Enhanced accumulation of pericardial fluid ferritin in patients with coronary artery disease

Selmeci, L.; Antal, M.; Horkay, Ferenc; Merkely, Béla; Szokodi, István; Biró, Lajos; Székely, Mária; Jobbágy, Judit; Szépvölgyi, J.; Tóth, Miklós

doi:10.1097/00019501-200002000-00010

Cited by 19 publications

(5 citation statements)

References 19 publications

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“…The pericardial fluid is regarded by some as an ultrafiltrate of the plasma[ 25 ], whereas others consider it as representative of the cardiac interstitium[ 26 ]. The pericardial fluid-to-plasma ratio, including the ratio as a fraction of the total protein concentration of the investigated proteins showed a strong relationship with molecular weight from a high ratio for small molecules (8.5 kDa for NT-pBNP, 15 kDa for FABP4, 16 kDa for leptin, and 25 kDa for lipocalin-2) to a lower ratio with increasing molecular weight (29 kDa for proteinase-3, 29.5 kDa for neutrophil elastase, 120 kDa for hsCRP, and > 250 kDa for adiponectin).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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BackgroundThe pericardial fluid may be representative of the interstitium of the heart. The aim of this study was to discriminate in cardiovascular disease patients between adipocytokines that are produced locally by the heart and those supplied by the circulation.MethodsEnzyme-linked immunosorbent assays (ELISA) were used to determine levels of N-terminal pro-brain natriuretic peptide (NT-pBNP), fatty acid-binding protein 4 (FABP4), leptin, lipocalin-2, neutrophil elastase, proteinase-3, high sensitivity C-reactive protein (hsCRP) and adiponectin in venous plasma and pericardial fluid harvested during elective cardio-thoracic surgery (n = 132–152).ResultsIn pericardial fluid compared to plasma, the levels were significantly smaller (p < 0.001) for leptin, lipocalin-2, neutrophil elastase, proteinase-3, hsCRP and adiponectin. For these biomarkers, the ratio of pericardial fluid-to-plasma level ([PF]/[P], median (interquartile range)) was 0.65 (0.47–1.01), 0.78 (0.56–1.09), 0.23 (0.11–0.60), 0.17 (0.09–0.36), 0.14 (0.08–0.35), and 0.25 (0.15–0.34), respectively. In contrast, pericardial fluid was significantly enriched (p < 0.001) in NT-pBNP ([PF]/[P]: 1.9 (1.06–2.73)) and even more so for FABP4 ([PF]/[P]: 3.90 (1.47–9.77)). Moreover, in pericardial fluid, the adipocytokines interrelated all significantly positive and correlated negative to hsCRP, whereas for NT-pBNP only a significantly positive correlation with adiponectin was found. These interrelations were distinct from those in the plasma, as were the correlations of the pericardial biomarkers with patient characteristics compared to plasma.ConclusionsIn cardiovascular disease patients, the pericardial cavity is a distinct adipocytokine microenvironment in which especially FABP4 is mainly derived from the heart.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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“…Control of pericardial fluid composition is however poorly understood. Some authors consider it a protein poor ultrafiltrate of the plasma [ 46 , 47 ] while others emphasize similarities to the interstitium of the heart [ 21 , 22 , 47 ]. Our observations of comparable contributions of low and high molecular weight APN isoforms in plasma and pericardial fluid and of different pericardial to plasma ratios for leptin and A-FABP along with earlier findings of elevated levels of lactate dehydrogenase (140 kDa) in pericardial fluid [ 46 ], are not compatible with the former view.…”

Section: Discussionmentioning

confidence: 99%

“…The composition of the pericardial fluid (PF) surrounding the heart has been proposed to be comparable to that of the interstitium of the heart [ 21 , 22 ]. Several angiogenic growth factors, cytokines, natriuretic peptides and classical vasoactive hormones are present at higher concentration in the PF than in the circulating plasma (P) of patients with ischemic heart disease or heart failure [ 21 , 23 – 25 ].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

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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.

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“…Thus ferritin, primarily a liver-derived, iron-binding protein, may act as an indirect antioxidant by sequestering iron. The augmentation of intracellular ferritin through HO-1 reduces the cytotoxic effects of heme and hydrogen peroxide in vascular endothelial cells (33), and may protect against ischemia-reperfusion injury through its cytoprotective effects on the endothelium and its ability to keep labile iron pools low and thereby reduce oxidant-induced lipid peroxidation (34). However, one hesitates to leap to the conclusion that these relationships are causal.…”

Section: Biochemistry and Genetics Of Ho-1mentioning

confidence: 99%

Hemoxygenase-1 in Cardiovascular Disease

Idriss

Blann

Lip

2008

Journal of the American College of Cardiology

129

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Hemoxygenase (HO)-1 is an inducible isoform of the first and rate-controlling enzyme of the degradation of heme into iron, carbon monoxide, and biliverdin, the latter being subsequently converted into bilirubin. Several positive biological effects exerted by this enzyme have gained attention, as anti-inflammatory, antiapoptotic, angiogenic, and cytoprotective functions are attributable to carbon monoxide and/or bilirubin. Thus, the physiological induction of HO-1 may be an adaptive and beneficial response to several possibly noxious stimuli, including heme itself, suggesting a potentially autoprotective and autodefensive role in several pathophysiological states including acute coronary syndromes and stroke. This review article provides a comprehensive overview of the biochemistry, physiology, and pathophysiology of HO-1 in relation to cardiovascular disease (CVD). Furthermore, we present some of the emerging evidence in support of the view that the induction of the HO-1 gene may be a new opportunity to target the pathophysiology of CVD, with therapeutic implications for management.

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Enhanced accumulation of pericardial fluid ferritin in patients with coronary artery disease

Cited by 19 publications

References 19 publications

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

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

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

Hemoxygenase-1 in Cardiovascular Disease

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