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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/μg vs 39 908 ± 5309 copies/μg; 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. [ABSTRACT FROM AUTHOR]

Introduction. Cardiac syndrome X (CSX) is defined by typical chest pain, ST segment depression on ECG and normal coronary angiography. Pathology of CSX may involve microvascular dysfunction related to inflammation and abnormal pain sensitivity. Kinins are labile peptides participating in vasodilation, inflammation and pain. Their effects are mediated by two receptors: B1 and B2. The aim of the study was to assess gene expression of kinin receptors in peripheral blood mononuclear cells (PBMC) from patients with CSX. Methods. The study was carried out in 34 patients with cardiac syndrome X, 13 with unstable angina and ten healthy subjects. Total mRNA was extracted from PBMC and the number of mRNA copies was assessed by quantitive reverse transcriptase polymerase chain reaction. Results and Conclusion. The study showed 7-fold higher transcriptional activity of B1R in CSX vs. control and 3.5 higher vs. UA. B2R expression was 2.5-fold higher in CSX group vs. control and UA, while in the letter two groups it was similar. Such disturbance in kinin signaling may participate in local vasoconstriction and may reflect disturbances in kinin signaling leading to nociceptive disturbances in these patients. [ABSTRACT FROM AUTHOR]

Abstract Background  Cardiac syndrome X is typically characterized by effort induced anginal pain with ST segment depression suggestive of myocardial ischemia and normal coronary arteries at angiography. The possible mechanism that may participate in the pathology of CSX is a microvascular dysfunction related to inflammatory process affecting endothelium. Interferon γ (IFN-γ) is an important cytokine in inflammatory reaction. It acts through its specific receptor composed of 2 subunits IFN-γ R1 (ligand binding) and R2 (signal transduction). The expression and proportion of these subunits influences IFN-γ activity. The aim of the study was to assess the gene expression of IFN-γ and its receptors in peripheral blood mononuclear cells (PBMC) from patients with syndrome X. Methods  The study was carried out in 36 patients aged 44–77 (average 57 years old) with cardiac syndrome X and 23 sex- and age-matched healthy subjects (control group). To evaluate gene expression of IFNγ and its receptor total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitive reverse transcriptase polymerase chain reaction (QRT-PCR). Results  We have not observed statistically significant differences in INFγ gene expression between studied group and control. Genes encoding IFNγ receptor subunits showed higher expression in PBMCs from patients with cardiac syndrome X vs control subjects (IFNγR1, 97,244  26,956 c/μg vs 12,120  2,940 c/μg, p p  Conclusion  Variation in transcriptional activity of genes encoding INF-γ receptor subunits may affect function of microvasculature and thereby participate in the pathology of cardiac syndrome X. [ABSTRACT FROM AUTHOR]

Abstract: Acute coronary syndromes (ACS) are one of the major causes of mortality nowadays. Although much is known about factors involved in atherogenesis and acute coronary events, there are still many cases in which a lack of classical risk factors, together with family history, suggests the presence of an unrevealed genetic predisposition and molecular mechanisms. This paper reviews genetic predisposition to ACS. It also indicates which genes are linked to the processes of destabilization and rupture of atherosclerotic plaque and thus may be potential targets for more effective prophylaxis and treatment. [Copyright &y& Elsevier]

Abstract: Background: Recent data report altered gene expression of numerous pro- and anti-inflammatory factors involved in pathology of acute coronary syndromes (ACS). Transforming growth factor β (TGFβ) signaling is engaged in a wide range of processes. Its effect on vessels seems to be protective due to its anti-inflammatory and anti-atherogenic action. However, it also seems to be engaged in such negative effects as neointima formation and fibrosis. The aim of the study was to assess the expression of the genes encoding TGFβ and its receptors (type I, II, and III) in patients with ACS. Methods: The study was carried out on 24 patients with acute coronary syndrome (7 with unstable angina [UA] and 17 with myocardial infarction [MI]) and 10 age-matched healthy subjects (control). To evaluate gene expression of TGFβ and its receptors total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR). Results: MI and UA patients demonstrated significantly lower TGFβ gene expression compared to control (2789±418 c/μg vs. 20262±2548 c/μg; p <0.001, and 3390±518 c/μg vs. 20262±2548 c/μg; p <0.001, respectively), as well as noticeably lower transcriptional activity of genes encoding its type I (3295±447 c/μg vs. 12859±1929 c/μg; p <0.001, and 3258±721 c/μg vs. 12859±1929 c/μg; p <0.01, respectively) and type II receptors (2364±346 c/μg vs. 19003±2357 c/μg; p <0.001, and 2680±522 c/μg vs. 19003±2357 c/μg; p <0.01, respectively). Also, gene expression of the type III receptor was inferior in the studied group compared to the control, although the difference was significant only for the UA group vs. control. Expressions of the studied genes did not differ between patients with MI and those with UA. Conclusion: Our report shows that the decreased activity of TGFβ in patients with ACS is at least partly due altered transcriptional activity of genes encoding both TGFβ and its receptors, what may be responsible for the evolution of atherosclerotic lesions. [Copyright &y& Elsevier]