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articles nature publishing group Bariatric surgery The Effect of Surgical Weight Reduction on Left Ventricular Structure and Function in Severe Obesity Chin-Feng Hsuan1,2, Chih-Kun Huang2,3, Jou-Wei Lin4, Lung-Chun Lin5, Thung-Lip Lee1, Chi-Ming Tai1, Wei-Hsian Yin6, Wei-Kung Tseng1,7, Kwan-Lih Hsu1 and Chau-Chung Wu5 The aim of this study was to examine the effect of surgical weight reduction on cardiac structure and function and to seek the determinants of these changes. Sixty-six severely obese adults (BMI ≥35 kg/m2) who received bariatric surgery underwent echocardiographic examination before and 3 months after surgery. At 3 months after surgery, BMI and systolic blood pressure (BP) decreased (43.3 ± 6.3 to 34.1 ± 5.6 kg/m2, P < 0.001, and 146 ± 12 to 130 ± 14 mm Hg, P < 0.001, respectively). In left ventricular (LV) geometry, the relative wall thickness (RWT) and LV mass index decreased significantly (0.43 ± 0.05 to 0.35 ± 0.05, P < 0.001, and 50 ± 11 to 39 ± 11 g/m2.7, P < 0.001, respectively) without changes in chamber size. Multivariate analyses showed change in systolic BP to be an independent predictor for the changes in RWT and LV mass index. In myocardial performance, peak systolic mitral annular velocity and all diastolic indexes showed significant improvements. We concluded that LV hypertrophy and function improved rapidly after bariatric surgery in severely obese adults. BP reduction was the major determinant for the regression of LV hypertrophy in the early stage of surgical weight reduction. Obesity (2010) doi:10.1038/oby.2010.42 Introduction Obesity is associated with abnormalities in cardiac structure and function, including increased left ventricular (LV) wall thickness, chamber size, LV mass, and systolic and diastolic dysfunction (1–5). These structural and functional changes, especially LV hypertrophy, are independent risk factors for cardiovascular disease (6). Studies have shown that weight reduction by diet and exercise programs may induce regression of LV mass; however, the magnitude of weight reduction and changes in cardiac structure and function were subtle (7). Bariatric surgery is a more effective and rapid method for weight reduction (8,9). Studies evaluating the effect of surgical weight reduction demonstrated significant improvements in LV mass and some demonstrated improvements on diastolic function (10–15). Nonetheless, little is known about the determinants for improvement in LV structure and function after this procedure. We, therefore, conducted a prospective study in severely obese patients receiving bariatric surgery to evaluate the effect of surgical weight reduction on LV structure, systolic and diastolic function, to examine the association of weight reduction with changes in hemodynamics, LV geometry and function, and, most importantly, to seek the predictors of these changes. Methods and Procedures Study population From May 2007 to August 2008, all severely obese (BMI ≥40 kg/m2 or ≥35 kg/m2 with comorbidities) adults (≥20 years of age), being scheduled for bariatric surgery (laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy) at a single medical center in the southern part of Taiwan after evaluation by a multidisciplinary team, were assessed for eligibility. Studied patients received echocardiographic evaluations before and 3 months after surgery. Patients with heart failure, valvular heart disease, coronary artery disease, regional wall motion abnormality, congenital heart disease, left bundle branch block or atrial fibrillation determined on the basis of previous history, physical examination, electrocardiography, and echocardiography were excluded from this study. Patients with an image inadequate for analysis were also excluded. The study protocol was approved by the hospital ethics committee, and all studied patients gave informed consent. Clinical and demographic data Before surgery, studied patients’ age, sex, and medical history were obtained. A detailed physical examination and 12-lead electrocardiography were performed. Weight, height, waist circumference, and blood pressure (BP) were measured before and 3 months after surgery by a well‑trained nurse. BMI was calculated as weight (Kg)/height × height (m2). Percent of excess BMI lost was calculated as (preoperative BMI−current BMI)/(preoperative BMI−23) × 100 1 Department of Internal medicine, E-Da Hospital, Kaohsiung, Taiwan; 2Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung, Taiwan; 3Department of Surgery, E-Da Hospital, Kaohsiung, Taiwan; 4Cardiovascular Center, National Taiwan University Hospital Yun-Lin Branch, Yun-Lin, Taiwan; 5 Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; 6Division of Cardiology, Cheng-Hsin General Hospital, Taipei, Taiwan; 7 Department of Medical Imaging and Radiological Sciences, I-Shou University, Kaohsiung, Taiwan. Correspondence: Wei-Kung Tseng ([email protected]) Received 18 October 2009; accepted 5 February 2010; advance online publication 18 March 2010. doi:10.1038/oby.2010.42 obesity 1 articles Bariatric surgery (16,17). BP was measured according to the recommendations described by Chobanian et al. (18). Echocardiography Echocardiographic studies were performed using a Sonos 7500 (Philips Ultrasound, Bothell, WA) ultrasound system equipped with a 1.6-3.2 MHz phased-array transducer. All echocardiographic images were digitally stored on optical discs for off-line analysis. Each parameter was measured off-line and quantified with the average of measurements of three consecutive cardiac cycles by a single experienced sonographer who was blinded to the patients’ clinical information. Two-dimensional guided M-mode echocardiographic tracings in the parasternal long axis view were performed to measure the left atrial (LA) diameter and the parameters of the LV geometry, including the LV end-diastolic dimension (LVEDD), end-diastolic interventricular septal thickness (IVSd) and LV posterior wall thickness (LVPWd) (19). LV endocardial fractional shortening was calculated as (LVEDD−LVESD)/ LVEDD. The relative wall thickness (RWT) was calculated as (IVSd + LVPWd)/LVEDD. LV mass was calculated using the corrected American Society of Echocardiography convention proposed by Devereux et al.: LV mass (g) = 0.8 × 1.04 × ((LVEDD + LVPWd + IVSd)3−LVEDD3) + 0.6 (20). For more appropriate normalization of LV mass in obese patients, LV mass was indexed by dividing by height2.7 (21). LV hypertrophy was defined as LV mass index >51 g/m2.7 (22), and LV concentricity was determined using RWT >0.45 as a cutoff point (23). The LV geometries of the studied patients were categorized into four groups: concentric LV hypertrophy, eccentric LV hypertrophy, concentric LV remodeling, and normal. Using pulsed-wave Doppler, early diastolic mitral inflow velocity (E-wave), late diastolic mitral inflow velocity (A-wave) and isovolumetric relaxation time were measured in apical 4-chamber and 5-chamber view, and an E/A ratio was calculated. Myocardial velocities was measured through the apical 4-chamber view with the Doppler beam parallel to the motion of the part of the LV of interest. Peak systolic and early diastolic tissue velocities were recorded over the septal and lateral mitral annulus. Representative values of peak systolic (Sa) and early (Ea) diastolic mitral annular velocities were obtained from the average of measurements of septal and lateral annulus. An E/Ea ratio was applied to estimate the LV filling pressure (24). Statistical analysis Statistical analyses were performed with SPSS, version 11.0 (SPSS, Cary, NC). All continuous variables were expressed as mean ± s.d. Differences in variables before and after surgery were assessed using the paired t-test. Pearson’s correlation analysis was used to estimate the relationships between BMI, waist circumference, hemodynamics, and echocardiographic variables preoperatively and, also, to determine the relationships between changes in these variables after surgery. At baseline, age, sex, and systolic BP were entered in the multiple linear regression analyses for adjustment of the possible relationship with the examined dependent variables. Hierarchical multiple linear regression analyses were also applied to examine the association between dependent variables, including the change in measurements of LV geometry and the indexes of systolic and diastolic function, and independent variables. The independent variables were selected if a significant correlation with the dependent variable was found in univariate analysis; and factors such as age, sex, and other clinically important baseline data were forced to remain in the model. A P value <0.05 was considered significant. Results Patient characteristics and echocardiographic measurements at baseline Sixty-six consecutive patients (23 men and 43 women; mean age 31 ± 9 years, range 20–58 years) were studied. All were 2 of Chinese ethnicity. Fifty-four patients received laparoscopic Roux-en-Y gastric bypass, and the other 12 patients received laparoscopic sleeve gastrectomy. Preoperative characteristics and echocardiographic measurements are summarized in Table 1. BMI ranged from 35 to 65.3 kg/m2 with a mean of 43.3 ± 6.3 kg/m2. Regarding LV geometry, the LV mass, LV mass index, and LVEDD correlated with BMI and waist circumference in all patients (Table 2), and in those with or without hypertension (systolic BP ≥ 140 mm Hg as a cutoff point) (data not shown). The RWT and LV mass, but not the LVEDD, correlated with systolic BP, and the LV mass index showed Table 1 Clinical characteristics and echocardiographic parameters of the study population at baseline and 3-month follow-up Preoperative Age (years) Postoperative P value 95 ± 18 <0.001 31 ± 9 Sex (male:female) 23: 43 Weight (kg) 121 ± 21 43.3 ± 6.3 34.1 ± 5.6 <0.001 Waist circumference (cm) BMI (kg/m ) 123.4 ± 14.2 106.9 ± 13.3 <0.001 Systolic BP (mm Hg) 146 ± 12 130 ± 14 <0.001 Diastolic BP (mm Hg) 90 ± 10 81 ± 13 <0.001 <0.001 2 Heart rate (beats/min) 86 ± 11 76 ± 13 LVEDD (cm) 5.00 ± 0.37 5.00 ± 0.37 0.869 IVSd (cm) 1.09 ± 0.15 0.89 ± 0.15 <0.001 LVPWd (cm) 1.04 ± 0.13 0.87 ± 0.13 <0.001 RWT 0.43 ± 0.05 0.35 ± 0.05 <0.001 LV mass (g) 201 ± 51 157 ± 45 <0.001 50 ± 11 39 ±11 <0.001 Concentric hypertrophy 19.7% 3.0% Eccentric hypertrophy 24.2% 13.6% Concentric remodeling 15.2% 1.5% Normal 40.9% 81.8% LV mass index (g/m ) 2.7 LV concentricity FS (%) 40.4 ± 2.8 40.1 ± 3.4 0.492 LA diameter (cm) 4.11 ± 0.41 4.02 ± 0.43 0.02 E/A ratio 1.32 ± 0.38 1.62 ± 0.45 <0.001 IVRT (ms) 93 ± 14 82 ± 15 <0.001 Ea (cm/s) 10.5 ± 2.4 12.6 ± 2.3 <0.001 Sa (cm/s) 8.1 ± 1.2 8.6 ± 1.3 0.001 E/Ea ratio 8.6 ± 1.9 7.6 ± 1.6 <0.001 Values are mean ± s.d. BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow velocity; Ea, early diastolic mitral annular velocity; FS, endocardial fractional shortening; IVRT, isovolumetric relaxation time; IVSd, end-diastolic interventricular septal thickness; LA, left atrial; LV, left ventricular; LVEDD, left ventricular enddiastolic dimension; LVPWd, end-diastolic left ventricular posterior wall thickness; RWT, relative wall thickness; Sa, peak systolic mitral annular velocity. www.obesityjournal.org articles Bariatric surgery Table 2 Correlations of age, systolic BP, BMI, waist circumference with LV geometry and diastolic function at baseline Age Systolic BP BMI Waist circumference RWT 0.23 0.26* 0.06 0.21 LV mass 0.13 0.32* 0.46** 0.54** 0.21 0.23 0.55** 0.45** −0.01 0.18 0.46** 0.42** LV mass index LVEDD RWT LV mass index E/A ratio −0.64** −0.05 0.18 −0.01 −0.42** −0.21 Ea −0.48** −0.09 0.05 −0.12 −0.44** −0.37* IVRT 0.24 −0.07 0.15 0.17 −0.03 0.29* E/Ea ratio 0.01 0.07 0.31* 0.26* 0.14 0.39** −0.16 0.13 0.38** 0.35* 0.20 0.36** LA diameter Values are Pearson’s coefficient; *P < 0.05; **P < 0.001. BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow velocity; Ea, early diastolic mitral annular velocity; IVRT, isovolumetric relaxation time; LA, left atrial; LV, left ventricular; LVEDD, left ventricular end-diastolic dimension; RWT, relative wall thickness. Weight, BP, and heart rate changes after bariatric surgery Weight, BMI, and waist circumference showed significant reductions 3 months after bariatric surgery (121 ± 21 to 95 ± 18 kg, 43.3 ± 6.3 to 34.1 ± 5.6 kg/m2, and 123.4 ± 14.2 to 106.9 ± 13.3 cm, respectively). The percent of excess BMI lost was 45.1% at 3 months. Systolic, diastolic BP, and heart rate decreased significantly after bariatric surgery (Table 1). Changes in systolic BP correlated with the percent change in BMI and percent of excess BMI lost (r = 0.28, P = 0.025 and r = 0.33, P = 0.007, respectively). Changes in LV mass and geometry after bariatric surgery The effects of weight reduction on LV mass and the parameters of LV geometry are listed in Table 1. Three months after baria tric surgery, except LVEDD, there were significant reductions in IVSd, LVPWd, RWT, LV mass, and LV mass index. The results remained the same in subgroup analyses (either in patients with or without hypertension, and either in patients with concentric or eccentric LV geometry) (data not shown). Univariate analysis revealed the changes in RWT and LV mass index correlated with change in systolic BP (r = 0.49, P < 0.001; obesity a 0.15 r = 0.49 P < 0.001 Change in RWT 0.05 –0.05 –0.15 –0.25 –50 –25 0 25 50 Change in systolic BP (mm Hg) b 15 Change in LV maa index (g/m2.7) a trend toward correlation with systolic BP (Table 2). The observation was similar in patients with hypertension, but not in those without hypertension. The associations of LV mass, LV mass index, and LVEDD with BMI and waist circumference persisted even after adjustment for age, sex, and systolic BP (regression coefficient (B) = 0.51, P < 0.001; B = 0.63, P < 0.001; B = 0.48, P < 0.001, respectively, for BMI and B = 0.44, P < 0.001; B = 0.46, P < 0.001; B = 0.38, P = 0.003, respectively, for waist circumference). In diastolic indexes, the E/A ratio and Ea correlated well with RWT (Table 2), even after adjustment for age, sex, and systolic BP. On the other hand, Ea and isovolumetric relaxation time correlated with LV mass index. LA diameter and the E/Ea ratio, representing LV filling pressure, correlated with BMI and waist circumference. There was no correlation between the hemo dynamic measurements (systolic, diastolic, mean BP, and heart rate) and systolic or diastolic function. r = 0.38 P < 0.001 5 –5 –15 –25 –35 –50 –25 0 25 50 Change in systolic BP (mm Hg) Figure 1 Correlation between (a) change in relative wall thickness (RWT) and change in systolic blood pressure (BP), and (b) change in left ventricular (LV) mass index and change in systolic BP after weight reduction induced by bariatric surgery. r = 0.38, P = 0.001, respectively) (Figure 1). There were no associations among change in BMI, the percent of excess BMI lost, or change in waist circumference and changes in LV mass, LV mass index, RWT, or LVEDD. Multivariate linear regression analyses showed changes in systolic BP and baseline RWT to be independent predictors for the change in RWT, and changes in systolic BP and baseline LV mass index were independent predictors for the change in LV mass index (Table 3). In subgroup analysis, regardless of the existence of hypertension at baseline, the most powerful predictor for changes in 3 articles Bariatric surgery RWT and LV mass index was still the change in systolic BP (Supplementary Table S1 online). Changes in systolic and diastolic function after bariatric surgery The fractional shortening remained stable 3 months after baria tric surgery. Nonetheless, Sa increased significantly (Table 1), and the magnitude of Sa increase correlated with the magnitude of BMI decrease (r = −0.36, P = 0.003) and the percent of excess BMI lost (r = −0.29, P = 0.017). Regarding LV diastolic function, the E/A ratio and Ea increased significantly after surgery. Isovolumetric relaxation time, LA size, and LV filling pressure (E/Ea ratio) also decreased significantly (Table 1). These changes represented improvements in diastolic function 3 months after bariatric surgery. Univariate analysis revealed that the change in the E/A ratio correlated with percent of excess BMI lost and change in waist circumference (r = −0.34, P = 0.005 and r = −0.26, P = 0.035, respectively), and the change in Ea correlated with percent of excess BMI lost (r = −0.26, P = 0.039) (Table 4). Discussion The results of the present study are consistent with previous reports that weight reduction after bariatric surgery could significantly improve LV hypertrophy and hemodynamics. Table 3 Multivariate analysis for determinants of changes in RWT and LV mass index Change in RWT R2 = 0.509 B P value Age 0.2 0.039 Sex −0.09 0.377 Baseline LV mass index Baseline RWT Change in LV mass index R2 = 0.327 B −0.01 P value 0.902 0.07 0.566 −0.363 0.004 −0.56 <0.001 Change in systolic BP 0.43 <0.001 0.51 <0.001 Percent of excess BMI lost 0.02 0.843 −0.16 0.202 B, regression coefficient; BP, blood pressure; LV, left ventricular; RWT, relative wall thickness. However, it provides some new information in addition to previous ones. It was the first study to show that subclinically impaired LV systolic function can be reversed after weight reduction. We also demonstrated that all diastolic indexes were improved after surgical weight reduction. Most importantly, our results indicated that, shortly after bariatric surgery, systolic BP reduction was the major determinant for the improvements in RWT and LV mass index. LV hypertrophy, especially the concentric type, has been demonstrated to be an important predictor for cardiovascular disease, heart failure or sudden death, even though an obesity paradox exists (6,25–27). Earlier studies reported obesity is related to eccentric hypertrophy, a compensatory hypertrophy to volume overload (28,29). Recent studies involving cardiac remodeling in obesity have shown that LV wall thickness appeared to increase to a greater extent than the internal dimension, which implies that LV hypertrophy in obesity may represent more than simple volume compensation (1–4,30). In agreement with most of the previous studies, the present results showed BMI was independently correlated with LV mass, LV mass index, and chamber size. An increase in RWT and a substantial percentage of concentric hypertrophy or remodeling of LV were also found in obese patients (Table 1), regardless of the existence of hypertension. This observation further confirmed that LV hypertrophy in obesity is not always of the eccentric type. The effect of weight reduction on LV geometry and mass through diet control and exercise programs was reported to be minor and even variable (7,31). The relatively small magnitude of weight loss in these programs may explain this result. Bariatric surgery offers an intervention that induces more vigorous and rapid weight reduction (8,9), and significantly improves the LV structure (11–15). However, there were few data from these reports to define the determinants for improving LV mass and geometry after bariatric surgery. Clinical trials have documented that weight loss could result in reduction of BP (32). On the other hand, reduction of BP by antihypertensive agents may induce regression of LV hypertrophy (33). Whether the regression of LV hypertrophy after bariatric surgery in severe obesity occurs because of reduction of BP, weight reduction itself, or other mechanism is unclear. Karason et al. and Ippisch et al. found that the regression of LV mass was better predicted by the weight Table 4 Correlations of changes in systolic BP, BMI, waist circumference, and LV geometry with changes in diastolic function Δ Systolic BP Δ BMI %EBL Δ Waist circumference Δ RWT Δ LV mass index Δ E/A ratio −0.24 −0.14 −0.34* −0.26* −0.19 −0.09 Δ Ea −0.08 −0.15 −0.26* −0.20 −0.07 0.11 0.10 0.11 −0.06 0.07 0.09 0.11 −0.10 0.02 −0.09 0.04 −0.04 −0.07 0.02 0.08 0.08 0.15 0.06 Δ IVRT Δ E/Ea ratio Δ LA diameter 0.27* Values are Pearson’s coefficient; *P < 0.05. BP, blood pressure; E/A ratio, the ratio of early to late diastolic mitral inflow velocity; Ea, early diastolic mitral annular velocity; IVRT, isovolumetric relaxation time; LA, left atrial; LV, left ventricular; RWT, relative wall thickness; Δ, change in; %EBL, percent of excess BMI loss. 4 www.obesityjournal.org articles Bariatric surgery loss than by the reduction of BP (11,15). Both studies had a relatively longer follow-up period (10–12 months). Another study with a shorter follow-up period after bariatric surgery (mean 4.6 ± 1.1 months) showed that change in LV mass index was positively correlated with change in systolic BP and percent overweight (10). The present study with 3 months of follow-up after baria tric surgery demonstrated significant BP reduction. Also, our results showed that the short-term effect of bariatric surgery on the LV structure was prominent except for that on the chamber size regardless of the baseline LV geometry. No sufficient time for remodeling might be the reason for no change in LV chamber size. Therefore, the improvements in LV mass, LV mass index, and RWT in this early stage after bariatric surgery resulted mainly from the improvement in LV wall thickness. Furthermore, this study found that the magnitude of systolic BP reduction had the strongest correlation with the improvements in LV mass index and RWT 3 months after bariatric surgery. These findings implied that BP reduction play an important role in the regression of LV mass and improvement of concentricity in the early stage of weight reduction after bariatric surgery. A regain of BP was observed 1 year after bariatric surgery (34), which may be a possible reason to explain why BP reduction becomes less important in the regression of LV hypertrophy in the long-term after bariatric surgery. Results of studies evaluating LV systolic function in obesity were variable. Most studies reported that LV ejection fraction or fraction shortening is preserved in obese patients. Nonetheless, increased endocardial shortening in LV hypertrophy may overestimate the LV systolic function in obesity (35). Several recent studies using newer and more sensitive methods, such as midwall fractional shortening or systolic myocardial velocity, detected subclinical depression of LV systolic function in obese patients (2,3). Some studies of the results of depressed LV systolic function in obese patients showed that duration of obesity was a determinant for LV systolic dysfunction (33,37). These findings suggested that obesity may have an impact on LV systolic function that may be subtle in the early stage of obesity. The results of our study further demonstrated that, after weight reduction, the subtle and possibly preclinical depressed LV systolic function can be reversed to avoid future deterioration. As with the findings for systolic function, studies on assessing LV diastolic function in obese patients with conventional Doppler methods to measure mitral inflow velocities showed inconsistent results (38–41). Recently, a newer echocardiographic technique using tissue Doppler imaging to measure myocardial velocity offers a more sensitive and load-independent method to assess LV diastolic function (42). Three recent studies applying this method consistently found decreased early diastolic mitral annular velocity (Ea) in obese patients (2,4,43). In the present study, we observed that Ea and the E/A ratio were independently associated with RWT rather than BMI, suggesting that the LV concentric geometry related to obesity, not obesity itself, had an influence on ventricular diastolic function, causing abnormal ventricular relaxation. obesity The E/Ea ratio has been widely used to estimate the LV filling pressure (24). Also, LA enlargement reflects chronic elevation of LV filling pressure (44,45). Elevation of the E/Ea ratio and LA enlargement in obese patients has been reported previously (2–4,40). A positive correlation between BMI and the E/Ea ratio and LA diameter in the present study indicated that elevated LV filling pressure may be related to volume expansion in obese patients. Importantly, the present study demonstrated that all diastolic indexes, including the E/A ratio, Ea, isovolumetric relaxation time, E/Ea ratio, and LA size, significantly improved after bariatric surgery, representing improvement in LV relaxation and decrease in LV filling pressure. However, only the changes in E/A ratio and Ea showed weak correlations with the percent of excess BMI lost. Further investigation is needed to clarify the mechanism of the improvement of diastolic dysfunction. Our study had several limitations. First, other comorbidities accompanying obesity, including insulin resistance, and some factors such as the duration of obesity, that may affect cardiac performance were not evaluated. Second, we used office BP in this study, which is inferior to 24-h average BP in the assessment of LV hypertrophy or dysfunction (46). Finally, this study demonstrated the improvements in cardiac structure and function echocardiographically without investigating the long-term benefit on survival or major adverse cardiac events. Further studies addressing these issues are needed. In conclusion, obesity was associated with increased LV mass, wall thickness and impaired LV function. Rapid weight reduction after bariatric surgery could induce a dramatic and rapid regression of LV mass and wall thickness, and improve not only diastolic but also systolic function of the heart in severely obese patients. More importantly, the present study indicated that BP was the major determinant for the regression of LV hypertrophy in the early stage of rapid weight reduction after bariatric surgery. 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