TY - JOUR
AU - Donal, Erwan
AB - Abstract Aims Secondary tricuspid regurgitation (STR) is commonly found in patients with aortic stenosis and is associated with increased morbidity. The study sought to evaluate the prevalence of pre-operative STR and its progression after surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI). Also, it sought to analyse the predictors of post-operative changes in STR. Methods and results We prospectively evaluated 116 patients (aged 75.1 ± 9.8 years, predominantly male) who undergo SAVR or TAVI for severe aortic stenosis (AS) from September 2013 to April 2015. Patients with associated valve disease requiring intervention, significant coronary artery disease or left ventricular ejection fraction (LVEF) <50% were excluded. Clinical and echocardiographic data, including TR grade and right ventricular (RV) size and function, were assessed at baseline and at the 1-year follow-up. At baseline, significant TR was documented in 13 patients (11.1%) and non-significant TR was documented in 103 patients (88.9%). Atrial fibrillation (AF) was more prevalent in patients with a tricuspid annulus diameter ≥40 mm (P < 0.0051). At the 1-year follow-up, the TR grade had improved in 17 patients (14.7%), was unchanged in 68 patients (58.6%) and had worsened in 31 patients (26.7%). Moderate to severe TR was found in 30 patients (25.8%). Tricuspid annulus diameter >40 mm was the only echocardiographic predictor of significant postoperative TR (relative risk (RR) = 2.12 [1.26–3.54], P = 0.004). Right heart function and size were not independent predictors. Conclusion Significant TR was present pre-operatively in 11.1% of patients. Post-operative progression was observed in 26.7% of patients. Only tricuspid annulus size >40 mm was an independent echocardiographic predictor of moderate to severe TR at the 1-year follow-up. secondary tricuspid regurgitation, aortic stenosis, tricuspid annulus Introduction ‘Functional’ or secondary tricuspid regurgitation (STR) refers to tricuspid regurgitation that occurs secondary to conditions that cause right ventricular and/or right atrial dilatation, such as left-sided heart disease, chronic atrial fibrillation (AF) or pulmonary hypertension, in the absence of organic lesions of the tricuspid valve apparatus. Approximately 80–90% of all tricuspid regurgitations (TR) are functional or secondary according to current guidelines. A total of 20–30% of patients undergoing cardiac surgery for left-sided valve disease present with significant TR. This is most common in conjunction with mitral valve disease; however, it is also frequently associated with aortic valve pathology, particularly aortic valve stenosis. Accordingly, discussions of aortic valve treatment in elderly patients deserve dedicated attention to STR.1–3 Until recently, the avoidance of surgical tricuspid valve repair was common in patients with STR because of the misconception that TR would disappear once the primary left-sided defect is treated. This conservative approach still influences surgical practice today, and tricuspid valve repair remains an infrequent procedure at most surgical centres. However, it has become evident that STR does not regress after the appropriate correction of the left-sided valvular disease in a significant number of cases. Thus, STR has been associated with increased postoperative morbidity and mortality.4–6 Several studies have reported the risk factors related to STR and their prognostic implications. These investigations have provided evidence favouring a more aggressive surgical approach to STR. However, this frequently poses a challenge for physicians because of the potentially high surgical risk in these patients.7 Recently, guidelines have been issued for the management of STR; however, the indication and optimal treatment strategies have remained controversial.8–10 Aims of the present study were: to determine the baseline prevalence of STR, to describe the post-procedural changes in STR and to identify the predictors of STR progression at 12-month follow-up (FU). Methods Study protocol We prospectively, reviewed data from patients with severe symptomatic native aortic stenosis (AS) (aortic valve area <1 cm2 or <0.6 cm/m2) who underwent a trans-catheter aortic valve replacement (TAVR) or surgical aortic valve replacement (SAVR) between September 2013 to April 2015. The type of procedure was determined by our institutional heart-team (and unknown at the inclusion in this prospective study). We excluded patients having a left ventricular ejection fraction (LVEF) <50%, or having a severe coronary artery disease (CAD) requiring coronary artery bypass graft, or having a concomitant significant valve disease requiring a double or triple valve procedure. Diseases with right heart problems including primary/secondary pulmonary parenchyma disease, pulmonary vascular disease (pulmonary embolism), congenital heart disease, primary tricuspid valvular problem (endocarditis), and tricuspid regurgitation related to leads of any device (pacemaker, Implantable cardiac defibrillator and cardiac resynchronization therapy implanted before the inclusion in the study) were excluded. Patients who underwent tricuspid repair during follow-up were not excluded but none of the patient from the cohort got any tricuspid valve surgery. The decision to propose a tricuspid repair was based on the degree of tricuspid annulus enlargement, the degree of TR, the qualitative assessment of RV function, the operating risk, the lung function and the global assessment performed by the anesthesiologist, the cardiologist and the surgeon. A total of 116 patients agreed to participate in the study. 14 patients were then excluded from further analysis because of missing tracking data. In total, 102 patients were eligible for statistical analysis. Clinical and echocardiographic data were recorded for all patients at baseline (inclusion, signature of the inform consent) and 1 year after the procedure. The study was conducted in accordance with the ‘Good Clinical Practice’ guidelines as stated in the Declaration of Helsinki. The study was reviewed by the independent ethics committees. All of the patients provided written informed consent (ethic committee authorization: CPP Ouest V. EudraCT number: 2012-AO1323-40). Clinical data Data concerning demographic status (age, gender), clinical assessment (New York Heart association functional class (NYHA), history of angina, hypertension, hypercholesterolemia, diabetes, hypertension and smoking), laboratory data (hemoglobin, creatinine, NT-proBNP), comorbidities (CAD, atrial fibrillation, and kidney failure estimated by the Modification of Diet in Renal Disease (MDRD) formula), presence of pace-maker and/or implantable cardioverter defibrillator (ICD) and therapeutic regimen were collected at patient enrolment. Echocardiographic data 2D standard transthoracic echocardiography and speckle tracking echocardiography were performed at baseline (inclusion) and at 12-month FU. by board-certified physicians, using high-end scanners and following current recommendations .10,11 LVEF was measured by the biplane Simpson method. Stroke volume was measured in the LV outflow tract and indexed to the body surface area. Early diastolic mitral inflow was measured at mitral valve leaflet tips with a pulse-wave Doppler unit. Tissue Doppler imaging was used to estimate mitral annular velocities (e′ wave) and the E/e′ ratio was used to evaluate LV filling pressure. Left atrial (LA) volume was calculated using the biplane area length method at the end systole. Aortic valve area (AVA) was measured using the continuity equation.9 Aortic trans-prosthetic mean pressure gradients (TMPGs) were calculated using the Bernoulli equation. Right ventricular (RV) and atrial dimensions were measured. RV systolic function was assessed by an integrative approach according to recent recommendations.12 We used the RV Fractional Area Change (FAC), the tricuspid annular plane systolic excursion (TAPSE), the Right ventricular Index of Myocardial Performance (RIMP), the tissue Doppler-derived tricuspid lateral annular systolic velocity (s′) and RV free wall (RV-GLS) strain. The tricuspid annulus diameter was measured in early diastole from a right ventricle–focused apical 4-chamber view as recommended9,10 (Figure 1) Figure 1 View largeDownload slide Example of the measurement of the tricuspid annulus diameter in early diastole in a patient with a sinus rhythm (A) and in atrial fibrillation (B). Figure 1 View largeDownload slide Example of the measurement of the tricuspid annulus diameter in early diastole in a patient with a sinus rhythm (A) and in atrial fibrillation (B). TR severity was assessed using an integrated approach, including TV morphology; the right ventricular/right atrial and inferior vena cava size; the vena contracta width, and the proximal flow convergence radius. TR severity was graded as none, mild (grade 1), moderate (grade 2), and severe (grade 3) according to current guidelines8,9 (Figure 2). Figure 2 View largeDownload slide Echocardiographic imaging of tricuspid regurgitation after AVR. Figure 2 View largeDownload slide Echocardiographic imaging of tricuspid regurgitation after AVR. Figure 3 View largeDownload slide According to the size of the tricuspid annulus: number of TR and its evolution after treatment of the aortic valve stenosis. No patient was treated on the tricuspid annulus or valve. Figure 3 View largeDownload slide According to the size of the tricuspid annulus: number of TR and its evolution after treatment of the aortic valve stenosis. No patient was treated on the tricuspid annulus or valve. Moderate and severe TR were considered ‘significant’ This semi-quantitative assessment of TR has been previously deemed reasonable8,9 (Table 1). Table 1 Echocardiographic parameters used for grading TR severity   Mild  Moderate  Severe  Qualitative parameters  Tricuspid valve morphology  Normal/abnormal  Normal/abnormal  Abnormal/flail/large coaptation defect  Color flow TR jet  Small, central  Intermediate  Very large central jet or eccentric wall-impinging jet  CW signal of TR jet  Faint/parabolic  Dense/parabolic  Dense/triangular with early peaking (peak < 2 m/s in massive TR)  Semi-quantitative  VC width (mm)  Not defined  <7  >7  PISA radius (mm)  ≤5  6–9  >9  Hepatic vein flow  Systolic dominance  Systolic blunting  Systolic flow reversal  Tricuspid inflow  Normal  Normal  E-wave dominant (≥1 m/s)  Quantitative  EROA (mm2)  Not defined  Not defined  ≥40  R Vol (mL)  Not defined  Not defined  ≥45  RV/RA/IVC size  Normal  Normal or dilated  Dilated    Mild  Moderate  Severe  Qualitative parameters  Tricuspid valve morphology  Normal/abnormal  Normal/abnormal  Abnormal/flail/large coaptation defect  Color flow TR jet  Small, central  Intermediate  Very large central jet or eccentric wall-impinging jet  CW signal of TR jet  Faint/parabolic  Dense/parabolic  Dense/triangular with early peaking (peak < 2 m/s in massive TR)  Semi-quantitative  VC width (mm)  Not defined  <7  >7  PISA radius (mm)  ≤5  6–9  >9  Hepatic vein flow  Systolic dominance  Systolic blunting  Systolic flow reversal  Tricuspid inflow  Normal  Normal  E-wave dominant (≥1 m/s)  Quantitative  EROA (mm2)  Not defined  Not defined  ≥40  R Vol (mL)  Not defined  Not defined  ≥45  RV/RA/IVC size  Normal  Normal or dilated  Dilated  CW, continuous wave; EROA, effective regurgitant orifice area; IVC, inferior vena cava; PISA, proximal isovelocity surface area; RA, right atrium; RV, right ventricule; R Vol, regurgitant volume; TR, tricuspid regurgitation; VC, vena contracta. Systolic pulmonary arterial pressure was calculated by adding the peak TR systolic gradient too the estimated central venous pressure. Statistical analysis Continuous variables were compared by the Wilcoxon test. Categorical variables were compared by the χ2 or exact Fisher test. The reasons for non-measurements were also described. We then tried to identify the echocardiographic predictor of tricuspid regurgitation at 12-months follow-up (primary outcome). The primary outcome (TR severity) was binary as follows: low or moderate to severe (defined as TR class II or above). The following five candidate variables potentially associated with the primary outcome were identified: mean aortic gradient, left atrial volume index (LAVI), E/e′, tricuspid annulus and TAPSE. These variables were measured at 12 months and were compared between patients with moderate to severe TR and those with mild TR using Wilcoxon tests. We used generalized additive models fit by the GAM procedure in SAS 9.4 (SAS institute, Cary, North Carolina, USA) to uncover relationships that might otherwise be missed between the independent continuous variables and the primary outcome. An estimate of the change in odds when the independent continuous variable increased by one standard deviation (or rounded value) was calculated along with its 95% confidence interval. Interaction with treatment (surgery or TAVI) was tested by introducing a product term in the logistic model. The variables of age, sex, treatment and all of the statistically independent candidate variables were incorporated into a multivariable logistic regression model. Backward selection was then performed using the 0.05 significance level; however, age, sex, treatment and any terms significantly interacting with treatment (at a P-value less than 0.15) were forced into the final model. Model discrimination was assessed using the c statistic. The Hosmer and Lemeshow goodness-of-fit statistic was also reported. The same process was applied to the secondary outcome (TAPSE was excluded as an independent variable). Reproducibility of tricuspid annulus diameter measurement was tested in 10 randomized patients. The coefficient de variation according to the Bland and Altman method was calculated for the intra and the inter-observer variability.13 Results Patient baseline characteristics and operative data The patient profiles are summarized in Table 2. Among the 116 patients included in this study, the majority were male (60.34%), and the mean age was 75.1 ± 9.8 years. Table 2 Baseline patient characteristics   Number of patients  Frequency  Clinical characteristics  Age [years]  116  75.1 ± 9.8  Male [n (%)]  116  70 (60.34%)  NYHA functional class  116     No dyspnea  12  10.33%   I  5  4.31%   II  70  60.34%   III  25  21.54%   IV  4  3.48%  Angina [n (%)]  115  16 (13.91%)  Hypertension  116  80 (68.96%)  Diabetes  116  16 (13.79%)  Dyslipidemia  116  68 (58.62%)  Smoker  115     No  87  75.65%   Active  5  4.34%   Former  23  20.01%  Atrial fibrillation  116  23 (19.82%)  CAD  116  21 (18.10%)  Pacemaker  116  3 (2.58%)  TAVI  116  32 (27.58%)  Surgery  116  84 (72.41%)  Electrocardiogram  Normal conduction  116  74 (63.79%)  BAV 1  108  27 (24.55%)  LBBB  116  4 (3.44%)  Incomplete LBBB  116  27 (23.27%)  RBBB  116  8 (6.89%)  Incomplete RBBB  116  1 (0.86%)  Laboratory  Estimated glomerular filtration rate by MDRD method  116  73.3 ± 21.9  NT-pro-BNP  54  1012 ± 1108.7  Hemoglobin  116  13.2 ± 1.5  Medication  Beta-blockers  116  55 (47.41%)  ACEi/ARB  116  55 (47.41%)  Diuretic agents  72  10 (13.88%)  Statins  116  60 (51.72%)    Number of patients  Frequency  Clinical characteristics  Age [years]  116  75.1 ± 9.8  Male [n (%)]  116  70 (60.34%)  NYHA functional class  116     No dyspnea  12  10.33%   I  5  4.31%   II  70  60.34%   III  25  21.54%   IV  4  3.48%  Angina [n (%)]  115  16 (13.91%)  Hypertension  116  80 (68.96%)  Diabetes  116  16 (13.79%)  Dyslipidemia  116  68 (58.62%)  Smoker  115     No  87  75.65%   Active  5  4.34%   Former  23  20.01%  Atrial fibrillation  116  23 (19.82%)  CAD  116  21 (18.10%)  Pacemaker  116  3 (2.58%)  TAVI  116  32 (27.58%)  Surgery  116  84 (72.41%)  Electrocardiogram  Normal conduction  116  74 (63.79%)  BAV 1  108  27 (24.55%)  LBBB  116  4 (3.44%)  Incomplete LBBB  116  27 (23.27%)  RBBB  116  8 (6.89%)  Incomplete RBBB  116  1 (0.86%)  Laboratory  Estimated glomerular filtration rate by MDRD method  116  73.3 ± 21.9  NT-pro-BNP  54  1012 ± 1108.7  Hemoglobin  116  13.2 ± 1.5  Medication  Beta-blockers  116  55 (47.41%)  ACEi/ARB  116  55 (47.41%)  Diuretic agents  72  10 (13.88%)  Statins  116  60 (51.72%)  Values are expressed as mean ± SD or frequency [n (%)]. ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BAV, atrioventricular block; CAD, coronary artery disease; LBBB, left bundle branch block; MDRD, modification of diet in renal disease; NHYA, New York Heart Association; NT-pro-BNP, serum amino terminal pro B-type natriuretic peptide; RBBB, right bundle branch block; TAVI, trans-catheter aortic valve implantation. Preoperatively, 29 (25%) patients had moderate or severe symptoms of heart failure (NHYA functional class III or IV). Only 16 patients (13.91%) had angina. Among the cardiovascular risk factors, hypertension (n = 80, 68.96%) and dyslipidemia (n = 68, 58.62%) were the most prevalent. A total of 21 patients (18.10%) had a history of CAD. Paroxysmal or persistent AF was present in 23 patients (19.82%). Five patients among the 11 patients with significant TR (at 45.45%) had paroxysmal or permanent AF. Three patients (2.58%) had a pacemaker or an ICD (but with no TR at baseline) during follow-up. SAVR (Trifecta, Mosaic) was performed in 84 patients (72.41%), the remaining patients (n = 32, 27.58%) underwent TAVR (Sapiens 2 or CoreValve). Echocardiographic data Baseline echocardiographic data, according to the tricuspid annulus size, are shown in Table 3. Patients with a tricuspid annulus ≥40 mm presented with significantly more STR (P = 0.0025), a higher peak TR velocity (P < 0.001), larger RV (P < 0.0001) and larger RA (P < 0.0001). This group also had higher E/e′ ratios (P = 0.0084) and larger left LAVI (P = 0.0005), reflecting higher LV-filling pressure (Figure 3). Table 3 Echocardiographic parameters at index date according to tricuspid annulus value Variables  Missing (n)  Tricuspid annulus <40 mm N = 93 median (IQR)  Tricuspid annulus ≥40 mm N = 19 median (IQR)  P  ZVA (mmHg/mL/m2)  1  4.73 (1.57)  4.75 (1.18)  0.37  LVEF (%)  1  68 (11)  65 (19)  0.60  LV-mass-ASE (g)  2  131 (43)  136 (37)  0.41  LV stroke volume index (mL/m2)  0  47.72 (15.49)  44.39 (17.83)  0.84  Peak aortic valve velocity (m/s)  0  4.54 (0.75)  4.60 (0.75)  0.94  Mean aortic gradient (mmHg)  0  53 (18)  60 (22)  0.81  Permeability index (%)  1  0.21 (0.07)  0.21 (0.05)  0.58  AVA (cm2)  0  4.84 (1.58)  5.55 (2.79)  0.29  TR  5  0.50 (1.00)  1.00 (2.00)  0.0025  e′ medium (cm/s)  8  6.00 (2.00)  6.50 (1.50)  0.81  s′ medium (cm/s)  10  6.00 (2.00)  5.50 (1.00)  0.48  E/e′ mean (ratio)  9  13.66 (5.89)  18.50 (12.25)  0.008  FAC (%)  12  0.45 (0.11)  0.45 (0.21)  0.28  TAPSE (mm)  1  23 (5)  23 (11)  0.34  s′ tricuspid velocity (cm/s)  8  14 (3)  13 (5)  0.16  Peak TR velocity (m/s)  36  2.65 (0.59)  3.13 (0.70)  0.0010  IVA (m/s2)  22  2.83 (1.85)  2.60 (0.96)  0.57  RV basal diameter (mm)  8  34 (7)  41 (5)  <0.0001  Tricuspid annulus diameter (mm)  0  34 (5)  42 (5)  <0.0001  RA volume (mL)  1  48.50 (22.00)  82.00 (59.00)  <0.0001  LAVI (mL/m2)  1  39.00 (15.68)  56.22 (41.09)  0.0005  Strain LV IS base (%)  19  −13.00 (5.00)  −12.00 (3.00)  0.30  GLS LV (%)  17  −17.47 (4.28)  −16.39 (4.51)  0.15  Strain RV bl (%)  21  −26.00 (9.00)  −22.61 (14.50)  0.12  GLS RV (%)  21  −21.50 (6.33)  −17.14 (8.03)  0.03  Variables  Missing (n)  Tricuspid annulus <40 mm N = 93 median (IQR)  Tricuspid annulus ≥40 mm N = 19 median (IQR)  P  ZVA (mmHg/mL/m2)  1  4.73 (1.57)  4.75 (1.18)  0.37  LVEF (%)  1  68 (11)  65 (19)  0.60  LV-mass-ASE (g)  2  131 (43)  136 (37)  0.41  LV stroke volume index (mL/m2)  0  47.72 (15.49)  44.39 (17.83)  0.84  Peak aortic valve velocity (m/s)  0  4.54 (0.75)  4.60 (0.75)  0.94  Mean aortic gradient (mmHg)  0  53 (18)  60 (22)  0.81  Permeability index (%)  1  0.21 (0.07)  0.21 (0.05)  0.58  AVA (cm2)  0  4.84 (1.58)  5.55 (2.79)  0.29  TR  5  0.50 (1.00)  1.00 (2.00)  0.0025  e′ medium (cm/s)  8  6.00 (2.00)  6.50 (1.50)  0.81  s′ medium (cm/s)  10  6.00 (2.00)  5.50 (1.00)  0.48  E/e′ mean (ratio)  9  13.66 (5.89)  18.50 (12.25)  0.008  FAC (%)  12  0.45 (0.11)  0.45 (0.21)  0.28  TAPSE (mm)  1  23 (5)  23 (11)  0.34  s′ tricuspid velocity (cm/s)  8  14 (3)  13 (5)  0.16  Peak TR velocity (m/s)  36  2.65 (0.59)  3.13 (0.70)  0.0010  IVA (m/s2)  22  2.83 (1.85)  2.60 (0.96)  0.57  RV basal diameter (mm)  8  34 (7)  41 (5)  <0.0001  Tricuspid annulus diameter (mm)  0  34 (5)  42 (5)  <0.0001  RA volume (mL)  1  48.50 (22.00)  82.00 (59.00)  <0.0001  LAVI (mL/m2)  1  39.00 (15.68)  56.22 (41.09)  0.0005  Strain LV IS base (%)  19  −13.00 (5.00)  −12.00 (3.00)  0.30  GLS LV (%)  17  −17.47 (4.28)  −16.39 (4.51)  0.15  Strain RV bl (%)  21  −26.00 (9.00)  −22.61 (14.50)  0.12  GLS RV (%)  21  −21.50 (6.33)  −17.14 (8.03)  0.03  T-test or Wilcoxon non parametric test. ASE, American Society of Echocardiography; AVA, aortic valve area; FAC, fractional area change; GLS, global longitudinal strain; IP, index of permeability; IVA, isovolumic acceleration; LAVI, left atrium volume indexed; LVEF, left ventricular ejection fraction; RA, right atrium; RV, right ventricular; TAPSE, tricuspid annular plane systolic excursion; TR, tricuspid regurgitation; ZVA, valvulo-arterial impedance. LVEF with RR = 0.82 [0.62–1.08], P = 0.16; but also, GLS (global longitudinal strain, RR = 0.91 [0.65–1.29], P = 0.62) were not predictor, in the present series, of significant TR at 12-month after treatment of the AS. At the 12-month follow-up, patients with tricuspid annulus ≥40 mm again presented with significantly more STR (P < 0.0039), higher peak TR velocity (P = 0.0048), larger RV (P = 0.017), and larger RA (P < 0.0001). RV Global longitudinal strain (RV-GLS) was worse in patients with larger tricuspid annulus (P = 0.044). Interestingly, no difference in other RV parameters, including FAC, TAPSE and s′ (P = 0.237) were found between the two groups of patients (Tables 3 and 4). Table 4 Echocardiographic parameters at 1 year according to baseline tricuspid annulus value Variables  Missing (n)  Tricuspid annulus <40 mm N = 93 median (IQR)  Tricuspid annulus ≥40 mm N = 19 median (IQR)  P  ZVA (mmHg/mL/m2)  63  3.63 (1.69)  3.53 (1.33)  0.52  LVEF (%)  8  63.50 (18.00)  66.50 (9.00)  0.55  LV-mass-ASE (g)  12  94 (41)  97 (31)  0.67  LV stroke volume index (mL/m2)  5  41.08 (13.60)  45.22 (7.10)  0.90  Peak aortic valve velocity (m/s)  0  2.33 (0.68)  2.50 (0.96)  0.34  Mean aortic gradient (mmHg)  1  11.50 (7.00)  12.00 (11.00)  0.48  IP (%)  2  0.46 (0.10)  0.50 (0.18)  0.97  AVA (cm2)  3  4.47 (1.30)  5.24 (2.71)  0.51  TR  14  1.00 (0.50)  1.50 (1.00)  0.003  e′ medium (cm/s)  10  7.50 (2.00)  7.00 (2.00)  0.44  s′ medium (cm/s)  14  6.00 (2.00)  6.00 (2.00)  0.85  E/e′ mean (ratio)  11  11.56 (6.99)  14.86 (11.00)  0.19  FAC (%)  22  0.44 (0.13)  0.45 (0.12)  0.53  TAPSE (mm)  3  18.00 (4.00)  18.50 (5.00)  0.40  s′ tricuspid velocity (cm/s)  11  10.50 (3.00)  12.00 (3.00)  0.23  Peak TR velocity (m/s)  25  2.56 (0.45)  2.87 (0.86)  0.004  IVA (m/s2)  16  2.33 (1.33)  2.42 (1.53)  0.72  RV basal diameter (mm)  15  34 (9)  38 (5)  0.017  Tricuspid annulus diameter (mm)  10  33 (7)  38 (7)  0.008  RA volume (mL)  6  52.50 (32.50)  81.00 (41.00)  <0.0001  LAVI (mL/m2)  3  38.00 (18.00)  47.21 (30.49)  0.002  Strain LV IS base (%)  15  −15.00 (6.00)  −12.00 (7.00)  0.26  GLS LV (%)  15  −18.50 (5.10)  −18.62 (6.78)  0.62  Strain RV bl (%)  39  −24.00 (8.00)  −14.00 (18.00)  0.04  GLS RV (%)  36  −19.10 (5.90)  −15.80 (9.70)  0.11  Variables  Missing (n)  Tricuspid annulus <40 mm N = 93 median (IQR)  Tricuspid annulus ≥40 mm N = 19 median (IQR)  P  ZVA (mmHg/mL/m2)  63  3.63 (1.69)  3.53 (1.33)  0.52  LVEF (%)  8  63.50 (18.00)  66.50 (9.00)  0.55  LV-mass-ASE (g)  12  94 (41)  97 (31)  0.67  LV stroke volume index (mL/m2)  5  41.08 (13.60)  45.22 (7.10)  0.90  Peak aortic valve velocity (m/s)  0  2.33 (0.68)  2.50 (0.96)  0.34  Mean aortic gradient (mmHg)  1  11.50 (7.00)  12.00 (11.00)  0.48  IP (%)  2  0.46 (0.10)  0.50 (0.18)  0.97  AVA (cm2)  3  4.47 (1.30)  5.24 (2.71)  0.51  TR  14  1.00 (0.50)  1.50 (1.00)  0.003  e′ medium (cm/s)  10  7.50 (2.00)  7.00 (2.00)  0.44  s′ medium (cm/s)  14  6.00 (2.00)  6.00 (2.00)  0.85  E/e′ mean (ratio)  11  11.56 (6.99)  14.86 (11.00)  0.19  FAC (%)  22  0.44 (0.13)  0.45 (0.12)  0.53  TAPSE (mm)  3  18.00 (4.00)  18.50 (5.00)  0.40  s′ tricuspid velocity (cm/s)  11  10.50 (3.00)  12.00 (3.00)  0.23  Peak TR velocity (m/s)  25  2.56 (0.45)  2.87 (0.86)  0.004  IVA (m/s2)  16  2.33 (1.33)  2.42 (1.53)  0.72  RV basal diameter (mm)  15  34 (9)  38 (5)  0.017  Tricuspid annulus diameter (mm)  10  33 (7)  38 (7)  0.008  RA volume (mL)  6  52.50 (32.50)  81.00 (41.00)  <0.0001  LAVI (mL/m2)  3  38.00 (18.00)  47.21 (30.49)  0.002  Strain LV IS base (%)  15  −15.00 (6.00)  −12.00 (7.00)  0.26  GLS LV (%)  15  −18.50 (5.10)  −18.62 (6.78)  0.62  Strain RV bl (%)  39  −24.00 (8.00)  −14.00 (18.00)  0.04  GLS RV (%)  36  −19.10 (5.90)  −15.80 (9.70)  0.11  T-test or Wilcoxon non parametric test. ASE, American Society of Echocardiography; AVA, aortic valve area; FAC, fractional area change; GLS, global longitudinal strain; IP, index of permeability; IVA, isovolumic acceleration; LAVI, left atrium volume indexed; LVEF, left ventricular ejection fraction; RA, right atrium; RV, right ventricular; TAPSE, tricuspid annular plane systolic excursion; TR, tricuspid regurgitation; ZVA, valvulo-arterial impedance. Table 5 Univariable and adjusted estimates for predictors of moderate/severe tricuspid regurgitation based on 98 patients (28 having the outcome)   Univariable estimates   Multivariable full model   Multivariable estimates   RR  95% CI  RR  95% CI  RR  95% CI  P-value  TAVI/surgery  2.17  1.24–3.80  0.99  0.54–1.72  1.23  0.98–2.25  0.48  10-year increase in Age  2.14  1.40–3.27  1.20  0.91–1.57  1.79  1.12–2.85  0.01  Male vs. female gender  0.71  0.40–1.28  0.91  0.61–1.34  0.79  0.46–1.37  0.40  Tricuspid annulus >40 mm  2.62  1.56–4.40  1.31  0.78–2.20  2.12  1.26–3.54  0.004  15-unit increase of aortic mean gradient  0.79  0.57–1.10  0.97  0.78–1.21        18-unit increase in LAVI  1.24  0.98–1.56  1.04  0.84–1.30        5-unit increase in mean E/e′  1.44  1.13–1.84  1.03  0.86–1.24        4 units increase of TAPSE  0.77  0.56–1.04  0.94  0.76–1.16          Univariable estimates   Multivariable full model   Multivariable estimates   RR  95% CI  RR  95% CI  RR  95% CI  P-value  TAVI/surgery  2.17  1.24–3.80  0.99  0.54–1.72  1.23  0.98–2.25  0.48  10-year increase in Age  2.14  1.40–3.27  1.20  0.91–1.57  1.79  1.12–2.85  0.01  Male vs. female gender  0.71  0.40–1.28  0.91  0.61–1.34  0.79  0.46–1.37  0.40  Tricuspid annulus >40 mm  2.62  1.56–4.40  1.31  0.78–2.20  2.12  1.26–3.54  0.004  15-unit increase of aortic mean gradient  0.79  0.57–1.10  0.97  0.78–1.21        18-unit increase in LAVI  1.24  0.98–1.56  1.04  0.84–1.30        5-unit increase in mean E/e′  1.44  1.13–1.84  1.03  0.86–1.24        4 units increase of TAPSE  0.77  0.56–1.04  0.94  0.76–1.16        LAVI, left atrium volume indexed; TAVI, trans-catheter aortic valve implantation; TAPSE, tricuspid annular plane systolic excursion. Predictors of significant tricuspid regurgitation at FU: At 1-year FU, moderate to severe TR was present in 30 patients (25.8%). TR improved in 17 patients (14.7%), was unchanged in 68 patients (58.6%) and worsened in 31 patients (26.7%) (Figures 1 and 2). The mean Nt-proBNP was 625 with a standard deviation of 1044pg/mL. Eight patients were hospitalized in cardiology for dyspnea (with unchanged or worsened TR) and two in neurology for a stroke (only one with a TR). The main predictors of moderate/severe TR at FU included TAVI (RR = 2.17, IC = 1.24 to 3.80), age (RR = 2.14, IC = 1.40 to 3.37), tricuspid annulus size (RR = 2.62, IC = 1.56 to 4.40) and E/e′ ratio (RR = 1.44, CI = 1.13 to 1.84). A multivariable analysis, age and tricuspid annulus >40 mm were the only predictors of significant tricuspid regurgitation (Figure 2; Table 5). Replacing tricuspid annulus diameter per indexed tricuspid annulus diameter lead to a slightly less convincing result (RR = 1.85 [0.99–3.46]; P = 0.05). Reproducibility of tricuspid annulus diameter measurement According to the 10 patients randomly re-analysed (blindly and with more than one month between the first and the second analysis), the difference between 2 measurements performed by one reader was 1.30 ± 0.58 mm (for an average diameter = 33.65 ± 5.68 mm). The difference between two independent readers was 1.35 ± 0.62 mm. Discussion Patients presenting with late TR after left heart valve procedures have poor clinical outcomes. The few existing studies on the prognostic significance of TR also suggest that it carries a considerable impact on morbidity and mortality.4–6 According to current recommendations, patients with TR without severe RV dysfunction could benefit from surgical correction at the time of left heart valve procedure if the TR is significant or the tricuspid annulus is dilated (≥40 mm or >21 mm/m2).10 Despite this, the level of evidence to support a tricuspid valve surgery in patients with non-severe TR remains weak. (Level of evidence C10) Several studies have reported the risk factors related to STR and their prognostic implications. However, their scope has been principally limited to TR associated with mitral valve disease, which occurs more commonly than TR associated with AS.14,15 Our study was focused on patients with severe AS undergoing AVR. The degree of tricuspid annulus dilatation was an independent and relevant parameter. In AS-patients, a dedicated attention should be, thus, paid to the right heart and the size of the tricuspid annulus. Echocardiography measurement of the tricuspid annulus according to current recommendation is nevertheless imperfect.16 Miglioranza et al.17,18 highlighted the presence of a gap in the scientific literature by providing normative data for tricuspid annulus diameters measured by 2D echocardiography imaging. Lindman et al.19 recently reported among 542 patients treated by aortic transcatheter valves, that TR was associated with increased 1-year mortality but essentially in patients having a mitral regurgitation . According to the current guidelines,8–10 tricuspid annulus dilatation is defined as a measure performed in early-diastole and in an apical 4-chamber view. The present study demonstrates that if the measurement is performed on optimized 4-chamber views in early-diastole, then, the intra and inter observer variability satisfied the precision required for the clinical routine. But, age, gender, RA and RV volumes have been found to be independently correlated with TA diameter.17,18 So, the best method for determining the severity of STR remains to be established. Dreyfus et al.16 have proposed a new staging system using TR severity, annular dilatation and mode of tricuspid leaflet coaptation as the 3 parameters to more accurately reflect the disease severity . Future developments in 3-D echocardiography may provide comprehensive imaging tools and quantitative software that are currently unavailable.20 Secondary TR develops or progresses after a left heart valve procedure mainly because of RV geometric alterations. It has recently been shown that while LV hypertrophy decreases after an AVR, this reverse remodelling is incomplete as observed in our study. Also, the degree of diffuse interstitial myocardial fibrosis remains essentially unchanged.21 Diffuse myocardial fibrosis has been linked with diastolic dysfunction and elevated LV end-diastolic pressures that promote post-capillary pulmonary hypertension. Elevated pulmonary pressure induces RV pressure overload which is associated with RV-dilation, distortion of the tricuspid valvular apparatus and eventually significant TR.22 The occurrence of significant TR initiates a vicious circle that propagates further RV dilatation and dysfunction, tricuspid annular dilatation and consequently worsening TR.19 The assumption that late secondary TR after a left heart valve procedure develops because of post-capillary pulmonary hypertension is supported by the more prominent left atrial dilation and higher estimated pulmonary artery pressures in patients with severe TR observed in our study (Table 3).23 Thus, pulmonary hypertension caused by left heart disease can cause significant TR, which means that correcting TR with an annuloplasty may not be sufficient to assure a stable TR reduction and to modify the outcome of these patients. In the PROTECT-PACE trial, TR was mainly related to the impact of the interventricular septum motion on the tricuspid septal leaflet.24 In the post-operative period, an altered motion of the interventricular septum and a restriction of the tricuspid septal leaflet motion might contribute to the progressive in TR. In a recent prospective long-term observational study, the impact of late significant TR after heart valve procedures was examined in 571 patients.25,26 Although significant TR was strongly associated with mortality by uni-variable Cox and Kaplan–Meier analyses, only RV-function was associated with outcomes in the multivariable model. Additionally, Kammerlander et al.25,26 showed that RV-function seems to be a more important predictor of outcomes in these patients. However, the same team did not reach the same conclusion when analysing a cohort of 465 consecutive patients who underwent only aortic valve replacement for AS.27 Significant TR was present in 26 (5.6%) patients at baseline. Patients with TR presented with a higher EuroSCORE I, more pulmonary hypertension and more dilated RV with more frequent RV-dysfunction. A multivariable Cox regression analysis found that TR was an independent marker of overall mortality after a median 5-year FU 8 years. Kaplan–Meier analysis revealed significantly lower survival rates in patients with significant TR compared with those without.27 Even if severe, TR may be well-tolerated for years. However, without treatment, TR may cause irreversible RV dysfunction, heart failure and death. Song et al.28 retrospectively investigated more than 600 patients after left heart valve procedures, including AS, and showed that significant late TR was associated with poorer outcomes, defined as either cardiovascular death, need for revision surgery and hospital admission due to congestive heart failure.19 They identified AF as an independent factor associated with the development of late TR. Atrial fibrillation, especially if chronic, can be an important factor in the development of STR primarily through its effect on tricuspid annular dilation. These data are consistent with our findings showing the significant role of TR dilatation in the development of significant TR after AVR in AS. Moreover, we found that AF was a frequent finding in patients with tricuspid annulus >40 mm (Table 6) and associated with the risk of late TR. Kwak et al.29 evaluated 335 patients after left heart valve procedures. Their endpoints of cardiovascular death or revision surgery were more frequently reached after 10 years of follow-up by patients with significant TR . In this study, preoperative AF was identified as the only independent predictor of late TR. Table 6 Clinical characteristics at index date according to tricuspid annulus value Variables  Missing data (n)  Tricuspid annulus <40 mm N = 93 % (n)  Tricuspid annulus ≥40 mm N = 19 % (n)  P  Clinical characteristics  Male  0  59.1 (55)  68.4 (13)  0.450  NYHA [functional class]  0         No dyspnea    10.8 (10)  5.3 (1)  0.615   I    5.4 (5)  0 (0)     II    58.1 (54)  73.7 (14)     III    22.6 (21)  15.8 (3)     IV    3.2 (3)  5.3 (1)    Age [years]  0  77 (14)  80 (7)  0.169  NT-pro-BNP  58  572 (902)  855 (2356)  0.279  Haemoglobin  0  13.4 (1.6)  13 (2.9)  0.998  Angina  1  14.1 (13)  10.5 (2)  0.675  HTA  0  68.8 (64)  68.4 (13)  0.972  Diabetes  0  16.1 (15)  10.5 (2)  0.535  Dyslipidemia  1  61.3 (57)  55.6 (10)  0.648  Smoker  1         No    72.8 (67)  89.5 (17)  0.271   Active    5.4 (5)  0 (0)     Former    21.7 (20)  10.5 (2)    Atrial fibrillation  0  16.1 (15)  47.4 (9)  0.005  CAD  0  21.5 (20)  5.3 (1)  0.118  Pacemaker    3.2 (3)  0 (0)    TAVI  0  26.9 (25)  36.8 (7)  0.381  Electrocardiogram  Normal conduction  0  64.5 (60)  52.6 (10)  0.381  BAV 1  8  25.6 (23)  14.3 (2)  0.358  LBBB    4.3 (4)  0 (0)    Incomplete LBBB    21.5 (20)  31.6 (6)    RBBB    6.5 (6)  15.8 (3)    Medication  Beta-blockers  0  41.9 (39)  57.9 (11)  0.202  ACEi/ARB  0  44.1 (41)  63.2 (12)  0.129  Diuretic agents  40  12.5 (8)  25 (2)  0.335  Statins  0  51.6 (48)  52.6 (10)  0.935  Variables  Missing data (n)  Tricuspid annulus <40 mm N = 93 % (n)  Tricuspid annulus ≥40 mm N = 19 % (n)  P  Clinical characteristics  Male  0  59.1 (55)  68.4 (13)  0.450  NYHA [functional class]  0         No dyspnea    10.8 (10)  5.3 (1)  0.615   I    5.4 (5)  0 (0)     II    58.1 (54)  73.7 (14)     III    22.6 (21)  15.8 (3)     IV    3.2 (3)  5.3 (1)    Age [years]  0  77 (14)  80 (7)  0.169  NT-pro-BNP  58  572 (902)  855 (2356)  0.279  Haemoglobin  0  13.4 (1.6)  13 (2.9)  0.998  Angina  1  14.1 (13)  10.5 (2)  0.675  HTA  0  68.8 (64)  68.4 (13)  0.972  Diabetes  0  16.1 (15)  10.5 (2)  0.535  Dyslipidemia  1  61.3 (57)  55.6 (10)  0.648  Smoker  1         No    72.8 (67)  89.5 (17)  0.271   Active    5.4 (5)  0 (0)     Former    21.7 (20)  10.5 (2)    Atrial fibrillation  0  16.1 (15)  47.4 (9)  0.005  CAD  0  21.5 (20)  5.3 (1)  0.118  Pacemaker    3.2 (3)  0 (0)    TAVI  0  26.9 (25)  36.8 (7)  0.381  Electrocardiogram  Normal conduction  0  64.5 (60)  52.6 (10)  0.381  BAV 1  8  25.6 (23)  14.3 (2)  0.358  LBBB    4.3 (4)  0 (0)    Incomplete LBBB    21.5 (20)  31.6 (6)    RBBB    6.5 (6)  15.8 (3)    Medication  Beta-blockers  0  41.9 (39)  57.9 (11)  0.202  ACEi/ARB  0  44.1 (41)  63.2 (12)  0.129  Diuretic agents  40  12.5 (8)  25 (2)  0.335  Statins  0  51.6 (48)  52.6 (10)  0.935  χ2 test or Fisher’s exact test. ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CAD, coronary artery disease; LBBB, left bundle branch block; RBBB, right bundle branch block; TAVI, trans-catheter aortic valve implantation. Study limitations This is a single-centre prospective study conducted on relatively limited number of patients. However, the major advantages of limiting data collection to a prospective single centre are as follows: ( i) inclusion of a homogenous patient population; (ii) adherence to a consistent clinical routine; (iii) consistent quality of echocardiographic work-up; and (iv) consistent follow-up (prospective study). It is difficult to precisely determine RV-dysfunction in the presence of significant TR because RV unloading due to TR may be misleading findings.12,30,31 One of the limitation of our analysis is that it is an echocardiography driven multivariable analysis. If we added atrial fibrillation in the multivariable model, age (RR = 1.77[1.03 –3.09], P = 0.03) and Atrial Fibrillation (RR = 2.55[1.51 –4.29], P = 0.0004) were the two parameters that were also independently and significantly associated with the prognosis. Conclusion In this study, moderate to severe STR was prevalent in 11.1% of patients with AS. This finding was more frequent in the case of a tricuspid annulus size >40 mm. Significant STR was found in 25.8% of patients 1 year after the procedure. Multivariable analysis found that tricuspid annulus size >40 mm was the only independent echocardiographic predictor of moderate to severe TR at the 1-year follow-up. RV function and size were not significantly associated with TR during followed-up of patients undergoing valve replacement for AS. Acknowledgements They thank deeply the CORECT and the CHU-Rennes for supporting the study (Acronym; AoMyoc). Conflict of interest: None declared. 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TI - Pre- and postoperative tricuspid regurgitation in patients with severe symptomatic aortic stenosis: importance of pre-operative tricuspid annulus diameter
JF - European Heart Journal – Cardiovascular Imaging
DO - 10.1093/ehjci/jex031
DA - 2018-03-01
UR - https://www.deepdyve.com/lp/oxford-university-press/pre-and-postoperative-tricuspid-regurgitation-in-patients-with-severe-WWy4DGMRLx
SP - 319
EP - 328
VL - 19
IS - 3
DP - DeepDyve
ER -