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The Effects of Bariatric Surgery on Cardiac Structure and Function: a Systematic Review of Cardiac Imaging Outcomes
Running Title: Bariatric Surgery and Cardiac Function
Ravi Aggarwal BA(Hons.) MBBS MRCS,1 Leanne Harling PhD MRCS,1,2 Evangelos
Efthimiou MD FRCS,1,3 Ara Darzi KBE FMedSci,1 Thanos Athanasiou MD PhD
FRCS FETCS,1,2 Hutan Ashrafian* PhD MRCS1,3
1Department of Surgery and Cancer, Imperial College London
2Department of Cardiothoracic Surgery, Imperial College Healthcare NHS Trust
3Department of Bariatric Surgery, Chelsea and Westminster Hospital
*Corresponding author: Hutan Ashrafian, The Department of Surgery and Cancer, Imperial
College London. 10th Floor, Queen Elizabeth the Queen Mother (QEQM) Building, Imperial
College Healthcare NHS Trust at St Mary’s Hospital, Praed Street, London, W2 1NY, United
Kingdom. E-mail: [email protected]. Telephone: +44 (0)20 7886 7651, Fax: +44
(0)20 7886 6309.
Manuscript type: Systematic Review
Financial disclosure: None
Conflict of Interest: The authors declare that they have no conflict of interest.
Word Count: 2361
Number of figures: 2
Number of tables: 2
Supplementary appendix: 0
Number of References: 75
Abstract
Background
Obesity is associated with cardiac dysfunction, atherosclerosis and increased
cardiovascular risk. It can be lead to obesity cardiomyopathy and severe heart failure,
which in turn raise morbidity and mortality whilst carrying a negative impact on
quality of life. There is increasing clinical and mechanistic evidence on the metabolic
and weight loss effects of bariatric surgery on improving cardiac structure and
function in obese patients.
Objectives
To quantify the effects of bariatric surgery on cardiac structure and function by
appraising cardiac imaging changes before and after metabolic operations.
Methods
A comprehensive systematic review of studies reporting pre-operative and post-
operative echocardiographic or magnetic resonance cardiac indices in obese patients
undergoing bariatric surgery. Studies were quality scored and data were meta-
analyzed using random effects modeling.
Results
Bariatric surgery is associated with significant improvements in the weighted
incidence of a number of cardiac indices including a decrease in left ventricular mass
index (11.2%, 95%CI 8.2-14.1%), left ventricular end diastolic volume (13.28ml,
95%CI 5.22-21.34ml), left atrium diameter (1.967mm, 95%CI 0.980-2.954). There
were beneficial increases in Left Ventricular Ejection Fraction (1.198%, 95%CI -
0.050-2.347) and E/A ratio (0.189%, 95%CI -0.113-0.265).
Conclusions
Bariatric surgery offers beneficial cardiac effects on diastolic function, systolic
function and myocardial structure in obese patients. These may derive from surgical
modulation of an enterocardiac axis. Future studies must focus on higher evidence
levels to better identify the most successful bariatric approaches in preventing and
treating the broad spectrum of obesity-associated heart disease whilst also enhancing
treatment strategies in the management of obesity cardiomyopathy.
Key Words: 'Bariatric Surgery'; 'Metabolic Surgery'; 'Imaging'; 'Cardiac function';
'Cardiac Structure'; ‘Obesity Cardiomyopathy’.
Abbreviation List
LVMI (left ventricular mass index), LVEF (left ventricular ejection fraction) LVESV (left ventricular end-systolic volume), LVESD (left ventricular end-systolic diameter), LVEDV (left ventricular end-diastolic volume), LVEDD (left ventricular end-diastolic diameter), LVEF (left ventricular ejection fraction)LVMI (left ventricular mass index), PWT (posterior wall thickness), IVST (interventricular septal thickness), RWT (relative wall thickness), IVRT (Isovolumic relaxation time).
Introduction
The global prevalence of both obesity and cardiovascular disease continues to rise.
Obesity has doubled since 1980 where an estimated 39% of adults globally are
overweight and 13% of adults are obese [1], whilst cardiovascular disease and cardiac
failure carry an impact of 31% of all global deaths in 2012 [2].
Obesity is recognized as a risk factor for cardiac dysfunction, atherosclerosis and
cardiovascular disease [3]. When combined with other risk factors such as
hypertension, dyslipidaemia and diabetes mellitus, it is known as ‘metabolic
syndrome’ which in itself is an independent predictor of cardiac dysfunction and
cardiovascular disease [4].
Evidence from epidemiological studies (such as the Framingham Heart Study and the
National Health and Nutrition Examination Survey) in addition to cardiac imaging
trials suggest that long-term obesity can lead to LV dilation and hypertrophy with
resultant cardiac failure [3, 5]. These structural changes cause a deterioration of
ventricular contractile function and distortion of shape and cavity resulting in
maladaptive LV remodeling, which can progress to non-ischaemic dilated
cardiomyopathy [3, 6].
The literature suggests that weight loss achieved by any means may improve cardiac
structure and function (through reverse re-modeling) and decreased cardiovascular
risk [7]. However, lifestyle (diet and exercise) and pharmacotherapy have not yet
demonstrated sustainable long-term weight loss in the majority of patients [8, 9].
Bariatric surgery offers the most efficacious and sustained weight loss in morbidly
obese individuals; which in turn can result in favorable modulation of cardiac function
cardiovascular risk factors [3].
The beneficial effects of bariatric procedures on cardiac functional imaging endpoints
(such as echocardiogram and MRI) have been demonstrated in a number of studies.
Although previous systematic reviews in this field have been performed [10, 11], our
objective was to accrue all the available data in this area which almost doubles the
study number of the last literature analysis [10]. Our aim was to complete the largest
and most comprehensive systematically review and meta-analysis to date examining
the data from cardiac imaging studies to quantify the impact of bariatric surgery on
cardiac structure and function in obese patients.
Methods
Literature Search
A literature search was performed using PubMed, Embase, Ovid and Cochrane
databases using combinations of the terms ‘bariatric surgery’ or ‘metabolic surgery’
or ‘weight loss surgery’ or ‘obesity surgery’ and ‘echocardiography’ or ‘magnetic
resonance imaging’ or ‘cardiac imaging’ or ‘cardiac dimensions’ or ‘ventricular
dimensions’. The last date for this search was 11th June 2015. Figure 1 outlines our
search strategy. All studies are listed in Table 1.
Inclusion and Exclusion Criteria
All studies reporting echocardiographic or magnetic resonance cardiac parameters of
structure and function were included. Studies were excluded from analysis if:
inconsistency of data did not allow valid extraction; studies did not report both pre-
operative and post-operative data. A minimum follow up of 3 months post surgery
was required for inclusion, and quality scoring was performed utilizing the
Newcastle-Ottawa scale.
Statistical Analysis
Meta-analysis was performed in line with recommendations from the Cochrane
Collaboration and PRISMA guidelines. Analysis was conducted using Stata version
12 (StateCorp LP, College Station, TX).
Data was analyzed using a random effects model. Continuous data were investigated
using weighted mean difference (WMD) and 95% confidence intervals (CI).
Proportion difference between outcomes was also calculated and pooled through
DerSimonian and Laird random-effects modeling. Results were computed and
represented on forest plots. Inter-study heterogeneity was explored using the I2-
statistic: a value of <30% was considered low, 30-60% as moderate, >60% is high.
The Newcastle-Ottawa scale was utilized for quality scoring.
Results
Forty studies were found that fulfilled the inclusion criteria, producing a pooled data
set of 1486 patients (Table 1). Twenty-six of these studies were non-randomized
prospective observational studies and fourteen were retrospective cohort studies. Two
studies [12, 13] had two different cohorts within the same study so these were
analyzed individually. Five studies used MRI (CMR) to visualize cardiac parameters
and thirty-seven used echocardiography. The types of operation performed and the
parameters reported across the forty publications varied markedly and are shown in
Table 1. Some publications used the same cohort of patients with the same outcomes;
consequently we only utilized the single most up-to-date study on these cohorts for
these outcomes. The overall weighted mean follow-up was 18.2 months for patients
with a BMI of 47.2Kg/m2. Cardiac imaging outcome parameters are listed in Table 2.
Cardiac Geometry
LV Mass (LVM)
Absolute LVM was reported in 24 studies. Pooled analysis demonstrated a weighted
mean decrease in the LVM 29.80g (95%CI 24.06-35.54 p<0.001) after surgery, there
was moderate heterogeneity between studies (I2-55%).
LV Mass Index (LVMI)
Three studies reported on LVM indexed to height (m), thirteen indexed to height
(m2.7) and six to body surface area (m2). Proportional analysis of cardiac imaging
findings in the total 22 studies demonstrated a weighted mean decrease of 11.2%
(95%CI 0.082-0.141 p<0.001) in LVMI after surgery, there was a moderate
heterogeneity between studies (I2-32.8%).
LV End-Diastolic Volume
13 studies reported on of LV End-Diastolic Volume (LVEDV) to reveal a decrease of
13.28ml (95%CI 5.22-31.34ml, p=0.001), there was high heterogeneity between
studies (I2-85.9%).
LV End-Systolic Volume
10 studies reported on of LV End-Systolic Volume (LVESV) to reveal a decrease of
4.99ml (95%CI 0.35-9.62ml, p=0.035), there was high heterogeneity between studies
(I2-87.3%).
Diastolic function
E/A ratio
Twenty one studies reported on the E/A ratio before and after surgery to reveal a
weighted mean increase of 0.189 (95%CI 0.113-0.265 p<0.001) from a baseline of
1.16. There was high heterogeneity between studies (I2-82.0%).
Left atrium (LA) Diameter
Fifteen studies reported on the LA diameter before and after surgery. Pooled analysis
of cardiac imaging findings demonstrated a weighted mean decrease in the LA
diameter of 1.967mm (95%CI 0.980-2.954 p<0.001) after surgery, there was a high
heterogeneity between studies (I2-79.7%).
Systolic Function
LV Ejection Fraction (LVEF)
Twenty two studies reported on LVEF before and after surgery. Pooled analysis of
cardiac imaging findings demonstrated a weighted mean increase in LVEF of 1.198%
(95%CI 0.050-2.347 p=0.041) after surgery, there was a high heterogeneity between
studies (I2-74.2%).
Body Mass Index
Pooled data from all studies reporting pre- and post-operative BMI figures
demonstrated a weighted mean reduction of 13.51 BMI points post-surgery (95%CI
12.36-14.66, p<0.001 from a baseline of 47.2, there was a high heterogeneity between
studies (I2-83.9%).
Discussion
Overall, our analysis demonstrates that cardiac structure and function are both
consistently improved in bariatric surgical subjects. These global changes include
statistically significant improvements in cardiac geometry, diastolic function and
systolic function. The beneficial effects are demonstrated after significant weight loss
(weighted mean reduction of BMI by 13.51Kg/m2) and across changing modalities of
cardiac imaging including echocardiography and MRI. Our systematic review and
meta-analysis represents the largest and most comprehensive to date, with forty
studies included (almost doubling previous systematic assessments). Although
research in this field largely consists of small sized studies, the findings confirm and
extend the previous evidence with improvements in cardiac geometry and diastolic
function. A novel finding is a small but statistically significant improvement increase
in systolic function identified through LV ejection fraction and a demonstrable
proportional change in measures of cardiac mass index to accommodate all data sets
available. Three studies were included which used CMR to evaluate cardiac indices
rather than echocardiography which has been shown to be more precise and
accurate[14] in estimating LV mass.
Cardiac Geometry
Obesity is a recognized driver of increasing left ventricular mass [15] with obese men
showing predominantly concentric hypertrophy and obese women exhibiting both
eccentric and concentric hypertrophy [16]. Our results demonstrate a statistically
significant weighted proportional decrease of 11.2% in LVMI after surgery (p<0.001)
supporting the notion that LV reverse remodeling occurs after bariatric surgery.
There was also a substantial drop in LV mass as a measure of improvement in left
ventricular hypertrophy (LVH) which may account for the long-term decrease in
cardiovascular mortality observed in bariatric patients [3].
This may result from the reversal of pathological diastolic dysfunction and reduced
ventricular filling [17], depressed ventricular contractility, reduced coronary reserve,
and arrhythmogenic electrical dysfunction. Additionally, our results demonstrating an
improvement in posterior wall thickness, inter-ventricular septal thickness and relative
wall thickness also support the concept of beneficial reverse remodeling of left
ventricular hypertrophy toward a less concentric pattern in bariatric subjects. Both
measures of end-systolic and end-diastolic volume and diameter dimensions also
demonstrated improvements, indicating increased filling and relaxation of the left
ventricle after bariatric surgery.
Diastolic dysfunction
Our meta-analysis demonstrates that bariatric surgery beneficially modulates
echocardiographic markers of diastolic dysfunction. Postoperative E/A ratio is
increased in all but one study. This is likely to be an improvement in pseudonormal
(grade II) diastolic dysfunction associated with obesity. Furthermore we demonstrate
a significant improvement in LA diameter (p<0.001). LA enlargement reflects chronic
exposure to increased LV filling pressure and therefore is an important measure of
diastolic function [18]. LVMI is also an independent predictor of LA enlargement,
which in turn is associated with adverse cardiovascular outcomes. Furthermore
increasing LA diameters are associated with a risk of developing atrial fibrillation so
that a trend towards normalization of this chamber reflects the favorable impact of
bariatric surgery on diastolic function and concurrent decreased risk of
arrhythmogenesis. Additionally, left atrium size is well recognized to be associated
with obstructive sleep apnea, which has also been demonstrated to decrease
significantly after bariatric surgery [19, 20].
LV systolic function
Morbid obesity has long been established as impairing LV systolic function, although
in many cases this is only subclinical and only seen on echocardiogram. Our meta-
analysis demonstrated a modest yet significant increase in LVEF after surgery with
high heterogeneity between studies. This novel finding may be due to the large
dataset applied within this study (as individual reports and previous analyses may
have been underpowered). Alpert et al [21] demonstrated that improvements in
systolic function only occur in those obese individuals whose systolic function was
depressed preoperatively and that the best improvement of systolic parameters after
surgery occurs in those who have been morbidly obese for longer periods of time
[22]. However, bariatric surgery might lead to symptomatic improvement in all
stages of obesity-related cardiomyopathy, and can improve systolic function even in
patients with severe heart failure who are waiting a heart transplant [23]. The overall
weighted baseline LV ejection fraction across all studies was 62%. This normal value
may suggest that many of the patients in reported studies suffered from uncomplicated
obesity (without cardiac sequelae) or even a selection bias for surgery for those
without cardiac dysfunction. Nevertheless, the finding of a significant improvement in
this parameter is noticeable and may represent the supra-physiological activity of
metabolic operations. These include the possibility of direct gut hormonal inotropic
action on the myocardium through an entero-cardiac axis [3].
Mechanisms accounting for the profound improvements in cardiac imaging after
bariatric surgery derive from models explaining how these operations achieve
beneficial reverse remodeling. The classical haemodynamic or mechanical weight-
dependent effect of bariatric surgery (with a decreasing circulating volume) is no
longer thought to be solely responsible for the reverse remodeling seen after surgery,
as the beneficial effects can be independent from changes in blood pressure [11, 24].
Consequently bariatric cardiac effects are also considered to derive from the profound
metabolic (weight independent) effects of bariatric surgery, so that the reverse
remodeling of cardiac geometry and function can result from the joint effects of
weight loss and metabolic enhancement [25]. The recent combined metabolic and
haemodynamic hypothesis [25] may better explain favorable surgical effects. Here
metabolites such as leptin and other adipokines are reported to drive ventricular
hypertrophy in early obesity and then increasing circulating volume contributing to
ventricular dilatation and hypertrophy in morbid obesity [25, 26]. Following bariatric
surgery, the reversal of metabolic dysfunction can then contribute to improved cardiac
structure and function.
The metabolic components of bariatric surgery that contribute to cardiac reverse
remodeling include the systemic BRAVE effects (Bile flow alteration, Reduction in
gastric size, Anatomical gut rearrangement, Vagal manipulation and Enteric gut
hormone manipulation) [27]. These effects occur almost instantaneously after surgery
[20, 27-29], and may offer a paradigm to identify the profound downstream
mechanisms that achieve improvements in glucose metabolism, insulin resistance, gut
hormonal release, microbiota and adipokine modulation [28, 30] demonstrated by
these operations which in turn may offer the resolution of obesity-associated cardiac
dysfunction.
Manipulation of enteric gut hormones has been shown to demonstrate beneficial
effects on cardiac function via the entero-cardiac axis [3, 25, 31]. Hormones such as
secretin (produced in the duodenum), glucagon (produced in the pancreas), and
vasoactive intestinal peptide (produced in the pancreas, gut and brain), act as
inotropes by activating cardiac membrane adenylate cyclase, a key enzyme in cardiac
cell communication [32]. The mechanisms for this are currently unclear, but it is
thought that cardiac energy metabolism is enhanced through TCA cycle
intermediaries, cardiorenal protective activity, and biochemical caloric restriction [33,
34].
Moreover two key hormones; Glucagon-like peptide-1 (GLP-1) and ghrelin also
modulate cardiac function. GLP-1 is well documented to raise satiety, improve
insulin secretion and is increased after bariatric surgery[31]. It has been shown to
improve LV systolic dysfunction after myocardial infarction in humans [35] and
improve functional status in patients with chronic heart failure [36].
There is conflicting data on the appetite-stimulating hormone Ghrelin following
bariatric surgery [31], however studies suggest that when it is infused into patients
with cardiac failure, stroke volume index, ejection fraction and cardiac index are all
improved with a decrease in LV wall stress [37]. Finally adipokines such as Leptin,
TNFα and adiponectin demonstrate cardiovascular activity and have been shown to
significantly decrease for up to 2 years after bariatric surgery [38]. Circulating leptin
levels correlate well with LV mass in morbid obesity both before and after bariatric
surgery [39] and may therefore also contribute to the beneficial cardiac effects of
bariatric operations.
Strengths and Limitations
This meta-analysis statistically appraises pooled data collected from 1486 patients in
40 studies. It is the largest study to date of cardiac indices pre- and post- bariatric
surgery. However the results presented here should be considered in the context of a
number of limitations. Firstly, the heterogeneity of the studies identifying cardiac
structural and functional change represents a significant interpretive limitation.
Patient selection and demographics, follow-up time, cardiac imaging technique and
bariatric procedure performed all vary between studies. The quality scoring of the
studies was generally very low, with only 7 studies scoring greater than 7 on the
Newcastle-Ottawa Scale. Echocardiographic studies are also vulnerable to
subjectivity and reporting biases of interpreting echocardiograms. This can be
difficult in obese patients, with limited acoustic windows and suboptimal data. There
was also great variation in the year of publication, ranging from 1990 to 2014. As
such, our analysis may not reflect the difference between current and older weight
loss therapies, or improvements in echocardiographic or CMR techniques.
Secondly, all of the trials included are limited by their study design. The majority
were prospective observational studies, with fourteen retrospective studies. There
were no randomized control trials. Therefore there may be a degree of publication
bias of these positive results.
Conclusion
In summary, our meta-analysis and systematic review on the effect of bariatric
surgery on cardiac structure assessed by imaging suggests that these procedures are
associated with a significant improvement in cardiac morphology and function. This
supports the role of bariatric surgery on beneficial reverse cardiac remodeling after
surgery although the significant heterogeneity between studies limits our
interpretation of results. Further studies, in particular randomized control trials with
mechanistic studies are justified to clarify the role of surgery in obesity and cardiac
dysfunction, and may help to better select patient cohorts and appropriate procedures
to address the severe mortality and morbidity of obesity-associated cardiac disease.
Ethical Approval: For this type of study, formal consent is not required
Conflict of interest: The authors declare that they have no conflict of interest
Financial disclosure: None
Acknowledgements: We would like to acknowledge Dr Oliver Rider of the Division
of Cardiovascular Medicine, The Radcliffe Department of Medicine (RDM),
University of Oxford, who kindly shared original data from his study.
Table 1. Bariatric surgical studies reporting on changes in cardiac structure and function
VBG = vertical banded gastroplastyLAGB = Laparoscopic adjustable gastric bandingSG = sleeve gastrectomyRYGB = Roux-en-Y Gastric BypassBPD-DS = Biliopancreatic diversion with duodenal switchTG = Tubular GastrectomyNS = not stated
Author Year Design Quality Score (0-9)
Intervention Total Participants
Follow up (months)
Pre-op BMI (SD)
Post-op BMI (SD)
Imaging Technique
Cardiac indices
Alpert[40] 2015 Prospective 4 VBG 67 5 46.2 (5.3) 34.5 (5.7) Echo E/A, DT, LVEDD, LVMI (g/m2.7),Kaier[41] 2014 Prospective 6 SG, RYGB 52 6 44.2 (8.7) 42.4 (4.6) 3D strain
EchoLA diameter, A, E, E/A, DT, IVRT, LVESV, LVEDV, LVSV, LVEF, LVM, RVESV, RVEDV, RVSV, RVEF, RVM
Van Schinkel [42] 2014 Prospective 3 RYGB 9 4 41.3 (4.3) 34.1 (2.8) CMR E/A, LVEF, LVMI (g/m2)Graziani[43] 2013 Prospective 7 NS 51 24 47.9 (6.9) 35.7 (5.9) Echo LA diameter, A, E, E/A ratio, DT,
LVESV, LVESD, LVEDV, LVEDD, LVEF, LVM, LVMI (g/m2), PWT,
IVST,Iancu[44] 2013 Prospective 5 SG 34 12 43.6 (11.9) 28.9 (5.8) Echo LVESV, LVESD, LVEDV, LVEDV,
LVM, LVMI (g/m2.7), PWT, IVST,Martin[45] 2013 Prospective 7 BPD-DS 70 12 41.5 (10.7) 49.4 (7.1) Echo LA diameter, A, E, E/A ratio, DT,
LVESD, LVEDD, LVEF, LVM, LVMI (g/m2.7), PWT, IVST,
Kokkinos G1[12] 2012 Prospective 5 RYGB 14 6 47.9 (6) 34.5 (4.7) Echo LA diameter, LVEF, LVM,Kokkinos G2[12] 2012 Prospective 5 SG 23 6 51.6 (7.5) 38.3 (5.9) Echo LA diameter, LVEF, LVM,
Damiano[46] 2012 Retrospective 5 RYGB 26 8 49.7 (5.8) 39.9 Echo LA diameter, E/A ratio, DT, LVEDD, LVEF, LVM, LVMI(g/m2.7),
RWTLuaces[47] 2012 Prospective 4 RYGB, TG 61 12 47.4 (5) 30.6 (5.07) Echo A, E, E/A, LVESD, LVEDD, LVSV,
LVMI(g/m2.7), RWTKoshino[48] 2013 Retrospective 7 RYGB, BPD-
DS,ns GB29 22.7 51 (9) 37 (10) Echo E/A ratio, DT, LVESD, LVEDD,
LVSV, LVEF, LVMI(g/m2)Cavarretta[49] 2012 Retrospective 5 SG 16 12-20 46.4 (10.3) 44.8 (8) Echo LA diameter, LVESD, LVEDD,
LVEF, LVMI(g/m2.7), PWT, IVST, RWT,
Luaces[50] 2012 Prospective 4 NS 41 12 47.41 (5) 30.43 (5.47) Echo DT, IVRT, LVEF, PWT, IVST,Michalsky[51] 2012 Retrospective 4 RYGB, GB 10 9.4 50.3 (10.2) 34.6 (4.16) CMR LVEDV, LVM,McCloskey[52] 2011 Retrospective 4 RYGB, GB, SG 14 6 50.8(2) 36.8(1.72) Echo LVEF
Lin[53] 2011 Prospective 8 RYGB 10 16 44(7) 29(5) Echo E/A, LVEDV, LVEF, LVM, LVMI(g/m2.7)
Valezi[54] 2011 Prospective 5 RYGB 43 12 41.8(4.4) 28.4(3.8) Echo E, A, E/A, LVEF, LVM, PWT, IVST,Schneiter[55] 2011 Prospective 5 LAGB 11 15.4 42.5 (3.1) 33.2 CMR LVESV, LVEDV, LVEF, LVM
Owan[56] 2011 Prospective 8 RYGB 338 24 47.9(7) 32.2(7.8) Echo LVESV, LVEDV, LVEDD, LVEF, LVMI (g/m2.7), PWT, IVST, RWT,
RVEDA, RVESAAlgahim[57] 2010 Prospective 6 RYGB, GB 15 24 46.7 32.4 Echo LVMI(g/m2.7)
Syed[58] 2010 Prospective 5 NS 22 6 44(11.4) 34.7(7.4) Echo LVEDD, LVM, PWT, IVST,Hsuan[59] 2010 Prospective 5 RYGB, SG 66 3 43.3(6.3) 34.1(5.6) Echo LA diameter, E/A ratio, IVRT,
LVEDD, LVM, LVMI(g/m2.7), PWT, IVST, RWT
Garza[24] 2010 Retrospective 7 RYGB 57 45 49(9) 35(8) Echo LVESD, LVEDD, LVEF, LVM, LVMI(g/m2), PWT, IVST, RVEDA,
RVESARider[60] 2009 Prospective 7 RYGB, GB 13 12 39.7 (7.6) 32.2 (5.3) CMR LVESV, LVEDV, LVSV, LVEF, LVM,
LVMI (g/m2), RVM, RVEDV, RVESV, RVEF
Jhaveri[61] 2009 Prospective 5 RYGB, GB 13 17 44.1(4.2) 29.9(4.7) CMR LVESV, LVEDV, LVSV, LVEF, LVM, LVMI(g/m2), RVESV, RVEDV,
RVEF, RVM,Leichman[62] 2008 Prospective 4 RYGB, GB 43 3 51(1.7) 43.3 Echo LVMI(g/m2.7)
Ippisch[63] 2008 Retrospective 6 RYGB 38 10 60(9) 40(8) Echo LA diameter, E, A, E/A, LVEDD, LVM, LVMI(g/m2.7), PWT, IVST,
RWT,Di Bello[64] 2008 Prospective 3 NS 13 6-24 47(8.1) 36(5) Echo LA diameter, E, A, E/A, DT, IVRT,
LVESV, LVEDV, LVEDD, LVEF, LVMI(g/m2), PWT, IVST,
Nault[65] 2007 Prospective 6 BPD-DS 10 6.8 52.3(7.6) 37.7(5.3) Echo LA diameter, E/A, IVRT, LVESD, LVEDD, LVEF, LVM, PWT, IVST,
Maniscalco[66] 2007 Prospective 6 GB 12 12 43.2(3.6) 31.7(4) Echo LVESV, LVEDV, LVEF, RVEDDCunha Lde[67] 2006 Prospective 5 RYGB 23 36 48.8(8.8) 31.8(5.3) Echo LA diameter, E, A, E/A, IVRT,
LVEDD, LVEF, LVM, LVMI(g/m2), PWT, IVST,
Ikonomidis[68] 2007 Prospective 8 RYGB 60 36 48.68(7.8) 32(6) Echo LA diameter, E/A. DT, IVRT, LVESD, LVESV, LVEDD, LVM,
LVMI(g/m2.7), PWT, IVST,Leichman[69] 2006 Prospective 4 RYGB, GB 22 3 46.8(1.4) 40.1(1.5) Echo E, A, E/A, DT, LVEF, RWT
Willens[70] 2005 Retrospective 5 RYGB 17 7.4 54(11) 40(11) Echo LA diameter, E, A, E/A, DT, LVEDD, LVMI(g/m), PWT, IVST,
RVEDD,Kanoupakis[71] 2001 Prospective 5 VBG 16 6 49(8) 34(7) Echo E, A, E/A, IVRT, LVESD, LVEDD,
LVM, PWT, IVST,Karason[72] 1998 Prospective 7 VBG 38 12 39(4) 29(3) Echo E, A, E/A, IVRT, LVESV, LVEDV,
LVEF, LVM,Gahtan[73] 1997 Prospective 5 VBG 13 18 52.5(1.9) 35.7(1.7) Echo LVM, LVMI(g/m), PWT, IVST,Alpert[74] 1995 Retrospective 3 VBG 25 4.5 NS NS Echo E, AAlpert[21] 1994 Retrospective 3 VBG 39 4.5 NS NS Echo LVESD
Alaud-din[75] 1990 Prospective 4 VBG 12 13 50(1.4) NS Echo LA diameter, LVESD, LVEDD, LVM
Table 2. Results Summary
Abbreviations: LVMI (left ventricular mass index), LVEF (left ventricular ejection fraction) LVESV (left ventricular end-systolic volume), LVESV (left ventricular end-systolic diameter), LVEDV (left ventricular end-diastolic volume), LVEDD (left ventricular end-diastolic diameter), LVEF, LVMI (g/m2.7), PWT (posterior wall thickness), IVST (interventricular septal thickness), RWT (relative wall thickness), IVRT (Isovolumic relaxation time).
Cardiac Indices No. of studies reporting
Baseline (weighted mean)
Weighted mean change post surgery
95% CI P value Heterogeneity I2
(%)Cardiac GeometryLVMI (proportion analysis)
22 -11.2% -14.1% – -8.2% <0.001 32.8
LVMI (g/m) 3 129.92 -0.032g/m -0.107 – 0.043 0.400 33.4LVMI (g/m2) 6 45.0 -0.098 g/m2 -0.153 – -0.044 <0.001 0LVMI (g/m2.7) 13 53.28 -0.133 g/m2.7 -0.168 – -0.099 <0.001 25.2LV mass 24 217.8g -29.798g -35.539 – -24.058 <0.001 55.0Posterior Wall Thickness
18 10.67mm -1.207mm -1.490 – -0.924 <0.001 69.2
Relative Wall Thickness
8 45.3mm -0.035mm -0.067 – -0.003 0.032 95.4
IVST 18 11.07mm -1.318mm -1.627 – -1.008 <0.001 67.9LVSV 5 42.15ml -4.667ml -12.168 – 2.835 0.223 71.2LVESD 12 31.45mm -0.410mm -1.500 – 0.679 0.461 81.9
LVEDD 20 50.77mm -0.668mm -1.343 – 0.007 0.052 54.9LVESV 10 42.15ml -4.987ml -9.624 – -0.351 0.035 87.3LVEDV 13 112.3ml -13.283ml -21.344 – -5.222 0.001 85.9Diastolic FunctionA wave 13 69.2 cm/s - 5.246 cm/s -7.757 – -2.734 <0.001 60.2E wave 13 77.6 cm/s 4.262 cm/s 1.267 – 7.258 0.005 72.0E/A ratio 21 1.16 0.189 0.113 – 0.265 <0.001 82.0Deceleration time 11 204.7ms -5.687ms -15.977 – 4.603 0.279 85.7IVRT 9 90.23ms -16.173ms -25.930 – -6.415 0.001 93.9LA diameter 15 39.18mm -1.967mm -2.954 – -0.980 <0.001 79.7Systolic FunctionLVEF 23 62.04 1.198% 0.050 – 2.347 0.041 74.2
Figures
Figure 1. Search Strategy
Figure 2. Forest plots demonstrating changes in (a) left ventricular mass and (b) left ventricular end diastolic volume following bariatric surgery
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