How to diagnose splenic abscesses?

Splenic abscess is a rare but potentially fatal entity, occurring mainly in patients with underlying risk factors. Mortality of the disease depends on the time of diagnosis and treatment. Due to low sensitivity and specificity of clinical symptoms and laboratory markers, imaging plays the vital role in the diagnostic work-up. The aim of this article is to give a concise overview of the methods of splenic abscess diagnosis.

Significant narrowing of the circumflex artery leads to worse outcomes than right coronary artery narrowing in patients with anterior myocardial infarction treated invasively.

BACKGROUND: Occlusion of the circumflex artery (Cx) often does not present signs in the ECG. It can lead to delayed angiography during ST-elevation myocardial infarction (STEMI). The aim of this analysis was to determine if Cx narrowing is related to diverse outcomes in comparison with right coronary artery (RCA) stenosis in patients with STEMI, treated with percutaneous coronary intervention (PCI) of the left descending artery (LAD). METHODS AND RESULTS: Inclusion criteria were as follows: first STEMI treated with PCI of the LAD and additional significant (≥ 70 %) Cx or RCA narrowing-two-vessel disease. A total of 234 consecutive patients with STEMI were included. Total mortality was estimated during long-term follow-up, at mean 639 (± 224) days after STEMI. Patients with Cx narrowing constituted 46 % (N = 108) of the study population, and patients with RCA narrowing amounted to 54 % (N = 126). Patients with narrowing of the Cx had worse long-term outcomes in terms of mortality than patients with RCA narrowing (22 vs. 11 %, p < 0.05, respectively). Multiple regression analysis showed independent risk factors for death during long-term follow-up such as: age, ejection fraction and Cx narrowing. CONCLUSION: Significant Cx narrowing leads to worse outcomes than RCA narrowing in patients with STEMI treated with PCI of the LAD.

Interleukin 6 is not necessary for STAT3 phosphorylation and myocardial hypertrophy following short term beta-adrenergic stimulation.

PURPOSE: In recent years several reports have suggested involvement of interleukin 6 (IL-6) in beta-adrenergic effects on myocardium, particularly in enhancement of STAT3 phosphorylation (downstream signal transducer of IL-6). Here we present a study of isoproterenol effects on hearts of IL-6 deficient mice. METHODS: Male 12 week old C57Bl6/J mice and age and sex matched mice from IL-6 knockout strain (C57Bl6/J(IL6-/-)) received a single intraperitoneal bolus of either isoproterenol (15 mg/kg) or placebo (0.9% NaCl) and were sacrificed after 1 or 24 hours (n=8 in each group). Another group of mice from both genotypes received a three-day isoproterenol treatment (20 mg/kg every 8h). Activation of STAT3 and MEK/ERK pathways were assessed after a single dose of isoproterenol by means of western blotting. RESULTS: After injection of placebo a significantly lower level of STAT3 phosphorylation was observed in IL-6 KO animals. This difference was abolished after isoproterenol both at 1 and 24-hour time points. Isoproterenol produced potent and rapid activation of both STAT3 and MEK/ERK pathways that returned to the levels of placebo treated controls after 24 hours. Lack of IL-6 did not affect phosphorylation of ERKs. Three-day treatment with isoproterenol caused significant increase of indices of RV and LV hypertrophy in both WT and IL-6 KO animals with no significant differences between genotypes. CONCLUSION: IL-6 is not necessary for isoproterenol induced STAT3 phosphorylation, but may affect activation of this pathway by mild non-specific stimuli. Lack of IL-6 does not affect activation of MEK/ERK pathway nor cardiac hypertrophy by beta-adrenergic agonists.

Early and long-term prognosis of patients with coronary artery disease treated with percutaneous coronary interventions in 2005. Experience of single large-volume PCI center.

PURPOSE: The progress which has been made in interventional cardiology contributes to the gradual improvement of the results of CHD (coronary heart disease) therapy. The aim of the study was the assessment of early and long-term prognosis in all the patients with CHD treated invasively in one large-volume PCI center in 2005. MATERIAL AND METHODS: 1390 consecutive patients with CHD treated with PCI in 2005 were included in the analysis. Patients with ST-elevation myocardial infarction (STEMI) accounted for 50% of cases, patients with stable angina (SA) amounted to 25%, and patients with non-ST elevation acute coronary syndromes (NSTE-ACS) constituted 25%. Mean follow-up was 738 (±237) days. RESULTS: The highest mortality during the hospitalization was noted within the STEMI group(SA vs. NSTE-ACS vs. STEMI; 0% vs. 0.3% vs. 4.1%, respectively; p<0.001). The highest mortality during a 2-year follow-up was also observed in the STEMI group (SA vs. NSTE-ACS vs. STEMI, 6.3% vs. 8.5% vs. 13.8%, respectively; p<0.001). Multiple regression model showed that independent risk factors for death during the follow-up were: age, glycaemia at admission, heart rate, blood pressure, ejection fraction, STEMI, ineffective PCI (R=0.3613; F(10.131)=19.672; p<0.0001 for the model). CONCLUSIONS: The highest relative increase of mortality after the discharge of patients with CHD undergoing PCI referred to the patients with NSTE-ACS. However, in the real life PCI practice STEMI patients have the worst hospital and long-term prognosis. Well recognized risk factors for death in patients with CHD are still of great importance in negative prognosis of patients undergoing PCI.

Serum myeloperoxidase levels and platelet activation parameters as diagnostic and prognostic markers in the course of coronary disease.

Early prediction of coronary artery disease complications is vital for the prevention and effective treatment of patients with coronary cardiac disease. It has been reported that inflammatory markers play a key role in the progression of cardiovascular diseases. Platelet count and platelet morphological parameters were analyzed on a fully-automated hematological analyzer ADVIA 2120 (Siemens). Serum myeloperoxidase (MPO) level was determined with an enzyme immunoassay (BioCheck). The measuring range of this assay is between 0 and 40 ng/ml. We demonstrate that serum MPO concentration and platelet activation increase systematically with the advancement of coronary artery disease. Moreover, MPO level is significantly higher in patients with unstable coronary artery disease and myocardial infarction compared with healthy subjects and patients with stable angina. The diagnostic sensitivity of these parameters was higher than of TnI (cardiac troponin I), CK-MB (creatine kinase-heart type), CRP (C-reactive protein), and fibrinogen and DD (D-dimers). MPO, L-PLT (large platelet), MPV (mean platelet volume), and MPC (mean platelet component concentration) may serve as attractive diagnostic and prognostic markers in the assessment of the risk for unstable atheroma in the course of coronary artery disease.

Oxidative stress and antioxidative defense parameters early after reperfusion therapy for acute myocardial infarction.

Reperfusion of ischemic myocardium evokes rapid release of free radicals in experimental models. The aim of the study was to investigate the oxidative stress and antioxidative defense during first minutes after reopening of the infarct related artery in patients treated for acute myocardial infarction. The study group consisted of 15 patients with first ST elevation myocardial infarction (STEMI) due to left anterior descending artery occlusion. The control group included ten patients with stable ischemic heart disease (IHD). Blood samples from coronary sinus were drawn before, immediately after and about 15 min after angioplasty. Activity of superoxide dysmutase (SOD), concentration of glutathione as well as the concentrations of lipid peroxides, malodialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) were measured. There was significantly higher concentration of MDA and HNE and higher SOD activity in STEMI patients before the reperfusion, as compared to the stable IHD group. After the reperfusion concentration of HNE in erythrocytes from STEMI patients was higher than in IHD group. At the same time the activity of SOD significantly decreased in patients with impaired tissue perfusion (myocardial blush grade <2). In conclusion, there is a slightly higher concentration of oxidative stress parameters in patients with STEMI. Diminished antioxidative defense after reperfusion is associated with impaired myocardial perfusion.

IL-6 deficiency increases fatty acid transporters and intramuscular lipid content in red but not white skeletal muscle.

IL-6 is a biologically active substance which appears to be involved in regulating skeletal muscle lipid oxidation. Ablation of IL-6 (IL-6(-/-)) may therefore be expected to increase intracellular lipid accumulation, possibly via a concurrent increase in fatty acid transporters such as FAT/CD36 and FABPpm. This however may only occur in oxidative muscles which utilize fatty acids at a greater rate than glycolytic muscles. In the present study we examined the fatty acid transporter protein expression as well as the lipid content and profiles of free fatty acids (FFA), diacylglycerols (DGs) and triacylglycerols (TGs) in skeletal muscles of IL-6 deficient mice at 4 and 12 months of age. FAT/CD36 and FABPpm protein content was increased in red muscles in IL-6(-/-) mice compared to WT mice at 4 (RG) and 12 months (soleus and RG). Along with this, FFA, DG and TG concentrations were also increased in these red IL-6(-/-) muscles. In addition, the IL-6(-/-) genotype increased the saturated FA acid composition of the intramuscular TG fraction. In contrast, in white gastrocnemius muscle the IL-6(-/-) genotype has no effect on the expression of fatty acid transporters as well as the lipid content and composition at either 4 mo or 12 months of age. IL-6 ablation increases fatty acid transporter expression and intramuscular lipid accumulation, particularly the saturated fatty acids. These effects however were confined to oxidative muscles, as glycolytic muscles were not affected.

The effects of moderate physical exercise on cardiac hypertrophy in interleukin 6 deficient mice.

PURPOSE: Prolonged physical training leads to compensatory changes in cardiovascular system. One of the most important of them is cardiac hypertrophy. The knowledge, which factors contribute to cardiomyocyte hypertrophy caused by physical exercise is still incomplete. Interleukin 6 (IL6) secreted by contracting skeletal muscles may affect cardiac hypertrophy and remodeling. The aim of the study was to investigate the role of IL6 in exercise induced cardiac hypertrophy. MATERIAL AND METHODS: Female mice lacking functional IL6 gene C57BL6/J(IL6-/-tm1Kopf) (IL6KO) and age and sex matched controls C57BL6/J (WT) were subjected to 6 week swimming regime. Twenty-four hours after the last training session the mice were sacrificed, hearts were excised and weighed. Two other groups of sex and strain matched mice (9 in each group) not subjected to physical training, were sacrificed and served as controls. Weights of the heart and the left ventricle were related independently to the body weight and the tibia length as measures of hypertrophy. Statistical analysis was performed using multifactorial ANOVA and the Fisher test. RESULTS: There was significantly higher heart/body weight ratio in both groups of mice which were trained as compared to the respective sedentary animals [F(3,30) = 31.085 p < 0.001] There were, however, no significant differences between respective WT and IL6KO groups. Similar relations were found for the left ventricle and also when the weights of the heart and the LV were related to the tibia length. CONCLUSION: IL6 is not necessary for cardiac hypertrophy induced by prolonged moderate physical exercise in mice. Additional study is warranted to elucidate this phenomenon.

High cholesterol in patients with ECG signs of no-reflow after myocardial infarction.

PURPOSE: Despite successful restoration of blood flow in epicardial artery after myocardial infarction (MI), some patients do not benefit sufficiently from modern revascularisation methods due to the impairment of microcirculation, also called no-reflow phenomenon. Hyperlipidaemia is well established risk factor of coronary heart disease and its detrimental actions on vessels are widely acknowledged. We attempted to investigate possible relations between hyperlipidaemia and electrocardiographic signs of no-reflow in myocardial infarction after successful primary angioplasty. MATERIAL AND METHODS: A total of 150 consecutive patients with acute myocardial infarction (AMI) with ST elevation who underwent successful primary angioplasty were studied. ECG was obtained directly before and 30 minutes after successful reperfusion. ST segment deviation was measured. Lack of 50% reduction of ST-segment elevation in the lead with maximal initial elevation, 30 minutes after angioplasty was defined as ECG sign of no-reflow. RESULTS: ST-segment resolution occurred in 116 patients (77%), whereas 34 presented ECG signs of no-reflow (23%). Patients with persistent ST-segment elevation had higher blood LDL and total cholesterol (TC) levels than group with ST-segment restoration (146.5 vs. 128.7 p < 0.01 and 219.5 vs. 200.9, p < 0.05 respectively). Triglyceride, HDL, glucose on admission and fasting glucose levels did not differ significantly between groups. ECG signs of no-reflow were observed more often in patients with anterior AMI, history of prior myocardial infarction and longer pain-to-balloon time (p < 0.05). CONCLUSIONS: Positive relation between impaired tissue perfusion and high TC and LDL blood levels suggests that lipids may play a role in the pathogenesis of no-reflow phenomenon, possibly by impairment of endothelial function.

Transformation of maize (Zea mays L.) protoplasts and regeneration of haploid transgenic plants.

Transgenic haploid maize (Zea mays L.) plants were obtained from protoplasts isolated from microspore-derived cell suspension cultures. Protoplasts were electroporated in the presence of plasmid DNA containing the gus A and npt II genes encoding ß-glucuronidase (GUS) and neomycin phosphotransferase II (NPT II), respectively. Transformed calli were selected and continuously maintained on kanamycin containing medium. Stable transformation was confirmed by enzyme assays and DNA. analysis. Stably transformed tissue was transferred to regeneration medium and several plants were obtained. Most plants showed NPT II activity, and some also showed GUS activity. Chromosome examinations performed on representative plants showed that they were haploid. As expected, these plants were infertile.