2018 Volume 82 Issue 3 Pages 886-894
Background: Uncertainties remain regarding the course of existing tricuspid regurgitation (TR) after aortic valve replacement (AVR), and its long-term impact on outcome. We investigated changes in existing TR after isolated AVR for severe aortic stenosis (AS), the impact of preoperative TR on long-term outcome, and predictors of late significant TR.
Methods and Results: After excluding mild mitral regurgitation and severe TR, 226 consecutive patients undergoing isolated AVR for severe AS between 2002 and 2015 were reviewed. Patients were classified into a non-TR (none/trivial preoperative TR, n=159) and a TR group (mild/moderate preoperative TR, n=67). During follow-up (median, 4.3 years), late significant TR was more prevalent in the TR group (n=20; 35.0%) than in the non-TR group (n=13; 9.6%; HR, 10.0; 95% CI: 4.44–24.7; P<0.001). The TR group developed more right heart failure (n=3; 5% vs. no patients in the non-TR group, P=0.007), and had a decreased estimated glomerular filtration rate (relative to baseline) until 5 years postoperatively. The tricuspid annulus diameter index was an independent predictor of late significant TR development.
Conclusions: Preoperative mild or moderate TR is aggravated after isolated AVR, resulting in a high incidence of renal dysfunction and right heart failure. Concomitant tricuspid valve intervention should be considered in patients undergoing AVR for severe AS with mild or moderate TR accompanied by dilated tricuspid annulus.
In recent decades, the management of tricuspid regurgitation (TR) has become a great concern, given that moderate or severe TR, at the time of mitral valve surgery (MVS), is associated with poor prognosis.1 With regard to the natural history of untreated TR in MVS, functional TR can worsen with time, significantly impairing long-term outcome.2,3 Additionally, several studies have suggested that tricuspid annuloplasty should be considered during MVS when tricuspid annular dilatation is present.2,4–6 Current guidelines state that tricuspid valve repair should be considered in patients undergoing left-sided valve surgery who have mild-moderate primary TR and a dilated annulus, as well as those with primary severe TR.7,8 Almost all of the studies referenced in these guidelines, however, investigated the indication for tricuspid valve surgery in concomitant MVS; few studies have focused on the indication for tricuspid valve surgery in concomitant aortic valve surgery. Thus, changes in existing TR after aortic valve replacement (AVR) and the associated long-term impact on outcome remain uncertain. The aims of this study were therefore to (1) investigate the impact of preoperative TR on early and long-term survival and freedom from major adverse cardiac events (MACE) after isolated AVR for severe aortic stenosis (AS); (2) examine the changes in existing TR; and (3) determine the risk factors for late significant TR.
The hospital ethics committee approved this study. Between January 2002 and December 2015, 252 patients underwent isolated AVR for severe AS at the present institution. Of these, 25 patients with moderate or severe preoperative mitral regurgitation (MR) were excluded to avoid contained bias. Patients with severe preoperative TR were also excluded. Additionally, 1 patient was excluded because of loss to follow-up ≤30 days after surgery. The remaining 226 patients were examined retrospectively: 159 patients had no or trivial TR preoperatively (non-TR group), and 67 patients had mild or moderate TR preoperatively (TR group).
AVR and TR Management StrategyAVR was performed using conventional cardiopulmonary bypass with bicaval cannulation and bidirectional cardioplegia infusion. The choice of prosthetic valve was mainly dependent on surgeon discretion, but a bioprosthetic valve was preferred for patients aged >65 years.
For patients with mild or moderate TR, surgical intervention was not performed unless structural valve deterioration existed (e.g., prolapse, perforation, or torn chordae).
Echocardiographic ParametersTransthoracic echocardiography was routinely performed by experienced medical technologists before surgery, 1 week after surgery, and at postoperative visits, as appropriate. The left ventricular (LV) dimensions were obtained in the parasternal M-mode view and the ejection fraction (LVEF) was calculated using the Teichholz method. The aortic valve area and trans-native or prosthetic aortic valve mean pressure gradients were calculated using the continuity equation and the Bernoulli equation, respectively. TR severity was assessed using the ratio of the maximum jet area to the corresponding right atrial area, averaged across the parasternal and apical views.9 TR was graded as none/trace, mild, moderate, or severe. The tricuspid annulus diameter (TAD) was measured in the transthoracic apical 4-chamber view in late diastole at the time of maximum tricuspid opening.10 The TAD index was calculated by dividing TAD by the body surface area. Six patients (2.7%) were excluded from TAD index analysis due to lost records. Preoperative, postoperative, and late TR data were obtained ≤30 days before and after surgery, and at the latest follow-up visit, respectively. Late significant TR was defined as moderate or greater TR recorded at least twice on echocardiography, with the latter date defined as the date of late significant TR.
Postoperative Management and Follow-upAll patients received antiplatelet and anticoagulation therapy with warfarin and aspirin once adequate hemostasis had been achieved. For patients with a mechanical valve, warfarin was given permanently and was adjusted, as needed, to achieve a target international normalized ratio (INR) of 2.0–2.5. For patients with a bioprosthetic valve, warfarin was given for the first 3 months, with a target INR of 1.5–2.0. Additionally, aspirin (100 mg daily) was given permanently to all patients, regardless of valve type. Diuretics were initiated orally at estimated systolic pulmonary pressure ≥50 mmHg or moderate or greater TR (assessed via echocardiography) was observed during follow-up; the dosage was adjusted depending on the heart failure severity.
The primary endpoint was the characterization of the changes in existing TR after isolated AVR, and the impact of preoperative TR on long-term survival and freedom from re-admission for congestive heart failure. All clinical follow-up data were obtained by reviewing the medical records or interviewing patients (or their families) via telephone. Complete follow-up data were obtained for 216 patients (96%) postoperatively, and for 196 patients (87%) at late follow-up. The median follow-up period was 4.3 years (IQR, 2.2–7.0 years).
Definitions and Data CollectionAll cardiac and non-cardiac events, including death, were recorded. Early mortality was defined as in-hospital mortality, while late mortality was defined as death occurring beyond this period. MACE was defined as sudden death, cardiac-related death, myocardial infarction, readmission due to heart failure, and cardiac arrhythmia requiring an implantable pacemaker or cardioverter defibrillator. Heart failure was further subdivided into left and right heart failure, according to symptoms. Left heart failure was defined as heart failure accompanied by left heart failure symptoms (i.e., any dyspnea concomitant with increased body weight, LV dysfunction, or pulmonary congestion). Right heart failure was defined as right heart failure symptoms (i.e., liver dysfunction, ascites, or lower leg edema), requiring adjustments in neurohormonal agents, diuretics, and/or inotropes. The effective orifice area (EOA) index for each prosthesis was derived from reference normal values of EOA, divided by body surface area. Prosthesis-patient mismatch (PPM) was defined as clinically non-significant (i.e., mild or no PPM) for EOA index >0.85 cm2/m2; as moderate for EOA index >0.65 cm2/m2 or ≤0.85 cm2/m2; and as severe for EOA index ≤0.65 cm2/m2.11 The estimated glomerular filtration rate (eGFR) was calculated as follows: eGFR=186×(serum creatinine/88.4)−1.154×(age)−0.203×(0.742 if female).12
Statistical AnalysisContinuous variables are presented as mean±SD or as median (IQR); categorical variables are summarized as frequencies and percentages. Preoperative and postoperative data were compared using paired t-test. Group differences were evaluated using 2-sample t-test and Mann-Whitney U-test. Kaplan-Meier analysis was used to assess freedom from all-cause death, MACE, and readmission due to heart failure; group differences were evaluated using the log-rank test. Cox hazard models were used to identify preoperative predictors of the development of late significant TR during follow-up. Factors statistically significant on univariate analysis were entered into a subsequent multivariate analysis. In addition, receiver operating characteristic (ROC) analysis was used to determine the TAD index cut-off predicting the development of late significant TR. Statistical analysis was performed using JMP version 12 (SAS Institute, Cary, NC, USA). P<0.05 was considered statistically significant.
Baseline characteristics are listed in Table S1. The TR group was significantly older and had a greater prevalence of atrial fibrillation (AF) compared with the non-TR group. The 2 groups were similar with regard to laboratory data. On preoperative echocardiography, the TR group had a higher prevalence of mild MR, higher TR pressure gradient, and larger TAD, compared with the non-TR group. Postoperative and late echocardiographic results are listed in Table S2. The TR group had a significantly greater prevalence of mild MR and a tendency toward higher TR pressure gradient (TRPG) postoperatively, but there were no group differences in these parameters at late follow-up. Regarding LV systolic function, LVEF was similar between the 2 groups postoperatively and at late follow-up. Regarding prosthetic valve function, the prosthetic valve area did not differ between the groups postoperatively, but the TR group had a relatively smaller area at late follow-up compared with the non-TR group. Furthermore, the TR group more frequently presented with AF and progressive MR at late follow-up compared with the non-TR group.
Clinical OutcomeThe early- and long-term clinical outcomes are listed in Table 1. There were no significant group differences in operative, cardiopulmonary bypass, or aortic cross-clamp times. In addition, the prevalence of bioprosthesis implantation, size of bioprosthesis, PPM, and EOA index were similar between the 2 groups. Postoperative stroke was more prevalent in the TR group (9%) compared with the non-TR group (2%, P=0.020). There were no deaths ≤30 days after surgery in either group.
| Non-TR group (n=159) |
TR group (n=67) |
P-value | |
|---|---|---|---|
| Early clinical outcomes | |||
| Operative results | |||
| Operation time (min) | 266±70 | 249±60 | 0.069 |
| CPB time (min) | 140±38 | 137±46 | 0.609 |
| Cross-clamp time (min) | 101±27 | 95±28 | 0.130 |
| Bioprosthesis | 143 (90) | 64 (96) | 0.144 |
| Prosthetic valve size (mm) | 21±2 | 20±2 | 0.105 |
| EOA index | 1.03±0.16 | 1.02±0.15 | 0.742 |
| PPM | 16 (10) | 6 (9) | 0.796 |
| Early complications | |||
| Re-exploration for bleeding | 9 (6) | 5 (7) | 0.622 |
| Cardiac tamponade | 6 (4) | 2 (3) | 0.760 |
| Stroke | 3 (2) | 6 (9) | 0.020 |
| Prolonged ventilation | 7 (4) | 5 (7) | 0.192 |
| Renal failure requiring hemodialysis | 3 (2) | 1 (1) | 0.830 |
| AF | 57 (36) | 32 (48) | 0.103 |
| Pacemaker implantation | 8 (5) | 6 (9) | 0.279 |
| Postoperative results | |||
| ICU stay (days) | 2 (2–3) | 2 (1–4) | 0.083 |
| 30-day mortality | 0 (0) | 0 (0) | – |
| Long-term clinical outcomes | |||
| Late mortality | 32 (20) | 9 (13) | 0.222 |
| Cardiac-related mortality | 6 (3) | 2 (4) | 0.766 |
| Sudden death | 1 (1) | 0 (0) | 0.401 |
| Prosthetic valve endocarditis | 3 (2) | 0 (0) | 0.145 |
| AMI | 0 (0) | 1 (1) | 0.118 |
| Left heart failure | 2 (1) | 1 (1) | 0.889 |
| MACE | 32 (20) | 14 (21) | 0.896 |
| Sudden death | 1 (1) | 0 (0) | 0.401 |
| Cardiac tamponade | 0 (0) | 1 (1) | 0.118 |
| Prosthetic valve failure | 5 (3) | 0 (0) | 0.059 |
| Prosthetic valve endocarditis | 10 (6) | 1 (1) | 0.090 |
| AMI/unstable angina | 3 (2) | 1 (1) | 0.835 |
| Left heart failure | 7 (4) | 4 (6) | 0.623 |
| Right heart failure | 0 (0) | 3 (4) | 0.007 |
| PMI for arrhythmia | 6 (3) | 4 (6) | 0.475 |
Data given as mean±SD, median (IQR) or n (%). AF, atrial fibrillation; AMI, acute myocardial infarction; CPB, cardiopulmonary bypass; EOA, effective orifice area; ICU, intensive care unit; MACE, major adverse cardiac event; PMI, pacemaker implantation; PPM, prosthesis-patient mismatch; TR, tricuspid regurgitation.
Late mortality and cardiac-related mortality were similar between the 2 groups. Regarding MACE, although the total incidence did not differ between the groups, the incidence of right heart failure was greater in the TR group (n=3; 5%) compared with the non-TR group (no patients, P=0.007). On Kaplan-Meier analysis, the overall survival rates at 1, 3, and 5 years after surgery were similar between the 2 groups (non-TR group, 96.1%, 88.9%, and 87.7%; TR group, 95.5%, 92.2%, and 82.6%, respectively; P=0.893; Figure 1A). The groups also did not differ significantly in freedom from MACE at postoperative years 1, 3, and 5 (non-TR group, 93.0% 90.1% and 85.5%; TR group, 89.5%, 87.8% and 70.6%, respectively; P=0.163; Figure 1B).
(A) Overall survival rate and (B) freedom from major adverse cardiac events (MACE) according to presence of preoperative tricuspid regurgitation (TR).
The serial change in TR is shown in Figure 2A. At discharge, 41 patients (27.0%) in the non-TR group had developed mild TR, while none had developed significant TR. During follow-up, 11 patients (8.1%) and 1 patient (0.7%) in the non-TR group presented with moderate and severe TR, respectively. In contrast, 56 patients (86.2%) in the TR group had ≤mild postoperative TR at discharge, and 9 patients (16.4%) had developed moderate TR. At the latest follow-up, 17 patients (28.3%) and 4 patients (6.7%) in the TR group had moderate and severe TR, respectively. Freedom from late significant TR at postoperative years 1, 3, and 5 was significantly higher in the non-TR group (100%, 98.1%, and 92.1%, respectively) compared with the TR group (91.6%, 75.7% and 58.6%, respectively; P<0.001; Figure 2B).
(A) Serial change in tricuspid regurgitation (TR) following aortic valve replacement and (B) freedom from late significant TR according to presence of preoperative TR.
Group differences in postoperative changes in end-organ function were evaluated in patients who did not require permanent hemodialysis preoperatively (Figure 3A). The eGFR in the TR group was significantly lower at 5 years postoperatively relative to the preoperative level (P<0.001). In addition, the postoperative reduction in eGFR was significantly greater in the TR group compared with the non-TR group at 6 months (−7.8±13 mL/min vs. +0.2±12 mL/min, respectively, P<0.001) and at 1 year postoperatively (−9.1±10 mL/min vs. −0.4±13 mL/min, respectively, P<0.001). There were, however, no significant group differences or chronological change in total bilirubin (Figure 3B).
Serial change in (A) estimated glomerular filtration rate (eGFR; excluding hemodialysis [HD] patients) and (B) total bilirubin in all patients according to presence of preoperative tricuspid regurgitation (TR). *P<0.05 compared to non-TR group; #P<0.05 compared to preoperative value.
Long-term clinical outcome of late significant TR is listed in Table 2. During follow-up, 33 patients (17%) developed late significant TR. Of these, 12 patients (36%) had late AF and the other 21 patients had sinus rhythm. The prevalence of late AF was significantly higher in patients with late significant TR compared with patients without late significant TR (36% vs. 10%, P<0.001). Although there was no difference in late mortality, there was a tendency toward higher MACE occurrence in patients with late significant TR compared with patients without late significant TR (P=0.080). Specifically, left heart failure (P=0.013) and right heart failure (P<0.001) developed significantly more frequently in patients with late significant TR compared with patients without late significant TR. Three patients had right heart failure, all of whom were in the TR group (preoperative TR: mild, n=2; moderate, n=1) with increased TAD, and had developed late significant TR without any LV or prosthetic valve function impairment at late follow-up.
| No late significant TR (n=163) |
Late significant TR (n=33) |
P-value | |
|---|---|---|---|
| Late AF | 16 (10) | 12 (36) | <0.001 |
| Late mortality | 21 (20) | 7 (13) | 0.233 |
| Cardiac-related mortality | 5 (3) | 1 (3) | 0.991 |
| Prosthetic valve endocarditis | 1 | 1 | 0.278 |
| AMI | 1 | 0 | 0.543 |
| Left heart failure | 3 | 0 | 0.291 |
| MACE | 27 (17) | 10 (30) | 0.080 |
| Sudden death | 1 | 0 | 0.401 |
| Cardiac tamponade | 0 | 1 | 0.543 |
| Prosthetic valve failure | 5 | 0 | 0.172 |
| Prosthetic valve endocarditis | 6 | 1 | 0.851 |
| AMI/unstable angina | 4 | 0 | 0.835 |
| Left heart failure | 5 | 5 | 0.013 |
| Right heart failure | 0 | 3 | <0.001 |
| PMI for arrhythmia | 6 | 1 | 0.851 |
Data given as n (%). Abbreviations as in Table 1.
On Kaplan-Meier analysis, freedom from left heart failure at postoperative years 1, 5, and 10 was significantly lower in patients with late significant TR compared with patients without late significant TR (100%, 79.7%, and 79.7% vs. 100%, 96.6%, and 94.8%, respectively; P=0.006, Figure 4A). Freedom from right heart failure at postoperative years 1, 5, and 10 was also significantly lower in patients with late significant TR compared with patients without late significant TR (97.0%, 92.6%, and 82.3% vs. 100%, 100%, and 100%, respectively; P=0.006; Figure 4B).
Freedom from (A) left heart failure (LHF) and (B) right heart failure (RHF), according to presence of late significant tricuspid regurgitation (TR).
On univariate analysis, older age, female sex, preoperative TR ≥mild, higher preoperative TRPG, larger preoperative TAD index, and postoperative/late AF were significantly associated with the development of late significant TR (P<0.05; Table 3). On subsequent multivariate analysis, preoperative TAD index was the only independent predictor of the development of late significant TR.
| Univariate analysis | Multivariate analysis | |||
|---|---|---|---|---|
| HR (95% CI) | P-value | HR (95% CI) | P-value | |
| Preoperative variables | ||||
| Older age | 1.122 (1.059–1.193) | <0.001 | 1.042 (0.968–1.128) | 0.278 |
| Female sex | 2.314 (1.110–5.278) | 0.024 | 1.624 (0.530–6.108) | 0.411 |
| Body mass index | 0.917 (0.832–1.008) | 0.074 | ||
| Hypertension | 1.459 (0.718–3.147) | 0.302 | ||
| Diabetes mellitus | 0.565 (0.135–1.603) | 0.313 | ||
| Hemodialysis | 1.189 (0.351–3.039) | 0.752 | ||
| COPD | 1.665 (0.488–4.329) | 0.376 | ||
| Rheumatic etiology | 2.181 (0.645–5.570) | 0.186 | ||
| AF | 1.700 (0.574–4.071) | 0.307 | ||
| History of PMI | 1.090 (0.057–5.860) | 0.938 | ||
| NYHA class | 1.007 (0.588–1.717) | 0.981 | ||
| LVEF | 1.000 (0.968–1.035) | 0.973 | ||
| Mild MR | 1.587 (0.774–3.262) | 0.206 | ||
| TR ≥mild | 7.965 (3.709–18.56) | <0.001 | 2.187 (0.702–7.674) | 0.180 |
| TRPG | 1.082 (1.035–1.128) | <0.001 | 1.030 (0.970–1.085) | 0.315 |
| TAD index | 1.311 (1.220–1.403) | <0.001 | 1.192 (1.063–1.340) | 0.003 |
| Postoperative variables | ||||
| AF | 2.832 (1.117–6.332) | 0.030 | 1.523 (0.442–5.603) | 0.510 |
| Aortic valve area | 0.642 (0.102–2.877) | 0.589 | ||
| Aorta-LV peak PG | 0.995 (0.958–1.029) | 0.774 | ||
| PPM | 0.782 (0.186–2.228) | 0.678 | ||
| Late variables | ||||
| Atrial fibrillation | 2.941 (1.398–5.908) | 0.006 | 2.353 (0.754–6.597) | 0.135 |
COPD, chronic obstructive lung disease; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; NYHA, New York Heart Association; PG, pressure gradient; TAD, tricuspid annular diameter. Other abbreviations as in Table 1.
On ROC analysis, a TAD index cut-off of 21.0 mm/m2 had optimal sensitivity (72.7%) and specificity (91.8%) in predicting the development of late significant TR (area under the curve, 0.879; P<0.001). Patients with a TAD ≥21.0 mm/m2 had a significantly higher incidence of late significant TR compared with those with TAD <21.0 mm/m2 (Figure 5A). Patients were further subdivided into 4 subgroups according to preoperative TR grade (non-TR/TR) and TAD index (≥ or <21.0 mm/m2). Patients with TR and increased TAD (group IV) had the lowest rate of freedom from late significant TR (1 year, 76.0%; 3 years, 54.6%; 5 years, 23.0%) of the 4 subgroups (Figure 5B).
Freedom from late significant tricuspid regurgitation (TR) according to (A) preoperative tricuspid annular diameter (TAD) index, and (B) preoperative TAD index and preoperative TR grade (I, no TR and non-increased TAD; II, TR and non-increased TAD; III, no TR and increased TAD; IV, TR and increased TAD).
The primary findings of the present study were as follows: (1) untreated TR progressed during follow-up after AVR, particularly in patients with mild or moderate preoperative TR; (2) patients with preoperative TR more frequently developed right heart failure and renal dysfunction during follow-up compared with those without preoperative TR; (3) late significant TR adversely affected the development of heart failure, especially right heart failure; and (4) a preoperative, increased TAD index was an independent predictor for the development of late significant TR.
In the present study, only half of the patients in the non-TR group (as well as a few patients in the TR group) remained unchanged in terms of TR after isolated AVR. Kusajima et al reported that freedom from moderate or severe TR after MVS was 64.2% at 5 years and 46.7% at 10 years in patients with mild preoperative TR, when the TR was not surgically treated.13 Similarly, Jeong et al recently examined changes in TR after AVR for AS and found that functional TR did not improve in half of the patients with mild or moderate preoperative TR.14 In the present study, approximately one-third of the patients in the TR group developed late significant TR during follow-up. In addition, late significant TR, which was more prevalent in patients with mild or moderate preoperative TR, was associated with a high incidence of right heart failure. Similarly, residual significant TR untreated at the time of MVS was associated with a higher long-term mortality rate, lower New York Heart Association (NYHA) class, lower quality of life, and reduced exercise capacity.2,5,15,16 Therefore, concomitant tricuspid valve surgery should be considered when there is a high risk of worsening TR. Residual late significant TR could be partly explained by progressive renal dysfunction, given that the incidence of late significant TR was associated with an exacerbation of renal function in the present study. A greater decline in eGFR in the TR group relative to that in the non-TR group emerged postoperatively and remained significant 1 year after AVR. Furthermore, eGFR remained decreased relative to the preoperative level, in the TR group until 5 years after AVR. An association between renal function impairment and renal congestion has been demonstrated, with renal dysfunction in heart failure more likely to be caused by passive backward venous congestion than by low forward renal perfusion.17,18 Although right heart catheter examination was not performed in the present study, echocardiographic preoperative and postoperative LV systolic function, and postoperative prosthetic valve function were similar in the non-TR and TR groups. Thus, backward congestive renal dysfunction due to worsening TR may result in systemic volume overload, precipitating a vicious cycle between worsening TR and further backward congestive renal dysfunction.
In the present study, only increased preoperative TAD index was an independent predictor of late significant TR. Various factors have been reported as risk factors for the persistence or late worsening of TR,2,4–6,19–24 but Goldstone et al reported that the TAD index was the only significant risk factor for late significant TR in patients with mild or no preoperative TR.25 In addition, Van de Veire et al reported that the worsening of untreated TR after MVS was mainly determined by the tricuspid annular dimension, not by preoperative TR.6 Importantly, the present study has shown that current guidelines pertaining to the TAD index for the indication of tricuspid valve surgery,7,8 which were derived from reports on concomitant MVS alone,2,4,6 can be applied in isolated AVR for AS.
The mechanisms underlying the links between TR and aortic valve disease remain unclear. Given that AS causes concentric myocardial hypertrophy and diastolic dysfunction, elevated endo-diastolic LV pressure leads to pulmonary hypertension, which eventually leads to right ventricular (RV) dysfunction. Consequently, RV dilatation and subsequent tricuspid annulus dilatation could worsen TR. Furthermore, Jeong et al showed that post-AVR diastolic dysfunction could cause late significant TR.14 Although parameters related to AVR (e.g., severity of aortic valve stenosis or postoperative prosthetic valve function) were not associated with the development of late significant TR in the present study, we believe that increased TAD may be the ultimate phenotype caused by RV dilatation due to elevated RV end-diastolic pressure derived from AF or pulmonary hypertension.19 It is noteworthy that a similar TAD index cut-off (21 mm/m2) was obtained by Colombo et al for MVS patients.4 Therefore, we speculate that a TAD of 21.0 mm/m2 is an important threshold, reflecting significant tricuspid annular dilatation, regardless of the type of left heart valve dysfunction.
Study LimitationsThere were several limitations in the present study. First, the present study was a single-center retrospective study with a limited number of patients. Second, the echocardiographic follow-up data were incomplete (follow-up rate, 87%). Third, although regional LV wall motion abnormality is usually unrecognized in these patients, estimation of LVEF using the Teichholz method can lead to error and should not be used in such patients. Fourth, we could examine TAD only as RV function on echocardiography. Data regarding the dimensions or ejection fraction of the right heart were not evaluated. Finally, data regarding medication use, including the amount of diuretics, were absent.
Mild or moderate preoperative TR worsened after isolated AVR in patients with increased TAD, and the worsening of TR was associated with a high incidence of right heart failure. Thus, concomitant tricuspid valve intervention should be considered in patients with mild or greater preoperative TR and a dilated tricuspid annulus at the time of AVR for severe AS. Prospective interventional studies, however, are needed to reach a definitive conclusion.
The authors declare no conflict of interest.
Supplementary File 1
Table S1. Patient characteristics vs. presence of preoperative TR
Table S2. Postoperative and late echocardiography
Please find supplementary file(s);
http://dx.doi.org/10.1253/circj.CJ-17-0996
