Obese Heart Failure Research Articles

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.

SURVIVAL ADVANTAGE FOR OVERWEIGHT AND OBESE PATIENTS PERSISTS IN A RURAL HEART FAILURE PATIENT POPULATION

A survival advantage termed the “obesity paradox” for improved survival in overweight and obese heart failure (HF) patients has been previously demonstrated. To our knowledge this relationship has not been demonstrated in a rural population, therefore we examined this relationship in a rural,

Obesity and Cardioprotection.

The incidence of obesity and diabetes is increasing rapidly worldwide. Obesity and metabolic syndrome are strictly linked and represent the basis of different cardiovascular risk factors, including hypertension and inflammatory processes predisposing to ischemic heart disease, which represent the most common causes of heart failure. Recent advances in the understanding of ischemia/reperfusion mechanisms of injury and mechanisms of cardioprotection are briefly considered. Resistance to cardioprotection may be correlated with the severity of obesity. The observation that heart failure obese patients have a better clinical condition than lean heart failure patients is known as "obesity paradox". It seems that obese patients with heart failure are younger, making age the most important confounder in some studies. Critical issues are represented by the "obesity paradox" and heart failure exacerbation by inflammation. For heart failure exacerbation by inflammation, an important role is played by NLRP3 inflammasome, which is emerging as a possible target for heart failure condition. These critical issues in the field of obesity and cardiovascular diseases need more studies to ascertain which metabolic alterations are crucial for alleged beneficial and deleterious effects of obesity.

Optimizing The Management of Obese HFpEF Phenotype: Can We Mind Both The Heart and The Kidney?

The adverse prognostic implications of significant renal dysfunction during treatment of acute decompensated heart failure (HF) in patients with obese HF and preserved ejection fraction (HFpEF) provide strong rationale for development of therapeutic strategies that enhance decongestion while preserving renal function in this cohort. The combination of preload sensitivity, intrinsic renal dysfunction related to obesity, glomerular hyperfiltration, reversible renal hypoperfusion (poor renal arterial perfusion and renal venous congestion), and decreased systemic vascular resistance in obesity may predispose patients to renal hemodynamic compromise during diuresis. Thus, serum creatinine increase should not be evaluated in isolation but rather considered in the context of the entire clinical picture in patients with obese HFpEF.

Abstract 943: Circulating Mirnome in Obese and Lean Heart Failure Patients: A Case-control Study

Background: Obesity is a risk factor for cardiovascular diseases; however, in obese heart failure (HF) patients live longer than lean HF patients, this observation is known as obesity paradox. MicroRNAs (miRs) regulate processes involved in both cardiac remodeling and obesity. Objective: We investigated whether the levels of circulating miRs in HF patients are influenced by obesity. Methods: In this case–control study, twenty HF patients (10 obese and 10 lean) and 10 healthy control individuals were analyzed using Affymetrix GeneChip miRNA 4.0 Array following manufacturer's instruction. Raw data was normalized using the Robust Multiarray Average method, batch effect was adjusted with Surrogate Variable Analysis, pairwise differential expression analysis was carry-out with Limma R package, and miRPath v3.0 was used to interrogate pathways enriched for the dysregulated miRNAs based on validated targets from Tarbase v7.0 and KEGG pathways annotation database. Bioinformatics and statistical analysis were performed using R and a p-value <0.01 was considered significant. Results and conclusions: We discovered a set of 36 and 48 miRNAs that were differentially expressed in obese HF and lean HF, respectively, in relation to controls. Thirteen miRNAs were commonly dysregulated in both HF groups. In addition, we found hsa-miR-451a to be up-regulated in obese HF in relation to controls, as well as to lean HF patients, suggesting that obesity may accentuate its dysregulation. On the other hand, hsa-miR-4738-5p, hsa-miR-1260a, and hsa-miR-98-5p were differentially expressed in lean HF in relation to both remaining groups. Pathways enrichment analysis suggested that hsa-miR-451a regulates genes from the mTOR signaling pathway (p=0.002), whereas hsa-miR-1260a modulates Hippo (p=0.02) and AMPK (p=0.03) signaling pathways, all of which have been previously related to cardiac hypertrophy. Further investigation and validation of their targets may contribute to a better understanding of the obesity paradox.

Hemodynamic Effects of Weight Loss in Obesity: A Systematic Review and Meta-Analysis

ObjectivesThe authors aimed to explore whether weight loss may improve central hemodynamics in obesity. BackgroundHemodynamic abnormalities in obese heart failure with preserved ejection fraction patients are correlated with the amount of excess body mass, suggesting a possible causal relationship. MethodsRelevant databases were systematically searched from inception to May 2018, without language restriction. Studies reporting invasive hemodynamic measures before and following therapeutic weight loss interventions in patients with obesity but no clinically overt heart failure were extracted. ResultsA total of 9 studies were identified, providing data for 110 patients. Six studies tested dietary intervention and 3 studies tested bariatric surgery. Over a median duration of 9.7 months (range 0.75 to 23.0 months), a median weight loss of 43 kg (range 10 to 58 kg) was associated with significant reductions in heart rate (−9 beats/min, 95% confidence interval [CI]: −12 to −6; p < 0.001), mean arterial pressure (−7 mm Hg, 95% CI: −11 to −3; p < 0.001), and resting oxygen consumption (−85 ml/min, 95% CI: −111 to −60; p < 0.001). Central cardiac hemodynamics improved, manifested by reductions in pulmonary capillary wedge pressure (−3 mm Hg, 95% CI: −5 to −1; p < 0.001) and mean pulmonary artery pressure (−5 mm Hg, 95% CI: −8 to −2; p = 0.001). Exercise hemodynamics were assessed in a subset of patients (n = 49) in which there was significant reduction in exercise pulmonary artery pressure (p = 0.02). ConclusionsTherapeutic weight loss in obese patients without HF is associated with favorable hemodynamic effects. Randomized controlled trials evaluating strategies for weight loss in obese patients with heart failure such as the obese phenotype of heart failure with preserved ejection fraction are needed.

Characterization of the Obese Phenotype of Heart Failure With Preserved Ejection Fraction: A RELAX Trial Ancillary Study

ObjectiveTo characterize the obese heart failure with preserved ejection fraction (HFpEF) phenotype in a multicenter cohort. Patients and MethodsThis was a secondary analysis of the randomized clinical trial RELAX (Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejection Fraction) performed between October 1, 2008, and February 1, 2012. Patients with HFpEF were classified by body mass index (BMI) as obese (BMI≥35 kg/m2) and nonobese (BMI<30 kg/m2) for comparison. ResultsObese patients with HFpEF (n=81) were younger (median age, 64 [interquartile range (IQR), 67-79] years vs 73 [IQR, 56-70] years; P<.001) but had greater peripheral edema (31% [25] vs 9% [6]; P<.001), more orthopnea (76% [56] vs 53% [35]; P=.005), worse New York Heart Association class (P=.006), and more impaired quality of life (P<.001) as compared with nonobese patients with HFpEF (n=70). Despite more severe signs and symptoms, obese patients with HFpEF had lower N-terminal pro B-type natriuretic peptide level (median, 481 [IQR, 176-1183] pg/mL vs 825 [IQR, 380-1679] pg/mL [to convert to pmol/L, multiply by 0.118]; P=.007) and lower left atrial volume index (median, 38 [IQR, 31-47] mL/m2 vs 54 [IQR, 41-63] mL/m2; P<.001). Serum C-reactive protein (median, 5.0 [IQR, 2.4-9.9] mg/dL vs 2.7 [IQR, 1.6-5.4] mg/dL [to convert to mg/L, multiply by 10−3]; P<.001) and uric acid (median, 7.8 [IQR, 6.1-8.7] mg/dL vs 6.8 [IQR, 5.5-8.3] mg/dL; P=.03) levels were higher in obese HFpEF, indicating greater systemic inflammation, than in nonobese HFpEF. Peak oxygen consumption was impaired in obese HFpEF (median, 11.1 [IQR, 9.6-14.4] mL/kg per minute vs 13.1 [IQR, 11.3-14.7] mL/kg per minute; P=.008), as was submaximal exercise capacity (6-minute walk distance, 272 [IQR, 200-332] m vs 355 [IQR, 290-415] m; P<.0001). ConclusionObese HFpEF is associated with decreased quality of life, worse symptoms of heart failure, greater systemic inflammation, worse exercise capacity, and higher metabolic cost of exertion as compared with nonobese HFpEF. Further study is required to understand the pathophysiology and potential distinct treatments for patients with the obese phenotype of HFpEF. Trial Registrationclinicaltrials.gov Identifier: NCT00763867

The Obesity Paradox in Cardiovascular Diseases

The Obesity Paradox in Cardiovascular Diseases

Cardiopulmonary remodeling in fattened beef cattle: a naturally occurring large animal model of obesity-associated pulmonary hypertension with left heart disease.

The obesity epidemic in developed societies has led to increased cardiovascular diseases including pulmonary hypertension associated with left heart disease (PH-LHD), the largest and fastest-growing class of PH. Similar to obese humans, PH and heart failure (HF) are increasingly recognized in North American fattened beef cattle. We hypothesized that PH and HF in fattened beef cattle are novel, phenotypically distinct manifestations of bovine PH arising from left ventricular (LV) dysfunction similar to obesity-related PH-LHD in humans. We conducted a semi-quantitative histopathological assessment of cardiopulmonary tissues obtained from fattened beef cattle suffering end-stage HF compared to asymptomatic cattle of equivalent age undergoing the same fattening regimens. In HF animals we observed significant LV fibrosis, abundant cardiac adipose depots, coronary artery injury, and pulmonary venous remodeling recapitulating human obesity-related PH-LHD. Additionally, striking muscularization, medial hypertrophy, adventitial fibrosis, and vasa vasorum hyperplasia in the pulmonary arterial circulation were associated with sequela of pathologic right ventricular (RV) remodeling suggesting combined pulmonary venous and arterial hypertension. The association between obesity, pathologic cardiopulmonary remodeling, and HF in fattened beef cattle appears to recapitulate the complex pathophysiology of obesity-associated PH-LHD in humans. This novel, naturally occurring, and large animal model may provide mechanistic and translational insights into human disease.

IL-1 Blockade in Patients With Heart Failure With Preserved Ejection Fraction.

Background Enhanced inflammation may lead to exercise intolerance in heart failure with preserved ejection fraction. The aim of the current study was to determine whether IL (interleukin)-1 blockade with anakinra improved cardiorespiratory fitness in heart failure with preserved ejection fraction. Methods and Results Thirty-one patients with heart failure with preserved ejection fraction and CRP (C-reactive protein) >2 mg/L were randomized to anakinra (100 mg subcutaneously daily, N=21) or placebo (N=10) for 12 weeks. We measured peak oxygen consumption (Vo2), ventilatory efficiency (VE/Vco2 slope), and high-sensitivity CRP and NT-proBNP (N-terminal pro-B-type natriuretic peptide) at 4, 12, and 24 weeks. Twenty-eight patients completed ≥2 visits, 18 women (64%), 27 (96%) obese. There were no differences in peak Vo2 or VE/Vco2 slope between groups at baseline. Peak Vo2 was not changed after 12 weeks of anakinra (from 13.6 [11.8-18.0] to 14.2 [11.2-18.5] mL·kg-1·min-1, P=0.89), or placebo (14.9 [11.7-17.2] to 15.0 [13.8-16.9] mL·kg-1·min-1, P=0.40), without significant between-group differences in changes at 12 weeks (-0.4 [95% CI, -2.2 to +1.4], P=0.64). VE/Vco2 slope was also unchanged with anakinra (from 28.3 [27.2-33.0] to 30.5 [26.3-32.8], P=0.97) or placebo (from 31.6 [27.3-36.9] to 31.2 [27.8-33.4], P=0.78), without significant between-group differences in changes at 12 weeks (+1.2 [95% CI, -1.8 to +4.3], P=0.97). Within the anakinra-treated patients, high-sensitivity CRP and NT-proBNP levels were lower at 4 weeks compared with baseline ( P=0.026 and P=0.022 versus placebo [between-group analysis], respectively). Conclusions Treatment with anakinra for 12 weeks failed to improve peak Vo2 and VE/Vco2 slope in a group of obese heart failure with preserved ejection fraction patients. The favorable trends in high-sensitivity CRP and NT-proBNP with anakinra deserve exploration in future studies. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT02173548.

Differential protein profiling as a potential multi-marker approach for obese patients with heart failure: A retrospective study

Identification of novel circulating biomarkers predicting death and major cardio-metabolic events in obese patients with heart failure (HF) remains a research priority. In this study, we compared multi-marker profile of non-obese (NOB) and obese (OB) HF patients in relation to mortality outcome. The new multiplex proximity extension assay technology was used to analyze the levels of 92 proteins in plasma samples from HF patients according to body mass index (BMI) categories. At 2-year follow-up, all-cause mortality rates were significantly greater in NOB patients (BMI < 30 kg/m2) compared to the OB patients (BMI > 30 kg/m2) with HF (odds ratio 26; 95% CI: 1.14–624, p < 0,04). Quantitative proteomic analysis revealed thirteen distinct proteins expression profiles of OB and NOB HF patients. Among these proteins, RAGE, CXCL6, CXCL1, CD40, NEMO, VEGF-A, KLK6, PECAM1, PAR1, MMP1, BNP and NTproBNP were down-regulated, whereas leptin was up-regulated in OB HF patients. In addition, an inverse correlation between plasma BNP levels and leptin in OB HF patients was observed (r = −0.58 p = 0.02). This study identifies specific plasma protein signature in OB and NOB patients with HF in relation to mortality outcome.

Invited Commentary

Hospital readmission is a metric that is increasingly being scrutinized in health care. This, combined with the nearly $17 billion of Medicare spending devoted to hospitalization of patients with heart failure, along with the rising use of left ventricular assist devices (LVADs) in the heart failure population, certainly make the current report by Han and colleagues [1Han J. Mauro C.M. Kurlansky P.A. et al.Impact of obesity on readmission in patients with left ventricular assist devices.Ann Thorac Surg. 2018; 105: 1192-1199Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar] timely [2Rosamond W. Flegal K. Furie K. et al.Heart disease and stroke statistics–2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.Circulation. 2008; 117: e25-e146Crossref PubMed Scopus (3025) Google Scholar, 3Kilic A. Sultan I. Yuh D.D. et al.Ventricular assist device implantation in the elderly: nationwide outcomes in the United States.J Card Surg. 2013; 28: 183-189Crossref PubMed Scopus (21) Google Scholar]. The authors note a 30-day readmission rate of 22% after LVAD implantation. By comparison, 30-day readmission rates for coronary artery bypass grafting and valve operations have similarly been shown to be between 10% and 25% [4Shahian D.M. He X. O’Brien S.M. et al.Development of a clinical registry-based 30-day readmission measure for coronary artery bypass grafting surgery.Circulation. 2014; 130: 399-409Crossref PubMed Scopus (53) Google Scholar, 5Kilic A. Magruder J.T. Grimm J.C. et al.Development and validation of a score to predict the risk of readmission after adult cardiac operations.Ann Thorac Surg. 2017; 103: 66-73Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar]. The authors report higher overall rates of readmission, driven by higher readmission rates for device failure and right heart failure, in patients with higher body mass indices. There are several plausible explanations for these findings. Obese patients likely have higher rates of obstructive sleep apnea and pulmonary hypertension that may increase right ventricular afterload and predispose to right heart failure. With respect to device failure, obese patients have been shown to have more severe prothrombotic states and higher rates of pump thrombosis. Furthermore, pump positioning may be more challenging in obese patients, leading to pump migration or kinking or to compression of the outflow graft, which then lead to device failure. Importantly, the authors demonstrate similar survival after LVAD operations in obese vs nonobese patients. These findings collectively suggest that we should not be averse to implanting LVADs in obese heart failure patients, but rather remain vigilant in surgical technique and optimization, prevention, and management of device failure and right heart failure in this susceptible cohort. More frequent outpatient follow-up and heightened awareness and attention to these issues may also help reduce the readmission burden in this higher risk subset. Impact of Obesity on Readmission in Patients With Left Ventricular Assist DevicesThe Annals of Thoracic SurgeryVol. 105Issue 4PreviewHospital readmissions have an adverse effect on the quality of life in patients with end-stage heart failure. We examined the temporal pattern, predictors, and outcomes of readmission in continuous flow left ventricular assist device–supported patients. Full-Text PDF

Modeling heart failure risk in diabetes and kidney disease: limitations and potential applications of transverse aortic constriction in high-fat-fed mice.

There is an increased incidence of heart failure in individuals with diabetes mellitus (DM). The coexistence of kidney disease in DM exacerbates the cardiovascular prognosis. Researchers have attempted to combine the critical features of heart failure, using transverse aortic constriction, with DM in mice, but variable findings have been reported. Furthermore, kidney outcomes have not been assessed in this setting; thus its utility as a model of heart failure in DM and kidney disease is unknown. We generated a mouse model of obesity, hyperglycemia, and mild kidney pathology by feeding male C57BL/6J mice a high-fat diet (HFD). Cardiac pressure overload was surgically induced using transverse aortic constriction (TAC). Normal diet (ND) and sham controls were included. Heart failure risk factors were evident at 8-wk post-TAC, including increased left ventricular mass (+49% in ND and +35% in HFD), cardiomyocyte hypertrophy (+40% in ND and +28% in HFD), and interstitial and perivascular fibrosis (Masson's trichrome and picrosirius red positivity). High-fat feeding did not exacerbate the TAC-induced cardiac outcomes. At 11 wk post-TAC in a separate mouse cohort, echocardiography revealed reduced left ventricular size and increased left ventricular wall thickness, the latter being evident in ND mice only. Systolic function was preserved in the TAC mice and was similar between ND and HFD. Thus combined high-fat feeding and TAC in mice did not model the increased incidence of heart failure in DM patients. This model, however, may mimic the better cardiovascular prognosis seen in overweight and obese heart failure patients.

LINKS BETWEEN RENIN-ANGIOTENSIN SYSTEM GENETIC POLYMORPHISMS AND LEPTIN SECRETION IN OBESE HEART FAILURE PATIENTS.

Chronic heart failure (CHF) and obesity are two conditions frequently associated and which, despite all the advances made in their management in the recent years, their prevalence continues to rise. Obese patients present unique challenges in the diagnosis of CHF and also therapeutic particularities. The genetic differences may be a possible explanation for the fact that some people, irrespective of their lifestyle and common classical cardiovascular risk factors, are more susceptible to develop heart failure. Moreover, the adipose tissue, a huge endocrine organ which secretes adipokines, is also a well-established source of all renin-angiotensin-aldosterone system components, being strongly involved in the pathogenesis of CHF. That is why this review will explore the possible links between the RAS genetic polymorphisms and leptin secretion in obese HF patients, trying to bring a more precise understanding of this relationship, which will undoubtedly facilitate a more appropriate treatment of HF in obese patients. We also try to explain the possible incriminated mechanisms, and plausible biological explanations for the relationship between RAS genetic polymorphisms and adipokines secretion in obese heart failure patients.

The correlation between body mass index, routine clinical and laboratory parameters and in-hospital survival in patients with acutely decompensated heart failure

Introduction: Recent studies have investigated the existence of so-called “obesity paradox” in heart failure (HF) patients, suggesting that obese patients might have a better prognosis than underweight and normal weight patients. It seems that body mass index (BMI) may be an independent prognostic factor in patients with acute and chronic HF. Patients and Methods: We investigated the correlation between BMI, in- hospital survival and routine clinical and laboratory parameters in patients hospitalized for acutely decompensated HF. Results: Total number of 145 patients (mean age 76±10.2 years) were divided in three groups: 37 with normal body weight (20-24.9 kg/m2), 64 overweight (25- 29.9 kg/m2), and 44 obese patients (≥30 kg/m2) patients. At the end of approximately 9 days of hospitalization, 24 of all patients died (16.5%). In-hospital mortality was significantly lower in obese patients (7% ; p=0.05). Patients with normal body weight were older than obese patients: 80 (75-87) compared to 72 (65-80) ; p=0.001 and significant negative correlation between BMI and patients age existed (r=-0.383 ; p<0.001). There was no significant difference in left ventricular ejection fraction between three compared groups of patients. Obese patients had significantly lower NT-proBNP (pmol/l): 319 (182-758) compared to overweight 862 (342-3013) and compared to normal body weight 1209 (616-2378) ; p=0.001, hs-cTnT (ng/l): 23 (15-57) compared to overweight 38 (27-70) and compared to normal body weight 44 (29-60) ; p=0.009 and serum urea (mmol/l) concentration: 8.1 (6.2-12.3) compared to overweight 9.7 (6.6-12.3) and compared do normal body weight 11.3 (8.2-14.7) ; p=0.039. No significant difference in serum creatinine, uric acid and hemoglobin existed, but significant negative correlation between BMI and NT-proBNP was found (r=-0.22 ; p=0.013). Conclusions: In-hospital mortality was significantly lower in obese HF patients. Obese patients had significantly lower NT-proBNP, hs- cTnT and serum urea concentrations. There was significant negative correlation between BMI and NT-proBNP.

The presence of obesity paradox in Greek patients with chronic heart failure

PurposeTo investigate the effect of body mass index (BMI) values on 1- and 2-year mortality rates in patients with chronic heart failure (HF).Patients and methodsWe conducted a retrospective cohort study of 112 patients with confirmed HF who visited the HF outpatient unit of a tertiary hospital of Athens, Greece, during a 5-month period (December 2012 – April 2013). These patients were assigned to four groups based on their BMI category. Data collection was carried out through a review of the medical patient records and the filling in of a structured questionnaire, including information on the demographic and clinical patient variables. Additionally, 1- and 2-year patient mortality was recorded. The statistical significance was two-tailed, and p-values of less than 0.05 were considered significant. The statistical analysis was performed with Mann–Whitney U test, χ2 test, and Student’s t-test using the SPSS software (IBM SPSS 21.0 for Windows).ResultsObese patients had significantly lower 1-year (13% vs 34.6%, p=0.039) and 2-year (4% vs 21.4%, p=0.022) mortality rates compared with those with normal BMI values. Additionally, we found clinically and not statistically significant lower mortality in overweight and obese patients, when compared with normal BMI and overweight patients, respectively.ConclusionObesity paradox seems to be present in our study, translating to significantly lower long-term mortality rates of obese patients compared to those with normal BMI. The significantly higher left ventricular ejection fraction and hematocrit levels among obese HF patients could justify our study findings. Further research is needed due to the inherent weaknesses of BMI and the other study limitations.

197 - Impact of Obesity on in-Hospital Survival in Acute Heart Failure Hospitalizations: Observations From Nationwide Inpatient Sample 2003–2011

Introduction: Prior studies have shown that obesity is paradoxically associated with improved survival in heart failure(HF) patients. However, majority of the studies have focused on HF with reduced ejection fraction patients (HFrEF). The association of obesity with survival in HF with preserved ejection (HFpEF) and hypertensive emergency-HF(HTN-HF) patients(pts) has not been well examined. Methods: We queried the 2003–2011 National Inpatient Sample databases to identify all admissions aged > 18 years with a primary diagnosis of HF. HF was then subgrouped into HFrEF, HFpEF and HTN-HF. Obese patients were then identified using a comorbidity variable (CM_obese) based on ICD-9 codes and diagnosis related groups. In-hospital mortality was compared between obese and non-obese patients using multivariate logistic regression (adjusted for patient demographics, hospital and admission characteristics, and clinically relevant cardiovascular and non-cardiovascular comorbidities. Results: Of 9,908,782 patients who were admitted with HF diagnosis, 81.3% were HFrEF, 11.4% were HFpEF and 7.3% were HTN-HF pts. Among these, pts with a diagnosis of obesity constituted 10.1% of HFrEF, 17.8% of HFpEF and 15.6% of HTN-HF admissions. A diagnosis of obesity was associated with lower in-hospital mortality among all three subgroups when compared with non-obese patients: HFrEF (1.8% vs. 3.9%), HfpEF (1.5%vs.2.8%) and HTN-HF (1.3% vs. 2.9%)(all P < .001). Interestingly even after multivariate analysis, this association of obesity with improved survival persisted (P < .001). Conclusion: In this retrospective observational analysis of a large nationwide inpatient database comparing in-hospital mortality in obese vs. non-obese HF patients, we observed higher survival in obese pts in HFrEF subgroup consistent with previous reports. Additionally, this paradoxical effect was also seen in HFpEF and HTN-HF pts.

The effect of BMI, serum leptin, and adiponectin levels on prognosis in patients with non-ischaemic dilated cardiomyopathy.

The recent studies demonstrated that obese heart failure patients have better prognosis - "obesity paradox". The aim of the study was to evaluate the relationship between body mass index (BMI), leptin and adiponectin concentrations and prognosis in patients with heart failure due to non ischeamic dilated cardiomyopathy (NIDCM). 128 patients with NIDCM were included and followed-up for three years. Leptin and adiponectin were measured at baseline using commercially available ELISA tests. Clinical data, routine laboratory parameters, NT-proBNP were assessed as risk factors for reaching the study endpoints: urgent heart transplantation (B), death (C), or combined endpoint death or urgent heart transplantation (D). Patient with adverse outcome had lower BMI and higher NT-proBNP concentration. Leptin was significantly elevated in group C and adiponectin was higher in groups B and D than in survived patients. Patients with leptin concentration below median or with adiponectin concentration above median were more often transplanted in three years follow-up (p = 0.029, p = 0.022, respectively). The cumulative probability of death was greater in patients with concentration of leptin above median (p = 0.024). In the multivariable Cox proportional hazards analyses, increasing leptin and lower BMI were predictors of death. Adiponectin was associated with higher risk of heart transplantation. Both an inverse association of BMI and positive association of leptin and adiponectin with combined endpoint were discovered. Further adjustment to established risk factors abolished association between combined endpoint and BMI, and modestly attenuate with adiponectin and leptin concentration. Evaluation of adiponectin and leptin concentrations was more useful than BMI in prediction of unfavourable outcome in patients with NIDCM. (Endokrynol Pol 2017; 68 (1): 26-34).

Midregional proadrenomedullin and growth differentiation factor-15 are not influenced by obesity in heart failure patients.

Obesity is a risk factor for heart failure (HF) and identification of symptomatic, and obese HF patients are challenging, because obesity can mimic HF symptoms. We aimed to evaluate novel biomarkers for HF in obese subjects of the general population. Midregional proadrenomedullin (MR-proADM), growth differentiation factor-15 (GDF-15), midregional pro-atrial natriuretic peptide (MR-proANP), and NT-proBNP were measured in 5000 individuals of the population-based Gutenberg Health Study (GHS), including 1204 obese individuals (BMI≥30kg/m2) and 107 individuals with HF. NT-proBNP and MR-proANP were lower in obese vs. non-obese HF individuals (p=0.013 and p=0.01, respectively), whereas GDF-15 was similar and MR-proADM was higher in obese vs. non-obese HF individuals. All biomarkers increased the odds ratio (OR) for prevalent HF. For NT-proBNP and MR-proANP, this increase was lower in obese vs. non-obese individuals, whereas it was comparable for MR-proADM and GDF-15. All biomarkers were associated with increased all-cause mortality (median follow-up 7.3years, 211 events). Results were validated in 8373 individuals (n=1734 with BMI≥30kg/m2) of the FINRISK study with a median follow-up of 13.8years (1030 events). Using a dichotomized biomarker cutoff for HF, the best predictor for all-cause mortality in obese subjects was GDF-15 (p<0.001). All biomarkers were associated with HF and higher risk for all-cause mortality in the general population. In contrast to the natriuretic peptides NT-proBNP and MR-proANP, the novel biomarkers MR-proADM and GDF-15 were not lower in obese HF individuals, indicating their potential to facilitate HF diagnosis and prognosis in an increasingly obese HF population.

Prevalence, Profile, and Prognosis of Severe Obesity in Contemporary Hospitalized Heart Failure Trial Populations

ObjectivesThis study evaluated the prevalence, profile, and prognosis of severe obesity in a large contemporary acute heart failure (AHF) population. BackgroundBetter prognosis has been reported for obese heart failure (HF) patients than nonobese HF patients, but in other cardiovascular populations, this effect has not been demonstrated for severely obese patients. MethodsA cohort of 795 participants with body mass index (BMI) measured at time of admission and complete follow-up were identified from enrollment in 3 contemporary AHF trials (DOSE [Diuretic Strategies Optimization Evaluation], CARRESS-HF [Cardiorenal Rescue Study in Acute Decompensated Heart Failure], and ROSE [Renal Optimization Strategies Evaluation in Acute Heart Failure]). Patients were divided into 4 BMI categories according to standard World Health Organization criteria, as follows: normal weight: 18.5 to 25 kg/m2 [n = 128]; overweight: 25 to 29.9 kg/m2 [n = 209]; mild-to-moderate obese: 30 to 39.9 kg/m2 [n = 301]; and severely obese: ≥40 kg/m2 [n = 157]). The relationship between BMI and 60-day composite outcome (death, rehospitalization, or unscheduled provider visit) was investigated. ResultsPatients with severe obesity (19.7%) were younger, more often female, hypertensive, diabetic, and more likely to have higher blood pressures and left ventricular ejection fraction, and lower N-terminal pro-B-type natriuretic peptide and troponin I levels than other BMI category patients. Following admission for AHF, patients with normal weight showed the highest risk of 60-day composite outcome, followed by patients who were severely obese. Overweight and mild-moderately obese patients showed lowest risk. ConclusionsNearly one-fifth of AHF patients enrolled in contemporary randomized clinical trials are severely obese. A U-shaped curve for short-term prognosis according to BMI is seen in AHF. These findings may help to better inform both HF clinical care and future clinical trial planning.