Expression of Cytokine and Adhesion Molecule mRNA in Atherectomy Specimens From Patients With Coronary Artery Disease

Ishibashi, Toshiyuki; Kijima, Mikihiro; Yokoyama, Keiko; Shindo, Joji; Nagata, Kenji; Hirosaka, Akira; Techigawara, Masaaki; Abe, Yukihiko; Satô, Eiichi; Yamaguchi, Naohito; Watanabe, Nozomi; Saito, Tomiyoshi; Maehara, Kazuhira; Ohmoto, Yasukazu; Maruyama, Yukio

doi:10.1253/jcj.63.249

Cited by 14 publications

(7 citation statements)

References 24 publications

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“…These inflammatory cells may then continue to drive inflammation locally through the release of inflammatory cytokines such as IL-1, TNFα, IL-6 and CD40 ligand [45,46]. Indeed, atherectomy specimens of patients with ACS have higher m-RNA levels of inflammatory cytokines and adhesion molecules compared with patients with stable CAD [47]. The changes associated with a perturbed endothelium are shown in Figure 1B.…”

Section: The Endothelial Response In Acsmentioning

confidence: 99%

Pathological Changes in Acute Coronary Syndromes: The Role of Statin Therapy in the Modulation of Inflammation, Endothelial Function and Coagulation

Ray

Cannon

2004

J Thromb Thrombolysis

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Considerable progress has been made in our understanding of the pathophysiology of coronary artery disease (CAD), their acute presentations as acute coronary syndromes (ACS) and the role of LDL cholesterol. In particular there is clear evidence that atherosclerosis is far from being a process that leads to an amorphous flow limiting lesion on an angiogram, but rather involves a complex interplay between the endothelium, inflammatory cells and the coagulation cascade occurring throughout the coronary vascular bed. While a culprit flow limiting lesion may be effectively treated by a drug eluting stent or coronary bypass surgery, this will have little impact on the global molecular processes that determine recurrent plaque instability at non-culprit sites. The search for systemic long term therapy, which is safe and effective and reduces the changes in inflammation, endothelial function and thrombosis that are the hallmark of ACS, has pushed statins to the forefront. A number of recent clinical trials have shown the benefits of early statin therapy in the treatment of ACS. In addition to their effects on LDL cholesterol, statins have a number of properties collectively referred to as pleiotropic effects, which enable them to modulate the adverse biological changes that are associated with ACS. The purpose of this review is to acquaint the reader with the biological changes that accompany ACS, highlight how these pathways may be modulated for clinical benefit by statins and identify potential novel targets for future therapy.

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Section: The Endothelial Response In Acsmentioning

confidence: 99%

Pathological Changes in Acute Coronary Syndromes: The Role of Statin Therapy in the Modulation of Inflammation, Endothelial Function and Coagulation

Ray

Cannon

2004

J Thromb Thrombolysis

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“…IL‐1 is known to be upregulated in the endothelium of patients with atherosclerosis, and in particular ACS [10,11]. Hence the endothelium of patients carrying the *2 allele may be more vulnerable to an IL‐1‐based inflammatory stimulus, which may result in greater endothelial activation, as these cells possess less intrinsic anti‐inflammatory capacity.…”

Section: Introductionmentioning

confidence: 99%

A potential pharmacogenomic strategy for anticoagulant treatment in non‐ST elevation acute coronary syndromes: the role of interleukin‐1 receptor antagonist genotype

Ray

Francis

Crossman

2005

Journal of Thrombosis and Haemostasis

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To cite this article: Ray KK, Francis S, Crossman DC. A potential pharmacogenomic strategy for anticoagulant treatment in non-ST elevation acute coronary syndromes: the role of interleukin-1 receptor antagonist genotype. J Thromb Haemost 2005; 3: 287-91.Summary. Objectives: Our aim was to determine a pharmacogenomic approach to heparin use in non-ST elevation acute coronary syndromes, specifically the impact of interleukin (IL)-1 receptor antagonist polymorphisms upon von Willebrand factor (vWF) responses to unfractionated heparin (UFH) and low molecular weight heparin (LMWH). Background: In acute coronary syndromes (ACS), identification of specific biological or genetic targets to direct pharmacological treatment remains a challenge. vWF has been shown to predict future cardiovascular risk and the response to anticoagulant treatments during non-ST elevation ACS. IL-1 receptor antagonist (IL-1RN) polymorphisms predict the change in vWF between 24 and 48 h (D vWF) during non-ST elevation ACS. Methods: We genotyped at the IL-1 locus, 67 patients with non-ST elevation ACS who received either LMWH or UFH, and measured vWF levels at 24 and 48 h. Results: LMWH was superior to UFH in reducing the rise in vWF between 24 and 48 h in the cohort as a whole. However, when patients were stratified by IL-1RN genotype, LMWH was superior to UFH in reducing D vWF only in allele *2 carriers (0.51 iU mL )1 vs. 1.37, P < 0.01), but not in non-carriers () 0.03 iU mL )1 vs. 0.15, P ¼ NS). Conclusion: IL-1RN genotype may be a useful marker to identify patients that benefit from LMWH in non-ST elevation ACS.

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“…The surface of all myocardial cells undergoes modification as a result of expression of adhesion molecules. Adhesion molecules are expressed at the border between the endothelium and necrotic cardiomyocytes, both on the surface of the endothelium as well as in the plasma, as soluble adhesion molecules [6]. Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is also expressed on endothelial cells.…”

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confidence: 99%

Role of complement factors and their inhibitors in the myocardial infarction

Ilczuk

Wasiutyński²

2013

cejoi

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Cardiovascular diseases and ischemic heart disease in particular with its extreme form -myocardial infarction, are responsible for approximately 40% of deaths in Poland and worldwide and therefore constitute one of the main problems of contemporary medicine. Despite widespread information, e.g. in the media, and multiple scientific publications, many aspects of these disorders remain unclear. Multiple factors can exacerbate ischemic heart disease, resulting in myocardial infarction: complete occlusion of an artery by a clot resulting from a ruptured atherosclerotic plaque [1]; an embolus originating from thrombi formed on the left ventricular valves; sudden increase of myocardial oxygen demand with coexisting impairment of coronary reserve; arteritis [2,3]. At the current stage of development of biomedical sciences, the disease progression is thought to be modulated by multiple immunological, biochemical and biophysical factors determined by genetic and environmental circumstances [4].Damage of the barrier between cardiomyocyte cytoplasm and extracellular environment resulting from ischemia is an important factor for the involvement of immunological mechanisms. Synthesis of ATP that is required for preservation of integrity of the cellular membrane and lysosomal membranes, is reduced, resulting in sarcolemmal damage. The mechanism of ionic exchange is disturbed, what results in inhibition of metabolite removal with subsequent accumulation of lactate, phosphate, ammonium and sodium ions in the cardiomyocytes. Increased osmotic pressure results in edema and cardiomyocyte rupture. Increased sarcolemmal permeability is also caused by the presence of superoxide and hydroxyl free radicals in higher amounts in the ischemic myocardium with simultaneous reduction of contents of inactivators [5]. The surface of all myocardial cells undergoes modification as a result of expression of adhesion molecules. Adhesion molecules are expressed at the border between the endothelium and necrotic cardiomyocytes, both on the surface of the endothelium as well as in the plasma, as soluble adhesion molecules [6]. Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is also expressed on endothelial cells. These molecules are located on side surfaces of endothelial cells but also exist on peripheral blood

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Expression of Cytokine and Adhesion Molecule mRNA in Atherectomy Specimens From Patients With Coronary Artery Disease

Cited by 14 publications

References 24 publications

Pathological Changes in Acute Coronary Syndromes: The Role of Statin Therapy in the Modulation of Inflammation, Endothelial Function and Coagulation

Pathological Changes in Acute Coronary Syndromes: The Role of Statin Therapy in the Modulation of Inflammation, Endothelial Function and Coagulation

A potential pharmacogenomic strategy for anticoagulant treatment in non‐ST elevation acute coronary syndromes: the role of interleukin‐1 receptor antagonist genotype

Role of complement factors and their inhibitors in the myocardial infarction

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