ABSTRACT
BACKGROUND: Inflammation plays a critical role in all stages of atherogenesis, including plaque destabilization leading to the rupture and local thrombosis, clinically manifested as unstable angina (UA) or myocardial infarction (MI). Recent data report enhanced expression of numerous pro-inflammatory genes in patients with acute coronary syndrome (ACS) both in plaque and in inflammatory cells. Kinins are peptides involved in vasodilation, vascular permeability, pain and inflammation. Their effects are mediated by two receptors, B1 and B2. As the role of kinins in ACS is not clear, the aim of the study was to assess the expression of the genes encoding kinin receptors in patients with ACS. METHODS: The study was carried out on 40 patients with ACS and 10 age-matched healthy subjects (control (C)). To evaluate gene expression of B1 and B2 kinin receptors, total mRNA was extracted from peripheral blood mononuclear cells and the number of mRNA copies was assessed by quantitative reverse transcriptase-polymerase chain reaction. RESULTS: In patients with MI and UA, the B1 receptor (B1R)/B2 receptor (B2R) ratio was inversed compared with healthy subjects (C group) (MI vs C: 1.54 +/- 0.39 vs 0.36 +/- 0.04; P < 0.01; UA vs C: 2.13 +/- 0.98 vs 0.36 +/- 0.04; P < 0.05 respectively). B2R gene mRNA level was markedly lower in MI group versus C group (24 216 +/- 5409 copies/microg vs 39 908 +/- 5309 copies/microg; P < 0.05). The difference in B1R gene expression between MI and C group was negligible. We have not observed differences in studied genes expression between UA and C groups. CONCLUSION: Patients with ACS show inverted B1R/B2R ratio. Such disturbance in kinin signalling may reflect increased activation of circulating mononuclears, which are important participants of atherosclerotic plaque development and eventually rupture.
Subject(s)
Acute Coronary Syndrome/blood , Acute Coronary Syndrome/genetics , Gene Expression Regulation/physiology , Leukocytes, Mononuclear/metabolism , Receptor, Bradykinin B1/biosynthesis , Receptor, Bradykinin B1/genetics , Receptor, Bradykinin B2/biosynthesis , Receptor, Bradykinin B2/genetics , Acute Coronary Syndrome/pathology , Adult , Aged , Female , Humans , Leukocytes, Mononuclear/pathology , Male , Middle Aged , Protein Isoforms/biosynthesis , Protein Isoforms/blood , Protein Isoforms/genetics , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Receptor, Bradykinin B1/blood , Receptor, Bradykinin B2/bloodABSTRACT
The prevalence of coronary artery disease (CAD) and acute coronary syndromes in patients with haemophilia is much lower than in general population and there is a lack of information regarding safe interventional or surgical treatment of CAD in haemophiliacs. This report presents a case of patient with moderate haemophilia A and unstable angina pectoris, who underwent successful coronary angioplasty. The patient was pretreated with factor VIII (before and after the procedure) and the incision site was sealed with vessel closure device. Additionally, the article discusses the issue of the safety of standard, postpercutaneous coronary intervention antiplatelet therapy in patients with haemophilia.
Subject(s)
Angina, Unstable/therapy , Angioplasty, Balloon, Coronary/methods , Coronary Artery Disease/surgery , Hemophilia A/complications , Stents , Angina, Unstable/complications , Anticoagulants/therapeutic use , Coronary Artery Disease/complications , Humans , Male , Middle Aged , Treatment OutcomeABSTRACT
OBJECTIVES: Glucose metabolism disorders usually coexist with dyslipidemia and coagulation/fibrinolysis disturbances. Increase of insulin resistance followed by hyperinsulinemia leads to enhanced protein synthesis, including production of apolipoproteins. As a result, the structure of Low Density Lipoprotein (LDL) becomes small and dense. This augments lipid infiltration into the arterial wall. Following this process monocyte adhesion to endothelium initiates atherosclerotic injury. One of the markers of this inflammatory reaction is Monocyte Chemoattractant Peptide-1 (MCP-1). A lot of inflammatory mediators affect both oxidative modification of LDL and coagulation processes being responsible for anti-fibrinolytic predominance. Plasminogen Activator Inhibitor-1 (PAI-1) is a marker of this state. Therefore the aim of this study is to evaluate the marker of the oxidation processes (oxLDL) as well as prothrombotic (PAI-1) and inflammatory state (MCP-1) markers in patients with Impaired Glucose Tolerance (IGT). METHODS: The study was carried out on 16 subjects: 10 with biochemically confirmed IGT and 6 age-matched healthy persons without such disorders. Following tests were performed: OGTT, HbA(1c) level as well as TCh, HDL, LDL and TG. Plasma concentrations of oxLDL, PAI-1 and MCP-1 were measured using ELISA method. RESULTS: In patients with Impaired Glucose Tolerance plasma levels of oxLDL were significantly higher compared to control group (67.6 +/- 0.9 U/l vs. 57.8 +/- 4.0 U/l; p < 0.01) in spite of LDL levels, which did not reveal such difference. MCP-1 plasma concentration compared to control group occurred to be significantly increased in experimental group as well (156.4 +/- 9.2 ng/ml vs. 125.4 +/- 1.9 ng/ml; p < 0.05). PAI-1 level revealed most significant difference (84.0 +/- 1.8 ng/ml vs. 43.7 +/- 2.7 ng/ml; p < 0.0001). CONCLUSIONS: It is concluded that patients with Impaired Glucose Tolerance should be considered as a group in which atherogenic modification of lipoproteins occurred. Also plasma inflammatory as well as prothrombotic markers concentration was elevated.