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1.
  • Herlitz, J, et al. (författare)
  • A short delay from out of hospital cardiac arrest to call for ambulance increases survival
  • 2003
  • Ingår i: European Heart Journal. - : Oxford University Press. - 1522-9645 .- 0195-668X. ; 24:19, s. 1750-1755
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim To describe the relative impact on survival of the delay from estimated time of collapse to call for an ambulance among patients who suffer from a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology. Methods A majority of all ambulance organizations in Sweden (covering 85% of Sweden inhabitants) participate in a National survey of out of hospital cardiac arrest. Results In all there were 9340 patients with a bystander witnessed cardiac arrest of a cardiac aetiology in whom cardiopulmonary resuscitation (CPR) was attempted participating in this survey. Survival at one month among patients with a delay between estimated time of collapse and call for ambulance of less than or equal to4 min (median) was 6.9% versus 2.8% among patients with a median of >4 min (P<0.0001). When adjusting for age, sex, initial rhythm, estimated interval between collapse and start of CPR, place of arrest and the interval between call for ambulance and arrival of the rescue team, the odds ratio for survival was 0.70 (0.95% Cl. 0.58-0.84) per unit increase of the natural logarithm of delay in minutes between collapse and call. Conclusion Among patients with a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology increased delay from estimated time of collapse to call for an ambulance decreased the chance of survival. (C) 2003 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
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2.
  • Cowie, MR, et al. (författare)
  • Clinical applications of B-type natriuretic peptide (BNP) testing
  • 2003
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 24:19, s. 1710-1718
  • Tidskriftsartikel (refereegranskat)abstract
    • Many claims have been made in recent years regarding the utility of plasma B-type natriuretic peptide (BNP) concentration measurements in the diagnosis, risk stratification and monitoring of patients with heart failure. This paper summarizes the current evidence and provides guidance for practising clinicians. Overall, plasma BNP testing appears to be of most value in the diagnostic arena, where it is likely to improve the performance of non-specialist physicians in diagnosing heart failure. In clinical practice, BNP testing is best used as a 'rule out' test for suspected cases of new heart failure in breathless patients presenting to either the outpatient or emergency care settings, it is not a replacement for echocardiography and full cardiological assessment, which will be required for patients with an elevated BNP concentration. Although work is ongoing in establishing the 'normal' values of BNP, heart failure appears to be highly unlikely below a plasma concentration of 100 pg/ml. However, as BNP levels rise with age and are affected by gender, comorbidity and drug therapy, the plasma BNP measurement should not be used in isolation from the clinical context.
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3.
  • Madler, C. F., et al. (författare)
  • Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography : optimal diagnostic models using off-line tissue Doppler in the MYDISE study
  • 2003
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 24:17, s. 1584-1594
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims To develop optimal methods for the objective non-invasive diagnosis of coronary artery disease, using myocardial Doppler velocities during dobutamine stress echocardiography. Methods and results We acquired tissue Doppler digital data during dobutamine stress in 289 subjects, and measured myocardial responses by off-line analysis of 11 left ventricular segments. Diagnostic criteria developed by comparing 92 normal subjects with 48 patients with coronary disease were refined in a prospective series of 149 patients referred with chest pain. Optimal diagnostic accuracy was achieved by logistic regression models, using systolic velocities at maximal stress in 7 myocardial segments, adjusting for independent correlations directly with heart rate and inversely with age and female gender (all p<0.001). Best cut-points from receiver-operator curves diagnosed left anterior descending, circumflex and right coronary disease with sensitivities and specificities of 80% and 80%, 91% and 80%, and 93% and 82%, respectively. All models performed better than velocity cut-offs alone (p<0.001). Conclusion Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography is best performed using diagnostic models based on segmental velocities at peak stress and adjusting for heart rate, and gender or age.
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4.
  • Norhammar, Anna, et al. (författare)
  • Under utilisation of evidence-based treatment partially explains for the unfavourable prognosis in diabetic patients with acute myocardial infarction
  • 2003
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 24:9, s. 838-844
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: The prognosis after an acute myocardial infarction is worse for patients with diabetes mellitus than for those without. We investigated whether differences in the use of evidence-based treatment may contribute to the differences in 1-year survival in a large cohort of consecutive acute myocardial infarction patients with and without diabetes mellitus. Methods: We included patients below the age of 80 years from the Register of Information and Knowledge about Swedish Heart Intensive care Admissions (RIKS-HIA), which included all patients admitted to coronary care units at 58 hospitals during 1995-1998. In all 5193 patients had the combination of acute myocardial infarction and diabetes mellitus while 20 440 had myocardial infarction but no diabetes diagnosed. Multivariate logistical regression analyses were performed to evaluate the influence of diabetes mellitus on the use of evidence-based treatment and its association with survival during the first year after the index hospitalisation. Results: The prevalence of diabetes mellitus was 20.3% (males 18.5%, females 24.4%). The 1-year mortality was substantially higher among diabetic patients compared with those without diabetes mellitus (13.0 vs. 22.3% for males and 14.4 vs. 26.1% for female patients, respectively) with an odds ratio (OR) (95% confidence interval (CI)) in three different age groups: <65 years 2.65 (2.23-3.16), 65-74 years 1.81 (1.61-2.04) and >75 years 1.71 (1.50-1.93). During hospital stay patients with diabetes mellitus received significantly less treatment with heparins (37 vs. 43%, p<0.001), intravenous beta blockade (29 vs. 33%, p<0.001), thrombolysis (31 vs. 41%, p<0.001) and acute revascularisation (4 vs. 5%, p<0.003). A similar pattern was apparent at hospital discharge. After multiple adjustments for dissimilarities in baseline characteristics between the two groups, patients with diabetes were significantly less likely to be treated with reperfusion therapy (OR 0.83), heparins (OR 0.88), statins (OR 0.88) or to be revascularised within 14 days from hospital discharge procedures (OR 0.86) while the use of ACE-inhibitors was more prevalent among diabetic patients compared to non-diabetic patients (OR 1.45). The mortality reducing effects of evidence-based treatment like reperfusion, heparins, aspirin, beta-blockers, lipid-lowering treatment and revascularisation were, in multivariate analyses, of equal benefit in diabetic and non-diabetic patients. Interpretation: Diabetes mellitus continues to be a major independent predictor of 1-year mortality following an acute myocardial infarction, especially in younger age groups. This may partly be explained by less use of evidence-based treatment although treatment benefits are similar in both patients with and without diabetes mellitus. Thus a more extensive use of established treatment has a potential to improve the poor prognosis among patients with acute myocardial infarction and diabetes mellitus.
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5.
  • Oldgren, Jonas, et al. (författare)
  • Myocardial Damage, Inflammation and Thrombin Inhibition in Unstable Coronary Artery Disease
  • 2003
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 24:1, s. 86-93
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM:Unstable coronary artery disease (CAD) is a multifactorial disease involving both thrombotic and inflammatory processes. We have assessed the time-course and the influence of thrombin inhibitors on changes in fibrinogen and C-reactive protein levels, and their relation to myocardial ischaemia in unstable CAD.METHODS AND RESULTS:Three hundred and twenty patients were randomized to 72 h infusion with three different doses of inogatran, a direct thrombin inhibitor, or unfractionated heparin. There were no significant differences between the treatment groups in fibrinogen or C-reactive protein levels. Overall, the fibrinogen levels were significantly increased in the first 24-96 h and still elevated at 30 days. The C-reactive protein levels showed a more pronounced increase during the first 24-96 h, but then markedly decreased over 30 days. Troponin-positive compared to troponin-negative patients had higher fibrinogen and C-reactive protein levels up to 96 h, although there was an increase compared to pre-treatment levels in both groups. A high fibrinogen level (pre-treatment top tertile) was associated with an increased rate of death or myocardial (re-)infarction at 30 days, 13% vs 5.6%, P=0.03, and increased long-term mortality. A high C-reactive protein level was related to increased 30-day mortality, 4% vs 0%, P=0.01.CONCLUSION:Myocardial cell injury was related to a high degree of inflammation, only some of which is an acutephase response due to tissue damage. The rise in fibrinogen was sustained, which might reflect low grade inflammation with long-term risk of thrombosis. The transient elevation of C-reactive protein levels might indicate a propensity to a pronounced inflammatory response and is associated with increased mortality.
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7.
  • Wallentin, Lars, et al. (författare)
  • Low molecular weight heparin (dalteparin) compared to unfractionated heparin as an adjunct to rt-PA (alteplase) for improvement of coronary artery patency in acute myocardial infarction - The ASSENT plus study
  • 2003
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 24:10, s. 897-908
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Current thrombolytic-antithrombotic regimens in acute myocardial infarction (AMI) are limited by incomplete early coronary reperfusion and by reocclusion and reinfarction. We compared the effects of low molecular weight heparin (LMWH) versus unfractionated heparin (UFH) as an adjunct to recombinant tissue-plasminogen activator (alteplase) on coronary artery patency and clinical outcomes in AMI. Methods: Patients with AMI treated with alteplase (n = 439) were randomised to either subcutaneous dalteparin (120 IU/kg every 12 h) for 4-7 days or intravenous infusion of UFH for 48 h. Coronary angiography was performed between day 4 and hospital discharge. Clinical events and safety were evaluated until day 30. Results: Overall there were higher thrombolysis in myocardial infarction (TIMI) flows in the infarct related coronary artery in the dalteparin group (p = 0.01 6). The predefined primary end-point, TIMI grade 3 flow, did not reach statistical significance (dalteparin 69.3% versus heparin 62.5%, p = 0.163). However, TIMI 0-1 flow (13.4 versus 24.4%, p = 0.006) and its combination with intraluminal thrombus (27.9 versus 42.0%, p = 0.003) were less common in the dalteparin group. During the period of randomised treatment there were less myocardial reinfarctions in the dalteparin group (p = 0.010) but after cessation of dalteparin there were more reinfarctions resulting in no difference in death or MI at 30 days. There were no significant differences in major bleeding or stroke after 30 days. Conclusions: In alteplase treated AMI adjunctive dalteparin for 4-7 days seems to reduce the risk of early coronary artery occlusion and reinfarction. However, early after cessation of treatment there is a raised risk of events, which might eliminate any long-term gains. ⌐ 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.
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8.
  • Aavik, Einari, et al. (författare)
  • Global DNA methylation analysis of human atherosclerotic plaques reveals extensive genomic hypomethylation and reactivation at imprinted locus 14q32 involving induction of a miRNA cluster
  • 2015
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 36:16, s. 993-U23
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims Genetics can explain just above 10% of the observed heritability in cardiovascular diseases. Epigenetics is about to provide some further explanations, but the information needed for that is in the accumulation phase. Genome-wide DNA methylation analysis has revealed thousands of genes, which are epigenetically differentially regulated in atherosclerotic plaques. Our results point to an additional level of complexity that needs to be integrated into the aetiology of atherogenesis.We conducted a genome-wide analysis to identify differentially methylated genes in atherosclerotic lesions. Methods DNA methylation at promoters, exons and introns was identified by massive parallel sequencing. Gene expression was analysed by microarrays, qPCR, immunohistochemistry and western blots. Results Globally, hypomethylation of chromosomal DNA predominates in atherosclerotic plaques and two-thirds of genes showing over 2.5-fold differential in DNA methylation are up-regulated in comparison to healthy mammary arteries. The imprinted chromatin locus 14q32 was identified for the first time as an extensively hypomethylated area in atherosclerosis with highly induced expression of miR127, -136, -410, -431, -432, -433 and capillary formation-associated gene RTL1. The top 100 list of hypomethylated promoters exhibited over 1000-fold enrichment for miRNAs, many of which mapped to locus 14q32. Unexpectedly, also gene body hypermethylation was found to correlate with stimulated mRNA expression. Conclusion Significant changes in genomic methylation were identified in atherosclerotic lesions. The most prominent gene cluster activated via hypomethylation was detected at imprinted chromosomal locus 14q32 with several clustered miRNAs that were up-regulated. These results suggest that epigenetic changes are involved in atherogenesis and may offer new potential therapeutic targets for vascular diseases.
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