Adipokine Imbalance in the Pericardial Cavity of Cardiac and Vascular Disease Patients

Abstract

AimObesity and especially hypertrophy of epicardial adipose tissue accelerate coronary atherogenesis. We aimed at comparing levels of inflammatory and atherogenic hormones from adipose tissue in the pericardial fluid and circulation of cardiovascular disease patients.Methods and ResultsVenous plasma (P) and pericardial fluid (PF) were obtained from elective cardiothoracic surgery patients (n = 37). Concentrations of leptin, adipocyte fatty acid-binding protein (A-FABP) and adiponectin (APN) were determined by enzyme-linked immunosorbent assays (ELISA). The median concentration of leptin in PF (4.3 (interquartile range: 2.8–9.1) μg/L) was comparable to that in P (5.9 (2.2–11) μg/L) and these were significantly correlated to most of the same patient characteristics. The concentration of A-FABP was markedly higher (73 (28–124) versus 8.4 (5.2–14) μg/L) and that of APN was markedly lower (2.8 (1.7–4.2) versus 13 (7.2–19) mg/L) in PF compared to P. APN in PF was unlike in P not significantly related to age, body mass index, plasma triglycerides or coronary artery disease. PF levels of APN, but not A-FABP, were related to the size of paracardial adipocytes. PF levels of APN and A-FABP were not related to the immunoreactivity of paracardial adipocytes for these proteins.ConclusionIn cardiac and vascular disease patients, PF is enriched in A-FABP and poor in APN. This adipokine microenvironment is more likely determined by the heart than by the circulation or paracardial adipose tissue.

Measuring non‐polyaminated lipocalin‐2 for cardiometabolic risk assessment

“…Among the 37 patients in the Danish cohort (31 male and six female subjects), most had been prescribed cholesterol‐lowering, renin–angiotensin system inhibitory, anti‐hypertensive, and anti‐diabetic medications . When compared with those of the Hong Kong healthy volunteers, the plasma pLcn2/npLcn2 ratios were reduced more than four‐fold, owing mainly to the increased npLcn2 levels ( Table ).…”

“…The healthy volunteer cohort included 37 lean (BMI < 23 kg/m 2 ), 27 overweight (BMI = 23–24.9 kg/m 2 ), and 36 obese (BMI ≥ 25 kg/m 2 ) individuals, according to the Asia‐Pacific guidelines of obesity classification . In addition, 37 patients who underwent elective coronary artery bypass grafting (26 subjects), valve replacement surgery (six subjects), or both (five subjects) were recruited at the Odense University Hospital for a study approved by the Medical Ethics Committee of the Region of Southern Denmark (S‐20100044) . The demographic and clinical characteristics of all study subjects are summarized in Table .…”

“…Triglycerides, total cholesterol (TC), high density lipoprotein (HDL), and low density lipoprotein (LDL) cholesterol levels in serum samples were analysed using respective LiquiColor test kits from Stanbio Laboratory (Boerne, TX, USA). Circulating lipid and haemoglobin A1c (HbA1c) levels in plasma collected from the Danish patients were measured at the Odense University Hospital …”

Local enrichment of fatty acid-binding protein 4 in the pericardial cavity of cardiovascular disease patients

“…For instance, patients with coronary artery disease have increased expression of pro-inflammatory adipocytokines in epicardial adipose tissue compared to non-coronary artery disease patients, where expression of the anti-inflammatory adiponectin is decreased[ 4 ]. We recently determined the levels of fatty acid-binding protein 4 (FABP4), leptin, and adiponectin in not only the circulation but also the pericardial fluid from a small number of cardiovascular disease patients[ 5 ]. This fluid can be representative for the interstitium of the heart.…”

Investigating interactions between epicardial adipose tissue and cardiac myocytes: what can we learn from different approaches?

“…Going beyond the identification and quantitation of EAT, many studies of this fat depot have involved molecular and biochemical studies using either blood or tissue biopsies, obtained during elective cardiovascular surgery procedures. These studies have variously used elisa (Mazurek et al, ; Gao et al, ; Sacks and Fain, ; Teijeira‐Fernandez et al, ; Fosshaug et al, ; Venteclef et al, ; Elie et al, ), PCR (Mazurek et al, ; Fain et al, ; Gao et al, ; Teijeira‐Fernandez et al, ; Fosshaug et al, ), miR analysis (Vacca et al, ), transcriptome and secretome analysis (Guauque‐Olarte et al, ; Imoto‐Tsubakimoto et al, ; Gaborit et al, ; McAninch et al, ; Venteclef et al, ) to show that the molecular profile of EAT is different from that of other adipose depots, and can change during physiological challenges affecting the heart. This large body of data supports the site‐specific, localized role played by EAT, but does not elucidate the question of whether the observed changes are the cause or the effect of physiological disturbance.…”