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Archives of cardiovascular diseases
Volume 110, n° 1
pages 26-34 (janvier 2017)
Doi : 10.1016/j.acvd.2016.05.010
Received : 22 February 2016 ;  accepted : 12 May 2016
Prognostic significance of left ventricular concentric remodelling in patients with aortic stenosis
Valeur pronostique du remodelage ventriculaire gauche dans la sténose valvulaire aortique
 

Nicolas Debry a, Sylvestre Maréchaux b, c, Dan Rusinaru c, d, Marcel Peltier c, d, David Messika-Zeitoun e, Aymeric Menet b, c, Christophe Tribouilloy c, d,
a Department of Cardiology, Lille University Hospital, F-59000 Lille, France 
b Department of Cardiology, Groupement des Hôpitaux de l’Institut Catholique de Lille, F-59160 Lille, France 
c Inserm U-1088, Jules-Verne University of Picardie, F-80054 Amiens, France 
d Department of Cardiology, Amiens University Hospital, F-80054 Amiens, France 
e Department of Cardiology, Bichat University Hospital, F-75018 Paris, France 

Corresponding author. Department of Cardiology, Amiens University Hospital, avenue René-Laënnec, 80054 Amiens cedex 1, France.
Summary
Background

Four patterns of left ventricular (LV) geometry (normal, concentric remodelling, concentric hypertrophy and eccentric hypertrophy) have been described in aortic stenosis (AS). Although LV concentric remodelling (LVCR), characterized by normal LV mass despite increased LV wall thickness, is frequently observed in AS, its prognostic implication has been not specifically studied.

Aim

We aimed to assess, using echocardiography, the prognostic implication of LVCR in asymptomatic or minimally symptomatic patients with AS.

Methods

Overall, 331 patients (mean age 73±13 years; 45% women) with AS (aortic valve area1.3cm2) and an ejection fraction >50% were enrolled. The endpoints were mortality with conservative management and mortality with conservative and/or surgical management.

Results

Sixty-three (19%) patients died under conservative management (follow-up 29±1 months). The highest risk of mortality under conservative management compared with patients with normal LV geometry was observed for LVCR (adjusted hazard ratio [HR]: 3.53, 95% confidence interval [CI]: 1.19–10.46; P =0.023), followed by concentric LVH (adjusted HR: 2.97, 95% CI: 1.02–8.60; P =0.045). Aortic valve replacement was performed in 96 patients (29%) during the entire follow-up (37±1 months); 72 (22%) patients died. Only LVCR remained independently associated with an increased risk of mortality when surgical management during the entire follow-up was considered (adjusted HR: 2.93, 95% CI: 1.19–7.23; P =0.020).

Conclusions

Among the patterns of LV geometry in AS, LVCR portends the worst outcome. Patients with LVCR and AS have a considerable increased risk of mortality, regardless of clinical management.

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Résumé
Contexte

Quatre types de géométrie ventriculaire gauche (VG) (normal, remodelage concentrique, hypertrophie concentrique et excentrique) ont été décrits dans le rétrécissement aortique (RAo). Bien que le remodelage concentrique du VG (RCVG) caractérisé par une masse VG normale malgré une augmentation de l’épaisseur de la paroi VG soit fréquemment observée dans le RAo, son impact pronostic n’a pas été spécifiquement étudié.

Objectif

Nous avons évalué à l’aide de l’échocardiographie l’implication pronostique du RCVG dans une cohorte de patients porteurs de RAo a- ou pauci-symptomatiques.

Méthodes

Trois cent trente et un patients (âge moyen 73±13 ans ; 45 % de femmes) porteurs d’une sténose aortique (surface aortique1,3cm2), fraction d’éjection>50 % ont été inclus dans l’étude. Les critères d’évaluation étaient : (1) la mortalité sous traitement médical et (2) la mortalité sous traitement médical et/ou chirurgical.

Résultats

Soixante-trois (19 %) patients sont décédés sous traitement conservateur (suivi moyen 29±1 mois). Le risque de mortalité sous traitement médical le plus élevé en comparaison avec la géométrie VG normale était observé pour le RCVG (hazard ratio ajusté [HR] : 3,53, IC 95 % : 1,19–10,46 ; p =0,023) suivi par l’hypertrophie ventriculaire gauche concentrique (HR ajusté : 2,97, IC 95 % : 1,02–8,60 ; p =0,045). Le remplacement valvulaire aortique a été réalisé chez 96 patients (29 %) au cours de la totalité de suivi (37±1 mois), et 72 (22 %) patients sont décédés. Seul le RCVG est resté indépendamment associé à un risque accru de mortalité lorsqu’une éventuelle prise en charge chirurgicale lors du suivi était considérée (HR ajusté : 2,93, IC 95 % : 1,19–7,23 ; p =0,020).

Conclusion

Parmi les types de géométrie VG dans le RAo, le RCVG a le moins bon pronostic. Les patients atteints de RAo avec RVGC présentent une augmentation considérable du risque de mortalité, indépendamment de leur gestion clinique.

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Keywords : Aortic stenosis, Left ventricular remodelling, Echocardiography, Surgery

Mots clés : Rétrécissement aortique, Remodelage ventriculaire gauche, Echocardiographie, Chirurgie

Abbreviations : AS, AVA, AVR, CI, HR, LV, LVCR, LVEF, LVH, RWT


Background

Concentric hypertrophy of the left ventricle (LV) is a compensatory mechanism for the chronic pressure overload observed in aortic stenosis (AS). Both the 2007 European Society of Cardiology [1] and the 1998 American College of Cardiology/American Heart Association guidelines [2] categorised echocardiographically detected left ventricular (LV) hypertrophy as a class IIb indication for aortic valve replacement (AVR). However, given the scarcity of published data on the prognostic effect of LV hypertrophy in AS [3], this recommendation was removed from the most recent versions of these guidelines [1, 4, 5]. Although concentric LV hypertrophy is classical in AS, LV concentric remodelling (LVCR) – characterised by a normal mass despite increased LV wall thickness – is also frequent (found in about 20% of cases of AS) [6]. However, the prognostic implications of LVCR in relation to clinical management have not been specifically studied.

The aim of the present analysis was to study the link between LVCR and mortality in patients with AS, irrespective of clinical management, in a cohort of patients with asymptomatic or minimally symptomatic AS.

Methods
Study population

Patients aged18 years, diagnosed at the echocardiography laboratories of two French tertiary centres (Amiens and Lille) between 2000 and 2012 with AS (aortic valve area [AVA]1.3cm2) and a left ventricular ejection fraction (LVEF)50%, and managed medically for at least 3 months after diagnosis, were prospectively identified and included in an electronic database.

We excluded patients with >mild aortic and/or mitral regurgitation; patients with prosthetic valves, congenital heart disease (with the exception of bicuspid aortic valves), supravalvular or subvalvular AS, or dynamic LV outflow tract obstruction; patients with angina, syncope or heart failure symptoms; and patients who denied authorization for research participation.

The present analysis included 331 AS patients who were asymptomatic or minimally symptomatic at the time of diagnosis. Symptoms were ascertained by each patient's personal cardiologist. We considered as minimally symptomatic patients presenting with atypical chest pain and elderly patients with minimal dyspnoea not clearly related to AS.

The Charlson comorbidity index, summating the patient's individual comorbidities, was calculated [7]. The diseases recorded for calculation of this index and their corresponding point values were myocardial infarction (1); congestive heart failure (1); cerebrovascular disease with mild or no residual deficit (1); chronic lung disease (1); peripheral vascular disease (1); peptic ulcer disease (1); diabetes mellitus without end-organ damage (1); dementia (1); connective tissue disease (1); mild liver disease (1); hemiplegia (2); diabetes mellitus with organ damage (2); moderate or severe chronic renal impairment (2); solid organ malignancy (2); leukaemia (2); lymphoma (2); moderate or severe chronic liver disease (3); metastatic solid organ malignancy (6); and acquired immunodeficiency syndrome (6). Known coronary artery disease was defined as the presence of documented history of acute coronary syndromes, coronary artery disease previously confirmed by coronary angiography (reduction of the normal diameter by ≥50% in the left main coronary artery and by ≥70% in the right coronary, left anterior descending and circumflex arteries) or history of coronary revascularization, as previously reported [8].

We obtained institutional review board authorizations prior to conducting the study. The study was conducted in accordance with institutional policies, national legal requirements and the revised Helsinki Declaration.

Echocardiography

Doppler echocardiographic measurements included LV end-diastolic and end-systolic diameters, LVEF determined by the modified Simpson's biplane method, LV stroke volume measured in the LV outflow tract by pulsed wave Doppler, aortic peak velocity, mean transvalvular gradient determined by the simplified Bernoulli equation and AVA determined by the continuity equation. Valvuloarterial impedance (Zva ) was calculated using the following formula, as previously reported [9]: Zva =[mean transaortic gradient+systolic blood pressure]/stroke volume indexed to body surface area.

LV mass was calculated using the corrected formula of the American Society of Echocardiography, and indexed for body surface area [10]. LV wall thickness and dimensions were estimated, whenever possible, from M-mode imaging or by default from two-dimensional images obtained in the parasternal long-axis view using the leading edge methodology. LV hypertrophy (LVH) was defined as LV mass index>115g·m−2 in men and >95g·m−2 in women [10]. Relative wall thickness (RWT) was calculated for assessment of LV geometry using the following formula: (septal+posterior diastolic wall thickness)/LV diastolic diameter [10]. Patients were classified according to four patterns of LV geometry: concentric remodelling; concentric hypertrophy; eccentric hypertrophy; and normal. LVCR was classically defined by RWT>0.42 in the absence of LVH. Concentric and eccentric hypertrophy were defined when LVH was associated with RWT≤ and >0.42, respectively. Normal geometry was considered in the absence of LVH and RWT0.42.

Clinical decision and follow-up

After initial medical management, treatment was either conservative or surgical, as deemed appropriate by the patient's attending physician. Information on follow-up was obtained retrospectively by direct patient interview and clinical examination and/or by repeated follow-up letters, questionnaires, and telephone calls to physicians, patients, and (if necessary) next of kin.

The study endpoint was overall survival after diagnosis starting at baseline echocardiography, and was analysed according to conservative management, and conservative and/or surgical management. Survival analysis with conservative management was assessed until last follow-up with medical management (censored at surgery). Survival with conservative and/or surgical management encompassed medical and surgical management.

Statistical analysis

Continuous variables are expressed as mean±standard deviation or median (interquartile range); categorical variables are summarized as numbers and percentages. The relationship between baseline continuous variables and the four patterns of LV geometry was explored using one-way analysis of variance. The Shapiro–Wilk test was used to verify whether the residuals obtained on analysis of variance approximated a normal distribution. When this test failed, non-parametric analysis of variance (Kruskal–Wallis test) was used. Pearson's χ2 statistic or Fisher's exact test was used to examine the association between the four patterns of LV geometry and baseline categorical variables. The significance between normal LV geometry (referent subgroup) and the other subgroups was examined if there was a significant difference across categories. Post hoc comparisons were performed using either Tukey's comparison or Mann-Whitney U tests with Bonferroni's correction for multiple comparisons, as appropriate.

For analysis of outcomes under medical management, data were censored at the time of cardiac surgery (if performed). The entire follow-up was used to analyse outcomes under conservative and/or surgical treatments. The effect of AVR on outcome was analysed as a time-dependent covariate using the entire follow-up.

The Kaplan-Meier method was applied to estimate mortality in the subgroups of patients defined by the four patterns of LV geometry (concentric hypertrophy, concentric remodelling, eccentric hypertrophy and normal). Two-sided log-rank tests were applied to compare mortality in the normal geometry subgroup versus the three other subgroups. Cox proportional hazard models using univariate then multivariable analysis determined all-cause mortality. Risk of death in the three subgroups (concentric hypertrophy, concentric remodelling and eccentric hypertrophy) was estimated versus the normal geometry subgroup. Model-building techniques were not used. Covariates entered in the models were considered of potential prognostic impact on an epidemiological basis; these covariates were age, sex, comorbidity index, hypertension, asymptomatic status at baseline, known coronary artery disease, history of atrial fibrillation, AVA and LVEF. AVR as a time-dependant variable was also added into Cox multivariable models analysing outcomes under conservative and/or surgical treatments. As coronary angiography was not performed in every patient, and as distinction between asymptomatic and minimally symptomatic patients in an elderly population is challenging, multivariable models without these two variables were also performed. For continuous variables, the assumption of linearity was assessed by plotting martingale residuals against independent variables. The proportional hazards assumption was confirmed using statistics and graphs based on the Schoenfeld residuals. A P -value<0.05 was considered statistically significant. Statistical analyses and figures were obtained using PASW 18.0 (IBM, Inc., Bois-Colombes, France), R-3.0.3 (R Foundation for Statistical Computing, Vienna, Austria) and GraphPad Prism (GraphPad Software, La Jolia, CA, USA).

Results

The study population consisted of 181 (55%) men and 150 (45%) women, with a mean age of 73±13 years; 223 (67%) had a history of hypertension, 133 (40%) were dyslipidaemic, 95 (29%) were diabetic and 11 (3%) had chronic renal failure (Table 1). Fifty-seven (17%) patients had normal LV geometry, 155 (47%) had concentric LVH, 34 (10%) had eccentric LVH and 85 (26%) had LVCR.

Table 1 shows the baseline clinical and echocardiographic data according to LV geometry. Hypertension, diabetes, hyperlipidaemia, smoking, history of coronary artery disease and atrial fibrillation were equally common in patients with LVCR and in patients with normal LV geometry. Compared with patients with normal LV geometry, patients with LVCR had a smaller LV diameter and stroke volume index, a similar LV mass index and LVEF, and a higher RWT and systolic pulmonary arterial pressure. However, AVA and transvalvular gradients were not different between these two subgroups.

Patients with concentric LVH, compared with those with normal LV geometry, were more often women and hypertensive, had a similar LV diameter, stroke volume index and LVEF, and a higher LV mass index, RWT, left atrium size and systolic pulmonary arterial pressure. Despite similar AVA values, transvalvular gradients and velocities were greater in patients with concentric LVH compared with patients with normal LV geometry.

Patients with eccentric LVH were similar to patients with normal LV geometry. Systolic pulmonary arterial pressure was higher in these patients compared with in those with normal LV geometry.

Outcome with conservative management

During a mean follow-up with conservative management of 29±1 months, 63 (19%) patients died. Four-year event-free survival was 90±5% for patients with normal LV geometry, 76±10% for patients with eccentric LVH, 70±5% for patients with concentric LVH and 65±7% for patients with LVCR (Figure 1A). Compared with patients with normal LV geometry, event-free survival was significantly lower in patients with LVCR (P =0.009) and concentric LVH (P =0.011), but was not lower in patients with eccentric LVH (P =0.15). LVCR and concentric LVH were associated with an increased risk of mortality under conservative management: unadjusted hazard ratio [HR]: 3.83, 95% confidence interval [CI]: 1.30–11.27 (P =0.015) for LVCR; and unadjusted HR: 3.49, 95% CI: 1.24–9.82 (P =0.018) for LVH. Risk was not significantly increased in patients with eccentric LVH (unadjusted HR: 2.49, 95% CI: 0.67–9.29; P =0.17). Cox multivariable analysis showed that LVCR and concentric LVH remained associated with mortality risk under conservative management, the higher risk being observed in case of LVCR: adjusted HR: 3.53, 95% CI: 1.19–10.46 (P =0.023) for LVCR; and adjusted HR: 2.97, 95% CI: 1.02–8.60 (P =0.045) for concentric LVH (Table 2, Figure 2A). Removing known coronary artery disease and asymptomatic status from this multivariable model did not alter the relationship between LVCR (adjusted HR: 3.63, 95% CI: 1.22–10.74; P =0.020), concentric LVH (HR: 2.94, 95% CI: 1.02–8.48; P =0.046) and outcome under conservative management. The replacement of AVA by aortic peak velocity in this former model did not alter its results: adjusted HR: 3.65, 95% CI: 1.23–10.78 (P =0.019) for LVCR; and adjusted HR: 3.03. 95% CI: 1.05–8.72 (P =0.040) for concentric LVH.



Figure 1


Figure 1. 

Kaplan-Meier event-free survival curves in aortic stenosis patients according to their left ventricular (LV) geometric pattern, (A) with conservative management, and (B) with conservative and/or surgical management. LVCR: left ventricular concentric remodelling; LVH: left ventricular hypertrophy.

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Figure 2


Figure 2. 

Adjusted Cox proportional hazard mortality curves in aortic stenosis patients according to their left ventricular (LV) geometric pattern, (A) with conservative management, and (B) with conservative and/or surgical management. Curves were adjusted for (A) age, sex, comorbidity index, hypertension, asymptomatic status at baseline, known coronary artery disease, history of atrial fibrillation, aortic valve area and LV ejection fraction; and (B) age, sex, comorbidity index, hypertension, asymptomatic status at baseline, known coronary artery disease, history of atrial fibrillation, aortic valve area, LV ejection fraction and aortic valve replacement as a time-dependent covariate. LVCR: left ventricular concentric remodelling; LVH: left ventricular hypertrophy.

Zoom

Outcome with conservative and/or surgical management

During a mean overall follow-up with conservative and/or surgical management of 37±1 months, AVR was performed in 96 patients (29%), and 72 patients (22%) died. AVR was performed in 21 patients (37%) with normal LV geometry, 24 (28%) patients with LVCR, 41 (27%) patients with concentric LVH and 10 (29%) patients with eccentric LVH.

Four-year event-free survival was 89±4% for patients with normal LV geometry, 78±9% for patients with eccentric LVH, 70±4% for patients with concentric LVH and 65±6% for patients with LVCR (Figure 1B). Compared with patients with normal LV geometry, event-free survival was significantly lower in patients with LVCR (P =0.011) and concentric LVH (P =0.03), but not in patients with eccentric LVH (P =0.33). LVCR and concentric LVH were associated with a markedly increased risk of mortality under medical and/or surgical management compared with normal LV geometry, the higher risk being consistently observed in case of LVCR: unadjusted HR: 3.06, 95% CI: 1.25–7.49 (P =0.014) for LVCR; and unadjusted HR: 2.49, 95% CI: 1.05–5.92 (P =0.037) for concentric LVH. Patients with eccentric LVH did not display a significant increase in risk of mortality (unadjusted HR: 1.84, 95% CI: 0.56–6.04; P =0.313). At Cox multivariable analysis, only LVCR remained associated with an increased risk of mortality under conservative and/or surgical management (adjusted HR: 2.93, 95% CI: 1.19–7.23; P =0.020) (Table 2). Despite further adjustment on AVR as a time-dependent covariate, only LVCR remained associated with a major increase risk of mortality under conservative and/or surgical management compared with patients with normal LV geometry (adjusted HR: 3.12, 95% CI: 1.35–7.23; P =0.008) (Table 2, Figure 2B). Removing known coronary artery disease and asymptomatic status from this multivariable model did not alter the relationship between LVCR (adjusted HR: 3.22, 95% CI: 1.40–7.42; P =0.006) and outcome under conservative and/or surgical management. Similarly, the replacement of AVA by aortic peak velocity in this former model did not alter its results (adjusted HR for LVCR: 3.27, 95% CI: 1.42–7.52; P =0.005).

Discussion

To our knowledge, this is the first study to demonstrate the link between LVCR and a considerably increased risk of death in patients with asymptomatic or minimally symptomatic AS. Patients with AS and LVCR showed a threefold increase in the risk of death under medical management compared with patients with normal LV geometry. Moreover, our results show that LVCR is not just predictive of excess mortality under medical management, but is also an independent determinant of lower survival when surgical correction of AS during follow-up was taken into account in the analysis. Of the four patterns of LV geometry (i.e. LVCR, concentric LVH, eccentric LVH and normal LV geometry), patients with LVCR had the highest risk of mortality. As expected, concentric LVH was also associated with an increased risk of death under conservative management, but when surgical management was taken into account the association was no longer observed.

Pressure overload, as observed in the context of AS, classically elicits concentric hypertrophy, with a high ratio of LV wall thickness to radius (h/R). Increased wall thickness compensates for wall stress (afterload) according to Laplace's law, to ensure maintenance of LV contractile function. In the landmark report by Grossman et al., patients with AS had normal systolic and diastolic LV wall stresses, as concentric hypertrophy had successfully compensated for the effect of elevated systolic and diastolic LV pressures on LV wall stress [11]. Whether asymptomatic patients with AS and extensive concentric LVH should undergo AVR to prevent progression of LVH or whether they should be managed conservatively until symptoms develop remains a controversial issue [12, 13]. Concentric LVH is probably secondary not only to AS, but also to other comorbidities, such as diabetes mellitus [14], hypertension or a genetic predisposition, such as the DD genotype of the ACE gene [15]. In both settings, excessive LVH is accompanied by prominent LV fibrosis [16], which may, in theory, predispose patients to ventricular arrhythmias or sudden death. The present study confirms that concentric LVH is associated with poor outcome in AS patients under conservative management. Importantly, the detrimental prognostic value of concentric LVH was not observed when surgical management during follow-up was considered, suggesting that AVR has a positive impact in these patients. Eccentric LVH has been well described in the presence of volume overload and in patients with AS and heart failure because of LV systolic dysfunction [17]. This pattern was rare in the present study (11%; n =34), in which patients with more than mild aortic regurgitation or mitral regurgitation or with low LVEF were excluded. As a consequence, the present study was underpowered to evaluate the detrimental prognostic value of this pattern compared with patients with normal LV geometry.

Increased RWT in individuals with normal LV mass (i.e. LVCR) has been reported in 10–15% of uncomplicated hypertensive patients [18]. LVCR in hypertensive patients is a powerful individual cardiovascular risk factor, independent of LVH and other well-known clinical risk factors, including increased body mass index, atrial fibrillation, diabetes or smoking [19]. LVCR has been associated with depressed myocardial contractility as well as poorer clinical outcome in hypertensive populations [20]. LVCR with normal LV mass is frequent in AS, and was found in 26% of patients in the present report. Increased RWT, which denotes LVCR, has been associated previously with adverse periprocedural outcome and early mortality after AVR in AS [21, 22, 23]. The present study demonstrates that LVCR has a major negative prognostic impact under medical management, even after adjustment for confounders, such as age or comorbidities. Importantly, LVCR remained significantly associated with an increased risk of mortality when surgical management during follow-up was taken into account, even after adjustment for AVR as a time-dependent variable. Therefore, LVCR is associated with the worst outcome regardless of clinical management, and should be included as a predictor of adverse prognosis in a further prospective study of outcome in AS intended to refine guidelines.

Study limitations

Whereas echocardiographic data were collected prospectively, clinical and outcome data were obtained by review of medical records. Our study therefore has the limitations inherent to retrospective analyses. However, diagnosis was established by cardiologists experienced in valvular heart disease. Moreover, all surgical decisions were made in accordance with good practice guidelines. The prevalence of each of the four geometric patterns of LV cannot be ascertained from the present data because patients were recruited from patients attending the echocardiography laboratory, and patients who were operated on during the first 3 months after diagnosis were excluded. Compared with normal geometry, LV concentric geometry with or without hypertrophy is associated with poor outcome; our findings suggest that LVCR portends the worst outcome, but this needs to be externally validated. As the number of patients in the eccentric LVH group was small, the specific prognostic value associated with eccentric LVH in our study is less robust than with other LV geometric patterns. The follow-up period of the present study was relatively short; a longer follow-up period would add power to the present findings. Alteration of myocardial longitudinal strain has been associated with cardiac death and AVR in patients with asymptomatic AS [24]. Moreover, the presence of focal fibrosis or unrecognised myocardial infarction detected by cardiovascular magnetic resonance has been associated with an increased risk of mortality in patients with AS undergoing AVR [25]. Unfortunately, strain echocardiography and magnetic resonance data were not available in the present study. Plasma B-type natriuretic peptides were not available in the present study, and may refine the predictive value of LV geometry.

Conclusions

In the present study, LVCR was shown to be a powerful independent predictor of survival in patients with asymptomatic or minimally symptomatic AS under medical management. The pejorative effect of LVCR remained when surgical correction of AS during follow-up was taken into account. Among the four classical patterns of LV geometry, LVCR was associated with the highest risk of mortality under medical and/or surgical management. Therefore, the pattern of LV geometry must be determined in AS patients. The presence of LVCR, which is easily recognised on routine echocardiography, identifies a high-risk group of AS patients who should be closely followed. The impact of AVR on the outcome of patients with LVCR needs to be investigated in future prospective studies.

Authors’ contribution

N. D. and S. M. contributed equally to this study and the preparation of the manuscript.

Sources of funding

None.

Disclosure of interest

The authors declare that they have no competing interest.

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