Aim: The objective of this study was to evaluate prognostic impact of clinical factors on outcome of renal function in septic and non-septic acute kidney injury (AKI) patients. Methods: The prospective, observational, clinical study was performed at Nephrology Clinic and Clinic for Infectious Diseases, University Clinical Centre Sarajevo. One hundred patients with diagnosis of AKI were enrolled in the study, and divided into two groups: septic and non-septic AKI patients. Clinical parameters included causes and type of AKI, pre-existing comorbidities and different treatment modalities. Patients were followed up until discharge or death. Renal function outcome was defined by creatinine clearance values at discharge. Results: Septic AKI patients had significantly longer hospital stay (p=0.03), significantly worse renal function outcome (p<0.001), and higher burden of comorbidities (70.6% vs. 60.6%), compared to non-septic patients. Septic AKI patients were almost three times less likely to receive renal replacement therapy (8.8% vs. 24.4%) and they had significant delay in initiation of dialysis (p=0.03). By multivariate analysis, sepsis (95% CI 0.128-0.967, p=0.043) and hypertension (95% CI 0.114-0.788, p=0.015) were independent predictors of adverse renal function outcome in AKI patients. Postrenal type of AKI was independent predictor of renal function recovery in non-septic AKI patients (95% CI 1.174-92.264, p=0.035), while Failure, as third class of AKI, was independent predictor of non-recovered renal function only in septic AKI patients (95% CI 0.026 to 0.868, p=0.034). Conclusion: Septic AKI patients are clinically distinct compared to non-septic AKI patients with different prognostic factors and poorer renal function outcome.

Introduction: The diagnostic utility of B-type natriuretic peptide (BNP) has prompted interest in its use as an aid in the detection of early heart failure and assessment of diseases. The first objective of this study was measurement of BNP and troponin I (TnI) blood levels in patients with acute myocardial infarction (AMI) and unstable angina. The second objective of this study was to find a correlation between TnI and BNP in blood.Methods: The concentrations of BNP and TnI in 150 blood levels were determined using CMIA (chemiluminescent microparticle immunoassay) Architect and 2000 (Abbott diagnostics). The retrospective study included 100 patients who were hospitalized at the Department of Internal Medicine of the University Clinical Center Sarajevo and 50 healthy control. The reference blood range of BNP is 0-100 pg/mL and TnI is 0.00-0.4 ng/mL.Results: In the patients with AMI the mean value of BNP is 764.48 ± 639.52 pg/mL and TnI is 2.50 ± 2.28ng/mL. The patients with unstable angina have BNP 287.18 ± 593.20 pg/mL and TnI 0.10 ± 0.23 ng/mL. Our studies have shown that the correlation between BNP and TnI was statistically significant for p< 0.05 using Student t test with correlation coefficient r = 0.36. Conclusions: BNP and TnI levels can help to identify the patients with a high risk for cardiovascular diseases.

Background: For the assessment of the left ventricular function and infarct size in acute myocardial infarction, brain natriuretic peptide (BNP) and cardiac troponin I (cTnI) are useful for the prediction of a prognosis. The aim of the present study was to correlate left ventricular function and infarct size to the level of cTnI and BNP in acute myocardial infarction. Patients and Methods: We studied 40 patients (pts), with the first ST-segment elevation myocardial infarction (STEMI). We measured the level of BNP and cTnI on a single occasion at 96 hours after the onset of symptoms, and then compared it with echocardiography estimated systolic and diastolic ventricular function and infarct size — which was determined with numbers of ECG leads and classification into small and large infarct size (small infarct size 3-4 leads, large infarct size 6-9 leads). Results: Distribution of data was estimated by using the Shapiro-Wilk test. The data do not have normal distribution, so they are representative as a median and range. We used non-parametric statistic tests (Mann-Whitney tests) to compare and improve differences among the groups. For statistical correlation, we used the Sperman rank correlation. Data were analyzed using statistical program Arcus Quick Stat. There was significant inverse correlation between the level of BNP and EF (r = -0.504, P = 0.0016) and between BNP i E/A (r = -0.290, P = 0.00705). There was a strong inverse correlation between BNP and LV-EF in STEMI, such as between BNP and E/A, against cTnI no significant correlation with LV-EF and E/A in STEMI was found. There is no significant statistical difference between BNP and cTnI in small and large infarct size. Conclusion: A single BNP value at 96 hours after the onset symptoms of myocardial infarction proved useful for the estimation of LV systolic and diastolic function. In a direct comparison BNP disclosed a better performance for the estimation of LV-EF and E/A against cTnI. cTnI is useful for diagnosing early myocardial damage in acute myocardial infarction, suggesting an implementation of dual marker strategy in acute myocardial infarction for diagnostic and prognostic work-up.

OBJECTIVE To assess serum levels of tumor marker carbohydrate antigen 125 (CA125) in patients with heart failure (HF) and to investigate possible correlation with echocardiographic parameters and level of brain natriuretic peptide (BNP). PATIENTS AND METHODS We included 76 patients with different cardiac symptoms hospitalized at Clinic for heart disease and rheumatism. Control group (n = 26) was consisted of patients without signs and symptoms of HF, normal left ventricle ejection fraction (LVEF) and normal BNP level. Patients with diagnosis of HF (n = 50) were subdivided into 2 group depending on signs and symptoms of fluid overload: compensated (compHF, n = 10) and decompensated group (decompHF, n = 40). Serum CA125 and BNP were measured on admission and all patient underwent ECG recording and trans thoracic echocardiographic examination. RESULTS The median CA125 level in HF group was significantly higher compared to control group (71.05 [30.70-141.47]U/ml vs 10.75 [8.05- 14.32] U/ml, p < 0.0005). Higher CA125 levels were found in decompHF group compared to compHF group (94.90 [49.75-196.75]U/ml vs 11.90 [10.25-15.80]U/ml, p < 0.0005). In decompHF group 13 of patients had pleural and/or pericardial effusion- their CA125 levels were significantly higher compared to patients without serosal effusion (n = 27) (205.10 [106.50-383.90]U/ml vs. 71.50 [47.30-109.55] U/ml, p < 0.002). We found significant difference in CA125 levels between patients with atrial fibrillation and sinus rhythm (98.40 [48.20-242.70] U/ml vs. 47.30 [12.95-99.05] U/ml, p = 0.015). There was no significant difference in CA125 levels in group with enlarged left atrium compared to normal sized atrium (p = 0.282), as well as in group with moderate/severe mitral regurgitation compared to group with no/mild mitral regurgitation (p = 0.99). Finally, levels of serum CA125 positively correlated with serum level of BNP (r = 0.293, p = 0.039), but not with LVEF (p = 0.369) and left atrium diameter (p = 0.636). CONCLUSION Serum CA125 is elevated in decompensated HF patients: more pronounced elevation was found in patients with pleural and/or pericard effusion compared to patients with no serosal effusion. CA125 level correlated with BNP, but not with left atrium diameter nor with LVEF. Tumor marker CA125 could be used as a marker of systemic congestion and volume overload in decompensated HF. We hypothesized that high CA125 level indicates that measured high BNP is actually wet BNP.

INTRODUCTION Usage of fibrinolytic therapy leads to reperfusion of the occluded coronary arteries, rescue of ventricle myocardium and successful recovery of patient. GOAL The objective of this study was to compare the reperfusion effect of streptokinase and alteplase in acute myocardial infarction (AMI) by analyzing echocardiographic parameters and post-coronarography treatment. PATIENTS AND METHODS We observed 53 patients in AMI and divided them depending on applied therapy in streptokinase and alteplase group. Both groups were further divided into three subgroups depending on the time passed from chest pain occurrence to admission at Clinic. Observed echocardiographic parameters were: mitral regurgitation, left ventricular systolic and diastolic function and signs of ischemic cardiomyopathy. On coronary angiogram we analyzed severity of coronary artery disease as well as recommended treatment thereafter. RESULTS There were no significant difference in post-coronarography treatment, incidence and severity of mitral regurgitation and ischemic cardiomyopathy in alteplase vs streptokinase group- only significantly less diastolic dysfunction was noted in alteplase group (p=0.037). We noticed only significant difference when we took into consideration time from chest pain to admission at clinic. In alteplase first subgroup were more patients treated only with medications (without need for revascularization) vs streptokinase first subgroup (62,5% vs 28.6%, p=0.047). In alteplase first subgroup was lower incidence of mitral regurgitation (p =0.045), developed cardiomyopathy (p =0.009) and more preserved left ventricular diastolic function (p =0.008) compared to first streptokinase subgroup. CONCLUSION In our study we have found a significant difference between streptokinase and alteplase in echocardiographic parameters and post-coronarography treatment when we took into consideration time from occurrence of chest pain to admission at Clinic. The best outcomes had patients who were treated with alteplase within 1.5 hour from occurrence of chest pain.

Brain natriuretic peptide (BNP) is released from ventricular myocites due to their stretching and volume overload. In heart failure there is BNP release. Aim of this study was to observe BNP release in acute myocardial infarction (AMI). We measured BNP in 75 patients with AMI. Control group (n=61) was similar by age and gender to AMI group. We found statistically significant elevation of BNP compared to controls (462.875 pg/ml vs 35.356 pg/ml, p< 0.001). Patients with severe systolic dysfunction had the highest BNP levels, while patients with the preserved systolic function had the lowest BNP levels (Group with EF< 30% BNP= 1129.036 pg/ml vs Group with EF31-40 % BNP= 690.177 pg/ml vs Group with EF 41-50% BNP= 274.396 pg/ml vs Group with EF> 51% BNP= 189.566 pg/ml, p< 0.001). We found statistically significant light positive correlation between BNP and left ventricle end-diastolic diameter (LVDd) (r= 0.246, p<0.05). and real positive correlation between BNP and peak troponin levels (r= 0.441, p < 0.05). BNP levels were higher in anteroseptal allocation of AMI compared to inferior allocation (835.80 pg/ml vs 243.03 pg/ml, p< 0.001) and in patients who were treated with heparin compared to fibrinolitic therapy (507.885 pg/ml vs 354.73 pg/ml, p< 0.05). BNP is elevated in AMI and is a quantitative biochemical marker related to the extent of infarction and the left ventricle systolic dysfunction. Besides echocardiographic calculation, elevation of BNP could be used for quick and easy determination of the left ventricle systolic dysfunction.