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      The Impact of Obesity on Left Ventricular Assist Device Outcomes

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          Abstract

          Background and Objectives: The understanding of high body mass index (BMI) and outcomes after Left Ventricular Assist Device (LVAD) implantation continues to evolve and the relationship has not been established yet. In this study, we investigated the effects of obesity (BMI > 30 kg/m 2) on post–LVAD implantation outcomes. HeartWare LVAD and Heart Mate III LVAD were implanted. The primary outcome that was measured was mortality (in-hospital and on follow-up). The secondary outcomes that were measured were major adverse events. Materials and Methods : At our institution, the West German Heart and Vascular Center (Essen, Germany), from August 2010 to January 2020, a total of 210 patients received a long-term LVAD. Patients were stratified according to BMI ≥ 30 kg/m 2 representing the obesity threshold. The first group ( n = 162) had an average BMI of 24.2 kg/m 2 (±2.9), and the second group ( n = 48) had an average BMI of 33.9 kg/m 2 (±3.2). Baseline demographics were analysed alongside comorbidities per group. Results: Overall mortality was not significantly different between the obese group (51.1% n = 24) and the nonobese group (55.2%, n = 85) ( p = 0.619). The difference between the mean duration of survival of patients who expired after hospital discharge was insignificant (2.1 years ± 1.6, group 1; 2.6 years ± 1.5, group 2; p = 0.29). In-hospital mortality was unvaried between the two groups: group 1: n = 34 (44% out of overall group 1 deaths); group 2: n = 11 (45.8% out of overall group 2 deaths) ( p > 0.05). Postoperative complications were unvaried between the obese and the non-obese group (all with p > 0.05). However, a significant difference was found with regards to follow-up neurological complications (18.5% vs. 37.8%, p = 0.01) and LVAD thrombosis (14.7% vs. 33.3%, p = 0.01), as both were higher in the obese population. Conclusion: Obesity does not form a barrier for LVAD implantation in terms of mortality (in-hospital and on follow up). However, a significantly higher incidence of follow-up LVAD thrombosis and neurological complications has been found in the obese group of patients.

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          The medical risks of obesity.

          Obesity is at epidemic proportions in the United States and in other developed and developing countries. The prevalence of obesity is increasing not only in adults, but especially among children and adolescents. In the United States in 2003 to 2004, 17.1% of children and adolescents were overweight, and 32.2% of adults were obese. Obesity is a significant risk factor for and contributor to increased morbidity and mortality, most importantly from cardiovascular disease (CVD) and diabetes, but also from cancer and chronic diseases, including osteoarthritis, liver and kidney disease, sleep apnea, and depression. The prevalence of obesity has increased steadily over the past 5 decades, and obesity may have a significant impact on quality-adjusted life years. Obesity is also strongly associated with an increased risk of all-cause mortality as well as cardiovascular and cancer mortality. Despite the substantial effects of obesity, weight loss can result in a significant reduction in risk for the majority of these comorbid conditions. Those comorbidities most closely linked to obesity must be identified to increase awareness of potential adverse outcomes. This will allow health care professionals to identify and implement appropriate interventions to reduce patient risk and mortality. A systematic search strategy was used to identify published literature between 1995 and 2008 that reported data from prospective longitudinal studies of obesity and comorbid medical conditions. This article will review evidence for significant associations of obesity with comorbidities to provide information useful for optimal patient management.
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            INTERMACS profiles of advanced heart failure: the current picture.

            The current classification of patients with New York Heart Association Class IV symptoms does not offer adequate description to allow optimal selection of patients for the current options of medical and pacing therapies, cardiac transplantation and mechanical circulatory support. Seven clinical profiles and an arrhythmia modifier were developed and implemented into the first year of data collection for the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS). The INTERMACS Coordinators' Council provided ongoing feedback regarding the characterization of patients receiving implantable devices. The definition of 7 clinical profiles revealed that 80% of current devices are being used in the 2 profiles with the highest levels of clinical compromise. The INTERMACS Coordinators' Council helped to identify gaps in the characterization of hospitalized patients on temporary assist devices and of homebound patients with resting symptoms, which has led to revised definitions of Profile 3 and 4 and the addition of 2 new modifiers, for temporary circulatory support devices in the hospital, and for frequent rehospitalization of patients at home. Patients considered for mechanical circulatory support can now be classified using the 7 profiles plus 3 modifiers developed through INTERMACS. Further understanding these profiles and their impact on outcome should help to better select patients and therapies in the advanced stages of disease.
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              Inflammation, obesity, and thrombosis.

              Clinical and epidemiological studies support a connection between obesity and thrombosis, involving elevated expression of the prothrombotic molecules plasminogen activator inhibitor-1 and tissue factor (TF) and increased platelet activation. Cardiovascular diseases and metabolic syndrome-associated disorders, including obesity, insulin resistance, type 2 diabetes, and hepatic steatosis, involve inflammation elicited by infiltration and activation of immune cells, particularly macrophages, into adipose tissue. Although TF has been clearly linked to a procoagulant state in obesity, emerging genetic and pharmacologic evidence indicate that TF signaling via G protein-coupled protease-activated receptors (PAR2, PAR1) additionally drives multiple aspects of the metabolic syndrome. TF-PAR2 signaling in adipocytes contributes to diet-induced obesity by decreasing metabolism and energy expenditure, whereas TF-PAR2 signaling in hematopoietic and myeloid cells drives adipose tissue inflammation, hepatic steatosis, and insulin resistance. TF-initiated coagulation leading to thrombin-PAR1 signaling also contributes to diet-induced hepatic steatosis and inflammation in certain models. Thus, in obese patients, clinical markers of a prothrombotic state may indicate a risk for the development of complications of the metabolic syndrome. Furthermore, TF-induced signaling could provide new therapeutic targets for drug development at the intersection between obesity, inflammation, and thrombosis.
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                Author and article information

                Journal
                Medicina (Kaunas)
                medicina
                Medicina
                MDPI
                1010-660X
                1648-9144
                23 October 2020
                November 2020
                : 56
                : 11
                : 556
                Affiliations
                [1 ]Department of Thoracic and Cardiovascular Surgery, West German Heart and Vascular Center Essen, University Hospital of Essen, University Duisburg-Essen, 45122 Essen, Germany; konstantin.zhigalov@ 123456yahoo.com (K.Z.); lukasgoerdt@ 123456yahoo.de (L.G.); thomas.chrosch@ 123456unitybox.de (T.C.); alina.zubarevich@ 123456gmail.com (A.Z.); daniel.wendt@ 123456uk-essen.de (D.W.); Nikolaus.Pizanis@ 123456uk-essen.de (N.P.); Achim.Koch@ 123456uk-essen.de (A.K.); Bastian.Schmack@ 123456uk-essen.de (B.S.); Arjang.Ruhparwar@ 123456uk-essen.de (A.R.); alexander.weymann@ 123456uk-essen.de (A.W.)
                [2 ]International Thoracic and Cardiovascular Research Association (ITCVR), 26133 Oldenburg, Germany; michel_pompeu@ 123456yahoo.com.br (M.P.B.O.S.); robert.vardanyan16@ 123456imperial.ac.uk (R.V.); aronf.popov@ 123456gmail.com (A.-F.P.)
                [3 ]Department of Cardiovascular Surgery at the Pronto Socorro Cardiológico de Pernambuco (PROCAPE), Recife, University of Pernambuco, Recife 74970-240, Brazil
                [4 ]Department of Medicine, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK
                [5 ]Department of Cardiothoracic Surgery, Heart Center Essen Huttrop, University Hospital Essen, 45138 Essen, Germany; markus.kamler@ 123456heh.uk-essen.de
                [6 ]Department of Thoracic and Cardiovascular Surgery, University Medical Centre Tubingen, 72076 Tubingen, Germany; Rafal.Berger@ 123456med.uni-tuebingen.de
                Author notes
                Author information
                https://orcid.org/0000-0002-6440-3736
                https://orcid.org/0000-0001-5356-2996
                https://orcid.org/0000-0002-4931-4049
                https://orcid.org/0000-0002-8111-2084
                https://orcid.org/0000-0001-6608-8496
                https://orcid.org/0000-0002-8245-4457
                https://orcid.org/0000-0003-4226-3004
                Article
                medicina-56-00556
                10.3390/medicina56110556
                7690722
                33113962
                4c0276f2-c8e6-4ae1-913a-90ab2dd879f1
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 23 September 2020
                : 21 October 2020
                Categories
                Article

                left ventricular assist device,obesity,mechanical circulatory support,heart failure,cardiac assist and artificial heart

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