area in tricuspid regurgitation: clinical implementation and follow-up study. Am Heart J. 1994;128:927-933.
57. Sugeng L, Weinert L, Lang RM. Real-time 3-dimensional color Doppler flow of mitral and tricuspid regurgitation: feasibility and initial quantitative comparison with 2-dimensional methods. J Am Soc Echocardiogr. 2007;20:1050-1057.
58. Song JM, Jang MK, Choi YS, et al. The vena contracta in functional tricuspid regurgitation: a real-time three-dimensional color Doppler echocardiography study. J Am Soc Echocardiogr. 2011;24:663-670.
59. Rodriguez L, Anconina J, Flachskampf FA, et al. Impact of finite orifice size on proximal flow convergence. Implications for Doppler quantification of valvular regurgitation. Circulation Res. 1992;70:923-930.
60. de Agustin JA, Viliani D, Vieira C, et al. Proximal isovelocity surface area by single-beat three-dimensional color Doppler echocardiography applied for tricuspid regurgitation quantification. J Am Soc Echocardiogr. 2013;26:1063-1072.
61. Loeber CP, Goldberg SJ, Allen HD. Doppler echocardiographic comparison of flows distal to the four cardiac valves. J Am Coll Cardiol. 1984;4:268-272.
62. Meijboom EJ, Horowitz S, Valdes-Cruz LM, et al. A Doppler echocardiographic method for calculating volume flow across the tricuspid valve: correlative laboratory and clinical studies. Circulation. 1985;71:551-556.
63. Hahn RT, Meduri CU, Davidson CJ, et al. Early feasibility study of a transcatheter tricuspid valve annuloplasty: SCOUT trial 30-day results. J Am Coll Cardiol. 2017;69:1795-1806.
64. Velayudhan DE, Brown TM, Nanda NC, et al. Quantification of tricuspid regurgitation by live three-dimensional transthoracic echocardiographic measurements of vena contracta area. Echocardiography. 2006;23:793-800.
65. Chen TE, Kwon SH, Enriquez-Sarano M, et al. Three-dimensional color Doppler echocardiographic quantification of tricuspid regurgitation orifice area: comparison with conventional two-dimensional measures. J Am Soc Echocardiogr. 2013;26:1143-1152.
66. Chopra HK, Nanda NC, Fan P, et al. Can two-dimensional echocardiography and Doppler color flow mapping identify the need for tricuspid valve repair? J Am Coll Cardiol. 1989;14:1266-1274.
67. Gonzalez-Vilchez F, Zarauza J, Vazquez de Prada JA, et al. Assessment of tricuspid regurgitation by Doppler color flow imaging: angiographic correlation. Int J Cardiol. 1994;44:275-283.
68. Hahn RT, Zamorano JL. The need for a new tricuspid regurgitation grading scheme. Eur Heart J Cardiovasc Imag. In press.
69. Saremi F, Hassani C, Millan-Nunez V, Sanchez-Quintana D. Imaging evaluation of tricuspid valve: analysis of morphology and function with CT and MRI. AJR Am J Roentgenol. 2015;204:W531-W542.
70. van Rosendael PJ, Joyce E, Katsanos S, et al. Tricuspid valve remodelling in functional tricuspid regurgitation: multidetector row computed tomography insights. Eur Heart J Cardiovasc Imag. 2016;17:96-105.
71. Huttin O, Voilliot D, Mandry D, et al. All you need to know about the tricuspid valve: tricuspid valve imaging and tricuspid regurgitation analysis. Arch Cardiovasc Dis. 2016;109:67-80.
72. Saremi F, Kang J, Rahmanuddin S, Shavelle D. Assessment of post-atrial switch baffle integrity using a modified dual extremity injection cardiac computed tomography angiography technique. Int J Cardiol. 2013;162:e25-e27.
73. Kabasawa M, Kohno H, Ishizaka T, et al. Assessment of functional tricuspid regurgitation using 320-detector-row multislice computed tomography: risk factor analysis for recurrent regurgitation after tricuspid annuloplasty. J Thorac Cardiovasc Surg. 2014;147:312-320.
74. Maeba S, Taguchi T, Midorikawa H, et al. Four-dimensional geometric assessment of tricuspid annulus movement in early functional tricuspid regurgitation patients indicates decreased longitudinal flexibility. Interact Cardiovasc Thorac Surg. 2013;16:743-749.
75. Anwar AM, Soliman OI, Nemes A, et al. Value of assessment of tricuspid annulus: real-time three-dimensional echocardiography and magnetic resonance imaging. Int J Cardiovasc Imaging. 2007;23:701-705.
76. Westenberg JJ, Roes SD, Ajmone Marsan N, et al. Mitral valve and tricuspid valve blood flow: accurate quantification with 3D velocity-encoded MR imaging with retrospective valve tracking. Radiology. 2008;249:792-800.
77. Koskenvuo JW, Jarvinen V, Parkka JP, et al. Cardiac magnetic resonance imaging in valvular heart disease. Clin Physiol Function Imag. 2009;29:229-240.
78. Sommer G, Bremerich J, Lund G. Magnetic resonance imaging in valvular heart disease: clinical application and current role for patient management. J Magn Reson Imag. 2012;35:1241-1252.
79. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26:921-964.
80. Chan K-L, Veinot JP. Anatomic basis of echocardiographic diagnosis. London: Springer; 2011.
81. Badano LP, Agricola E, de Isla LP, et al. Evaluation of the tricuspid valve morphology and function by transthoracic real-time three-dimensional echocardiography. Euro J Echocardiogr. 2009;10:477-484.
82. Lang RM, Badano LP, Tsang W, et al. EAE/ASE recommendations for image acquisition and display using three-dimensional echocardiography. J Am Soc Echocardiogr. 2012;25:3-46.
Rebecca T. Hahn, MD
Columbia University Medical Center
New York-Presbyterian Hospital
New York, New York
(212) 342-0444; firstname.lastname@example.org
Disclosures: Principal Investigator for the SCOUT trial, but receives no compensation; speaker for Abbott Vascular, GE Medical, and St. Jude Medical.