Obesity Heart Failure Research Articles

Abstract 14347: Sleep Apnea and Left Atrial Dilatation in Patients With Atrial Fibrillation Prior to Catheter Ablation

Introduction: Sleep apnea and left atrial dilatation are both risk factors for an arrhythmia recurrence after catheter ablation (CA) of atrial fibrillation (AF). Negative intrathoracic pressure fluctuations during an obstructive apnea episode may cause the left atrium to distend and stretch its wall. Whether sleep apnea is associated with left atrial dilatation in patients receiving CA of AF remains unknown. Methods: This study was conducted under a retrospective, single-center, observational design. The data were derived from screening tests for sleep apnea, which were routinely performed in patients scheduled to receive CA of AF in our institution. After excluding patients who were already diagnosed with sleep apnea, we enrolled 1265 consecutive patients (age 65±11 years, 27.8% females, and 46.2% of non-paroxysmal AF) who underwent both home sleep apnea testing and multidetector computed tomography (MDCT) before the CA of AF. The severity of the sleep apnea was evaluated by the apnea-hypopnea index (AHI) using a watch-type peripheral arterial tonometry. Left atrial dilatation was evaluated by the left atrial maximum volume (LA max V) using 256-slice MDCT. Results: The age was 65±11 years, 27.8% were females, and 46.2% had non-paroxysmal AF. The mean AHI was 20.3±15.3 and LA max V 104.9±33.9 ml (R 2 =0.075, p<0.0001). LA dilatation, defined by an LA max V≥100 ml, was more frequently observed in patients with an AHI≥15 than those with an AHI<15 (62.5% vs. 40.2%, p<0.0001). We examined an LA max V≥100 ml as a predictor. After an adjustment by an advanced age (≥65 years), non-paroxysmal AF, male sex, obesity, hypertension, and congestive heart failure, all of which were significant predictors of an LA max V≥100ml in the univariate analysis, moderate or severe sleep apnea (AHI≥15) was a significant predictor of an LA max V≥100 ml (odds ratio 1.49, 95% confidence interval 1.13-1.97, p=0.0049). Conclusion: Among the patients scheduled to receive catheter ablation of AF, moderate or severe sleep apnea was independently associated with left atrial dilatation.

Insulin signaling in the heart.

Insulin receptors are highly expressed in the heart and vasculature. Insulin signaling regulates cardiac growth, survival, substrate uptake, utilization, and mitochondrial metabolism. Insulin signaling modulates the cardiac responses to physiological and pathological stressors. Altered insulin signaling in the heart may contribute to the pathophysiology of ventricular remodeling and heart failure progression. Myocardial insulin signaling adapts rapidly to changes in the systemic metabolic milieu. What may initially represent an adaptation to protect the heart from carbotoxicity may contribute to amplifying the risk of heart failure in obesity and diabetes. This review article presents the multiple roles of insulin signaling in cardiac physiology and pathology and discusses the potential therapeutic consequences of modulating myocardial insulin signaling.

476 Sleep-Disordered Breathing is More Predictive than Obesity of Increased Left Ventricular Mass Index in Bariatric Surgery Patients

Abstract Introduction Obesity and obstructive sleep apnea (OSA) are associated with left ventricular hypertrophy and increased cardiovascular risk. Alternatively, the “obesity paradox” describes an improved prognosis from heart failure in obesity, though potentially attributable to confounding/bias. We sought to determine the contributions of obesity and sleep-disordered breathing (SDB) to left ventricular function and morphology in bariatric surgery candidates. Methods Patients undergoing polysomnography prior to bariatric surgery from 2011–2018 had demographic (age, gender, race), anthropometric (body mass index [BMI], neck circumference), comorbidities (atrial fibrillation, coronary artery disease, diabetes, hypertension, hyperlipidemia), echocardiographic and sleep-disordered breathing (apnea-hypopnea index [AHI], peak end-tidal CO2 [etCO2]) variables retrospectively examined. The echocardiographic visit closest to polysomnogram within two years was selected with missing values filled by available values within 6 months. Linear regression assessed the relationship of BMI, AHI, and etCO2 with left ventricular mass index (LVMI) after adjustment of demographics and comorbidities. Echocardiographic measures were logarithm transformed before regression analysis. Coefficients and 95% confidence intervals (CI) were calculated by exponential transformation. The analysis was performed based on an overall significance level of 0.05 using SAS software (version 9.4, Cary, NC). Results The total of 832 patients had 24% males, mean age 48.8±12, 60% white, and BMI:49.4±9.5kg/m2. Ejection fraction (%) was 60.0±7.0, and LVMI (g/m2): 80.9±23.7. In adjusted models, LVMI decreased by 2.1% for each 5kg/m2 increase in BMI (coefficient=0.979, 95%CI 0.961–0.997, p=0.022) and increased by 4.3% for each 5 mmHg increase in etCO2 (coefficient=1.043, 95%CI 1.013–1.073, p=0.005). Without adjustment, patients with AHI ≥ 5 had 15.3% higher LVMI than non-OSA group (coefficient=1.153, 95%CI 1.034–1.286, p=0.011) and moderate/severe OSA was associated with a 7.6% higher LVMI than those with AHI<15 (coefficient 1.076, 95%CI 1.003–1.153, p=0.040), but not statistically significant after adjustment. Conclusion In obese patients, nocturnal hypoventilation rather than obesity may have adverse influences on left ventricular morphology. Future studies should focus on clarifying whether obesity is truly protective in terms of LV mass, i.e. reflective of paradox versus a product of bias. The potential benefit of identifying/treating SDB in bariatric surgery candidates to mitigate cardiovascular risk also deserves further investigation. Support (if any) Cleveland Clinic Transformative Resource Neuroscience Award

An analysis based on sex&gender in the chest pain unit of an emergency department during the last 12 years

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Josep Font 2019 Grant from Hospital Clinic de Barcelona Background Differences between female (F) and male (M) with coronary disease (CD) are related to time delays in detriment of women such as: hospital presentation, recognition of symptoms or an appropriate treatment. Further research based on sex and gender (S&G) is at important to confront the interplay of factors that shape health inequities. Purpose To do an analysis based on S&G of the admissions in the chest pain unit (CPU) of an emergency department (ED), comparing clinical features and also the physician’s initial diagnostic orientation after the first evaluation of the patients (FEoP) . Methods This is an observational descriptive unicentric study of consecutive cases. We retrospectively analysed all the cases admitted in a CPU from 2008-2019 and recorded the cardiovascular risk factors (cvrf), and the clinical and electrocardiographic (ECG) features. We also recorded the final diagnostic after all the management in the CPU and the FEoP [based on the clinical history, physical examination and ECG; before other complementary examinations like troponins (Tnc)]. The characteristics were compared according to sex (F or M). Results 41828 patients were included (42% F), with an older median age in F [Md (RIC) [65 (47-78) vs 59 (43-73)] y.o.; p < 0,001]. We found a significant greater number of late presenters (≥12hours from symptoms onset) in F (41%vs37%;p < 0,001). F were associated to greater rates of obesity, hypertension and previous heart failure; M had greater rates of diabetes mellitus, previous known coronary disease and smoke or cocaine use. When we considered the patients with typical chest pain (TCP), no significant differences based on S&G were found. Women’s ECG were more often interpreted as not having significant changes of ischemia. After the FEoP, the patients were classified as having an STEMI(♀1%vs♂2,5%;p < 0,001), non-STEMI (♀4,3%vs♂5,4%;p < 0,001) or non-diagnostic-ECG(93%). Among patients with non-diagnostic ECG, the physician’s initial diagnostic was a probable acute coronary syndrome (ACS) in 42% of cases. F were less likely to be considered as having an ACS (♀39%vs♂44,5%;p < 0,001). This significant differences were maintained when:1) patients had ≥3cvrf [♀OR0,72; IC95%(0,63-0,83)]; 2)patients had ≥2cvrf [♀OR0,79; IC95% (0,74-0,86)]; 3)patients had TCP [♀OR 0,69; IC95% (0,64-0,74)]; 4)patients had ≥2cvrf and TCP [♀OR 0,72; IC95% (0,63-0,82)]. After the management in the CPU, a 14% of patients with non-diagnostic ECG were finally diagnosed with an ACS (36% if≥2cvrf and TCP). 3% of ACS were initially misdiagnosed (♀5%vs♂3% ;p < 0,001). After a multivariate analysis F is an independent risk factor for an initial impression of non-ACS. Conclusions There is a gender gap in the first evaluation of chest pain with an underestimation of risk in women, not only by the patients who are more often late presenters, but also by the physicians, which entails a higher risk of being misdiagnosed or late diagnosed.

Quality of Life Is Associated with Cardiac Biomarkers, Echocardiographic Indices, and Mortality in CKD Stage 4–5 Patients Not on Dialysis

Introduction: Patients with CKD have an impaired health-related quality of life (QoL). Most studies have been conducted on dialysis patients, and less is known about QoL and its determinants in predialysis patients. We studied the association between QoL and comorbidities, cardiac biomarkers, echocardiography, and mortality in patients with CKD stage 4–5 not on dialysis. Methods: A total of 140 patients enrolled in the Chronic Arterial Disease, Quality of Life and Mortality in Chronic Kidney Injury (CADKID) study filled the Kidney Disease Quality of Life Short Form (KDQOL-SF) at the beginning of the study. Echocardiography and biochemical parameters were obtained at baseline. Patients were followed up for at least 2 years or until death. Results: The median age was 66 years, and 51 (36%) patients were female. The median estimated glomerular filtration rate was 13 mL/min per 1.73 m². Obesity, diabetes, atrial fibrillation, and congestive heart failure were associated with lower QoL scores in multiple KDQOL-SF domains. Cardiac biomarkers, troponin T (p = 0.02), N-terminal pro-B-type natriuretic peptide (p = 0.006), and the echocardiographic parameter of cardiac systolic function left ventricular global longitudinal strain (p = 0.02) were significant predictors of lower physical component summary (PCS) score in multivariable regression models after controlling for age, BMI, and diabetes. A low PCS score predicted mortality in a multivariable Cox proportional hazards model [HR 0.96 (95% CI 0.92–0.99), p = 0.03]. QoL was not associated with kidney disease progression. Conclusion: Impaired QoL in CKD stage 4–5 patients not on dialysis is associated with cardiac biomarker levels, echocardiographic indices, and mortality.

Sarcopenic Obesity in Heart Failure With Preserved Ejection Fraction.

Heart failure with preserved ejection fraction (HFpEF) is a public health epidemic that is projected to double over the next two decades. Despite the high prevalence of HFpEF, there are currently no FDA approved therapies for health-related outcomes in this clinical syndrome making it one the greatest unmet needs in cardiovascular medicine. Aging and obesity are hallmarks of HFpEF and therefore there is a high incidence of sarcopenic obesity (SO) associated with this syndrome. The presence of SO in HFpEF patients is noteworthy as it is associated with co-morbidities, worsened cardiovascular health, hospitalizations, quality of life, and mortality. Furthermore, SO plays a central role in exercise intolerance, the most commonly reported clinical symptom of this condition. The aim of this review is to provide insights into the current knowledge pertaining to the contributing pathophysiological mechanisms and clinical outcomes associated with HFpEF-related SO. Current and prospective therapies to address SO in HFpEF, including lifestyle and pharmaceutical approaches, are discussed. The urgent need for future research aimed at better understanding the multifaceted physiological contributions to SO in HFpEF and implementing interventional strategies to specifically target SO is highlighted.

Impact of body mass index on surgical coronary revascularization for ischaemic heart failure: insights from STICHES.

AimsPatients with obesity and ischaemic heart failure may counter‐intuitively have better outcomes compared with patients with normal body weight due to an ‘obesity paradox’. This study sought to determine if body mass index (BMI) impacts the treatment effects or safety outcomes of the treatment of ischaemic heart failure with coronary artery bypass grafting (CABG).Methods and resultsWe obtained and reviewed the Surgical Treatment of Ischaemic Heart Failure (STICHES) data for 1212 patients. We categorized obesity by the World Health Organization (WHO) classes to define baseline characteristics and test for treatment interactions for the primary and secondary STICHES outcomes by treatment groups. While CABG decreased the risk of death, there was no evidence of treatment interaction by BMI per 5 kg/m2 (P = 0.83) or WHO obesity class. For the overall cohort, there was no interaction by WHO obesity class for the cumulative incidence of death in either the medical therapy or CABG plus medical therapy (P‐interaction = 0.90). There was a non‐significant trend for higher BMI and a lower risk of death [hazard ratio 0.92, 95% confidence interval (CI) 0.85–1.00, P = 0.051]. Increasing body size (per 5 kg/m2) was associated with return to the operating room (odds ratio 2.48, 95% CI 1.45–4.26, P < 0.001) and infectious mediastinitis (odds ratio 2.09, 95% CI 1.10–3.97, P = 0.024) at 30 days but not other 30 day safety outcomes.ConclusionsThe benefit of CABG vs. medical therapy for ischaemic heart failure was consistent regardless of BMI or WHO obesity class for death or secondary clinical outcomes. However, higher BMI was associated with some short‐term post‐CABG complications.

Obesity paradox and heart failure.

There is scientific consensus that obesity increases the risk of cardiovascular diseases (CVD), including heart failure (HF). However, in CVD, many studies observed greater survival in overweight or class 1 obesity individuals. This counterintuitive observation was termed "obesity paradox" (OP). This article is a narrative overview of the relationship between OP and CVD, particularly HF. The sources used were MEDLINE/PubMed, CINAHL, EMBASE, and Cochrane Library, from 2001 to 31 May 2020, exception for a 1983 work of historical importance. Studies reporting association and prognostic impact of obesity in HF and the impact of body composition on cardiac structure and myocardial function in obesity were also included in this review. In addition, we examined references from the retrieved articles and explored several related websites. Ultimately, we chose 79 relevant documents. Fifty-three were specifically focused on OP and HF. In this review, we made a summary of the evidence coming from a series of studies investigating OP. Many of these studies do not take into consideration or underestimate some of the more important morpho-functional variables of patients suffering from HF: among these, body composition and visceral adiposity, sarcopenic obesity, muscle fitness (MF), and cardiorespiratory fitness (CRF). A high body mass index (BMI) represents a risk factor for HF, but it also seems to exert a protective effect under certain circumstances. Fat distribution, lean mass, and cardio fitness could play an essential role in determining the observed differences in the HF population. BMI does not distinguish between the metabolically healthy and metabolically unhealthy obesity. The obesity impact on morbidity and premature mortality can be underestimated and, therefore, may lead to incorrect clinical courses. Level V, Narrative review.

Longitudinal Changes in Cardiac Structure and Function in Severe Obesity: 11-Year Follow-Up in the Utah Obesity Study.

BackgroundProgressive cardiac remodeling and worsening myocardial function over time have been proposed as potential mediators of heart failure in obesity.Methods and ResultsWe serially assessed cardiac structure and function in 254 subjects participating in a longitudinal study of obesity. Demographic, clinical, laboratory, and echocardiographic features were determined at baseline and 2‐, 6‐, and 11‐year follow‐up. We measured body mass index (BMI) exposure as the area under the curve of the BMI at each of the 4 visits. At enrollment, mean age of the subjects was 47 years, 79% were women, mean BMI was 44 kg/m2, 26% had diabetes mellitus, 48% had hypertension, and 53% had hyperlipidemia. Between baseline and 11 years, BMI increased by 1.1 and 0.3 kg/m2 in men and women, respectively. There were modest increases in left ventricular (LV) end‐diastolic volume, LV mass, and left atrial volume, and significant decreases in early/late mitral diastolic flow velocity ratio and E wave deceleration time. However, there were no significant changes in LV ejection fraction or ratio of early mitral diastolic flow velocity/early mitral annular velocity, whereas right ventricular fractional area change increased. Significant predictors of the change in LV mass were male sex, baseline BMI, BMI area under the curve, and change in LV stroke volume, but not smoking, hypertension, or diabetes mellitus.ConclusionsIn long‐standing, persistent severe obesity, there was evidence of cardiac remodeling over a period of 11 years, but no clear worsening of systolic or diastolic function. Measures of remodeling were most strongly related to BMI. The observed changes might predispose to heart failure with preserved ejection fraction, but are not classic for an evolving dilated cardiomyopathy.

Screening for atrial fibrillation in high-risk nursing home residents.

BackgroundVarious methods have been implemented for screening of patients for atrial fibrillation (AF), but the yield has generally been low. Targeting high-risk patients may improve detection of asymptomatic AF, which could be of value if appropriate treatment could be initiated before a potential thromboembolic event.ObjectiveThe purpose of this study was to test screening of high-risk nursing home residents having ≥2 risk factors for AF and no previous history of AF using a smartphone-based electrocardiographic (ECG) monitoring device to determine whether it is an accurate, easy-to-use method of screening for asymptomatic AF.MethodsStudy participants had ≥2 risk factors, consisting of age ≥75 years, female sex, obstructive sleep apnea, peripheral vascular disease, diabetes mellitus, obesity, hypertension, and congestive heart failure. Using the monitoring device, 30-second heart rhythm recordings were obtained on 4 different occasions. All tracings were reviewed by a cardiologist and, if uncertain, by an electrophysiologist. The nursing facility was notified of any diagnosis of AF, prompting further evaluation by the primary physician.ResultsOf the 245 residents screened, 18 (7.4%) had a diagnostic tracing for AF, 15 (83.3%) of whom had AF on the initial screen. There were no significant differences in demographics or individual risk factors between residents with and those without AF.ConclusionIntermittent ECG screening of high-risk nursing home residents using a simple, handheld device provided a diagnostic yield in our population comparable to that observed in past studies. Such screening of high-risk individuals can aid in the early diagnosis of AF and initiation of appropriate treatment.

Particularities of arrhythmias and obesity in heart failure

Chronic heart failure and obesity are two conditions which despite all the advances made in the recent years, still represent two of the leading causes of morbidity and mortality worldwide. Moreover, a well-known fact is that the risk of sudden cardiac death, mostly related to malignant arrhythmias is higher in apparently healthy obese individuals in comparison with lean subjects. On the other hand, obese heart failure patients bring unique challenges in the diagnosis of heart failure, having a better prognosis than their normal or underweight counterparts. Taking into account the above-mentioned existing data, there are questions regarding whether cardiac arrhythmias such as atrial fibrillation or ventricular arrhythmias in this population have certain evolutive particularities. This paper describes various mechanisms of cardiac arrhythmias found in obese heart failure patients, such as myocardial architectural changes, neurohormonal and paracrine modifications.

B-type natriuretic peptide and obesity in heart failure: a mysterious but important association in clinical practice

B-type natriuretic peptide and obesity in heart failure: a mysterious but important association in clinical practice

P2496Results cardiopulmonary exercise testing in patients with obesity and chronic heart failure

Abstract Purpose Determination of exercise tolerance in patients with obesity and chronic heart failure. Methods An exercise cardiorespiratory testing (CPET) was performed using a spiroergometer in combination with treadmill using the modified BRUCE protocol in 222 patients divided into the following groups: Group 1: obesity I-II grade – 60 patients; Group 2: obesity I-II grade + chronic heart failure (CHF) – 49 patients; Group 3: grade III obesity – 60 patients; Group 4: grade III obesity + CHF – 53 patients. Results The results of CPET showed that the reason for the decrease in tolerance to physical activity in patients with obesity without CHF is detraining. Patients with obesity and CHF were characterized by a more pronounced decrease in exercise tolerance, which was reflected in a decrease in peak oxygen consumption (VO2peak), which in patients with obesity I-II + CHF was equal to 72.7±3.4% (moderate decrease), and in patients with obesity III + CHF – 50±2.1% (marked decrease); differences when compared with the groups without CHF were 44.3% and 24.4% (p&lt;0.001).The maximum aerobic performance of patients with obesity I-II + CHF was equal to 5.5±0.9 MET (moderate decrease), and in patients with obesity III + CHF – 3.8±0.4 MET (marked reduction); differences when compared with patients without CHF were significant at p&lt;0.001. A small reduction in the global pumping function of the heart was found only in patients with obesity III + CHF – the oxygen pulse was 9.4±2.2 ml/beats and was significantly different from the group of patients without CHF. In addition, a decrease in alveolar gas exchange (VE/VCO2) was observed in the groups of patients with obesity and CHF, which was equal to 32.1±1.5 units in the group of patients with obesity I-II degree and 33.6±2.5 units in the group of patients with obesity Grade III (the norm is less than 32), which is probably due to the presence of pulmonary hypertension and a decrease in the ventilation-perfusion ratio. Conclusion The development of CHF in patients with obesity leads to impaired alveolar ventilation, a decrease in aerobic muscle power and tolerance to physical exertion. In addition, it was found that when performing a stress test in patients with obesity and CHF (unlike patients without CHF), the anaerobic threshold is reached before the stage corresponding to their average daily exercise. This means that the usual physical activity of patients does not allow them to carry out effective fat oxidation, which may be the metabolic cause of the progression of obesity in patients with CHF. Acknowledgement/Funding Research No. 0529-2019-0061 Diagnostics, prevention and dietaterapy of patients with alimentary-dependent diseases

A172 The Role of Bariatric Surgery in Patients with Obesity and Advanced Heart Failure as a Bridge to Heart Transplantation: A Systematic Review and Meta-Analysis

A172 The Role of Bariatric Surgery in Patients with Obesity and Advanced Heart Failure as a Bridge to Heart Transplantation: A Systematic Review and Meta-Analysis

Genetic predictors of chronic heart failure in obese patients

BACKGROUND: the study of molecular genetic markers and pathogenetic mechanisms of neurohormonal activation, as well as their importance in the formation of heart failure in obesity, is an urgent problem of modern medicine, the solution of which will allow effective prevention of cardiovascular complications, optimize treatment and improve the prognosis of obese patients.&#x0D; AIMS: search for genetic markers presumably involved in the pathogenesis of secondary diastolic heart failure in patients with obesity.&#x0D; MATERIALS AND METHODS: PCR-diagnostics of whole blood of 104 patients with obesity was carried out, which were divided into 2 groups, depending on the presence of diastolic heart failure. The following candidate genes were analyzed: angiotensinogen AGT gene (C521T and T704C), angiotensin II receptor gene of the first type AGTR1 (A1166C), angiotensin II receptor gene of the second type AGTR2 (G1675A), aldosterone synthase gene CYP11B2 (C (-344) T).&#x0D; RESULTS: It is shown that the development of secondary diastolic heart failure in obese individuals of both sexes is associated with the mutation of the aldosterone synthase gene CYP11B2, namely, with the replacement of the C allele at the -344 position by the T allele and the presence of the T / T genotype. The relative risk of developing the disease with the T / T genotype was 5.93 times higher in men (p = 0.008) and 4.57 times in women (p = 0.014). For men, the mutation of the angiotensinogen AGT gene, namely the replacement of the allele C at position 521 by the T allele, is important. At the same time, the relative risk of development of SDS in the T / T genotype is increased by 4.26 times (p = 0.039). Mutations of the genes of the angiotensin II receptor of the first type AGTR1 (A1166C) and the angiotensin II receptor of the second type AGTR2 (G1675A) are not associated with the development of diastolic heart failure in obese patients.&#x0D; CONCLUSIONS: The data presented can be used to stratify the risk of secondary heart failure in obese individuals.

Alstrom syndrome: insulin resistance in young with congestive heart failure

Alstrom Hallgren syndrome is a rare ciliopathy first described in 1959. It is characterised by progressive cone-rod dystrophy leading to blindness, sensorineural hearing loss, childhood obesity and congestive heart failure. Its pathogenesis is related to development of insulin resistance, and type 2 diabetes mellitus. We report a case of a 20-year-old presenting with decompensated heart failure and had been blind since childhood who was eventually diagnosed as Alstrom syndrome based on clinical criteria.

Laparoscopic sleeve gastrectomy in patients with heart failure and left ventricular assist devices as a bridge to transplant

BackgroundObesity is an epidemic that is closely associated with heart failure. The ultimate treatment for end-stage heart failure is cardiac transplantation. Patients with morbid obesity are often excluded from receiving donor organs. Many transplant centers use body mass index (BMI) >35 kg/m2 as a contraindication to listing for heart transplant. Left ventricular assist devices (LVADs) were developed as a bridge to transplant for many heart failure patients, but bariatric surgery for LVAD patients has not been well described. ObjectivesThe purpose of our study was to evaluate the safety and efficacy of laparoscopic sleeve gastrectomy (LSG) in LVAD patients and the impact on heart failure recovery as a bridge to cardiac transplantation. SettingUniversity hospital. MethodsA retrospective study was conducted to evaluate the outcomes of patients with morbid obesity and LVADs who underwent LSG at a large academic medical center between 2013 and 2017. Age, BMI, percent excess weight loss, cardiac ejection fraction, listing status for transplantation, and success of transplant were reviewed. ResultsEleven patients were identified with morbid obesity and heart failure with LVAD support who underwent LSG. There were no perioperative deaths. Four patients (37%) achieved BMI <35 and were successfully listed for and received cardiac transplantation. An additional 3 patients (27%) achieved BMI <35 kg/m2 and are listed for cardiac transplantation. ConclusionsLSG can be safely used in patients with morbid obesity and end-stage heart failure requiring LVAD support to lower their BMI and become eligible for cardiac transplantation.

EET‐agonist Prevents and Reverses Heart Failure in Obesity Induced Diabetic Cardiomyopathy

Previously we demonstrated that an EET‐agonist has pleiotropic effects including inhibition of Soluble Epoxide Hydrolase expression and reversed cardiomyopathy by decreasing inflammatory molecules and increasing antioxidant signaling. We hypothesized that an EET agonist would increase PGC‐1α, which controls mitochondrial function and HO‐1 induction and negatively regulates the expression of the proinflammatory adipokine NOV in both cardiac and pericardial tissues. This pathway would be expected to further improve left ventricular systolic function as well as increase insulin receptor phosphorylation. The effect of an EET agonist was measured in cardiac and pericardial adipose tissues in db/db mice on oxygen consumption, fractional shortening, blood glucose levels, thermogenic and mitochondrial signaling proteins. Control db/db mice developed signs of metabolic syndrome including insulin resistance, hypertension, inflammation, LV dysfunction, and increased NOV expression in pericardial adipose tissue. EET agonist decreased pericardial adipose tissue expression of NOV, normalized FS, increased PGC‐1α, HO‐1 levels, insulin receptor phosphorylation and improved mitochondrial function. HO‐1‐ derived carbon monoxide (CO) levels, mitochondrial function (p&lt;0.01), insulin receptor phosphorylation (p&lt;0.05), ATP levels and VO2 (p&lt;0.05). Deletion of PGC‐1α reversed all of the above beneficial effects, increasing the expression of NOV and inflammatory cytokines in pericardial adipose tissue. These studies demonstrate that an EET agonist increases insulin receptor phosphorylation, mitochondrial and thermogenic gene expression, decreases cardiac and pericardial tissue NOV levels, and ameliorates cardiomyopathy in an obese mouse model of the metabolic syndrome. Further, this study demonstrated that EET‐mediated inhibition of NOV is a potential therapeutic target for the prevention of heart failure and the development of metabolic syndrome.Support or Funding InformationNational Institutes of Health grant (HL34300 to NGA)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Obesity and advanced heart failure, can bariatric surgery help?

Obesity and advanced heart failure, can bariatric surgery help?

The content of adiponectin, resistin in serum and their ratio in patients with chronic heart failure in overweight and obesity depending on severity of disease, body mass index, age, gender and myocardium contractile ability

Recently more and more attention of researchers is paid to determining of adiponectin and resistin role in the development, progression and outcomes of chronic heart failure (CHF) with overweight and obesity, given the continuing increase in the incidence of both pathologies. Purpose – to examine the contents of adiponectin and resistin in serum and their ratio in patients with CHF in overweight and obesity depending on severity of disease, body mass index, age, gender and contractile myocardial ability. Materials and Methods. We examined 100 patients of the main group who had CHF of II–III functional class (FC) on the background of normal, overweight and obesity I–III degree. The comparison group included 12 patients with cardiac pathology and normal weight without clinical and instrumental signs of CHF, matched by age and gender. The control group consisted of 12 healthy subjects with normal weight. The presence of normal, overweight and degree of obesity was calculated based on the body mass index (BMI). The level of adiponectin and resistin in the blood serum was determined with ELISA method. Results. In patients with CHF, overweight and obesity the content of adiponectin and resistin in serum is increased and depends on FC of disease and age. Increasing degree of overweight and reducing the myocardium contractile ability are characterized by higher levels of resistin. The resistin/adiponectin ratio in patients with CHF, overweight and obesity increases with increasing BMI, in relation to the adiponectin/resistin ratio opposite changes occur. Conclusions. In CHF patients with concomitant overweight and obesity is an excessive activation of adipocytokines system, which is manifested by increase in the content of adiponectin, resistin, resistin/adiponectin ratio and a reduction of adiponectin/resistin index.