scholarly journals Reciprocal Effects of Systemic Inflammation and Brain Natriuretic Peptide on Adiponectin Biosynthesis in Adipose Tissue of Patients With Ischemic Heart Disease

2014 ◽  
Vol 34 (9) ◽  
pp. 2151-2159 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Marios Margaritis ◽  
Patricia Coutinho ◽  
Janet Digby ◽  
Rikhil Patel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Systemic Inflammation ◽  
Ischemic Heart ◽  
Reciprocal Effects

scholarly journals Association between the level of plasma B-type natriuretic peptide and in-hospital mortality in patients with acute exacerbation of COPD without a history of coronary ischemic heart disease: a retrospective study

2021 ◽  
Author(s):  
Jiyun Cui ◽  
Jie Liu ◽  
Jing Wang ◽  
Meng Lv ◽  
Chunyan Xing ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Heart Disease ◽  
Hospital Mortality ◽  
Ischemic Heart Disease ◽  
Natriuretic Peptide ◽  
Invasive Mechanical Ventilation ◽  
Ischemic Heart ◽  
Composite Outcome ◽  
History Of ◽  
Secondary Outcomes

Abstract Background: Previous studies suggested that plasma B-type natriuretic peptide (BNP) level was often elevated in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and was associated with increased mortality. However, most studies did not consider the fact that conditions such as coronary ischemic heart disease can also increase BNP level. Therefore, we aimed to explore the association between BNP level and in-hospital mortality in patients with AECOPD without a history of coronary ischemic heart disease.Methods: In this retrospective cohort study, patients who were diagnosed with AECOPD using International Statistical Classification of Diseases and Related Health Problems, Nineth Revision (ICD-9 codes) between January 2017 and December 2019. All data were obtained from electronic patient files and medical data intelligence platform of Jinan Central Hospital. BNP level was determined within 24 hours after admission, and the value was log2 transformed. The primary outcome was in-hospital mortality, and the secondary outcome was a composite outcome of in-hospital mortality or invasive mechanical ventilation.Results: A total of 300 patients were included in this study. Univariate cox regression analysis showed that the unadjusted HRs of the primary and secondary outcomes were 1.85 (95% CI, 1.39-2.47) and 1.45 (95% CI, 1.20-1.75), respectively. After adjustment for age, sex, past medical history, smoking status, drinking status, CURB65 (Confusion, Urea > 7mmol/L, Respiratory rate≥30/min, Blood pressure systolic < 90 mmHg or diastolic <60 mmHg and age > 65 years), arterial partial pressure of O2(PaO2), the adjusted HRs of the primary and secondary outcomes were 3.65 (95% CI, 2.54-5.26) and 1.43 (95% CI, 1.14-1.97), respectively. The results of subgroup analysis by age, sex, and lung function were robust. This study was retrospective, so there was no clinical trial registration.Conclusions: The plasma log2BNP level was significantly associated with in-hospital mortality and a composite outcome of in-hospital mortality or invasive mechanical ventilation.

scholarly journals Adipokine-cytokine profile of adipocytes of epicardial adipose tissue in ischemic heart disease complicated by visceral obesity

2017 ◽  
Vol 14 (4) ◽  
pp. 38-45 ◽  
Author(s):  
Olga V. Gruzdeva ◽  
Daria A. Borodkina ◽  
Olga E. Akbasheva ◽  
Julia A. Dileva ◽  
Larisa V. Antonova ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Blood Serum ◽  
Epicardial Adipose Tissue ◽  
Visceral Obesity ◽  
Cytokine Profile ◽  
Ischemic Heart ◽  
Atherogenic Dyslipidemia ◽  
Soluble Receptor

Introduction. To date, cardiovascular diseases (CVD) remain the main cause of disability and mortality in population. The majority of ectopic fat deposits demonstrated a reliable association with cardiometabolic risks and clinical manifestations of most CVD. The elucidation of the metabolic features of adipocytes of epicardial adipose tissue localized in the immediate vicinity of the lesion in ischemic heart disease (IHD) can have both theoretical and practical significance for pathophysiology and cardiology. Aim. To study the adipokine-cytokine profile of epicardial adipocytes (EA) and subcutaneous adipose tissue (SCAT), blood serum in relation to the area of visceral adipose tissue (AVAT), biochemical and rhelinic characteristics of IHD patients. Methods. 84 patients (70 men and 14 women) with IHD were examined. In the presence of visceral obesity (VO), patients were divided into two groups. In patients with VO, adipocyte EA and SCAT were sampled, followed by cultivation and evaluation of adipokine and proinflammatory activity. The parameters of carbohydrate and lipid metabolism, adipokine and proinflammatory status in blood serum were determined. Results. It has been established that the adipokine-cytokine profile of the adipocytes EA and SCAT differ. Adipocytes of EA in IHD on the background of VO are characterized by an increase in IL-1, TNF-, leptin-adiponectin ratio and a decrease in the protective factors: adiponectin and anti-inflammatory cytokine IL-10. While adipocytes of SCAT were characterized by a decrease in the concentration of the soluble receptor to leptin and a more pronounced leptin resistance, and the increase in inflammatory cytokines was compensated by an increase in the concentration of IL-10, the presence of VO was associated with multivessel coronary disease, multifocal atherosclerosis, insulin resistance, atherogenic dyslipidemia, adipokine imbalance, and markers of inflammation. Thus, the value of the area of VO determined higher values of leptin concentration, TNF- in adipocytes and serum, lipid and carbohydrate metabolism and a lower soluble receptor for leptin content. The conclusion. Thus, in IHD with VO the state of adipocytes, EA is characterized as "metabolic inflammation" and may indicate the direct involvement of adipocytes in the pathogenesis of IHD due to the formation of adipokine imbalance and the activation of proinflammatory reactions.

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