Search

Objective: The aim of this study was to examine the clinical efficacy and safety of the duodenal-jejunal bypass liner (DJBL) while in situ for 12 months and for 12 months after explantation., Summary Background Data: This is the largest randomized controlled trial (RCT) of the DJBL, a medical device used for the treatment of people with type 2 diabetes mellitus (T2DM) and obesity. Endoscopic interventions have been developed as potential alternatives to those not eligible or fearful of the risks of metabolic surgery., Methods: In this multicenter open-label RCT, 170 adults with inadequately controlled T2DM and obesity were randomized to intensive medical care with or without the DJBL. Primary outcome was the percentage of participants achieving a glycated hemoglobin reduction of ≥20% at 12 months. Secondary outcomes included weight loss and cardiometabolic risk factors at 12 and 24 months., Results: There were no significant differences in the percentage of patients achieving the primary outcome between both groups at 12 months [DJBL 54.6% (n = 30) vs control 55.2% (n = 32); odds ratio (OR) 0.93, 95% confidence interval (CI): 0.44-2.0; P = 0.85]. Twenty-four percent (n = 16) patients achieved ≥15% weight loss in the DJBL group compared to 4% (n = 2) in the controls at 12 months (OR 8.3, 95% CI: 1.8-39; P = .007). The DJBL group experienced superior reductions in systolic blood pressure, serum cholesterol, and alanine transaminase at 12 months. There were more adverse events in the DJBL group., Conclusions: The addition of the DJBL to intensive medical care was associated with superior weight loss, improvements in cardiometabolic risk factors, and fatty liver disease markers, but not glycemia, only while the device was in situ. The benefits of the devices need to be balanced against the higher rate of adverse events when making clinical decisions., Trial Registration: ISRCTN30845205. isrctn.org; Efficacy and Mechanism Evaluation Programme, a Medical Research Council and National Institute for Health Research (NIHR) partnership reference 12/10/04., Competing Interests: Declaration of interests: A.R. received travel fees support from GI Dynamics. A.D.M. has received honoraria for presentations and advisory board contribution by Novo Nordisk, Boehringer Ingelheim, AstraZeneca, Johnson & Johnson and research grant funding from Fractyl. A.P.G. reports funding supported by UK Medical Research Council and Wellcome Trust, outside of the submitted work, is on a Data Safety Monitoring Board for Novo Nordisk, and has received honoraria for presentations and advisory board contribution by Janssen, Pfizer, Novo Nordisk, Zafgen, Soleno Therapeutics Inc, and Millendo Theapeutics Inc, and Merck. A.R.A. received educational grants from MSD and WL Gore. C.W.R. is a member of scientific advisory board for Herbalife, GI Dynamics, NovoNordisk, Keyron, Sanofi, has provided ad hoc consulting for Ethicon and Fractyl, occasional speaking engagement for MSD, Boehringer Ingelheim and Lilly. J.P.T. received travel fees support from GI Dynamics. The rest of the authors report no conflicts of interest. The authors report no conflict of interests., (Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Increased thoracic ascending aortic stiffness is thought to contribute to concentric left ventricular hypertrophy and increased mortality, a pattern seen in hypertension. As such, aortic stiffness and increased left ventricular mass are candidates by which obesity increases cardiovascular risk. However, obesity is characterized predominantly by increased abdominal aortic stiffness and with eccentric left ventricular hypertrophy., Methods: We aimed to establish whether or not, in addition to these changes, there is also an element of concentric remodeling in obesity that was predicted by ascending aortic stiffness. 301 subjects underwent cardiovascular magnetic resonance imaging to measure regional aortic distensibility and left ventricular morphology. To compare obesity with hypertension, subjects were separated into groups by hypertensive status and body mass index., Results: In comparison to normotensive subjects, hypertension was linked with concentric remodeling (a 17% increase in left ventricular mass:volume ratio (LVM:VR), (p<0.001)) and reduced ascending aortic distensibility (by 64%,p<0.001). LVM:VR was negatively correlated with ascending aortic distensibility (R=-0.36,p<0.01). Obesity, in the absence of hypertension, was associated with elevated left ventricular mass when compared to normal weight normotensive subjects (by 27%, p<0.01), in an eccentric pattern with cavity dilatation (p<0.01). However, LVM:VR was also 14% larger than in normal weight normotensive subjects (p<0.01), indicative of additional concentric remodeling. LVM:VR in obesity was, however, not correlated with ascending aortic distensibility when adjusted for mean arterial pressure (R=-0.14,p<0.14)., Conclusion: In summary, despite the predominantly eccentric pattern of left hypertrophy in obesity there is a concentric element of hypertrophy that, unlike in hypertension, is not linked to increased ascending aortic stiffness., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Aims: As obesity-related cardiovascular mortality, although elevated when compared with normal weight, is lower in females than in males at every body mass index (BMI) level, we aimed to investigate gender-specific differences in left ventricular (LV) hypertrophy in obesity, which themselves have been shown to have varying prognostic value., Method and Results: In total, 741 subjects (female, n = 399) without identifiable cardiovascular risk factors (BMI 15.7-59.2 kg/m(2)) underwent cardiovascular magnetic resonance (1.5 T) to determine LV mass, end-diastolic volume (EDV, mL), and LV mass/volume ratio (LVM/VR). Across both sexes, there was a strong positive correlation between BMI and LV mass (male r = 0.44, female r = 0.57, both P < 0.001), with males showing a greater LV hypertrophic response (male +2.3 vs. female +1.6 g per BMI point increase, P = 0.001). Concentric hypertrophy was present in both sexes and LVM/VR positively correlated to BMI (male r = 0.45, female r = 0.29, both P < 0.001) on linear regression analysis. However, the degree of concentric hypertrophy was greater in males (male +0.13 vs. female +0.06 LVM/VR increase per BMI point increase, P = 0.001). On the other hand, females showed a greater LV cavity dilatory response (female +1.1 vs. male +0.3 mL per BMI point increase, P < 0.001). Indeed, in contrast to females, where BMI and LV-EDV were positively correlated (r = 0.38, P < 0.001), BMI did not correlate with EDV in men (r = 0.03, P = 0.62)., Conclusion: In the absence of traditional cardiovascular risk factors, obese men show predominantly concentric hypertrophy, whereas obese women exhibit both eccentric and concentric hypertrophy. As concentric hypertrophy is more strongly related to cardiovascular mortality than eccentric hypertrophy, our observations may explain the observed gender difference in obesity-related mortality.

Obesity is associated with cardiac hypertrophy and increased aortic stiffness, which are independent predictors of cardiovascular risk. In the setting of obesity, bariatric surgical weight loss has been shown to reduce mortality. We present a case showing that, in a severely obese individual without comorbidities, these cardiovascular responses to excess weight are reversible during weight loss over a period of 1 year.

Obesity is an escalating global health problem associated with both an increased risk of death and an increased risk of cardiovascular events. Our goal was to use magnetic resonance imaging (MRI) to determine the effect of obesity and weight loss, in the absence of the traditional cardiovascular risk factors, on aortic pulse wave velocity (PWV) a reliable, reproducible, and accurate clinical measure of aortic stiffness linked to increased mortality. Fifty obese (BMI 38.3 ± 6.8 kg/m(2)) and eighteen normal-weight controls (BMI 22.0 ± 1.7 kg/m(2)) with no identifiable cardiovascular risk factors underwent vascular MRI to assess PWV between the ascending aorta at the level of the pulmonary artery and the abdominal aorta (AA). Twenty-eight subjects underwent repeat imaging after a 1-year period of weight loss. Both groups were well matched for age, systolic blood pressure, fasting glucose, and total cholesterol. Obesity was associated with a 14% increase in PWV (P = 0.021), and with elevated C-reactive protein (CRP) (P < 0.01) and leptin levels (P < 0.001) factors known to cause increase arterial stiffness. Weight loss (average 50% excess weight) was associated with a 14% improvement in PWV (P = 0.03), and with reductions in serum leptin levels (P < 0.01). Obesity, in the absence of the traditional cardiovascular risk factors, is associated with increased aortic PWV, a noninvasive clinical measure of aortic stiffness independently predictive of cardiovascular mortality. Significant weight loss results in improvements in aortic PWV. This may provide a potential link between both obesity and increased mortality, and the reduction in mortality that occurs with weight loss.