Intracardiac expression of markers of endothelial damage/dysfunction, inflammation, thrombosis, and tissue remodeling, and the development of postoperative atrial fibrillation

Kairevičiūtė, Diana; Lip, Gregory Y.H.; Balakrishnan, Balu; Uzdavinys, Giedrius; Norkūnas, Gediminas; Kalinauskas, Gintaras; Sirvydis, Vytautas; Aidietis, Audrius; Zanetto, Ulises; Sihota, H.; Maheshwari, M. C.; Blann, Andrew D.

doi:10.1111/j.1538-7836.2011.04523.x

Cited by 36 publications

(18 citation statements)

References 37 publications

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“…In contrast to other studies [21] the sP-sel levels were very low in our study population. As possible explanation would be continuous oral anticoagulation before and after procedure (each procedure was performed without cessation of vitamin K antagonists or NOACs) as well as peri-procedural ACT-driven anticoagulation with heparin during ablation.…”

Section: Discussioncontrasting

confidence: 99%

Effects of Radiofrequency Catheter Ablation of Atrial Fibrillation on Soluble P-Selectin, Von Willebrand Factor and IL-6 in the Peripheral and Cardiac Circulation

et al. 2014

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BackgroundCatheter ablation (CA) of atrial fibrillation (AF) is associated with inflammatory response, endothelial damage and with increased risk of thrombosis. However, whether these processes differ in peripheral and cardiac circulation is unknown.MethodsPlasma markers (von Willebrand factor (vWf), soluble P-selectin (sPsel) and interleukin-6 (IL-6)) were measured by ELISA at three time points in 80 patients (62±10 years, 63% males, 41% paroxysmal AF) undergoing CA. These were at baseline – from femoral vein (FV) and left atrium (LA) before ablation; directly after ablation – from the pulmonary vein (PV), LA and FV; and 24 hours after procedure – from a cubital vein (CV).ResultsThe levels of vWF and IL6 – but not sP-sel – increased significantly 24h after procedure (p<0.001). Baseline vWF was significantly associated with persistent AF (Beta = .303, p = 0.006 and Beta = .300, p = 0.006 for peripheral and cardiac levels, respectively), while persistent AF (Beta = .250, p = 0.031) and LAA flow pattern (Beta = .386, p<0.001) remained associated with vWF in cardiac blood after ablation. Advanced age was significantly associated with IL6 levels at baseline and after ablation in peripheral and cardiac blood. There were no clinical, procedural or anti-coagulation characteristics associated with sP-sel levels in cardiac blood, while peripheral sP-sel levels were associated with hypertension before (Beta = −.307, p = 0.007) and with persistent AF after ablation (Beta = −.262, p = 0.020).ConclusionsvWF levels are higher in persistent AF and are associated with LAA rheological pattern after AF ablation. Increase of peripheral vWF and IL6 levels after procedure supports current AF ablation management with careful control of post-procedural anticoagulation to avoid ablation-related thromboembolism.

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Section: Discussioncontrasting

confidence: 99%

Effects of Radiofrequency Catheter Ablation of Atrial Fibrillation on Soluble P-Selectin, Von Willebrand Factor and IL-6 in the Peripheral and Cardiac Circulation

et al. 2014

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“…Ultimately, it is the inflammatory response within the atrial tissue (remodelling) that might be critical in determining the onset of POAF. When investigating the expression of different pro-inflammatory markers in the left and right atrial appendage it was noted that the intensity of VWF expression in left atrial appendage tissue predicted patients who developed POAF after CABG (Kaireviciute, et al, 2011). TGF-β1 have also been implicated in the pathology of AF in animal models.…”

Section: Inflammatory Response and Factors That Alter Incidence Of Poafmentioning

confidence: 98%

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Zakkar

Ascione

James

et al. 2015

Pharmacology & Therapeutics

190

129

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Postoperative atrial fibrillation (POAF) is a common complication of cardiac surgery that occurs in up to 60% of patients. POAF is associated with increased risk of cardiovascular mortality, stroke and other arrhythmias that can impact on early and long term clinical outcomes and health economics. Many factors such as disease-induced cardiac remodelling, operative trauma, changes in atrial pressure and chemical stimulation and reflex sympathetic/parasympathetic activation have been implicated in the development of POAF. There is mounting evidence to support a major role for inflammation and oxidative stress in the pathogenesis of POAF. Both are consequences of using cardiopulmonary bypass and reperfusion following ischaemic cardioplegic arrest. Subsequently, several anti-inflammatory and antioxidant drugs have been tested in an attempt to reduce the incidence of POAF. However, prevention remains suboptimal and thus far none of the tested drugs has provided sufficient efficacy to be widely introduced in clinical practice. A better understanding of the cellular and molecular mechanisms responsible for the onset and persistence of POAF is needed to develop more effective prediction and interventions.

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“…IHC scoring was interpreted using a semi-quantitative scoring system that has been widely accepted and described previously [42,43] taking into account the staining intensity and the number of positive cells (area extent). MMP and TIMP stained sections were graded in a blinded manner by two independent experienced pathologists as absent (0), weak (1), moderate (2) or intense (3) staining.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Immunohistochemical determination of the extracellular matrix modulation in a rat model of choline‐deprived myocardium: the effects of carnitine

Strilakou

Perelas

Lazaris

et al. 2015

Fundamemntal Clinical Pharma

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Choline has been identified as an essential nutrient with crucial role in many vital biological functions. Recent studies have demonstrated that heart dysfunction can develop in the setting of choline deprivation even in the absence of underlying heart disease. Matrix metalloproteinases (MMPs) are responsible for extracellular matrix degradation, and the dysregulation of MMP-2 and MMP-9 has been involved in the pathogenesis of various cardiovascular disorders. The aim of the study was to investigate the role of MMPs and their inhibitors (TIMPs), in the pathogenesis of choline deficiency-induced cardiomyopathy, and the way they are affected by carnitine supplementation. Male Wistar Albino adult rats were divided into four groups and received standard or choline-deficient diet with or without L-carnitine in drinking water (0.15% w/v) for 1 month. Heart tissue immunohistochemistry for MMP-2, MMP-9, TIMP-1, and TIMP-2 was performed. Choline deficiency was associated with suppressed immunohistochemical expression of MMP-2 and an increased expression of TIMP-2 compared to control, while it had no impact on TIMP-1. MMP-9 expression was decreased without, however, reaching statistical significance. Carnitine did not affect MMP-2, MMP-9, TIMP-1 or TIMP-2 expression. The pattern of TIMP and MMP modulation observed in a choline deficiency setting appears to promote fibrosis. Carnitine, although shown to suppress fibrosis, does not seem to affect MMP-2, MMP-9, TIMP-1 or TIMP-2 expression. Further studies will be required to identify the mechanism underlying the beneficial effects of carnitine.

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Intracardiac expression of markers of endothelial damage/dysfunction, inflammation, thrombosis, and tissue remodeling, and the development of postoperative atrial fibrillation

Cited by 36 publications

References 37 publications

Effects of Radiofrequency Catheter Ablation of Atrial Fibrillation on Soluble P-Selectin, Von Willebrand Factor and IL-6 in the Peripheral and Cardiac Circulation

Effects of Radiofrequency Catheter Ablation of Atrial Fibrillation on Soluble P-Selectin, Von Willebrand Factor and IL-6 in the Peripheral and Cardiac Circulation

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Immunohistochemical determination of the extracellular matrix modulation in a rat model of choline‐deprived myocardium: the effects of carnitine

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