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Abstract Objective Type III Hyperlipoproteinemia is a rare lipid disorder with a frequency of 1-5 in 5000. It is characterized by the accumulation of triglyceride rich lipoproteins and patients are at increased risk of developping atherosclerosis. Type III HLP is strongly associated with the homozygous presence of the ε2 allele of the APOE gene. However only about 10% of subjects with APOE2/2 genotype develop hyperlipidemia and it is therefore assumed that further genetic and environmental factors are necessary for the expression of disease. It has recently been shown that variation in the APOA5 gene is one of these co-factors. The aim of this study is to investigate the development of cerebrovascular atherosclerosis in patients with Type III hyperlipoproteinemia (Type III HLP) and the role of variation in the APOA5 gene as a risk factor. Methods 60 patients with type III hyperlipidemia and ApoE2/2 genotype were included in the study after informed consent. The presence of cerebrovascular atherosclerosis was investigated using B-mode ultra-sonography of the carotid artery. Serum lipid levels were measured by standard procedures. The APOE genotype and the 1131T > C and S19W SNPs in the APOA5 gene and the APOC3 sstI SNP were determined by restriction isotyping Allele frequencies were determined by gene counting and compared using Fisher's exact test. Continuous variables were compared using the Mann Whitney test. A p value of 0.05 or below was considered statistically significant. Analysis was performed using Statistica 7 software. Results The incidence of the APOA5 SNPs, -1131T > C and S19W and the APOC3 sstI SNP were determined as a potential risk modifier. After correction for conventional risk factors, the C allele of the 1131T > C SNP in the APOA5 gene was associated with an increased risk for the development of carotid plaque in patients with Type III HLP with an odds ratio of 3.69. Evaluation of the genotype distribution was compatible with an independent effect of APOA5. Conclusions The development of atherosclerosis in patients with Type III HLP is modulated by variation in the APOA5 gene.

Aims: This work aimed to evaluate the antimicrobial activity of pure (ZnO) and doped (ZnMgO) zinc oxide (ZnO) nanoparticles on bacterial pathogens and Saccharomyces cerevisiae to confirm their applicability as an alternative to antibiotics and to estimate their biocompatibility. Methods and Results: Microbial growth inhibition on agar plates, microbial viability and adaptation tests in broth with ZnO nanoparticles, spore germination, random amplified polymorphic DNA and SDS‐PAGE analysis were conducted to evaluate the effects of ZnO nanoparticles on cell morphology, viability, DNA damage and protein production. For this purpose, Escherichia coli, Salmonella, Listeria monocytogenes, Staphylococcus aureus, Bacillus subtilis and S. cerevisiae were studied after the addition of ZnO nanoparticles to the growth media. The contact with ZnO nanoparticles produced changes in morphology, shape, viability, DNA arrangement (DNA fingerprints) and protein content (SDS‐PAGE) in treated cells. Conclusions: As reported in this study, ZnO nanoparticles have an antimicrobial effect on both prokaryotic and eukaryotic cells. Before using ZnO nanoparticles as antimicrobial agents, it is important to evaluate the target because their effect depends on their composition, size and dose. Significance and Impact of the Study: We believe that the results obtained can help to optimize manufactured metal oxide nanoparticles in terms of their composition, size and working concentration. The parameters obtained directly define the applicability and biocompatibility of ZnO nanoparticles and thus are essential for any utilization in food, medicine and industry where pathogen control is crucial. [ABSTRACT FROM AUTHOR]

Presents six month mortality and morbidity data from the Anglo-Scandinavian Study of Early Thrombolysis (ASSET). Patients received intravenous alteplase or placebo within five hours of suspected acute myocardial infarction.

One hundred and six patients with acute myocardial infarction admitted to hospital within four hours after the onset of symptoms were randomised to treatment with intravenous timolol (54 patients) or placebo (52 patients). Serum potassium concentrations were estimated at frequent intervals during the first 24 hours of admission. Patients in both treatment groups, who did not receive subsequent diuretic treatment, had a transient rise in serum potassium concentration, which was maximal after four hours. This rise was abolished by diuretic treatment in the placebo group but not in the timolol group, in which there was a pronounced and prolonged rise in serum potassium concentration. The change in serum potassium concentration in the first four hours after admission correlated with cumulative creatine kinase release in the placebo group, but not in the timolol group. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) occurred in 15 (28.8%) patients in the placebo group and in seven (13%) in the timolol group and was independent of infarct size. The frequency of hyperkalaemia was not increased in the timolol group. By increasing the serum potassium concentration and preventing hypokalaemia, the use of intravenous timolol early in acute myocardial infarction may have important clinical effects in addition to reducing infarct size. [ABSTRACT FROM PUBLISHER]

In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations. [ABSTRACT FROM PUBLISHER]

Serum potassium concentrations obtained on admission to hospital were inversely related to the incidence of ventricular fibrillation in 289 women and 785 men with acute myocardial infarction, 92 of whom developed ventricular fibrillation. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) was found in 122 patients (11.4%). The incidence of ventricular fibrillation was significantly greater in patients with hypokalaemia compared with those classified as normokalaemic (serum potassium concentration greater than or equal to 3.6 mmol/l) (17.2% v 7.4%). The increased risk of ventricular fibrillation in the hypokalaemic group was about the same for women and men. While they were in hospital patients with hypokalaemia developed ventricular fibrillation significantly earlier than did normokalaemic patients (median 0.3 hours v 7 hours). Hypokalaemia was more common in women (17.3%) than in men (9.2%), and 55% of the hypokalaemic patients had been treated with diuretics before admission compared with 22% of the normokalaemic group. Hypokalaemia on admission to hospital predicts an increased likelihood and early occurrence of ventricular fibrillation in patients with acute myocardial infarction. [ABSTRACT FROM PUBLISHER]

To examine the effect of short-term, high-dose anticoagulation on the subsequent occurrence of left ventricular (LV) thrombi after a first anterior wall acute myocardial infarction (AMI), 21 patients received placebo and 21 high-dose anticoagulants during the first 10 days of the acute infarction. They were studied with cross-sectional echocardiography 10 days and 1-3 and 6 months post infarction. At 1 month, 6 of 7 thrombi present in the placebo group at 10 days were still visible. No thrombi were detected at 10 days in the anticoagulation group, but 6 patients had developed a LV thrombus at 1 month. These 12 patients with LV thrombi were subsequently treated with oral warfarin for 2 months, after which all thrombi had disappeared. Warfarin was then discontinued, and a thrombus had recurred in 5 patients after 6 months. Apical akinesis at 10 days a predictor for thrombus with a sensitivity and specificity of 100% and 72.2% respectively.Three of the 13 patients with LV thrombi suffered stroke in contrast to none without thrombi (P=0.025).We conclude that after discontinuation of short-term high-dose anticoagulation therapy in anterior AMI, LV thrombi may develop rapidly and lead to embolic complications, particularly in patients with persisting apical akinesis. [ABSTRACT FROM PUBLISHER]

In a study of 1033 consecutive patients with acute myocardial infarction, serum potassium concentrations were determined on admission to hospital and studied with respect to the subsequent occurrence of atrial fibrillation and flutter and of ventricular tachycardia and fibrillation. The study cohort fulfilled the inclusion criteria for the Norwegian timolol trial in which they later took part. In multivariate analysis, with serum potassium concentrations as a continuous variable, age, the presence of ventricular tachycardia and fibrillation, and maximum level of aspartate aminotransferase greater than four times the upper limit of normal were significantly associated with the occurrence of atrial fibrillation and flutter, while serum potassium concentration was not. Serum potassium concentrations and time from onset of the infarction to hospital admission were significantly negatively associated with the occurrence of ventricular tachycardia and fibrillation; while age, cardiomegaly, transient hypotension, pathological Q-waves in the electrocardiogram, atrial fibrillation and flutter, and ventricular premature beats were positively related to these arrhythmias. [ABSTRACT FROM PUBLISHER]

Risk factors for systemic embolisation in patients with ventricular thrombi caused by an acute myocardial infarction were studied in 150 consecutive patients with an infarction of the anterior wall. Serial echocardiograms were performed 2-10 days after the acute event and patients were followed up for three months. Anticoagulation treatment was started only after the detection of thrombi. Of the 55 patients in whom a thrombus developed, 15 (27%) had peripheral emboli between 6-62 days; but only two (2%) of 95 patients without thrombus had emboli. Among 15 variables, the best single predictors of embolisation were age greater than 68 years (80% sensitive, 85% specific), pendulous thrombus (60%, 93%), and independent thrombus mobility (60%, 85%). Logistic regression analysis showed that a formula that included patient age, thrombus area, and the length of thrombus in the ventricular lumen predicted embolisation (sensitivity 87%, specificity 88%). There was no correlation between age and the thrombus variables. The risk of embolisation from left ventricular thrombi in acute anterior myocardial infarction can be accurately assessed from patient age and echocardiographic features. The risk of peripheral emboli is high in patients with left ventricular thrombi and those aged greater than 68. [ABSTRACT FROM PUBLISHER]