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Background: Psoriasis is a common autoimmune disease of unknown etiology. Recently, much attention has been paid to evidence that a local hypercoagulable state is an important contributing factor to the development of inflammatory skin diseases. Thus, the aim of this study was to characterize the local hemostasis in the affected skin of patients with psoriasis., Methods: Skin biopsies of psoriatic plaques were obtained from 73 consecutive patients (48M, 25F, average age 45 years) with at least a one year history of the disease. The studied patients had not received any specific systemic treatment for at least 4 weeks before the biopsy was done. As a control, normal skin biopsies were obtained from 16 healthy subjects. For immunohistological study, the En-Vision method (DAKO EnVision Kit ®/Alkaline Phosphatase detection system), and monoclonal antibodies anti-tissue factor (TF), anti-thrombomodulin (TM) and anti-von Willebrand Factor (vWF) were used. All these molecules were assessed semi-quantitatively in the frozen sections., Results: Clinically, the Body Surface Area index ranged between 1-90% and the Psoriasis Area Severity Index score ranged from 1.6 to 47. Immunohistochemistry revealed redistribution of TF antigens from the upper to lower layers of the epidermis as compared to the control. It was collaborated with the number of TF-positive cells in the psoriatic skin sections (78.3%) as compared with the healthy subjects (34.4%; P<0.001). In addition, TF was uniformly and moderately expressed on capillary endothelial cells of the plaque sections in 43 out of 73 patients (58.9%). As far as the thrombomodulin is concerned, TM was clearly down-regulated and localized mainly in the upper layers of the psoriatic epidermis. It was collaborated with the number of TM positive cells in the psoriatic skin sections (38.9%) as compared with the healthy subjects (66.7%; P<0.001). All capillary vessels found in the biopsy sections were positive for TM and vWF staining, with similar expression (≥2+) in both groups. In the current study, no relationship was found between the TF, TM and vWF expression and the PASI and BAS (NS)., Conclusions: A local procoagulable state found in psoriatic plaques suggests a significant role of local tissue hemostasis in pathogenesis of the disease. These findings indicate another potential target for a therapeutic approach in patients with psoriasis, although further research would help elucidate the exact mechanisms., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Introduction: It is generally accepted that mitochondria are a primary source of intracellular reactive oxygen species (ROS). Under physiological circumstances they are permanently formed as by-products of aerobic metabolism in the mitochondria. To counter the harmful effect of ROS, cells possess an antioxidant defence system to detoxify ROS and avert them from accumulation at high concentrations. Mitochondria-located manganese superoxide dismutase (MnSOD, SOD2) successfully converts superoxide to the less reactive hydrogen peroxide (H 2 O 2 ). To the best of our knowledge, there are no available data regarding immunohistochemical expression of MnSOD in colorectal neoplastic tissues., Aim: To investigate the immunohistochemical expression status of MnSOD in colorectal premalignant and malignant lesions., Material and Methods: This study was performed on resected specimens obtained from 126 patients who had undergone surgical resection for primary sporadic colorectal cancer, and from 114 patients who had undergone colonoscopy at the Municipal Hospital in Jaworzno (Poland). Paraffin-embedded, 4-µm-thick tissue sections were stained for rabbit polyclonal anti SOD2 antibody obtained from GeneTex (clone TF9-10-H10 from America Diagnostica)., Results: Results of our study demonstrated that the development of colorectal cancer is connected with increased expression of MnSOD both in adenoma and adenocarcinoma stages. Samples of adenocarcinoma with G2 and G3 grade showed significantly higher levels of immunohistochemical expression of this antioxidant enzyme. Moreover, patients with the presence of lymphovascular invasion and higher degree of regional lymph node status have been also characterised by higher levels of MnSOD expression. The samples of adenoma have been characterised by higher levels of MnSOD expression in comparison to normal mucosa as well. Interestingly, there was no significant correlation between expression and histological type of adenoma., Conclusions: Development of colorectal cancer is connected with increased expression of MnSOD both in adenoma and adenocarcinoma stages., Competing Interests: The authors declare no conflict of interest.

Notch signalling is an evolutionarily conserved signalling pathway, which plays a significant role in a wide array of cellular processes including proliferation, differentiation, and apoptosis. Nevertheless, it must be noted that Notch is a binary cell fate determinant, and its overexpression has been described as oncogenic in a broad range of human malignancies. This finding led to interest in therapeutically targeting this pathway especially by the use of GSIs, which block the cleavage of Notch at the cell membrane and inhibit release of the transcriptionally active NotchIC subunit. Preclinical cancer models have clearly demonstrated that GSIs suppress the growth of such malignancies as pancreatic, breast, and lung cancer; however, GSI treatment in vivo is associated with side effects, especially those within the gastrointestinal tract. Although intensive studies are associated with the role of γ-secretase in pathological states, it should be pointed out that this complex impacts on proteolytic cleavages of around 55 membrane proteins. Therefore, it is clear that GSIs are highly non-specific and additional drugs must be designed, which will more specifically target components of the Notch signalling.

The Epstein-Barr virus (EBV), also known as human herpesvirus 4, is a member of the Herpesviridae virus family. EBV infection can cause infectious mononucleosis (IM) in the lytic phase of EBV's life cycle. Past EBV infection is associated with lymphomas, and may also result in certain allergic and autoimmune diseases. Although potential mechanisms of autoimmune diseases have not been clearly elucidated, both genetic and environmental factors, such as infectious agents, are considered to be responsible for their development. In addition, EBV modifies the host immune response. The worldwide prevalence of autoimmune diseases shows how common this pathogen is. Normally, the virus stays in the body and remains dormant throughout life. However, this is not always the case, and a serious EBV-related illness may develop later in life. This explains the chronic course of autoimmune diseases that is often accompanied by exacerbations of symptoms. Based on the present studies, EBV infection can cause autoimmune diseases, such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), Sjögren's syndrome, and autoimmune hepatitis. The EBV has also been reported in patients with autoimmune thyroid disorders. Although EBV is not the only agent responsible for the development of autoimmune thyroid diseases, it can be considered a contributory factor.

Background: The "double-faced" effect of nitric oxide (NO) is thought to play an important role in triggering and progression of glaucoma., Material/methods: Iris samples were obtained during iridectomy in 35 patients (mean age of 65.4±5.3 years) with diagnosed primary open-angle glaucoma (POAG). The controls were collected postmortem from 10 donors with a mean age of 62.2±1.9 years. Visual field defects were evaluated by perimetry. The Hodapp-Parrish-Anderson classification was used to divide patients into 3 visual field defect groups. The intraocular pressure was measured 3 times before surgery using applanation tonometry. The phenotype activity of nitric oxide synthase (NOS) isoenzymes (endothelial--eNOS and inducible--iNOS) and expression of nitrotyrosine in iris vasculature was assessed., Results: Significant differences were found between glaucoma patients and the controls in eNOS and iNOS activity (Mann-Whitney test, U=35.5, Z=-2.037, p=0.04 and U=21, Z=2.69, p=0.007, respectively). In addition, the results showed an upregulation of nitrotyrosine in the capillary endothelial cells in the study group, which was associated with the duration of diagnosed glaucoma (R-Spearman of 0.33, p=0.0047) and visual field mean defect MD (R-Spearman of 0.29, p=0.019). Moreover, the activity of nitrotyrosine was significantly correlated with iNOS immunoreactivity (R-Spearman of 0.5, p=0.0001). However, the iNOS activity significantly varied among Hodapp-Parrish-Anderson groups (p=0.03)., Conclusions: Our observations confirmed the association between glaucomatous disturbances and upregulation of iNOS, together with increased nitrotyrosine storage.

Vimentin is an intermediate filament protein normally expressed in cells of mesenchymal origin, e.g. myofibroblasts, chondrocytes, macrophages, and endothelial cells. The expression of vimentin, which has been thought of as the main mesenchymal marker, is also detected in tumour tissue. In tumours of the gastrointestinal tract vimentin expression is usually correlated with advanced stage of tumour, lymph node metastasis, and patient survival.

Snail1 is a zinc-finger transcription factor, which plays a role in colorectal cancer development by silencing E-cadherin expression and inducing epithelialmesenchymal transition (EMT). During EMT tumour cells acquire a mesenchymal phenotype that is responsible for their invasive activities. Consequently, Snail1 expression in colorectal cancer is usually associated with progression and metastasis. Some studies revealed that about 77% of colon cancer samples display Snail1 immunoreactivity both in activated fibroblasts and in carcinoma cells that have undergone EMT. Therefore, expression of this factor in the stroma may indicate how many cells possess the abilities to escape from the primary tumour mass, invade the basal lamina and colonise distant target organs. Blocking snail proteins activity has the potential to avert cancer cell metastasis by interfering with such cellular processes as remodelling of the actin cytoskeleton, migration and invasion, which are clearly associated with the aggressive phenotype of the disease. Moreover, the link between factors from the snail family and cancer stem cells suggests that inhibitory agents may also prove their potency as inhibitors of cancer recurrence.

Aim: The aim of this study was to assess the relationship between late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR) and immunohistochemical markers of inflammation in patients with heart failure and a reduced ejection fraction (HFrEF)., Material and Methods: Endomyocardial biopsy and CMR were performed in 38 consecutive patients (24 males, average age 43.2 ± 6.9 years, New York Heart Association [NYHA] class II) with HFrEF and suspected myocarditis. The immunohistochemical evaluation was done by the En-Vision system using DAKO monoclonal antibodies. The presence of > 14 infiltrating cells together with myocardial damage and ≥ 2 + up-regulation of HLA class II was considered diagnostic for myocarditis. The results of LGE were compared with the immunohistochemical markers of inflammation. All patients underwent coronary angiography., Results: Twelve out of 38 (31.6%) patients met the immunohistological criteria for the diagnosis of myocarditis. Late gadolinium enhancement was present in 23 of 38 (60.5%) patients, mostly at the interventricular septum. No correlation was found between LGE and immunohistochemistry results (Kendall's tau; r = 0.21, p = 0.09)., Conclusions: Our study revealed no significant relationship between LGE cardiovascular magnetic resonance imaging and immunohistochemical markers of inflammation in patients with HFrEF.

Background: Previous reports have indicated the role of endothelium disturbances, as expressed by von Willebrand factor (vWF) release, in pathophysiology of glaucoma. The objective of this study was to investigate the vWF expression in iris vasculature of patients with primary open-angle glaucoma (POAG)., Material and Methods: Immunohistochemistry of vWF expression was performed on cryostat sections of samples collected at the time of peripheral iridectomy and controls collected from dead donors., Results: Twenty-seven Caucasians age 66.6±3.7 with 5.8±3.7-year history of treated PAOG and 10 controls age 62.2±1.92 with no history of glaucoma. The percentage of patients who presented normal and up-regulation of vWF phenotype expression differed statistically between examined and control groups: 48% versus 100% (p=0.035, chi-square test with Yates' correction). Sex, age, glaucoma duration, and visual field quantitative indices had no impact on vWF expression. A significant correlation between mean pre-surgery intraocular pressure and vWF expression was found (Spearman r=0.42, p=0.03)., Conclusions: Considering the results, it may be suggested that vWF is actively involved in the pathophysiology of glaucoma.

Introduction: Despite advances in medicine, chronic heart failure (CHF) still remains a significant clinical problem associated with poor outcome., Aim of the Study: To determine risk factors for major adverse cardiac events (MACE) in three-year follow-up in patients with CHF of nonischemic etiology., Material and Methods: The prospective study included consecutive hospitalized patients with stable CHF (LVEDD > 57 mm; LVEF < 40%) and symptom duration > 6 months. Study exclusion criteria were: serious neurological and/or psychiatric diseases, stenoses in epicardial coronary arteries in coronarography, active myocarditis confirmed by myocardial biopsy, diseases of the respiratory system with pulmonary hypertension, presence of heart defects, neoplastic or connective tissue disease, documented infectious diseases at least three months before inclusion in the study, diabetes, liver cirrhosis, chronic kidney disease (eGFR < 30 ml/min/1.73 m(2)), alcoholism, planned heart transplantation. Depression severity was assessed with the Beck and the Hamilton Scales. Depression was diagnosed based on the ICD-10 criteria. Clinical follow-up began on admission and lasted three years., Results: The analysis encompassed 199 patients aged 49 (41-54), who met the inclusion/exclusion criteria. Depression was diagnosed in 30% of the patients. Independent factors increasing the risk of MACE (death, transplantation, ventricular assist device, hospitalization) were: depression (HR: 2.26; p < 0.001), E/A index (HR: 1.31; p < 0.01), right ventricular dimension (HR: 1.06; p < 0.01), hsCRP level (HR: 1.06; p < 0.01) and alkaline phosphatase activity in blood serum (HR: 1.01; p < 0.05)., Conclusions: Factors affecting 3-year outcome are: depression, right ventricular dimension, the E/A index, alkaline phosphatase activity and the level of high-sensitivity C-reactive protein (hs-CRP).

Gastric cancer is one of the most common cancers in the world. More than 95% of gastric cancers are adenocarcinomas originating from the glandular epithelium of the stomach lining. Unfortunately, a large number of patients are diagnosed when the tumour is at unresectable stage. Therefore, it is very important to understand the mechanisms involved in gastric cancer pathogenesis. One of them is angiogenesis, which means the formation of new blood vessels from pre-existing vasculature. This process is dependent on interactions between the tumour and surrounding stromal cells which create the tumour microenvironment. Moreover, both tumour and stromal cells release a wide array of angiogenic factors that have an influence on endothelial cell recruitment and thus affect the process of angiogenesis. In this paper we discuss the role of tumour microenvironment in gastric cancer angiogenesis.

Notch signaling pathway is activated dynamically during evolution playing significant role in cell fate determination and differentiation. It has been known that alterations of this pathway may lead to human malignancies, including gastric cancer. Despite a decline in the overall incidence, this disease still remains an important global health problem. Therefore, a better understanding of the molecular alterations underlying gastric cancer may contribute to the development of rationally designed molecular targeted therapies. It has been reported that Notch1 receptor could become a prognostic marker of gastric cancer and novel target for gastric cancer therapy. Among the novel and targeted approaches for the treatment of gastric cancer is also the process of Notch receptors regulation by specific microRNA. γ-secretase inhibitors are also taken into consideration.

Inflammatory bowel disease (IBD) is characterized by a chronic inflammation accompanied by procoagulation settings. However, tissue hemostasis in IBD patients was only incidentally reported. Accordingly, the current study characterizes changes in tissue hemostasis components in a colon inflammatory setting. Serial cryostat sections of endoscopic mucosal biopsy specimens taken from 26 consecutive IBD patients diagnosed de novo and normal colon resection specimens taken from 6 patients were immunohistochemically stained with monoclonal anti-human tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombomodulin (TM), as well as CD3 and CD68 positive cells. The hemostatic components studied differed significantly from the control subjects. Up-regulation predominated in the case of TF while down-regulation was mainly found in TM and TFPI in IBD. In the control sections, TF was observed in a few fibroblast-shaped cells in the lamina propria, while in the majority of IBD sections, TF positively stained small microvessels, infiltrating mononuclear cells and fibroblast-shaped cells tightly surrounding the colon crypts. Thrombomodulin intensively stained the endothelium of the small capillary vessels in the control, whereas such staining mainly accompanied infiltrating mononuclear cells of the IBD subjects. Tissue factor pathway inhibitor positively stained the endothelium of the small capillary vessels in the control group, whereas in the IBD group endothelial cells presented only weak TFPI staining. The mean number of CD3-positive lymphocytes in IBD was 23.3 ± 14.3, but the mean number of CD68-positive cells was 114.5 ± 55.8. In the control sections, it was 4.1 ± 2.4 and 39.6 ± 17.9, respectively. There was no relationship between CD3 and CD68 (+) cells and the hemostasis markers studied. The results of the current study indicate a shift of tissue hemostasis toward the procoagulant state irrespective of the severity of inflammatory infiltration. In addition, TF distribution in the colon sections of IBD patients may indicate a role in the restoration of the barrier function in injured intestinal mucosa., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

In this review we try to answer the question whether and to what degree contemporary forensic pathology takes advantage of quantitative and qualitative troponin determinations. The report is simultaneously an introduction to discussing our results in this area. To perform this review we used the database "PubMed". Polish literature, concurrent with the objective of the study and not included in "PubMed" or included in "OLDMEDLINE" was also analyzed. The identified publications, which were concurrent with the aim of the study, were read and citations were checked. If among the cited papers we found one that was concurrent with the subject of the review, it was also included. While several studies support the use of post-mortem blood and body fluid levels of cardiac troponin T and I as a marker of sudden cardiac death, in our opinion, further research is required to determine the effects of post-mortem autolysis, microbial activity, metabolic derangement and the use of different sample matrices in autopsy cases.

Introduction: We determined retrospective analysis of the diagnostic value of virus serology in patients with non-ischemic systolic heart failure and parvovirus B19 infection., Material and Methods: Virus serology and endomyocardial biopsy were performed in 31 patients with non-ischemic systolic heart failure hospitalized from 2001 to 2006 in our clinic., Results: The serum specimens from 31 patients were tested for IgM and IgG antibody against parvovirus B19. IgM antibodies were identified in 3 patients and IgG antibodies were identified in 23 patients. All of the patients underwent endomyocardial biopsy which revealed chronic active myocarditis in 10 patients (32.4%), chronic persistent myocarditis in 14 patients (45.1%) and no myocarditis in 7 patients (22.5%)., Conclusions: Virus serology has no relevance for the diagnosis of non-ischemic systolic heart failure caused by parvovirus B19 infection. The result of serological tests are positive more frequently than the biopsy specimens results.

Inflammatory cytokines have an important role in the pathogenesis of myocarditis, but still little is known about the importance of interferon gamma (IFNg) in this disease. The aim of the study was to evaluate the prognostic value of the initial transcriptional activity of IFNg and two subunits of its receptor as measured with the use of QRT-PCR and SYBRGreen chemistry in the group of 63 patients with clinically confirmed myocarditis who were treated with statin or immunosupressive therapy. The initial values of IFNg and the ratio of IFNgRb/IFNgRa were statistically different in the analyzed group of patients. The prognostic value of IFNg and IFNgRb/IFNgRa was determined by logistic regression analysis.

Background: Renal ischaemia resulting from stenosis of the renal artery may result in two important sequelae: systemic arterial hypertension, and renal atrophy and nephron loss, resulting in an increased risk of progression to end-stage renal disease. Renal artery stenosis (RAS) may lead to both renovascular hypertension and ischaemic nephropathy - a potentially curable cause of renal failure., Aim: To assess the efficacy of g-intraluminal brachytherapy (ILBT) in prevention of restenosis after percutaneous transluminal renal artery angioplasty (PTRA) and the effects of this method of revascularisation on renal function., Methods: 71 patients aged 52+/-8 years with refractory renovascular hypertension were randomised to group I (PTRA + ILBT) or group II (PTRA). Both baseline and 9-month follow-up angiography, intra-vascular ultrasound and non-invasive examination were performed to assess the efficacy of PTRA on renal function., Results: The overall PTRA success rate was 87%: 33 patients from group I and 29 from group II underwent a successful procedure. A decrease of serum creatinine level was observed regardless of the treatment modality, directly after angioplasty: 20 micromol/l (17.5%) in group I and 26 micromol/l (22%) in group II (NS). Also in long-term follow-up this effect was sustained: 18 micromol/l (15.8%) in group I and 10 micromol/l (8.5%) in group II (NS). In the follow-up period a non-significant increase of serum creatinine level was observed in group I (from 94+/-19 to 96+/-25 micromol/l, NS). In group II the increase of serum creatinine level was significantly higher (from 92+/-39 micromol/l to 108+/-60 micromol/l, p=0.001)., Conclusions: PTRA improves renal function in patients with ischaemic nephropathy. In long-term observation the positive effect of PTRA on renal function is especially visible in patients with ILBT after PTRA.

Objectives: The long-term prognosis and predictors of adverse cardiac events in hypertension-related chronic systolic heart failure (CHF) remain uncertain. Therefore, we sought to determine the major adverse cardiac events (MACE) in this group of patients., Patients and Methods: One hundred and thirty two patients (83% males, age 48.6 +/- 8.2 years) in NYHA class II and III with hypertension-related chronic CHF were prospectively evaluated for three years. Hypertension was defined as blood pressure > or = 140/90 mmHg documented clinically twice for at least 5 years before the onset of CHF symptoms. All patients underwent coronary angiography to exclude coronary artery disease as a cause of CHF. Analysis of predictors of MACE (death, urgent heart transplantation and re-admission to the hospital due to CHF progression) during the 3 years of follow up was performed., Results: After follow up the frequency of MACE was 41.7%. The independent predictors of MACE occurrence were as follows: the symptoms of depression [hazard ratio (HR) 2.58 (95% CI 1.44-4.63, p < 0.01)], end-diastolic diameter of the right ventricular (EDDRV) [HR 1.07 (95% CI 1.02-1.12, p < 0.01)] and D-dimers [HR 2.24 (95% CI 1.08-4.67, p < 0.05)]. To define optimal prognostic accuracy of EDDRV and D-dimers the receiver operating characteristics curve analysis was performed. The cut-off for EDDRV was 28 mm (sensitivity 50%, specificity 67.6%, area under curve [AUC] 0.64, p < 0.01) and for D-dimers 0.23 microg/ml, (sensitivity 58%, specificity 64.2%, AUC 0.62, p < 0.05)., Conclusions: In analysed group the symptoms of depression, higher baseline right ventricular diastolic diameter and higher baseline D-dimers level were independent predictors of MACE.

Objectives: The aim of the study was to evaluate the occurence of death and major adverse cardiac events (MACE) in patients with normal (group A) and elevated (group B) plasma bilirubin levels., Patients and Methods: We evaluated 124 patients (83% males, mean age 50.1 +/- 7.7 yrs) in New York Heart Association class II and III with hypertension-related chronic heart failure. We assessed the occurence of death and MACE (death, urgent heart transplantation and readmission to hospital)., Results: Groups A and B comprised 77 and 47 patients respectively. The independent predictors of death in group B were: N-terminal pro-brain natriuretic peptide (NT-proBNP) level (per 100 pg/ml difference; 95% CI: 1.29-4.76; p = 0.005) and physical component summary score (per 10 point difference; 95% CI: 0.66-0.99; p = 0.03). The independent predictors of MACE in group B were: age (per 10 yrs; 95% CI: 0.1-1.8; p = 0.04), NT-proBNP level (per 100 pg/ml difference; 95% CI: 1.02-3.69; p = 0.04) and the symptoms of depression (95% CI: 1.02-2.5; p = 0.01). The independent predictors of MACE in group A were: NT-proBNP level (per 100 pg/ml difference; 95% CI: 1.31-5.32; p = 0.006) and mental component summary (per 10 point difference; 95% CI: 0.85-0.98; p = 0.01). In a two-year follow-up the death rate was 5.2% in group A, and 23.4% in group B (p = 0.002) and frequency of MACE 18.2% and 42.6% in group A and B (p = 0.003), respectively., Conclusions: Elevated bilirubin levels are associated with higher incidence of death and MACE during a two-year follow-up in patients with hypertension-related chronic heart failure. Thus, it may be used as a simple prognostic factor in such of patients.

Unlabelled: We aimed at assessing the frequency of death, myocardial infarction, unstable angina, repeat revascularization, cardiovascular hospitalisation during 12 months in patients assigned to early invasive strategy., Material and Method: We analysed 658 consecutive patients with acute coronary syndrome (ACS) without ST-segment elevation hospitalized between January 2000 and February 2003. Patients had to fulfill the following criteria: 1) rest angina within 24 hours prior to admission, 2) at least one of the following: ST-segment depression (> or = 0,05 mV), transient (< 20 min) ST-segment elevation (> or = 0,05 mV), T-wave inversion (> or = 1 mV) in at least 2 contiguous leads, positive serum cardiac markers., Results: All patients underwent coronary angiography followed by PCI (percutaneous coronary interventions) in 71.8% of patients. 18.2% were assigned to CABG (coronary artery bypass graft) and 8.7% of patients were treated conservatively. 1.3% of patients underwent PCI followed by an elective CABG surgery. In-hospital mortality rate was.,3%. 3.3% patients died after hospital discharge. The frequency of myocardial infarction, unstable angina and repeat PCI at 12 months was 2.1%, 16.8% and 11.5% respectively. The rate of cardiovascular hospitalisation was 15.6%. Multivariate analysis identified two independent predictors ofdeath: diabetes mellitus (OR: 7.02, 95% CI: 1.5-13.8, p = 0.03) and heart failure (OR: 12.6, 95% CI: 2.86-16.6 p = 0.005)., Conclusions: Early invasive strategy in analysed group yields good long-term outcomes with low rate of adverse ischemic events. Independent predictors of deaths were diabetes mellitus and heart failure.

Background: Early invasive strategy is one of alternative methods for management of acute coronary syndromes (ACS) without persistent ST-segment elevation., Hypothesis: The aim of the study was analysis of clinical characteristics, in-hospital outcome and factors of in-hospital mortality., Methods: The study group comprised 853 patients who were defined as high-risk, based on resting pain episodes within previous 24 hours, changes of ST-T segment in ECG, and elevated serum cardiac markers. All patients underwent coronary angiography followed by PCI (percutaneous coronary interventions) in 73.1% of patients. 16.7% were assigned to CABG (coronary artery bypass graft), 1.6% of patients underwent PCI and CABG and 8.6% of patients were treated conservatively., Results: Overall in-hospital mortality was 3%; 1.4% in the PCI group, 8.4% in the CABG group and 6.8% in conservatively treated patients. The independent risk factors of in-hospital deaths were: Braunwald's IIIC class angina (OR 7.8; 95%CI 3.6-12.37 p=0.004), recurrent angina after revascularization (OR 13.04; 95%CI 7.62-29.23 p=0.002), congestive heart failure (OR 11.45; 95%CI 8.01-18,38 p=0.00001) and evolving myocardial infarction with ST-segment elevation (OR 12.77; 95%CI 8.35-27.35 p=0.0001). Stent implantation was associated with decreased risk of in-hospital death (OR 0.12; 95%CI 0.07-0.41; p=0.003)., Conclusions: Early invasive strategy in patients with ACS without ST-segment elevation is efficacious method of treatment. Independent predictors of in-hospital deaths are: Braunwald's IIIC class angina, congestive heart failure, recurrent angina after revascularization, myocardial infarction complicating hospital course. Stent implantation improves in-hospital prognosis.

Unlabelled: Cardiogenic shock develops in 5-15% of patients hospitalised with acute myocardial infarction. It is responsible for more than a half of all hospital deaths with survival rate of about 20%. Conventional medical therapy with use of adrenergic, vasoactive, inotropic and thrombolytic agents has failed to improve survival. Treatment strategy combine hemodynamic stabilisation with restoration of coronary blood flow. The aim of the study was evaluation of mechanical restoration of coronary blood flow in infarction related artery and to assess its influence on mortality in patients with myocardial infarction complicated by cardiogenic shock. We retrospectively analysed 58 subjects: 26 patients treated by primary angioplasty, 25 patients with PTCA angioplasty after streptokinase treatment and 7 ones treated conservatively. TIMI 3 flow in angioplasty treated patients was achieved in 70.6% with in hospital mortality rate 14%, however, when reperfusion was unsuccessful the mortality was high (80%). 12 months follow-up mortality rate was 41.8%., Conclusion: Successful reperfusion with coronary angioplasty of the infarct-related artery can significantly reduce mortality rate in patients with cardiogenic shock. Patients who survived in-hospital period have favourable one-year prognosis.

Unlabelled: The inflammatory process in chronic heart failure (CHF) is the result of dysbalance between the function of inflammatory and natural antiinflammatory mediators. Tumor necrosis factor alpha (TNF-alpha) is increased in patients with severe CHF. Two soluble proteins, the extracellular domains of the TNF receptors (sTNF-RI and sTNF-RII) inhibit the TNF-alpha biological effect. The aim of the study was to examine the plasma levels of sTNF-RI and sTNF-RII in patients with CHF and its relation to clinical, biochemical parameters of CHF severity. 41 patients with CHF (NYHA III and NYHA IV) and 18 control subjects were enrolled in this study. Plasma levels of sTNF-RI and sTNF-RII were analyzed by immunosorbent assay (ELISA) kits R&D (Research and Diagnostics Systems) (pg/ml)., Results: CHF patients had significantly increased receptor plasma levels compared to controls (p < 0.001). Soluble sTNF-RI and sTNF-RII receptors levels were similar in class NYHA III and NYHA IV. Receptor sTNF-RII correlated negatively with sodium plasma levels (p < 0.001), and sTNF-RI positively correlated with urice acid plasma level (p < 0.05). No statistically significant correlations were found between those receptors and age and gender etiology and severity of CHF, body weight (BMI) or other examined parameters (clinical, hemodynamic, echocardiographic, holter)., Conclusions: Plasma level of sTNF-RI and sTNF-RII are increased in patients with CHF.