Abstract
Background:
Chronic severe mitral regurgitation is associated with poor clinical outcome because chronic volume overload leads to hemodynamic changes and left ventricular and left atrial remodeling. Few data are available regarding left atrial volume index regression (LAVIR) and left ventricular mass index regression (LVMIR) after valve surgery for mitral regurgitation. We aimed to identify predictive correlates of LAVIR and LVMIR and to assess the relationship between these regressions.
Hypothesis:
Volume overload in chronic severe mitral regurgitation may influence left atrial and ventricular remodeling and reverse remodeling.
Methods:
Eighty‐five patients who underwent valve repair for severe chronic mitral regurgitation were consecutively enrolled. Plasma N‐terminal fragment of the prohormone brain natriuretic peptide (NT‐proBNP) and echocardiographic measurements were performed before surgery, before discharge, and at 12 months after surgery. LAVIR and LVMIR were assessed using serial echocardiography.
Results:
There were significant decreases in left ventricular mass index (LVMI; from 125.9 ± 31.3 g/m2 to 94.8 ± 28.6 g/m2, P = 0.001) and left atrial volume index (LAVI; from 75.3 ± 33.5 mL/m2 to 41.7 ± 16.0 mL/m2, P = 0.001) after surgery. Preoperative LAVI positively correlated with preoperative LVMI (r = 0.437, P = 0.001) and LAVIR positively correlated with LVMIR (r = 0.347, P = 0.001). In multivariate stepwise linear regression analysis, preoperative LAVI, age, hypertension, and atrial fibrillation were independently predictive of LAVIR, and preoperative LVMI, hypertension, and NT‐proBNP were independently predictive of LVMIR.
Conclusions:
Volume overload in chronic severe mitral regurgitation may influence left ventricular remodeling and reverse remodeling, as well as left atrial remodeling and reverse remodeling. Preoperative lower LAVI, younger age, absence of hypertension, and absence of atrial fibrillation may predict LAVIR, and preoperative lower LVMI, lower NT‐proBNP levels, and absence of hypertension may predict LVMIR after surgery for chronic severe mitral regurgitation. Copyright © 2010 Wiley Periodicals, Inc.
The authors have no funding, financial relationships, or conflicts of interest to disclose.
Introduction
Chronic volume overload in chronic severe mitral regurgitation causes dilation of the left atrium (LA) and left ventricle (LV), which begets more mitral regurgitation. This vicious cycle leads to atrial fibrillation (AF), LA and LV failure, and poor clinical outcomes.1, 2, 3, 4 If severe mitral regurgitation persists, changes of the left atrial and/or ventricular chamber geometry and function become irreversible, despite surgical correction of mitral regurgitation.5 Preoperative LA and LV dysfunction and dimensions are known to be important predictors of poor outcome after surgical correction.6, 7, 8, 9 However, preoperative evaluation of LA and LV function has been found to be partially successful in determining postoperative clinical outcomes.6, 7, 8, 9 Accordingly, assessing whether the preoperative parameters are related to reverse remodeling of LA and/or LV after surgical correction is pertinent. However, few studies have been published on factors that influence the reverse remodeling of LA and LV after surgical correction of chronic severe mitral regurgitation. Furthermore, few data are currently available on the relationship of LAVI regression (LAVIR) and LVMI regression (LVMIR) after surgery. The aim of this study was to identify predictive factors of LAVIR and LVMIR and assess the relationship of LAVIR to LVMIR in patients about to undergo valve repair for chronic severe mitral regurgitation.
Methods
Study Subjects
Between January 2004 and December 2007, 85 patients about to undergo valve repair for chronic severe mitral regurgitation were consecutively enrolled. We included patients with either degenerative or rheumatic mitral regurgitation. Patients with other causes of mitral regurgitation, such as ischemic dilated cardiomyopathy, congenital heart disease, or infective endocarditis, were excluded. Patients who received any repair or reconstruction on the aortic valve were also excluded. Other exclusion criteria for this study were as follows: patients with coronary artery disease, mitral stenosis of ≥mild grade, aortic stenosis or insufficiency of ≥mild grade, uncontrolled thyroid disease, previous cardiac surgery, and chronic renal failure. The cause of mitral regurgitation was determined from the clinical history, the operative report of the surgeon, and the gross and microscopic pathologic findings. The protocol was approved by the Institutional Research Ethics Committee of Samsung Medical Center, Seoul, Korea, and the ethical recommendations of the revised version of the Declaration of Helsinki were met.
Hypertension (HT) was defined as repeated measurements of systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg, or previous antihypertensive drug treatment. Diabetes mellitus was defined as a serum glucose level of ≥126 mg/dL, a history of diabetes mellitus, or current use of antidiabetic therapy. Current smoking was defined as having smoked cigarettes in the year before surgery.
Echocardiography
Transthoracic echocardiographic examinations were performed in all patients with a 2.5 MHz transducer attached to a commercially available Doppler echocardiography machine, before and immediately after surgery (within 1 week), and 6 and 12 months after surgery. A standard echocardiographic examination was performed, which included LV end‐diastolic (LVEDD) and end‐systolic diameters (LVESD), and wall‐thickness measurement in accordance with the recommendations of chamber quantification.10 LV ejection fraction (LVEF) was calculated using the Teichholz method.10 LV mass (LVM) was calculated based on Devereux's formula and indexed by body surface area (LVMI).11 The postoperative percent change in LVMI was calculated as follows: (preoperative LVMI − postoperative LVMI) / preoperative LVMI ×100. The early diastolic mitral inflow velocity (E) was measured using pulse‐wave Doppler at the tip of the mitral valve leaflets as they opened. The early diastolic tissue Doppler velocity (E′) of the mitral annulus was acquired at the septum in apical four‐chamber view. Mitral regurgitation was qualified by color Doppler and quantified by vena contracta width and the proximal isovelocity surface area (PISA) method in accordance with the recommendations of the American Society of Echocardiography (ASE).12, 13 Tricuspid regurgitation (TR) was assessed by color Doppler flow mapping of spatial distribution of the regurgitant jet with the right atrium in accordance with the recommendations of the ASE.12, 13 In our study, significant TR was defined as TR of ≥mild degree. LA volume was determined by the prolate ellipse method12, 13 and indexed by body surface area (LAVI). The postoperative percent change in LAVI was calculated as follows: (preoperative LAVI − postoperative LAVI) / preoperative LAVI ×100.
Surgical Correction of Mitral Regurgitation
All procedures were performed through median sternotomy, using cardiopulmonary bypass with a bicaval venous drainage under moderate hypothermia and arrested heart. When performing a valve operation, the valve was first excised, then the modified Maze procedure was performed,14 followed by valve repair. Decisions regarding the use of different repair methods were made by the attending surgeon. Mitral valve repair was performed using resection of the prolapsing portion of the leaflet, neochordae, chordal shortening, chordal transfer, or edge‐to‐edge technique as needed, in isolation or in combination. A mitral annuloplasty, with or without prosthetic ring, was performed in 84 (99%) patients. The modified Maze procedure was conducted with cryoablation guided by direct visualization.14
Assay of N‐Terminal Fragment of the Prohormone Brain Natriuretic Peptide
Blood samples were taken from the antecubital vein using lithium heparin, centrifuged, and stored at −70°C until further analysis. Plasma N‐terminal fragment of the prohormone brain natriuretic peptide (NT‐proBNP) levels were measured using an Elecsys proBNP reagent kit (Roche Diagnostics, Indianapolis, IN) and an Elecsys 2010 (Roche Diagnostics).
Statistical Analysis
Statistical analysis was performed using SPSS version 13.0 software (SPSS, Inc., Chicago, IL). Data for continuous variables are expressed as mean ± SD. Plasma NT‐proBNP levels are given in terms of the median and interquartile range (IQR). The Mann‐Whitney nonparametric U test was used to compare the mean values between groups, and the χ 2 test was used to compare the categorical variables. Spearman correlation was used to estimate the correlation between 2 variables. The Wilcoxon rank sum test was used for comparison of preoperative and postoperative echocardiographic data and NT‐proBNP levels. The natural logarithm (ln) of NT‐proBNP levels (ln NT‐proBNP) was used to correlate the echocardiographic findings based on the Spearman correlation coefficient. Stepwise multiple linear regression analysis, including all significant parameters identified by univariate analysis, was used to identify the most important parameters of LAVIR and LVMIR. Differences were considered statistically significant when P values were <0.05.
Results
Clinical Characteristics
The clinical characteristics of the study population are presented in Table 1. The mean age of the patients was 54.7 ± 13.3 years. Of the 85 enrolled patients, 47 (55%) were women. The causes of mitral regurgitation in this study were myxomatous degeneration in 76 (89%) patients and rheumatic mitral valve disease in 9 (11%) patients. In 50 (59%) patients, tricuspid annuloplasty (TAP) was performed concomitantly. In 55 (65%) patients with AF, a modified Maze procedure was performed at the time of valve repair.
Table 1.
Clinical Characteristics
| N = 85 | |
|---|---|
| Age (y) | 54.7 ± 13.3 |
| Male sex, n (%) | 38 (45) |
| BMI (kg/m2) | 24.0 ± 3.0 |
| Body surface area (m2) | 1.7 ± 0.2 |
| Type of valvular disease | |
| Degenerative | 76 (89) |
| Rheumatic | 9 (11) |
| NYHA Fc, n (%) | |
| I | 3 (4) |
| II | 13 (15) |
| III | 46 (54) |
| IV | 23 (27) |
| HT, n (%) | 26 (31) |
| DM, n (%) | 9 (11) |
| AF, n (%) | 55 (65) |
| Smoking history, n (%) | 23 (27) |
| Thyroid dysfunction, n (%) | 2 (3) |
| β‐Blocker, n (%) | 20 (24) |
| ACEI or ARB, n (%) | 41 (48) |
| Diuretics, n (%) | 24 (28) |
| Systolic BP (mm Hg) | 118.0 ± 14.6 |
| Diastolic BP (mm Hg) | 72.9 ± 12.5 |
| Significant TR, n (%) | 50 (59) |
| TAP, n (%) | 50 (59) |
Abbreviations: BMI, body mass index; NYHA Fc, New York Heart Association functional class; HT, hypertension; DM, diabetes mellitus; AF, atrial fibrillation; ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; TR, tricuspid regurgitation; TAP, tricuspid valve annuloplasty.
Changes After Mitral Valve Surgery
Table 2 shows echocardiographic findings and NT‐proBNP levels before surgery and at the serial follow‐up after surgery. There were significant decreases in LVM, LVMI, LVEDD, LVESD, and LAVI after surgical correction. In contrast, LVEF and E/E′ increased significantly after surgery. Of note is that NT‐proBNP levels decreased significantly during follow‐up, from a median of 593 pg/mL (IQR: 176, 1399) to 146 pg/mL (IQR: 61, 354) (P = 0.001).
Table 2.
Echocardiographic Findings and NT‐proBNP Levels
| Preoperative | Postoperative, 1 Wk | Postoperative, 6 Mo | Postoperative, 12 Mo | P Value | |
|---|---|---|---|---|---|
| LVEF (%) | 58.5 ± 9.3 | 55.4 ± 9.7 | 58.0 ± 9.7 | 62.7 ± 7.2 | 0.001a |
| LVEDD (mm) | 60.3 ± 7.7 | 52.9 ± 6.8 | 51.2 ± 6.3 | 50.4 ± 6.0 | 0.001a |
| LVESD (mm) | 36.8 ± 7.3 | 36.6 ± 7.7 | 33.4 ± 7.6 | 32.8 ± 6.9 | 0.001a |
| LVM (g) | 213.3 ± 57.8 | 183.8 ± 52.3 | 168.4 ± 49.5 | 160.3 ± 49.8 | 0.001a |
| LVMI (g/m2) | 125.9 ± 31.3 | 108.5 ± 27.9 | 99.3 ± 27.8 | 94.8 ± 28.6 | 0.001a |
| E/E′ | 17.0 ± 12.2 | 22.4 ± 9.6 | 22.9 ± 8.6 | 22.9 ± 8.2 | 0.002a |
| LAVI (mL/m2) | 75.3 ± 33.5 | 48.4 ± 19.2 | 41.8 ± 17.3 | 41.7 ± 16.0 | 0.001a |
| NT‐proBNPb | 593 (176, 1399) | 584 (355, 926) | NA | 146 (61, 354) | 0.001a |
Abbreviations: LVEF, left ventricular ejection fraction; LVEDD, left ventricular end‐diastolic diameter; LVESD, left ventricular end‐systolic diameter; LVM, left ventricular mass; LVMI, left ventricular mass index; E/E', early diastolic mitral inflow velocity/early diastolic mitral annular velocity; LAVI, left atrial volume index; NT‐proBNP, N‐terminal fragment of the prohormone brain natriuretic peptide; NA, not available; IQR, interquartile range.
P < 0.05 postoperative 12‐month vs preoperative.
Expressed as median ± IQR.
Using the cutoff of 0% change of LAVI and LVMI at 12 months after surgery, a decrease in LAVI after surgery was seen in 78 (92%) patients, whereas 7 (8%) showed an increase in LAVI after surgery. Also, 74 (87%) patients showed a decrease in LVMI after surgery, whereas 11 (13%) showed an increase in LVMI after surgery.
Using the same cutoff, a decrease in LAVI after surgery was seen in 8 (89%) patients with rheumatic mitral regurgitation, whereas 70 (92%) patients with degenerative mitral regurgitation showed a decrease in LAVI. Also, 9 (100%) patients with rheumatic mitral regurgitation showed a decrease in LVMI, whereas 65 (86%) patients with degenerative mitral regurgitation showed an increase in LVMI after surgery. There were no significant differences in the decrease of LAVI (P = 0.740) and LVMI (P = 0.221) between these subgroups.
Correlation Between LAVI and LVMI, and Between LAVIR and LVMIR
Preoperative LAVI positively correlated with preoperative LVMI (r = 0.437, P = 0.001) and postoperative LAVIR positively correlated with postoperative LVMIR (r = 0.347, P = 0.001) (Figure 1). Patients with AF, when compared with patients with sinus rhythm, had significantly higher LAVI (79.8 ± 34.0 mL/m2 vs 54.5 ± 22.1 mL/m2, P = 0.003) and LVMI (129.9 ± 31.5 g/m2 vs 107.4 ± 22.9 g/m2, P = 0.034) (Figure 2). Patients with sinus rhythm had a significantly higher LAVIR (48.3 ± 11.9 % vs 38.2 ± 21.5%, P = 0.016) than patients with AF. However, there was no significant difference in LVMIR between patients with AF and patients with sinus rhythm (Figure 2).
Figure 1.
Correlation between LAVI and LVMI, and between LAVIR and LVMIR. Preoperative LAVI was positively correlated with preoperative LVMI (r = 0.437, P = 0.001), and postoperative LAVIR was positively correlated with postoperative LVMIR (r = 0.347, P = 0.001). Abbreviations: LAVI, left atrial volume index; LAVIR, left atrial volume index regression; LVMI, left ventricular mass index; LVMIR, left ventricular mass index regression; SEE, standard error of the estimate.
Figure 2.
Comparison of preoperative LAVI and LVMI and postoperative LAVIR and LVMIR in patients with AF and patients with sinus rhythm. Patients with AF had significantly higher LAVI (79.8 ± 34.0 mL/m2 vs 54.5 ± 22.1 mL/m2, P = 0.007) and significantly higher LVMI (129.9 ± 31.5 g/m2 vs 107.4 ± 22.9 g/m2, P = 0.011) than patients with sinus rhythm. Patients with AF had significantly lower LAVIR (38.2 ± 21.5% vs 48.3 ± 11.9%, P = 0.016) than patients with sinus rhythm. However, there was no significant difference in LVMIR between the 2 groups. Abbreviations: AF, atrial fibrillation; LAVI, left atrial volume index; LAVIR, left atrial volume index regression; LVMI, left ventricular mass index; LVMIR, left ventricular mass index regression.
Correlates of LAVIR and LVMIR
Simple correlation analysis shows that age (r = −0.318, P = 0.003), HT (r = −0.281, P = 0.009), AF (r = −0.319, P = 0.003), and LAVI (r = −0.510, P = 0.001) were negatively related to LAVIR. To identify independent predictors of LAVIR, we performed multivariate stepwise linear regression analysis and identified age, HT, AF, and preoperative LAVI as independent predictors of LAVIR (Table 3).
Table 3.
Correlates of Postoperative LAVIR and LVMIR
| β | P Value | |
|---|---|---|
| LAVIR | ||
| Age | −0.220 | 0.011a |
| HT | −0.199 | 0.022a |
| AF | −0.336 | 0.001a |
| Preoperative LAVI | −0.595 | 0.001a |
| LVMIR | ||
| HT | −0.239 | 0.018a |
| ln NT‐proBNP | −0.250 | 0.013a |
| Preoperative LVMI | −0.396 | 0.001a |
Abbreviations: LAVIR, left atrial volume index regression; HT, hypertension; AF, atrial fibrillation; LAVI, left atrial volume index; LVMIR, left ventricular mass index regression; ln, natural logarithm; NT‐proBNP, N‐terminal fragment of the prohormone brain natriuretic peptide; LVMI, left ventricular mass index.
P < 0.05, significant finding.
Simple correlation analysis shows that HT (r = −0.219, P = 0.044), preoperative LVMI (r = −0.330, P = 0.002), LVEDD (r = −0.251, P = 0.021), and ln NT‐proBNP (ρ = −0.226, P = 0.038) were negatively related to LVMIR. In multivariate stepwise linear regression analysis, independent predictors of LVMIR were HT, preoperative LVMI, and ln NT‐proBNP levels (Table 3).
Discussion
The main findings of this study are: (1) preoperative LAVI was positively correlated with preoperative LVMI, and postoperative LAVIR was positively correlated with postoperative LVMIR; and (2) age, HT, AF, and preoperative LAVI were independent predictors of LAVIR, and HT, preoperative LVMI, and ln NT‐proBNP levels were independent predictors of LVMIR after surgical repair of chronic severe mitral regurgitation.
We believe this is the first and largest study to investigate whether clinical characteristics, echocardiographic parameters, and NT‐proBNP levels could predict LAVIR and LVMIR in patients about to undergo valve repair for chronic severe mitral regurgitation, and the first to assess the relationship between LAVIR and LVMIR in such patients.
Postoperative Changes
Similar to results from previous studies,15, 16 most patients (92%) in our study showed a decrease in LAVI 12 months after valve repair for degenerative mitral regurgitation. Cardiac magnetic resonance imaging studies15, 17 have reported that LV reverse remodeling was observed at early follow‐up in the majority of patients, but a substantial percentage of patients showed LV reverse remodeling only at late follow‐up because the reverse remodeling process may need substantial time in some patients. Our findings indicated that a substantial percentage of patients (13%) did not show a decrease in LVMI 12 months after mitral valve repair. A possible explanation is that a substantial percentage of patients with irreversible structural changes caused by long‐standing severe mitral regurgitation may not show postoperative decreases in LAVI and LVMI, regardless of volume unloading early after surgery. Another possible explanation is that postoperative decreases in LAVI and LVMI may be long‐lasting processes in some patients.
It may be anticipated that patients with rheumatic mitral regurgitation may have better reverse remodeling because they tend to be younger than those with degenerative mitral regurgitation; however, our study did not show differences in decreases of LAVI and LVMI 12 months after surgery between these groups. The relatively small number of patients with rheumatic mitral regurgitation might have influenced these findings.
Correlation Between LAVI and LVMI, and Between LAVIR and LVMIR
To the best of our knowledge, no previously published studies have reported in detail on associations between LA and LV remodeling in patients with chronic severe mitral regurgitation.
In this study, preoperative LAVI was positively correlated with preoperative LVMI. Moreover, postoperative LAVIR was positively correlated with postoperative LVMIR. These findings may suggest that as a manifestation of chronic volume overload in chronic severe mitral regurgitation, structural remodeling of LV may parallel the structural and electrical remodeling of LA. According to previous studies,18, 19 LV remodeling causes LA enlargement, possibly through higher LV diastolic pressures or myocardial alterations, and LA enlargement reveals advanced hemodynamic alterations. This hypothesis is further supported by findings from an animal study,20 which demonstrated that in the presence of chronic volume overload, new sarcomeres are added in order to normalize elevated end‐diastolic stress resulting in eccentric hypertrophy with fiber elongation and LV enlargement. Therefore, we reasoned that the severity of LA and LV structural and/or electrical changes may reflect chronic history of mitral regurgitation.
In the present study, patients with AF had significantly higher LAVI than patients with normal sinus rhythm. Additionally, patients with normal sinus rhythm had significantly higher LAVIR than patients with AF. These findings are in concordance with previous studies14, 21 that show LA enlargement is a predictive factor for the development of AF in patients with organic mitral regurgitation and that AF itself produces LA enlargement and dysfunction. Thus, AF in chronic severe mitral regurgitation may exert a significant influence on LA remodeling and possibly reverse remodeling.
Interestingly, in this study, patients with AF had significantly higher LVMI than patients with normal sinus rhythm. However, no significant difference in LVMIR was observed between these 2 groups. These findings may suggest that AF itself may not be an important predictive factor of LVMIR, even though AF may reflect chronic history of mitral regurgitation.
Correlates of LAVI and LVMI Regressions
According to earlier studies, important factors determining the natural history after mitral valve surgery are LV function,1, 2, 3 LV size,6, 7, 8 LA size,9, 14 and AF.4, 21
In the present study, age, HT, AF, and LAVI were independent predictors of LAVIR in a multiple stepwise regression analysis. These findings may indicate that old age, HT, AF, and increased LAVI may hinder LA reverse remodeling after surgical repair of chronic mitral regurgitation. In the animal model,22 aging‐related changes in LA were interstitial fibrosis associated with variable conduction delay. Therefore, these pathological changes may be associated with lesser reverse remodeling of LA. According to previous studies,23, 24 insufficient LAVI regression in patients with HT is a consequence of impaired LV filling due to increased LV stiffness.
In accordance with previous studies,14, 16, 21 we found that preoperative AF and LAVI were predictive factors of LA reverse remodeling after surgical correction of mitral regurgitation. Therefore, we suggest that surgery at a younger age, or before the onset of AF and LA enlargement, may benefit patients with chronic severe mitral regurgitation.
The results of our stepwise multiple linear regression analysis indicate that HT, LVMI, and preoperative ln NT‐proBNP were independent predictors of LVMIR. According to a biopsy study of patients with severe chronic HT,25 collagen deposition and interstitial fibrosis in the myocardium are significantly increased in patients with HT compared with normotensive patients. Therefore, these pathological changes with HT may be associated with less reverse remodeling of LV. Based on these observations, we reasoned that a history of HT may adversely affect LVMIR after surgical repair of chronic severe mitral regurgitation. This study also showed that LVMI was negatively correlated with LVMIR. This may indicate that the change in LV mass as a time‐integrated marker of exposure to chronic severe mitral regurgitation may be a predictive factor for LVMIR after surgery.
In this study, preoperative ln NT‐proBNP was negatively correlated with LVMIR. This may indicate that NT‐proBNP levels are strongly associated with ventricular changes (remodeling). Recently published studies reported that brain natriuretic peptide (BNP) activation in mitral regurgitation reflects primarily ventricular and atrial consequences of mitral regurgitation, and higher BNP is a biomarker of adverse clinical outcomes.26, 27 The consistent findings of these studies,26, 27 in addition to the results of this study, indicate that preoperative lower NT‐proBNP levels at the time of surgery may be important predictors of LVMIR early after surgery.
Study Limitations
There are some limitations to be considered in our study. First, this was a retrospective analysis. Nonetheless, all patients were diagnosed and managed by protocol. Second, results of our study may be limited by the relatively small number of patients and short‐term follow‐up duration. The relatively small number of enrolled patients might result in a poor correlation coefficient despite the statistical relevance among continuous variables. However, this is the first study dedicated to the investigation of whether clinical characteristics, echocardiographic parameters, and NT‐proBNP levels can predict LA and LV reverse remodeling after repair of chronic severe mitral regurgitation. Finally, the value of quantitative Doppler echocardiographic methods has been debated; however, LV mass has been calculated based on Devereux's formula and used to describe LV remodeling. LA volume has been measured to describe LA remodeling, and mitral regurgitation has been quantified by 3 validated methods.
Conclusion
Volume overload in chronic severe mitral regurgitation may influence LV remodeling and reverse remodeling as well as LA remodeling and reverse remodeling. Preoperative lower LAVI, younger age, absence of HT, and AF may predict LAVIR, and preoperative lower LVMI, lower NT‐proBNP levels, and absence of HT may predict LVMIR after surgical repair of chronic severe mitral regurgitation.
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