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European Heart Journal Advance Access originally published online on June 26, 2007
European Heart Journal 2007 28(15):1886-1893; doi:10.1093/eurheartj/ehm181
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Physiological consequences of percutaneous pulmonary valve implantation: the different behaviour of volume- and pressure-overloaded ventricles

Louise Coats1,2, Sachin Khambadkone1,2, Graham Derrick1,2, Marina Hughes1,2, Rod Jones1,2, Bryan Mist3, Denis Pellerin3, Jan Marek1,2, John E. Deanfield1,2, Philipp Bonhoeffer1,2,* and Andrew M. Taylor1,2

1 UCL Institute of Child Health, London, UK
2 Cardiothoracic Unit, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, UK
3 The Heart Hospital, London, UK

Received 29 November 2006; revised 22 February 2007; accepted 13 April 2007; online publish-ahead-of-print 26 June 2007.

* Corresponding author. Tel: +44 2078138106; fax: +44 2078138262. E-mail address: bonhop{at}gosh.nhs.uk

See page 1793 for the editorial comment on this article (doi:10.1093/eurheartj/ehm261)


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Conclusions
 Acknowledgements
 References
 
Aims: To investigate the early clinical and physiological consequences of relieving chronic right ventricular (RV) volume overload with percutaneous pulmonary valve implantation (PPVI).

Methods and results: We selected 17 patients (age 21.2 ± 8.7 years), from a total of 125 who underwent PPVI, because they had important pulmonary regurgitation (PR) [regurgitant fraction > 25% on magnetic resonance (MR)] and an echocardiographic gradient < 50 mmHg across the RV outflow tract. Cardiopulmonary exercise testing, tissue Doppler and MR were performed before and within 3 months of PPVI. Following PPVI, PR (40.7 ± 7.3 to 4.1 ± 6.1%, P < 0.001) and RV end-diastolic volume fell (115.4 ± 33.1 to 98.9 ± 32.0 mL/m2, P = 0.001); effective RV stroke volume increased (34.3 ± 7.8 to 44.4 ± 9.3 mL/m2, P < 0.001). Left ventricular end-diastolic volume (66.6 ± 18.0 to 73.4 ± 16.5 mL/m2, P = 0.014), stroke volume (38.4 ± 11.1 to 46.4 ± 10.2 mL/m2, P = 0.001) and ejection fraction (57.8 ± 8.1 to 63.5 ± 5.2 mL/m2, P = 0.001) increased. Pulmonary artery diastolic pressure (8.9 ± 4.5 to 12.5 ± 5.2 mmHg, P = 0.041) and mitral E/Ea increased (from 9.0 ± 2.0 to 11.6 ± 3.1, P = 0.003). Patients felt better, but standard measures of exercise capacity were unchanged.

Conclusion: PPVI relieves PR and restores compensatory cardiac performance. The lack of improvement in exercise parameters suggests that, in contrast to pressure overload, the contractile reserve of chronically volume-overloaded myocardium is limited.

Key Words: Conduit dysfunction • Volume overload • Ventricular function • Physiology • Percutaneous valve


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Conclusions
 Acknowledgements
 References
 
Right ventricular (RV) to pulmonary artery conduit dysfunction, a common problem in patients with repaired congenital heart disease, is well recognized.1–3 There have been conflicting reports regarding the potential for RV recovery following surgical restoration of the pulmonary valve.4,5 Restoration of RV function following relief of pressure overload due to conduit obstruction was recently described by us.6 We decided to apply the same methodology to the study of regurgitant conduits, in order to elucidate the response of the RV to relief of chronic volume overload. Percutaneous pulmonary valve implantation (PPVI) provides a unique model with which to study this as it is not confounded by the effects of cardiopulmonary bypass or remodelling of the RV outflow tract (RVOT) that may be performed at surgery.7 The purpose of this study was to investigate the clinical and physiological consequences of relief of chronic pulmonary regurgitation (PR).


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Conclusions
 Acknowledgements
 References
 
Study population
From 125 patients who underwent PPVI for various indications between September 2000 and April 2006, the last 86 consecutive patients were investigated with a standardized protocol that included cardiopulmonary exercise testing, tissue Doppler echocardiography and magnetic resonance (MR) imaging. From these 86, we selected all patients (n = 30) with PR but no significant RVOT obstruction (peak RVOT gradient < 50 mmHg) on echocardiography. Thirteen patients, with moderate to severe PR on echocardiography, were unable to undergo MR and were therefore excluded from the study, as the PR could not be quantified. The remainder (n = 17) all had a pulmonary regurgitant fraction on MR > 25% and form the subjects of this study.

Acceptance for PPVI required suitable outflow tract anatomy (potential device implantation site diameter ≤ 22 mm) as well as a clinical indication for intervention.8 In the study group, 14 patients had symptomatic PR with impaired cardiopulmonary exercise capacity. Two patients, although reportedly asymptomatic, showed substantial deterioration in objectively assessed exercise capacity. The final patient, who was asymptomatic and had preserved exercise capacity, was treated because of severe RV dilatation [RV end-diastolic volume (RVEDV) 2.6 times the left]. None of the patients included in this study had an intra-cardiac shunt or bilateral branch pulmonary artery stenosis.

Cardiopulmonary exercise testing, tissue Doppler echocardiography and MR imaging were performed before and early after PPVI, together with assessment of New York Heart Association (NYHA) functional class. Separate investigators performed the clinical assessment (SK), exercise testing (GD), tissue Doppler echocardiography (LC), MR imaging (AT) and valve implantation (PB); all were blinded to the results of the other tests. Post-processing was performed in a random fashion. Because of the valved stent, the investigator could sometimes determine whether the investigations were performed before or after intervention; however, he/she had no knowledge to which patient the images belonged. The local research ethics committees approved the study, and all subjects (and/or a parent/guardian) gave informed consent.

Percutaneous pulmonary valve implantation
PPVI was carried out under general anaesthesia as previously described.7 Two patients additionally had a single bare stent placed in the left branch pulmonary artery to relieve a localized stenosis. RV peak systolic and end-diastolic pressure and pulmonary artery peak systolic and diastolic pressure were measured before and after PPVI.

Cardiopulmonary exercise testing
Cardiopulmonary exercise testing was performed on a mechanically braked bicycle ergometer (Sensormedics Ergoline 800, Blitz, Germany) with respiratory gas exchange analysis (Medgraphics, St Paul, MN, USA) before and at 21 ± 12 days following PPVI. Work rate was increased with a ramp protocol. A 12 lead electrocardiogram was monitored continuously, and blood pressure recorded every 2 min during exercise. Breath-by-breath respiratory gas exchange measurements were recorded throughout the test and averaged over a peak width of 20 s at the end of exercise to determine maximum values. Anaerobic threshold was assessed using the modified V-slope method.9

Conventional and tissue Doppler echocardiography
Trans-thoracic imaging of the heart was performed using a Vivid 7 (GE Vingmed, Horten, Norway), with a transducer frequency of 3.5 Mhz, before and 2 ± 1 days after PPVI. A subset of the population (n = 11, indicated in Table 1) who were able to return to our institutions for follow-up underwent further imaging at 1 and 3 months. RV systolic pressure was calculated from the continuous wave Doppler profile of the tricuspid regurgitation jet, and peak RVOT gradient was calculated in the same way from the continuous wave Doppler signal across the RVOT.10 A pulsed wave mitral inflow Doppler was recorded at end expiration, as has been described elsewhere, and peak early diastolic velocity (E) was measured.11 The RV free wall and left ventricular (LV) lateral wall were imaged from the apex during quiet breathing. Colour-coded velocities of the tricuspid and mitral annulus were acquired with a mean frame rate of 172 ± 37 s–1. A cineloop of three consecutive cardiac cycles was digitally stored for off-line analysis (Echopac, GE Vingmed, Horten, Norway). Myocardial velocities during early diastole (Ea) and late diastole (Aa) were also measured. Isovolumic acceleration (IVA), a relatively load independent measure of intrinsic myocardial contractility, and peak myocardial velocity during systole (Sa), which has been demonstrated to correlate with ejection fraction (EF), were measured at the lateral tricuspid and mitral annuluses to assess global systolic function.12–15 IVA was also measured in an age and sex matched control group. The region of interest was tracked to myocardial motion. Measurements were performed on three consecutive cardiac cycles and the average of these calculated. The E/Ea ratio was calculated as a non-invasive indicator of LV filling pressure.16


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  		Table 1 Patient characteristics

 
Magnetic resonance imaging
MR imaging was performed at 1.5 T (Avanto; Siemens Medical Systems, Erlangen, Germany) before and at 19 ± 29 (range 1–98) days after PPVI. Retrospective gated steady-state free precession cine MR images of the heart were acquired in the vertical long axis, four-chamber, short axis (9–12 slices) and two long axis views of the RVOT and LVOT for positioning of through-plane flow quantification.17 Each image was acquired during a single breath-hold. The cine sequence parameters were: TR 2.8 ms, TE 1.4 ms, flip angle 51°, slice thickness 8 mm, matrix 192 x 256, field of view 300–380 mm, temporal resolution 25–40 phases.

Assessment of LV and RV volumes was performed by manually defining the endocardial outline at end-diastole and end-systole in each short axis slice (Argus; Siemens Medical Systems, Erlangen, Germany). End-diastolic and end-systolic volumes were calculated using Simpson's rule for each ventricle and from these, the stroke volume and Ejection Fraction (EF) were derived.

Pulmonary artery flow data were acquired using a flow sensitive gradient echo sequence (TR 8 ms, TE 3.8 ms, flip angle 30°, slice thickness 6 mm, matrix 256 x 256) during free breathing. A phase correction filter was used to correct for phase errors introduced by eddy currents and Maxwell terms. Image planes were located at the midpoint of the pulmonary trunk/conduit pre-PPVI, and just above the stent following PPVI, to avoid stent artefact. Through-plane flow data (40 phases per cardiac cycle) were acquired using retrospective cardiac gating. The velocity-encoded peak velocity was varied according to the degree of pulmonary trunk/conduit flow. Flow was calculated from the phase contrast images using a semi-automatic vessel edge detection algorithm with operator correction. Regurgitant fraction was calculated as the percent backward flow over forward flow. All measurements were indexed for body surface area (Dubois formula) and expressed in mL/m2.

Statistical analysis
All continuous variables are expressed as mean ± standard deviation or as median and range. Normally distributed variables were compared before and after PPVI using a two-tailed, paired student's t-test and at subsequent follow-ups with repeated two-tailed ANOVA testing. Non-normally distributed variables were compared using the Mann–Whitney U test. Correlation between normally distributed variables was assessed using Pearson's test and between non-normally distributed variables using the Spearman's rho test. Statistical significance was inferred when P < 0.05. Intra- and inter-observer measurements of RV IVA were compared using the Bland–Altman method. All statistical testing and data analysis were performed with SPSS version 11 for Mac (SPSS Inc., Chicago, IL, USA).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Conclusions
 Acknowledgements
 References
 
Baseline characteristics
Demographics of the 17 patients (35% male, age 21.2 ± 8.7 years, 71% tetralogy of Fallot or subtype, median NYHA 2) studied are shown in Table 1. Patients had a median pulmonary regurgitant fraction of 41% (range 25–54%). All patients had mild tricuspid regurgitation or less. PPVI was performed successfully in 16 of the 17 subjects with one case complicated by obstruction of a tortuous branch pulmonary artery by the valved stent, necessitating homograft replacement on the same day. The patient made an uneventful recovery and has been omitted from the analysis.

Subjects who underwent successful PPVI had important RV dilatation with a ratio of RVEDV and LV end-diastolic volume (RVEDV:LVEDV) measured at 1.8 ± 0.5 on MR (normal value approximately 1.15).18 We found a similar relationship between RVEDV:LVEDV and RVEF (r = –0.600, P = 0.014) as previously reported in patients with RVOT obstruction.18 IVA was 0.85 ± 0.32 m/s2 at the tricuspid annulus. This was substantially reduced when compared with our age and sex matched control group (35% male, age 21.4 ± 10.0 years, IVA 2.14 ± 0.76 m/s2) and is likely to reflect impairment of intrinsic RV contractility. One patient had restrictive physiology defined by forward flow at end-diastole in the pulmonary artery throughout the respiratory cycle.19 This patient is identified in Table 1.

Although there was an association between VO2max and age at intervention (r = –0.657, P = 0.008), a stronger negative correlation was present between VO2max and age at primary repair (r = –0.820, P < 0.001, Figure 1).


Figure 1
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  		Figure 1 Relationship between VO2max and age at primary repair.

 
Excluded patients
Thirteen patients (77% male, age 21.2 ± 9.8 years, 62% tetralogy of Fallot or subtype, median NYHA 3) were not included in the study protocol because they were unable to undergo MR scanning for the following reasons: arrhythmia (n = 4), requirement for general anaesthesia (n = 5), permanent pacemaker (n = 1), claustrophobia (n = 1), in extremis (n = 1), and significant metallic artefact (n = 1).

Haemodynamics after percutaneous pulmonary valve implantation
In 16 subjects (procedure time 89.0 ± 31.8 min, fluoroscopy time 20.3 + 15.7 min), RV systolic pressure fell (51.3 + 13.6 to 42.0 + 9.7, P = 0.003), whereas end-diastolic pressure did not change (9.8 + 2.9 to 9.3 + 3.9, P = 0.479). Pulmonary artery systolic pressure was unchanged (31.3 + 8.9 to 28.0 + 8.1 mmHg, P = 0.253), but diastolic pressure increased (8.9 + 11.9 to 11.9 + 5.0, P = 0.041). There was a small reduction in RVOT gradient. Pressures measured at catheterization are shown in Table 2.


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  		Table 2 Pressures at catheterization

 
New York Heart Association
NYHA class improved from a median of 2 to 1 (P = 0.001), 1 month following PPVI.

Cardiopulmonary exercise testing
A total of 15 out of 16 patients completed maximal exercise tests (one patient was unable to co-operate due to his age and language difficulties). Following PPVI, there was no change in peak VO2 (23.5 ± 8.6 to 23.8 ± 6.8 mL/kg/min, P = 0.710), anaerobic threshold (13.6 ± 5.6 to 13.5 ± 4.8 mL/kg/min, P = 0.854), or workload (90.1 ± 31.4 to 93.5 ± 28.7, P = 0.277). There was a significant reduction in VE/VCO2 (40.3 ± 9.3 to 36.8 ± 8.4, P = 0.002). The patient with restrictive physiology performed almost identical exercise tests before and after valve implantation; VE/VCO2 however fell from 40 to 35. Exercise parameters are shown in Table 3.


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  		Table 3 Cardiopulmonary exercise testing

 
Conventional echocardiography
RV systolic pressure (43.0 ± 13.3 to 37.8 ± 12.3 mmHg, P = 0.158) and peak RVOT gradient (30.9 ± 9.4 to 26.6 ± 10.1 mmHg, P = 0.088) fell following PPVI. The discrepancy between echocardiographic and catheter measurement of RVOT gradient is likely to reflect both the conscious state of the patient and technical differences between the two techniques.20 There was no significant change in tricuspid regurgitation following valve implantation.

Tissue Doppler echocardiography
Peak systolic velocity remained unchanged following PPVI at both the tricuspid (5.5 ± 1.8 to 5.5 ± 1.7 cm/s, P = 0.957) and mitral annulus (5.0 ± 1.5 to 4.8 ± 1.7 cm/s, P = 0.373). In addition, IVA did not change significantly at the tricuspid (0.85 ± 0.32 to 0.81 ± 0.43 m/s2, P = 0.784) or at the mitral annulus (0.89 ± 0.26 to 0.99 ± 0.48 m/s2, P = 0.281). Although diastolic velocities at the tricuspid annulus showed no change, the early diastolic velocity (Ea) at the mitral annulus fell significantly (– 10.5 ± – 2.2 to – 8.8 ± – 2.1 cm/s, P = 0.003) resulting in an increase in the mitral E/Ea ratio (9.2 ± 2.0 to 11.6 ± 3.1, P = 0.003). The changes in mitral Ea and E/Ea after PPVI were maintained at 1 and 3 months. There was no change in other tissue Doppler parameters during follow-up. Intra- and inter-observer IVA measurements correlated well (r = 0.910, P < 0.001 and r = 0.752, P < 0.001, respectively) with no systematic bias on the Bland–Altman plots (Figure 2). Echo parameters are shown in Tables 4 and 5.


Figure 2
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  		Figure 2 Bland–Altman plots demonstrating (A) intra- and (B) inter-observer variability for isovolumic acceleration measurements.

 

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  		Table 4 Echocardiography before and immediately after PPVI

 

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  		Table 5 Echocardiography at 1 and 3 months in a subset of patients (n = 11)

 
Magnetic resonance imaging
Pulmonary regurgitant fraction fell significantly following PPVI (40.7 ± 7.3 to 4.1 ± 6.1%, P < 0.001). This was associated with a reduction in RV end-diastolic volume (116.7 ± 30.8 to 100.2 ± 30.3 mL/m2, P = 0.001, Figures 3 and 4) but no change in end-systolic volume (57.0 ± 24.3 to 53.0 ± 24.8 mL/m2, P = 0.212). Although the total RV stroke volume fell with relief of the PR, the effective stroke volume (the total forward flow minus the regurgitant flow) increased significantly (34.8 ± 7.1 to 45.4 ± 7.6 mL/m2 P < 0.001). RVEF did not change (52.7 ± 10.5 to 49.3 ± 10.5 mL/m2, P = 0.143). LVEDV increased (67.7 ± 16.9 to 74.4 ± 14.8 mL/m2, P = 0.014, Figures 2 and 3) and was associated with an improvement in LV stroke volume (39.0 ± 10.5 to 47.1 ± 9.1 mL/m2, P = 0.001), LV EF (57.8 ± 8.1 to 63.5 ± 5.2%, P = 0.001), and indexed cardiac output (2.5 ± 0.8 to 2.9 ± 0.9 mL/m2/min, P = 0.001). Changes in ventricular volumes in the patient with restrictive physiology mirrored that of the whole group. MR parameters are shown in Table 6.


Figure 3
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  		Figure 3 Balanced steady-state free precession short axis cine magnetic resonanceimage (A) before and (B) after percutaneous pulmonary valve implantation.

 

Figure 4
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  		Figure 4 Change in (A) right ventricular end-diastolic volume and (B) left ventricular end-diastolic volume following percutaneous pulmonary valve implantation.

 

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  		Table 6 Magnetic resonance imaging

 
Discussion
The timing of surgery for conduit dysfunction has long been debated in the paediatric and adult congenital heart disease population and is different according to the predominant lesion.

We have treated 125 patients with PPVI and selected those who had pure obstruction and those with pure regurgitation to improve our understanding of post-procedural ventricular recovery.6

The presence of symptoms, as for other valvular lesions, is an unequivocal indication for intervention. The asymptomatic population present a greater challenge, as predicting irreversible myocardial injury and time-related risks of arrhythmia, and sudden death is difficult and there is no ‘perfect valve’ available for replacement. Cardiopulmonary exercise testing and assessment of ventricular volumes at end-systole and end-diastole are increasingly used to determine appropriate timing for intervention.4,5,21–23

In our study, restoration of a competent pulmonary valve, without cardiopulmonary bypass or surgical remodelling, resulted in a reduction of RV end-diastolic volume. In contrast to the pressure-overloaded ventricle, however, RV end-systolic volume did not change, as there was no significant change in afterload.6 Although total RV stroke volume fell due to elimination of PR, the effective forward flow increased indicating, like in the pressure-overloaded ventricle, that RV ejection prior to intervention is sub-optimal. IVA did not change, therefore this improvement in effective stroke volume combined with the fall in RV end-diastolic volume implies that the RV is on the decompensatory limb of the Starling curve at baseline and shifts leftwards back to the compensatory limb following intervention. The lack of change in tricuspid annular velocities, following PPVI, may reflect the response of damaged myocardium to relief of chronic volume overload as compared with the fall in velocities that is observed in models in which intrinsic contractile function is preserved.24,25

Following PPVI, the LV increased in volume. This is likely to be a result of both increased pre-load, implied by the rise in RV effective forward flow, pulmonary artery diastolic pressure, and mitral E/Ea, and the change in ventricular configuration as septal behaviour alters. Ea, which reflects the ventricular dynamics during early diastole, falls in a similar manner to that seen following percutaneous atrial septal defect closure and is sustained during follow-up.25–27 Pulmonary valve competence, therefore, has important consequences for LV function in this population: leading to an increase in diastolic stretch, a rightward shift on the compensatory limb of the Starling curve and an increase in cardiac output and LV EF as the ventricle becomes better filled. Animal studies of chronic PR support these mechanisms and an increase in intrinsic contractility, which is not supported by our IVA measurements, is unlikely to be responsible.28

The ratio of RVEDV:LVEDV remained abnormal even after PPVI (1.8–1.4, normal 1.15) alluding to persistent abnormalities of ventricular interaction. The presence of LV dysfunction, often underestimated in these patients, has been reported to be associated with a high risk of sudden death in this population.29 The use of absolute or indexed RV volumes without considering the impact on LV dynamics may not be the best way of decision making in the management of chronic PR, particularly as the reported range of normality is too wide to be clinically useful.18

In contrast to the reported population with pressure overloaded RVs, VO2max and anaerobic threshold did not mirror the improvements in cardiac performance that were seen on MR following relief of chronic PR. Experimental work suggests that the volume-overloaded RV functions at a high level of performance at rest and that further functional increase, by either the Frank–Starling mechanism or by adrenergic stimulation, may be limited.28 We propose that the pressure-overloaded myocardium has a contractile reserve that is recruitable with reduction in afterload, whereas the over-performing volume-loaded RV, which is driven by myocardial stretch, does not. Peak exercise performance, which is often used to describe the functional status of patients, must therefore be interpreted in context of the loading conditions in the right heart. The reported symptomatic improvement following relief of PR is better explained by the increase in resting cardiac output, although a placebo effect cannot be entirely discounted. Further investigation is required to confirm these findings and to determine whether RV remodelling over the longer term can be translated into an improvement in objectively assessed exercise capacity. The improvement in VE/VCO2 that probably results from better pulmonary perfusion due to the increase in RV output is however encouraging because of its prognostic value.30,31

Studies in patients undergoing surgical pulmonary valve replacement have been unable to describe the physiology shown here, as they are confounded by the effect of cardiopulmonary bypass. Furthermore, the surgical intervention itself, which in some cases includes resection and remodelling of the RVOT, has confused the issue as it has been associated with a physical reduction in RV end-systolic volume alongside the diastolic volume change and thus an obligatory increase in RVEF.20,21,32 PPVI, for the first time, provides a pure model with which to study the effects of chronic volume overload in this patient population, whereas focus on effective stroke volume rather than EF permits better interpretation of the physiology.

Limitations of study
RV dilatation in the population described here is not as marked as that reported in some cohorts undergoing surgical pulmonary valve replacement.21,22 In our view, the main reason for this was the anatomical nature of the RVOT, which to ensure successful PPVI necessitated exclusion of patients with trans-annular patches and aneurysms of the pulmonary trunk and RVOT. Development of devices to treat PR in such outflow tracts is underway and will provide an important area for future study.33 The presence of mild conduit obstruction and the necessity for unilateral branch pulmonary artery stenting in two patients may have influenced the physiology observed. We believe, however, that the contribution is likely to be minimal and that the main changes can be ascribed to the relief of volume overload. Finally, not all patients were able to return for follow-up due to our wide referral base. Although this may introduce a degree of selection bias, these data are only provided to demonstrate the maintenance of the changes and are not the main focus of this study.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Conclusions
Acknowledgements
 References
 
Chronic PR has a detrimental effect on RV and LV function. Restoration of pulmonary valve competence with PPVI reduces RV volumes, improves efficacy of RV ejection and LV filling, and increases cardiac output. Despite this, in contrast to the pressure-overloaded ventricle, there is no improvement in standard measures of exercise capacity. Indications for intervention based solely on RV volumes may not, therefore, be adequate to determine timing of pulmonary valve implantation or replacement. The premise that chronic PR should be treated after the onset of symptoms or significant RV dilatation may need to be challenged and more robust markers for myocardial and functional recovery sought to prevent irreversible injury.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Conclusions
 Acknowledgements
References
 
L.C., J.E.D., and P.B. are funded by the British Heart Foundation (BHF). A.M.T. is funded by the Higher Education Funding Council for England (HEFCE).

Conflict of interest: P.B. is a consultant for NuMed and Medtronic.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Conclusions
 Acknowledgements
 References
 

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