Abstract 2387: Co-Localisation of C-Reactive Protein and the Terminal Complement Complex in Dilated Cardiomyopathy - Implications for Non-Ischaemic Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Oliver Zimmermann ◽  
Dimitar E Manolov ◽  
Ziya Kaya ◽  
Thomas P Zwaka ◽  
Magdalena Bienek-Ziolkowski ◽  
...  

Background: C-reactive protein (CRP) has been suggested as a risk factor in cardiovascular disease. Recently, it has been shown that CRP binds to ligands exposed in ischaemic damaged tissue and activates the complement system. Furthermore, CRP was demonstrated to be strongly and independently associated with the occurrence of heart failure in men. In this study we have investigated the presence of CRP and the Terminal Complement Complex (C5b-9) in the myocardium of patients suffering from non-ischaemic heart failure. Methods and Results: Endomyocardial biopsies were taken from 151 patients suffering from dilated cardiomyopathy. Biopsies were immunohistochemically analysed for the presence and distribution pattern of CRP and C5b-9. In 39 patients plasma levels of hsCRP and NT-proBNP were measured and correlated with myocardial biopsy findings. In 47 patients a positive staining for CRP and in 141 patients a positive staining for C5b-9 was detected. CRP and C5b-9 significantly co-localised within the myocardium. A negative correlation was observed for plasma hsCRP levels and myocardial CRP. Conclusions: This study shows for the first time that CRP is frequently present in the myocardium of patients suffering from non-ischaemic dilated cardiomyopathy and co-localises with the Terminal Complement Complex. CRP may contribute to myocardial damage in dilated cardiomyopathy via activating the complement system.

Author(s):  
Thona Wusu

Introduction: Schizophrenia is a severe mental disorder among nationalities of the world, which has a substantial social and economic effect. Scientific therapeutic drugs have proved abortive due to adverse effects. Aim: The study investigated the repression of the complement system by aqueous extract of alligator pepper on schizophrenia. Methods: Male mice were induced with schizophrenia using ketamine and dexamethasone; the mice were treated with aqueous extract of alligator pepper (200mg/ml and 400mg/ml) respectively for ten days. After which their brain was removed, and analysed for dopamine. Blood samples was collected from the animal and plasma was used to determine the level of complement component (3 and 4), and C-reactive protein spectrophotometrically. Phytochemical content of the aqueous extract was also done spectrophotometrically, and characterization was confirmed using FTIR. Result: The alligator plant extract constituent includes flavonoids, tannins, saponin, steroids, phlabotannis, terpenoids, and cardiac glycoside. With a tannins having a concentration of 1292.6 µg/ml and 726.8µg/ml, phenol had a concentration of 221.7 µg/ml and 94.2 µg/ml and flavonoids had a concentration of 105.3 µg/ml and 100.0 µg/ml at 200mg/ml and 400mg/ml plant concentration respectively. The alligator pepper reversed the effect of ketamine and dexamethasone induced schizophrenia by decreasing the level of C-reactive protein , complement component (3 and 4) and dopamine significantly (<0.0001) in a dose dependent manner, in all the groups compared to the control. Conclusion: The high phenolic and flavonoids content in alligator pepper may be responsible for the antipsychotic property of alligator pepper. Thus, probable natural therapy for schizophrenia.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Celina Wojciechowska ◽  
Ewa Romuk ◽  
Andrzej Tomasik ◽  
Bronisława Skrzep-Poloczek ◽  
Ewa Nowalany-Kozielska ◽  
...  

Background.The aim of study was to determine relationships between functional capacity (NYHA class), left ventricle ejection fraction (LVEF), hemodynamic parameters, and biomarkers of redox state and inflammation in patients with dilated cardiomyopathy (DCM).Methods. DCM patients (n=109, aged45.97±10.82years), NYHA class IIV, and LVEF2.94±7.1% were studied. Controls comprised age-matched healthy volunteers (n=28). Echocardiography and right heart catheterization were performed. Serum activities of superoxide dismutase isoenzymes (MnSOD and CuZnSOD), concentrations of uric acid (UA), malondialdehyde (MDA), and C-reactive protein (hs-CRP) were measured.Results. MnSOD, UA, hs-CRP, and MDA were significantly higher in DCM patients compared to controls. Except MDA concentration, above parameters were higher in patients in III-IV NYHA class or with lower LVEF. hsCRP correlated with of MnSOD (P<0.05) and CuZnSOD activity (P<0.01). Both isoenzymes positively correlated with mPAP and pulmonary capillary wedge pressure (MnSOD, resp.,P<0.01andP<0.05and CuZnSODP<0.05;P<0.05). UA positively correlated with MnSOD (P<0.05), mPAP (P<0.05), and PVRI (P<0.05). The negative correlation between LVEF and UA (P<0.01) was detected.Conclusion. There are relationships among the severity of symptoms of heart failure, echocardiographic hemodynamic parameters, oxidative stress, and inflammatory activation. Increased MnSOD activity indicates the mitochondrial source of ROS in patients with advanced heart failure.


2021 ◽  
Vol 12 ◽  
Author(s):  
Margrethe Flesvig Holt ◽  
Annika E. Michelsen ◽  
Negar Shahini ◽  
Elisabeth Bjørkelund ◽  
Christina Holt Bendz ◽  
...  

ObjectiveDysregulation of the complement system has been described in patients with heart failure (HF). However, data on the alternative pathway are scarce and it is unknown if levels of factor B (FB) and the C3 convertase C3bBbP are elevated in these patients. We hypothesized that plasma levels of FB and C3bBbP would be associated with disease severity and survival in patients with HF.MethodsWe analyzed plasma levels of FB, C3bBbP, and terminal C5b-9 complement complex (TCC) in 343 HF patients and 27 healthy controls.ResultsCompared with controls, patients with HF had elevated levels of circulating FB (1.6-fold, p &lt; 0.001) and C3bBbP (1.3-fold, p &lt; 0.001). In contrast, TCC, reflecting the terminal pathway, was not significantly increased (p = 0.15 vs controls). FB was associated with NT-proBNP, troponin, eGFR, and i.e., C-reactive protein. FB, C3bBbP and TCC were not associated with mortality in HF during a mean follow up of 4.3 years.ConclusionOur findings suggest that in patients with HF, the alternative pathway is activated. However, this is not accompanied by activation of the terminal pathway.


2001 ◽  
Vol 1 (S2) ◽  
Author(s):  
Niubel Diaz-Padilla ◽  
Wim KBleeker ◽  
C Erik Hack

2020 ◽  
pp. 30-34
Author(s):  
V. V. Boyko ◽  
D. O. Yevtushenko ◽  
I. V. Kryvorotko ◽  
I. A. Taraban ◽  
D. V. Minukhin ◽  
...  

Summary. The etiology of the development of adhesive disease — the most common postoperative complication — can be determined by epigenomic disorders related to various links of resistance and immunogenetic control. Purpose of the study. To study the epigenomic factors in the development of adhesive disease, the immune status of patients operated on in the abdominal cavity was studied. The comparison group included 55 patients with a complicated course of peritoneal commissural disease, the main group consisted of 59 patients operated on on the abdominal organs on the background of peritoneal commissural disease, the course of which was asymptomatic. Results and its discussion. The revealed epigenomic factors associated with the risk of developing adhesive disease: belongs to an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24.1 % in comparison with the comparison group — 13.25 %). Conclusions. The results of our studies showed that patients with adhesive disease have a wide range of epigenome trigger factors. Epigenomic factors associated with the risk of developing adhesive disease include an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24, 1 % compared with the comparison group - 13.25 %)


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