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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 MRCS 1,3 1 Department of Surgery and Cancer, Imperial College London 2 Department of Cardiothoracic Surgery, Imperial College Healthcare NHS Trust 3 Department of Bariatric Surgery, Chelsea and Westminster Hospital * Corresponding author: Hutan Ashrafian, The Department of Surgery and Cancer, Imperial College London. 10 th 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.

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Page 1: spiral.imperial.ac.ukspiral.imperial.ac.uk/bitstream/10044/1/38741/2/Bar...  · Web view2017. 5. 1. · 52.McCloskey CA, Ramani GV, Mathier MA, Schauer PR, Eid GM, Mattar SG, et

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

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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

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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).

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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

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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-

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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

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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

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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

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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.

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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

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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

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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.

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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].

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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.

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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.

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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

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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

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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

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Figures

Figure 1. Search Strategy

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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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