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Aim: Current knowledge on the role of obesity in causing cardiac dysfunction is insufficient. Several biomarkers reflecting biological processes that may play a role in the occurrence of cardiac dysfunction in obesity patients are available. Purpose: To compare cardiovascular biomarker profiles between obesity patients and nonobese controls, and between obesity patients with and without cardiac dysfunction, in order to better understand the underlying pathophysiology of cardiac dysfunction in obesity patients. Materials & methods: Blood samples were obtained from 100 obesity patients (BMI ≥35 kg/m 2 ) without known cardiovascular disease, and from 50 age- and gender-matched nonobese controls (BMI ≤30 kg/m 2 ). The third cardiovascular panel of the Olink Multiplex platform was used for the measurement of 92 biomarkers. Results: The majority (53%) of biomarkers were elevated in obesity patients compared with nonobese controls. Only 5% of the biomarkers were elevated in obesity patients with cardiac dysfunction compared with those without. Biomarkers discriminating cardiac dysfunction from no cardiac dysfunction in obesity patients differed from those discriminating obese from nonobese patients. An elastic net model for the prediction of cardiac dysfunction in obesity patients had a high area under the receiver operating curve of 0.87 (95% CI: 0.79-0.94; p < 0.001). The sensitivity of this model was 84% and the specificity was 79%. Conclusion: A multiplex immunoassay was used for the first time in obesity patients without known cardiovascular disease. These patients have cardiovascular biomarker profiles that are clearly different from nonobese controls. Comparison of obesity patients with and without cardiac dysfunction suggested an important role for inflammation, atherosclerosis and insulin resistance in the underlying pathophysiology of cardiac dysfunction in obesity patients.

Background: Despite a generally high specificity, electrocardiographic (ECG) criteria for the detection of left ventricular hypertrophy (LVH) lack sensitivity, particularly in obesity patients., Objectives: The aim of the study was to evaluate the accuracy of the most commonly used ECG criteria (Cornell voltage and Sokolow-Lyon index), the recently introduced Peguero-Lo Presti criteria and the correction of these criteria by body mass index (BMI) to detect LVH in obesity patients and to propose adjusted ECG criteria with optimal accuracy., Methods: The accuracy of the ECG criteria for the detection of LVH was retrospectively tested in a cohort of obesity patients referred for a transthoracic echocardiogram based on clinical grounds (test cohort, n = 167). Adjusted ECG criteria with optimal sensitivity for the detection of LVH were developed. Subsequently, the value of these criteria was prospectively tested in an obese population without known cardiovascular disease (validation cohort, n = 100)., Results: Established ECG criteria had a poor sensitivity in obesity patients in both the test cohort and the validation cohort. The adjusted criteria showed improved sensitivity, with optimal values for males using the Cornell voltage corrected for BMI, (RaVL+SV3)*BMI ≥700 mm*kg/m 2 ; sensitivity 47% test cohort, 40% validation cohort; for females, the Sokolow-Lyon index corrected for BMI, (SV1 + RV5/RV6)*BMI ≥885 mm*kg/m 2 ; sensitivity 26% test cohort, 23% validation cohort., Conclusions: Established ECG criteria for the detection of LVH lack sufficient sensitivity in obesity patients. We propose new criteria for the detection of LVH in obesity patients with improved sensitivity, approaching known sensitivity of the most commonly used ECG criteria in lean subjects., (© 2020 The Authors. Clinical Cardiology published by Wiley Periodicals, Inc.)

Aim: Epicardial adipose tissue (EAT) plays a role in obesity‐related heart failure with preserved ejection fraction. However, the association of EAT thickness with the development of cardiac dysfunction in subjects with severe obesity without known cardiovascular disease is unclear. The aim of this study was to determine the association between EAT thickness and cardiac dysfunction and describe the potential value of EAT as an early marker of cardiac dysfunction. Methods and results: Subjects with body mass index ≥35 kg/m2 aged 35 to 65 years, who were referred for bariatric surgery, without suspicion of or known cardiac disease, were enrolled. Conventional transthoracic echocardiography and strain analyses were performed. A total of 186 subjects were divided into tertiles based on EAT thickness, of whom 62 were in EAT‐1 (EAT <3.8 mm), 63 in EAT‐2 (EAT 3.8–5.4 mm), and 61 in EAT‐3 (EAT >5.4 mm). Parameters of systolic and diastolic function were comparable between tertiles. Patients in EAT‐3 had the lowest global longitudinal strain (GLS) and left atrial contractile strain (LASct). Linear regression showed that a one‐unit increase in EAT thickness (mm) was independently associated with a decrease in GLS (%) (β coefficient −0.404, p = 0.002), and a decrease in LASct (%) (β coefficient −0.544, p = 0.027). Furthermore, EAT‐3 independently predicted cardiac dysfunction as defined by a GLS <18% (odds ratio 2.8, p = 0.013) and LASct <14% (odds ratio 2.5, p = 0.045). Conclusions: Increased EAT thickness in subjects with obesity without known cardiac disease was independently associated with subclinical cardiac dysfunction. Our findings suggest that EAT might play a role in the early stages of cardiac dysfunction in obesity before this may progress to overt clinical disease. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to assess heart failure (HF) treatment in patients with and without obesity in a large contemporary real‐world Western European cohort. Methods: Patients with a left ventricular ejection fraction (LVEF) <50% and available information on body mass index (BMI) were selected from the CHECK‐HF registry. The CHECK‐HF registry included chronic HF patients in the period between 2013 and 2016 in 34 Dutch outpatient clinics. Patients were divided into BMI categories. Differences in HF medical treatment were analysed, and multivariable logistic regression analysis (dichotomized as BMI <30 kg/m2 and ≥30 kg/m2) was performed. Results: Seven thousand six hundred seventy‐one patients were included, 1284 (16.7%) had a BMI ≥30 kg/m2, and 618 (8.1%) had a BMI ≥35 kg/m2. Median BMI was 26.4 kg/m2. Patients with obesity were younger and had a higher rate of comorbidities such as diabetes mellitus, hypertension and obstructive sleep apnoea (OSAS). Prescription rates of guideline‐directed medical therapy (GDMT) increased significantly with BMI. The differences were most pronounced for mineralocorticoid receptor antagonists (MRAs) and diuretics. Patients with obesity more often received the guideline‐recommended target dose. In multivariable logistic regression, obesity was significantly associated with a higher likelihood of receiving ≥100% of the guideline‐recommended target dose of beta‐blockers (OR 1.34, 95% CI 1.10–1.62), renin–angiotensin system (RAS)‐inhibitors (OR 1.34, 95% CI 1.15–1.57) and MRAs (OR 1.40, 95% CI 1.04–1.87). Conclusions: Guideline‐recommended HF drugs are more frequently prescribed and at a higher dose in patients with obesity as compared to HF patients without obesity. [ABSTRACT FROM AUTHOR]

Summary: The prevalence of nonalcoholic fatty liver disease (NAFLD) and the more severe and inflammatory type, nonalcoholic steatohepatitis (NASH), is increasing rapidly. Especially in high‐risk patients, that is those with obesity, metabolic syndrome, and type 2 diabetes mellitus, the prevalence of NAFLD can be as high as 80% while NASH may be present in 20% of these subjects. With the worldwide increase of obesity, it is most likely that these numbers will rise. Since advanced stages of NAFLD and NASH are strongly associated with morbidity and mortality—in particular, cardiovascular disease, liver cirrhosis, and hepatocellular carcinoma—it is of great importance to identify subjects at risk. A great variety of noninvasive tests has been published to diagnose NAFLD and NASH, especially using blood‐ and imaging‐based tests. Liver biopsy remains the gold standard for NAFLD/NASH. This review aims to summarize the different mechanisms leading to NASH and liver fibrosis, the different noninvasive liver tests to diagnose and evaluate patients with severe obesity. [ABSTRACT FROM AUTHOR]

Background: Obesity is a risk factor not only for abdominal aortic aneurysm (AAA) but also for complications after vascular surgery. This study was to determine the effect of obesity on short-term mortality and post-intervention complications after AAA repair. Methods: A systematic review and meta-analysis were performed. A systematic search was performed in PubMed; the articles describing the differences in post-intervention complications after open or endovascular repair of an AAA between obese and non-obese patients were selected. The primary outcome was short-term mortality defined as in-hospital mortality or mortality within 30 days after AAA repair. The secondary outcomes were cardiac complications, pulmonary failure, renal failure, and wound infections. The meta-analysis was performed using OpenMeta. Results: Four articles were included in the meta-analysis; these articles included 35,989 patients of which 10,917 (30.3%) were obese. The meta-analysis showed no significant differences for short-term mortality (odds ratio [OR], 0.85; 95% confidence interval [CI], 0.69-1.04). Also, no significant difference was found in pulmonary failure (OR, 1.09; 95% CI, 0.85-1.42). However, obese patients were less likely to suffer from cardiac complications (OR, 0.73; 95% CI, 0.55-0.96). Nevertheless, there was a significantly higher risk of renal failure (OR, 1.16; 95% CI, 1.05-1.30) and wound infections (OR, 1.92; 95% CI, 1.55-2.38) in obese patients. Conclusion: Obesity is not a risk factor for short-term mortality after AAA repair compared to non-obesity. Moreover, obese patients suffer less from cardiac complications than non-obese patients. [ABSTRACT FROM AUTHOR]

Aims: We aimed to gain insight into the underlying pathophysiology of cardiac dysfunction in obesity patients and the improvement of cardiac function after weight loss. Methods: This is a longitudinal study in which 92 cardiovascular biomarkers were measured by multiplex immunoassays in obesity patients without known cardiovascular disease, before and one year after bariatric surgery. Results: Out of 100 eligible patients, 72 patients completed the follow-up. A total of 72 (78%) biomarkers changed significantly. The biomarkers with the highest relative changes represented processes linked mainly to insulin resistance and inflammation. In the patients with persistent subclinical cardiac dysfunction, the baseline values of 10 biomarkers were different from values in patients with normalization of cardiac function. Most of these biomarkers were linked to inflammation or atherosclerosis. Finally, a model was developed to investigate the relationship between changes in the biomarkers and persistent subclinical cardiac dysfunction. Seven biomarkers were retained in this model, mainly linked to inflammation, atherosclerosis, and hypercoagulability. Conclusion: The majority (78%) of cardiovascular biomarkers changed, pointing mainly to modulation of insulin resistance and inflammation. The baseline levels of 10 biomarkers, as well as pre- to post-bariatric surgery changes in seven biomarkers, were related to persistent subclinical cardiac dysfunction after bariatric surgery. [ABSTRACT FROM AUTHOR]