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Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Psychiatria Polska is the property of Editorial Committee of Polish Psychiatric Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tako-tsubo syndrome is a transient cardiomyopathy, which is also known as the apical ballooning syndrome. Tako-tsubo is characterised by transient systolic dysfunction involving left ventricular apex and ischemic ECG findings with the absence of significant obstructive coronary artery disease. The clinical manifestation of tako-tsubo is similar to acute coronary syndrome. The most frequent finding on admission is ST-segment elevation in precordial leads in ECG. Tako-tsubo cardiomyopathy is also present in patients with diabetes. We present a case of a 66-year-old female patient with tako-tsubo cardiomyopathy, in whom apical ballooning syndrome was diagnosed despite of the absence of typical ECG findings. [ABSTRACT FROM AUTHOR]

Copyright of Cardio-Diabetological Review / Przeglad Kardiodiabetologiczny is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aim of the study: In the case of atherosclerosis, therapeutic management depends on the advancement of the disease. The ever-present element of management in each clinical form of the disease is conservative treatment, including e.g. the elimination of risk factors for sclerosis, pharmacological treatment, and the treatment of comorbidities. The aim of the work was to evaluate the lifestyles of patients with lower extremity arterial disease and the patients' expectations concerning health education referring to the disease and the recommended lifestyle. Material and methods: The respondent group was composed of 50 patients with lower extremity arterial disease, of both sexes (including 61% of males), aged from 24 to 89 years. The research was carried out at the Invasive Cardiology Clinic of University Clinical Hospital in Bialystok and at the Nursing Home in Bialystok. A self-constructed survey questionnaire (including 44 questions) was used. Results: Most of the patients did not observe the recommendations about reducing consumption of saturated fats and increasing the consumption of complex carbohydrates and dietary fibre. They did not exercise regularly, and nearly half of them smoked. Only 16% of the patients had normal BMI. The respondents wanted, among others, information on foot care, complications, symptoms, risk factors for the disease, pharmacological treatment, and rehabilitation methods. Conclusions: Because of the high percentage of atherosclerosis complications occurring in the investigated group of patients and their failure to observe doctors' orders concerning an appropriate lifestyle, special attention should be given to educating patients and motivating them to observe therapeutic recommendations regarding non-pharmacological treatment. [ABSTRACT FROM AUTHOR]

Vitamin D is known for almost 100 years. Since time of its discovery, numerous studies on vitamin D function in the human body were performed. Considered from the beginning as an important factor in rickets prevention, thanks to the continuous development of knowledge, vitamin D is regarded now as an important factor from the point of view of the whole body homeostasis. Newly-find features of vitamin D allow to use this substance concentration in serum as a biomarker of general health and create opportunities of vitamin D use in the prevention and treatment of many diseases. The aim of this article is to present basic function of vitamin D in human body, sources of this substance, its metabolism and molecular mechanism of action, taking into account the evolution of the state of knowledge about Vitamin D - from early researches leading to its discovery, through the finding of its basic functions to the present studies on vitamin D mechanisms of action at molecular and genomic level.

Klotho, the gene encoding the antiaging protein, was discovered in 1997 and named after a Greek Goddes who spun the thread of life. Numerous experiments on mice confirmed that destruction of the klotho gene or loss of klotho function leads to an accelerated aging and premature death. In addition to shortened life span, klotho-deficient mice demonstrated changes in functioning of multiple organs, ectopic calcification, enhanced development of arteriosclerosis, osteoporosis and atrophy of skin. In contrast, overexpression of a gene in mice inhibited aging and prolonged survival. The multisystemic phenotype induced by Klotho deficiency indicates that Klotho works on a variety of organs. Klotho is highly expressed in the kidney, brain, and to a lesser extent in other organs. Protein Klotho exists in two forms: membrane and secreted which play different functions. Membrane Klotho function as an obligate co-receptor required for signaling for the phosphaturic factor FGF23, regulates calcium-phosphate homeostasis through renal ion transport in addition to modulation of PTH and 1,25(OH)2D3. Soluble klotho functions as a humoral factor and regulates the activity of several ion channels and transporters. The secreted Klotho can also inhibit oxydative stres and the insulin and insulin-like growth factor 1 (IGF-1) pathways. The discovery of the protein klotho led to the identification of new axes connecting endocrine disturbances in the homeostasis of the calcium-phosphate to the aging of the organism. Klotho deficiency may not only be a trigger for accelerated aging but also in development of age- -associated diseases, including hypertension, osteoporosis, cardiovascular disease, and CKD. Conceivably, better understanding of Klotho protein might provide a novel treatment strategy for aging and age-associated diseases.

Acute respiratory distress together with hypoxia could be an indication for admission to intensive care unit. It may also lead to acute kidney injury. In addition, mechanical ventilation may be an additional factor for development of acute kidney injury. The aim of the work was to assess the prevalence of acute kidney injury, including the need for renal replacement therapy in patients with acute respiratory distress treated in intensive care unit. In addition, the effect of acute kidney injury on outcome of patients with acute respiratory distress was evaluated. The studies were performed on 100 patients with acute respiratory distress treated in intensive care unit of the regional hospital. Patients were divided into 2 groups in respect to the presence or absence of acute kidney injury. Acute kidney injury was diagnosed in 22% of patients with acute respiratory distress, while 12% required renal replacement therapy, it was more often observed in patients with estimated GFR < 60 ml/min/1.73m2. Length of stay was similar irrespective of kidney function, however, the mortality was significantly higher in patients with eGFR < 60 ml/min/1.73 m2, particularly in those on hemodialyses. In addition, mortality was associated with older age and sepsis.

Introduction: Suicides around the world are a major public health problem. They are the most serious causes of death among patients with mental disorders. In many European countries, national programs and strategies for suicide prevention were developed. The progress of civilisation, changes in political and economic life, a too fast pace of life negatively affect human, causing the liberation of self-destructive behaviours., Aim: The aim of this study, which was based on medical records, was to analyse the course of psychiatric disorders, that ended with suicide., Material and Methods: Descriptions of the course of mental disorders which ended with suicide and self-harm codes according to ICD-10 in randomly selected patients have been presented. 1. A 68 year old patient with schizophrenia - the intending self-harm by hanging (X70); 2. A 46 years old patient with a diagnosis of schizoaffective disorder - the intentional self-harm by drug poisoning (X61); 3. A 51 years old patient with a diagnosis of bipolar disorder - suicide death under the wheels of the train (X8 1)., Conclusions: Risk of suicide in mental disorders requires the implementation conduct standards in a suicide crisis. In each case, it is necessary to assess the risk on the basis of the identification of suicide risk factors. Evaluation of risk factors is the basis of therapeutic action and determines how to support patients with a risk of suicidal death. Despite advances in the treatment of mental disorders, in some cases, there is still limited effectiveness of suicide preventio.

Background: Stress hyperglycaemia on admission is a predictor of mortality in patients with acute myocardial infarction (MI)., Aim: To establish what level of hyperglycaemia on admission indicates a significantly poorer long-term prognosis in patients with MI treated invasively., Methods: Glycaemia on admission was measured in patients with both ST-segment elevation MI (STEMI) and non-ST- -segment elevation MI (NSTEMI) treated with percutaneous coronary intervention (PCI). In-hospital and late mortality were evaluated during a 679.3 ± 202 day follow-up., Results: We enrolled 794 patients (564 men; 71%), mean age 63.8 ± 11.3 years. One per cent of the patients died during initial hospitalisation, and 10% during the two-year follow-up. The mean value of glycaemia in the whole population was 115 ± 36 mg/dL (6.32 ± 1.98 mmol/L). Admission glycaemia in patients who died in hospital was 194 ± 71 mg/dL (10.67 ± 3.91 mmol/L), while in the patients discharged home it was 114 ± 35 mg/dL (6.27 ± 1.93 mmol/L) (p 〈 0.0001). In terms of two-year mortality, the patients who died had also significantly higher glycaemia on admission (145 ± 48 mg/dL; 7.98 ± 2.64 mmol/L) vs 112 ± 31 mg/dL (6.16 ± 1.71 mmol/L, p 〈 0.0001). Apart from admission hyperglycaemia, we found the following risk factors of late mortality in univariate analysis: age, heart rate (HR), left ventricular ejection fraction (LVEF), glomerular filtration rate (GFR), creatinine level, number of significantly narrowed coronary vessels other than the infarct related artery (IRA), and unsuccessful PCI. In multivariate analysis, the following parameters correlated with death in the two-year follow-up: glycaemia on admission, age, HR, LVEF, GFR, creatinine level, total cholesterol, number of significantly narrowed coronary vessels other than the IRA, and unsuccessful PCI. Hyperglycaemia on admission was an independent risk factor of death even after adjustment for confounding variables such as age, sex and LVEF. We compared the areas under ROC curve for in-hospital mortality and the areas under ROC curve for late mortality according to glycaemia on admission. Both were significantly different from those of a random model (p 〈 0.001 and p 〈 0.001, respectively). A glycaemia value of 205 mg/dL (11.28 mmol/L) calculated from ROC curve had the highest sensitivity and specificity for late mortality. Apart from these findings, we observed a linear correlation between glycaemia and mortality., Conclusions: The best cut-off value for stress hyperglycaemia determined by ROC curve in patients with acute MI treated invasively is 205 mg/dL (11.28 mmol/L). Patients with glucose levels 〉 205 mg/dL (11.28 mmol/L) on admission have significantly higher late mortality compared to those with glucose levels 〈 205 mg/dL (11.28 mmol/L). Our results suggest that hyperglycaemia is a reliable marker of poor outcome in acute MI patients with and without previously diagnosed diabetes mellitus. This level of glucose may be used in risk stratification in patients with acute MI.

Rotational atherectomy is a valuable technique complementary to PCI in complex calcified coronary artery stenoses. A case of a 65 year-old man with non-ST elevation acute myocardial infarction (NSTEMI) treated with PCI with rotational atherectomy followed by two drug eluting stents (DES) implantation is presented.

Heart disease and renal failure occurring together, constitute a potential threat to life, especially in the elderly. Diseases of the cardiovascular system are the main factor in morbidity and mortality in patients with chronic kidney disease. On the other hand, chronic kidney disease is considered a risk factor for cardiovascular diseases. Identified major nephrological problems, especially chronic renal disease and acute kidney damage, as the most aggravating cardiac patients. Stressed the importance of clinical, preventive measures and prognosis in contrast nephropathy

The number of patients with chronic kidney disease-CKD is still growing. Overweight and obesity present also an important problem of world public health. However, there are not many data showing possible association between obesity and incresing risk of development of renal failure recently it has been demonstrated that in obese patients secondary focal segmental glomerulosclerosis and glomerular hypertrophy appear more frequently. The aim of this study was to estimate glomerular filtration rate-GFR in patients with normal serum creatinine concentration undergoing primary angioplasty according to body mass index. The study included 1413 patients udergoing primary angioplasty for acute myocardial infarction. The following parameters were assessed: age, gender, family history of cardiovascular disease, risk factors of cardiovascular disease (hypertension, diabetes mellitus, obesity etc.), previous myocardial infarction, pre-existing heart failure, treatment given, localization of infarct, coronary stenting, serum creatinine before angioplasty, cholesterol, LDL, HDL, triglycerides, glucose, blood pressure. Of a total of 1413 patients, 1337 (94.62%, 943 M, 394 F) had correct serum creatinine concentration (below 1.5 mg/dl for men, below 1.2 mg/dl for women). Glomerular filtration rate was calculated from serum creatinine levels by using the simplified Modification of Diet in Renal Disease Study formula--MDRD, Cockcroft-Gault equation and Jeliffe formula. An average value of GFR in study group was 79.94 +/- 24.51 ml/min (Cockcroft-Gault equation), 73.02 +/- 21.96 ml/min (Cockcroft-Gault adjusted to weight), 90.37 +/- 25.1 ml/min (MDRD equation) and 77.67 +/- 21.65 ml/min (Jeliffe formula). A significant lower serum creatinine levels and GFR (assessed by 3 formulas and Cockcroft-Gault using adjusted weight) were observed in women group. In the whole study group (with normal serum creatinine levels) substantial correlation was found between age and serum creatinine concentration (r = 0.13, p > 0.001), GFR (MDRD, r = -0.37, p < 0.001, Cockcroft-Gault, r = -0.62, p < 0.001, adjusted to weight r = -0.64, p < 0.001, Jeliffe r = -0.61, p < 0.001) and also between BMI and GFR (MDRD r = 0.28, p < 0.001, Cockcroft-Gault, r = 0.31, p < 0.001, adjusted to weight r = 0.08, p < 0.001, Jeliffe r = 0.341, p < 0.001), but not with serum creatinine concentration (r = 0.03, p = 0.3). In patients with normal serum creatinine levels percentage of patients with GFR below 60 ml/min ranges from 4.79% up to 30.74%. In patients with higher BMI, higher GFR may be partially caused by glomerular hyperfiltration. Overweight or obesity are significant, but potentially changeable risk factors for development of chronic renal failure. However, chronic kidney disease is one of the complications of obesity.

Unlabelled: Experimental and clinical reports suggest the role of antiphospholipid antibodies (aPL) in the pathogenesis of atherosclerosis and arterial thrombosis. The aim of our study was to evaluate IgM and IgG anti-beta2-glycoprotein I (anti-beta2-GPI), as well as IgG antiphosphatydylserine (aPS) antibodies in 80 consecutive patients (mean age 58.6+/-8.3 years) referred for coronary angiography, dependent on the extent of atherosclerotic lesions in coronary vessels and the disturbances of glucose tolerance. Antiphospholipid antibodies were measured by ELISA. The mean values of aPS and anti-beta2-GPI did not differ significantly between patients with 1- (n = 17), 2- (n = 15) or 3-vessel disease (n = 14) and subjects without significant changes in coronary arteries (n = 34), as well as between patients with unstable (n = 12) and effort angina (n = 68). Significantly higher levels of IgG anti-beta2-GPI were found in the subgroup with type 2 diabetes in comparison with the subjects with impaired glucose tolerance (median 3,8 (1.9 -9.3) U/ml vs 2,8 (1.5-5.0) U/ml, p = 0.027). Current smokers (n = 11) had significantly higher values of aPS than non smokers (55.8 +/- 30.7 - 64.7) U/ml vs 38.7 (5.7 +/- 82.6) U/ml, p = 0.017). Abnormal aPS values were found in 34 subjects (42,5%): 16 (6 diabetics) with normal angiograms (47.0%), 9 (26.5%) with 1-vessel disease, 3 (8,8%) with 2-vessel disease and 6 (17,6%) with 3- vessel disease. Increased IgG anti- (2-GPI levels were found in 8 (10%), and IgM anti-beta2-GPI - in 4 patients (5%). All subjects with high IgM anti-beta2-GPI values, as well as 5 persons with high IgG anti-beta2-GPI levels (62.5%) had significant coronary artery lesions. Multiple regression analysis revealed that factors independently influencing the levels of aPS were: patient's age (Beta = -0.8417, p = 0.0003) and glycaemia 120 min. after glucose load (Beta = 0.6453, p = 0.025)., Conclusions: our results do not confirm an association between aPS or/and anti-beta2-GPI antibodies and the extent of atherosclerotic lesions in coronary vessels, although they suggest an increased membrane phospholipids immunogenicity in relatively young patients with elevated postload glycaemia, as well as cigarette smokers.

The no-reflow phenomenon is an impairment of microcirculation after successful percutaneous coronary interventions (PCI). The no-reflow phenomenon is usually observed during acute myocardial infarction. This case-report describes no-reflow phenomenon in a patient undergoing elective PCI in the right coronary artery, occluded due to restenosis in implanted stent. After deflation of balloon during angioplasty in restenosed stent, no-reflow phenomenon occurred, followed by asystolia. The patient was successfully resuscitated. During resuscitation procedures, abciximab was administered what improved myocardial perfusion. This case demonstrates that no-reflow phenomenon can be a serious problem during elective PCI, leading even to a cardiac arrest. It shows also the necessity for administration of drugs improving tissue perfusion when no-reflow phenomenon occurs.

Background: Coronary stenting is associated with acute inflammation within the arterial wall followed by neointimal growth. Acute inflammatory response is expressed by a marked systemic elevation of the inflammatory biomarker C-reactive protein (CRP). It has been shown that the degree and extent of CRP increase may be related to clinical presentation or periprocedural treatment., Aim: To investigate whether an increase in CRP level is associated with the extent of arterial injury during stent deployment., Methods: CRP levels were measured with a high-sensitivity CRP (hsCRP) assay. Seventy-three patients (51 males) with normal baseline plasma CRP (<3 mg/L) underwent percutaneous coronary intervention (PCI) with stent implantation for stable coronary disease. Blood samples for hsCRP were drawn before the intervention, and 6, 12 and 24 hours after the procedure. Both quantitative (single vs multivessel coronary intervention) and qualitative analyses (including lesion classification according to the ACC/AHA grading system) were performed in all patients. The examined angiographic parameters and procedural data obtained included reference diameter, lesion location, lesion length, total stented segment length, diameter of stent after deployment, maximal deployment pressure, total inflation number and duration., Results: The mean hsCRP level increased in all patients between baseline and 24 hours (1.36+/-0.93 mg/L and 4.34+/-3.3 mg/L, p <0.0001). Single vessel procedure was performed in 51 patients and multivessel coronary intervention in 22 patients. Mean hsCRP was similar at baseline and after 6 hours in both groups and the increase after 12 and 24 hours was higher among patients with multivessel coronary intervention compared to patients with single vessel procedure (2.69+/-2.48 vs 4.15+/-3.17; p=0.039 and 3.76+/-3.13 vs 5.69+/-3.38; p=0.021, respectively). There was no correlation between hsCRP and the degree of lesion complexity. Multiple regression analysis showed that the total stented segment length (p=0.01) contributed to the hsCRP increase after 24 hours., Conclusions: The inflammatory response expressed by hsCRP levels is higher in patients with multivessel coronary intervention with longer total segment stented.

A case of a 61-year-old female with a history of stroke in a course of mitral stenosis with atrial fibrillation is reported. Mitral commissurotomy was conducted eight years after the diagnosis. The chest X-ray revealed large calcified mass in the left atrium. During surgical mitral valve replacement the mass has been removed and identified as calcified thrombus. Despite numerous risk factors, anticoagulation has not been introduced until a few months before the operation.

Unlabelled: Kidney disease and cardiovascular disease seem to be lethally synergistic and both approach level of epidemy. On the other hand, patients with ischemic heart disease often exhibit renal dysfunction due to concomitant diabetes, hypertension, congestive heart failure and dyslipidemia. Patients with chronic kidney disease are at increased risk of death after acute MI., Aim: Assessment of prevalence of kidney dysfunction in patients with normal serum creatinine using estimated GFR in a cohort of 922 consecutive patients undergoing primary PCI due to acute myocardial infarction., Results: Normal serum creatinine (less than 1.5 mg/dL in males and less than 1.2 mg/dL in females) was observed in 857 (93%) patients. Mean GFR was 69.0 +/- 21.15 ml/min (Cockcroft-Gault formula), 85.18 +/- 24.17 ml/min (MDRD) or 72.25 +/- 21.65 ml/min (Jeliffe). According to Cockcroft-Gault formula stage 2 chronic kidney disease-CKD i.e. GFR 60-89 ml/min was found in 378 patients (44.11%) and stage 3 CKD i.e. GFR 30-59 ml/min was found in 283 (33.02%) patients with normal serum creatinine. According to MDRD formula stage 2 CKD was found in 440 patients (51.32%) and stage 3 CKD was found in 71 (8.29%) patients, whereas according to Jeliffe formula stage 2 CKD was found in 405 patients (47.25%) and stage 3 CKD was found in 194 (22.63%) patients with normal serum creatinine., Conclusion: The prevalence of chronic kidney disease is high, up to almost 80% patients undergoing primary PCI despite normal serum creatinine. The risk of contrast nephropathy with worse outcomes is enhanced in these patients. In patients with risk factors for cardiovascular disease, GFR should be estimated since renal dysfunction is one more important risk for cardiovascular morbidity and mortality.

Repeated administration of t-PA and abciximab in a patient with anterior myocardial infarction - a case report. A case of a 40-year-old male with acute anterior myocardial infarction (MI) is presented. Due to the angiographic equipment failure, the patient did not undergo primary angioplasty and received heparin and 100 mg of t-PA. This treatment was associated with clinical and ECG signs of reperfusion, however, 30 minutes after completion of t-PA infusion, the patient developed clinical and ECG signs of re-occlusion. The decision was made to transfer the patient to a catheterisation laboratory for further invasive treatment, however, it was located 200 km from our centre. Because of that, the patient received another dose of 50 mg of t-PA and abciximab before transportation. Further course was uncomplicated and the patient underwent successful stent implantation in the other centre.

Circulating monocyte-platelet aggregates can release procoagulant, oxidative and mitogenic factors, thereby contributing to arterial thrombosis. The aim of our study was the estimation of heterophilic leukocyte-platelet aggregates in patients referred for coronary angiography, dependent on the degree of coronary stenosis and the disturbances of carbohydrate metabolism. Flow-cytometric analysis was performed in 50 consecutive patients with positive exercise test (age 54.2 +/- 6.4 years): 27 with normal glucose tolerance, 7 with impaired glucose tolerance and 16 with type 2 diabetes, and in 16 healthy subjects (age 44.8 +/- 14.1 years). We found that patients with coronary heart disease had increased leukocyte-platelet aggregate formation in comparison to the controls (the percentage of monocyte-platelet aggregates 47.5 +/- 23.0 vs 25.7 +/-12.8, p = 0.003, mean fluorescence intensity (MIF) 187.6 +/- 117.2 vs 79.3 +/- 42.8, p = 0.002, the percentage of granulocyte-platelet aggregates 20.7 +/- 10.4 vs 17.0 +/- 3.6, p = 0.009, MIF 64.2 +/- 41.3 vs 40.9 +/- 6.3, p = 0.008). The highest percentage of heterophilic aggregates was observed in patients with 1- and 2-vessel disease and those with "clean" vessels. In diabetic patients the percentage and MIF of granulocyte-platelet aggregates were decreased in comparison to the subjects with normal glucose tolerance (16.7 +/- 7.2 vs 22.8 +/- 9.8, p = 0.03 and 44.3 +/- 10.8 vs 74.4 +/- 48, p = 0.009, respectively). There was no increase in glycoprotein CD14 expression in any of the group studied. We found a positive correlation between the percentage of monocyte-platelet aggregates and fasting insulin level (r = 0.369, p = 0.04) and a negative correlation between MIF of monocyte-platelet aggregates and HDL level (r = -0.459, p = 0.012), between MIF CD14 and HDL level (r = -0.435, p = 0.02), and between the percentage of granulocyte-platelet aggregates and postprandial glycaemia (r = -0.4117, p = 0.03). We concluded that: 1. the patients with "clean" vessels represent a group of high atherothrombotic risk. 2. the patients with minimal coronary stenosis may benefit from anti-inflammatory and antiplatelet treatment.