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Unlabelled: Atherosclerosis is a permanently progressive chronic inflammatory disorder which nuclear factor kappaKB (NFkappaB) is involved. Therefore NFkappaB has become integral aspect of atherogenesis and its complications., The Aim of the Study: Estimation of genes expression involved in NFkappaB signaling pathway and separation genes differentiate patients with acute myocardial infarction from healthy subjects., Material and Methods: The examination was assess using the Affymetrix HG-U133A oligonucleotide microarray. Differentiating genes were determined using Bland-Altman graph analysis. Patients wasn't treated due to cardiac diseases before. All patients were subjected to 12-lead ECG, 2-D echocardiography, coronarography and laboratory studies including cardiac troponin, CK and CK-MB. The healthy individuals were subjected to coronarography and computed tomography (calcium score)--coronary artery disease was out of the question., Results: Hierarchical clusterization has demonstrated that the genes expression of patients with acute myocardial infarction was different from healthy individuals. It also demonstrated that the individual groups are homogeneous, especially the group of patients with acute myocardial infarction, regardless of diagnosis, number of risk factors and progression of coronary artery disease. Further Bland-Altman graph analysis showed three important differentiating genes: TLR2, TNFRSF1A i IKBKAP., Conclusions: Our results confirmed the share of genes involved in NFkappaB signaling pathway in acute complications of atherosclerosis. Noticed differences in genes expression of patients with acute myocardial infarction and healthy subjects can show important role isolated differentiating genes in destabilization of atherogenic plaque and acute myocardial infarction occurrence.

The pathology of cardiomyocyte death during and after myocardial infarction involves both necrosis and apoptosis. Although both mechanisms lead to cell death, participation of apoptosis in this process carries the potential of developing therapies influencing at least part of the population of dying cells. Therefore the aim of this study was to determine (using oligonucleotide microarrays) expression profiles of apoptosis-regulating genes in postinfarction myocardium, comparing chronically ischemic and healthy heart muscle. Tissue samples were obtained during elective surgery from the right cardiac auricles of three patients. The expression of 141 genes involved in fibrosis was assessed using the Affymetrix HG_U133A microarray. The patients' transcriptomes were compared using hierarchical clusterization. Differentiating genes were determined using regression analysis and Bland-Altman graph analysis. Hierarchical clusterization demonstrated that the profile of gene expression in postinfarction myocardium was different from that in the remaining specimens. Further statistical analysis showed two important differentiating genes: FOXO3A (underexpressed in post-MI sample) and CFLAR (overexpressed in post-MI sample). The expression of apoptosis-regulating genes is significantly different in post-MI myocardium from chronically ischemic and a nonischemic myocardium. Our results suggest that CFLAR is important in the induction of apoptosis in postinfarction cardiac tissue.

Unlabelled: Atherosclerosis is regarded as a chronic disease. Because of its progressive character the most advanced cases of atherosclerosis are expected to be found in elderly population., Aim of the Study: We decided to take a closer look at a population of patients above 80 years of age who were admitted to our Center because of ACS., Material and Methods: Included in our study were 50 consecutive cases of patients admitted with less than 12-hour history of symptoms of ACS . Their age ranged from 80 to 93 years with a mean of 82 years. All patients were subjected to: complete history and physical examination, 12-lead ECG, 2-D Echocardiography and laboratory studies including CPK, CK-MB, lipid profile, glucose and creatinine level. In the researched group 44 patients underwent coronary angiography and 32 of them required PTCA. Six patients in the group managed with invasive studies subsequently expired. Patients were analyzed in respect to: infarct site, coronary vessel lesion localization, cardiac enzymes levels, LV ejection fraction and renal insufficiency. We also compared groups with ST segment elevations, NSTEMI and unstable angina. Separately analysis of a group of deceased patients was conducted., Results: Six of our patients expired. Their mean age was higher than of the whole group. They also presented with significantly higher levels of cardiac enzymes. In majority of cases right coronary artery occlusion was found to be the culprit lesion., Conclusion: Therefore, in complicated cases of elderly with multi-vessel atherosclerotic changes not qualifying for surgical revascularisation attempts to improve blood supply in the territory of the RCA might be considered.

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 beta (TGFbeta) 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 TGFbeta 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 TGFbeta 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 TGFbeta gene expression compared to control (2789+/-418 c/microg vs. 20262+/-2548 c/microg; p<0.001, and 3390+/-518 c/microg vs. 20262+/-2548 c/microg; p<0.001, respectively), as well as noticeably lower transcriptional activity of genes encoding its type I (3295+/-447 c/microg vs. 12859+/-1929 c/microg; p<0.001, and 3258+/-721 c/microg vs. 12859+/-1929 c/microg; p<0.01, respectively) and type II receptors (2364+/-346 c/microg vs. 19003+/-2357 c/microg; p<0.001, and 2680+/-522 c/microg vs. 19003+/-2357 c/microg; 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 TGFbeta in patients with ACS is at least partly due altered transcriptional activity of genes encoding both TGFbeta and its receptors, what may be responsible for the evolution of atherosclerotic lesions.

Myocardial infarction (MI) is the direct cause of 40% of all deaths, independently of the high standard of medical treatment. The main aim of the study was to define the relationship between the declarative health model (declarations) and the real health activity of the sufferers (realization). The research was performed on 107 patients after acute MI, hospitalized in the Cardiology Department Medical University of Silesia. They were questioned in direct interviews. In addition, the modified form of Shalit's circle was applied. The results indicated the coexistence of two health models of patients. In declarations, there is a model of person with interior attribution of MI (90.65%) that has a feeling of ability to influence his/her health (e.g. through the lifestyle: 63.55%; an individual's character: 41.12%). In realization, there is a model of sick patient with exterior attribution of heart attack (e.g. political and economic crisis, innate predisposition). A similar tendency in the perception of health factors and planning of changes after MI was observed. For instance, 50.47% patients talked about "the increase caution" or "slowing down" as a new planned form of activity. Moreover, of 92% patients who have the social support only 33.64% consider that as an important factor for health. The results suggest a divergence between declarations and real health activity. The launched health model of beliefs seems to be too costly and not attractive enough. Taking into consideration the complete risk factors in MI and making the proposed health belief system more accessible seem to be essential for creating an adequate prevention program.

Background: Reperfusion therapy reduces mortality rate in patients with acute myocardial infarction with ST-segment elevation (STEMI)., Aim: The aim of the study was to access the early outcome of patiens (pts) with STEMI admitted to Upper Silesian Cardiology Centre in 2002., Methods: 957 pts with AMI were enrolled into the study. The influence of several factors on in-hospital mortality was analised., Results: Out of 957 pts 51 died during hospitalization (5,3%). Coronary angiography was performed in 98,0% of pts. Primary PTCA was performed in 94,5% of pts. Stents were implanted in 85,9% of patients who underwent PTCA. The following factors significantly contributed to increased mortality among pts with acute myocardial infarction: female sex (p<0,02), multivessel disease (p<0,05), age above 65 yrs (p<0,001), time from the onset of chest pain above 6 hours (p<0,01) and 12 hours (p<0,001). The use of GP IIB/IIIA inhibitors significantly reduced the mortality rate (p<0,05). Cardiogenic shock was the only independent factor of the increased risk of mortality in multivariate regression analysis (p<0,0001) with relative risk of death (RR 33,5). The mortality rate in pts with shock was 40,2%: 70,8% in case of conservative treatment, 70% in the group of failed PTCA and only 17,2% in the group of successful PTCA. Among pts who underwent primary PTCA the failure to restore coronary blood flow of the infarct related artery contributed to increased relative risk of death (RR 14,5) (p<0,001). Stents improved the survival rate (p<0,01). In PTCA group cardiogenic shock and failed PTCA were independent risk factors in multivariate regression analysis., Conclusions: The results of our study show low rate of in-hospital mortality in pts without cardiogenic shock (1,2%). PTCA is highly successful method of treatment of pts with shock with mortality rate 17,2% in pts who underwent successful procedure.

Introduction: Angiopoietin-2 (Ang-2) is a novel marker of coronary artery disease (CAD) and diabetes (DM). The aim was to evaluate Ang-2 as a potential new biomarker of non-ST elevation myocardial infarction (NSTEMI) in patients with or without type 2 DM (T2DM).Material and methods: This was a multi-center, prospective study that included 138 (males: 91/66%) consecutive patients hospitalized due to NSTEMI, T2DM, or different cardiac disorders. The subjects were divided into four study groups: group A: 28 patients with NSTEMI and T2DM; group B: 47 patients with NSTEMI without T2DM; group C: 31 patients with T2DM, without a history of CAD; group D: 32 patients as a control group. Patients with NSTEMI underwent urgent coronarography. Clinical characteristics including biomarkers (hs-CRP, hsTnT, NT-proBNP, VEGF, HbA1c), SYNTAX SCORE, type of intervention (PCI vs. CABG), and number of implanted stents were taken into account in the analysis.Results: Serum Ang-2 concentrations were significantly higher in patients with NSTEMI (group A: 1769 pg/ml; group B: 1757 pg/ml) and patients with T2DM (group C: 1993 pg/ml) as compared to the patients without CAD and without T2DM (group D: 866.8 pg/ml; p < 0.05). The prognostic accuracy of Ang-2 in NSTEMI diagnosis was determined with the area under the ROC curve (area under curve (AUC) = 0.63).Conclusions: Angiopoietin-2 serum concentration is elevated in the presence of NSTEMI in patients with and without T2DM and does not correspond to the degree of myocardial injury and hemodynamic status. Ang-2 remains elevated also in patients with T2DM without a history of CAD. [ABSTRACT FROM AUTHOR]

Abstract: Matrix metalloproteinases (MMPs) are an expanding group of proteolytic enzymes that participate in numerous physiological and pathological processes including embryogenesis, connective tissue turn-over, healing, angiogenesis, etc. Disturbances in matrixin activity are observed in carcinogenesis, some degenerative processes, and in inflammation, including atherogenesis. The role of matrixins in the pathology of the cardiovascular system seems to be particularly important in two processes: (1) atherosclerotic plaque development and rupture (leading to an acute coronary event) and (2) post-infarction remodeling of myocardium, leading to heart failure. The purpose of this paper is to gather and summarize information about the role of MMPs in acute coronary syndromes (ACS), in both the processes leading to coronary artery occlusion and the “myocardial consequence” of this event. In addition, some benefits and disadvantages of pharmacological intervention into this enzymatic network will be addressed. [Copyright &y& Elsevier]

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]