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Per Tornvall

Publications and source records attributed to Per Tornvall.

31 records · Page 2Linked to original sources
PubMed2004

Prognostic value of plasma interleukin-6 concentrations and the -174 G > C and -572 G > C promoter polymorphisms of the interleukin-6 gene in patients with acute myocardial infarction treated with thrombolysis.

The present study was performed to investigate the prognostic value of plasma interleukin-6 (IL-6) concentrations and promoter polymorphisms of the IL-6 gene in patients with acute myocardial infarction treated with thrombolysis. Two hundred and eight patients with myocardial infarction treated with thrombolysis were included and followed for 2-5 years. Plasma concentrations of IL-6 were measured at admission and 48 h after admission. Genotyping for the -174 G > C and -572 G > C IL-6 polymorphisms was performed. Patients who died of cardiovascular causes or suffered a new myocardial infarction during follow-up had increased plasma concentrations of IL-6 at admission (P < 0.002) and at 48 h after admission (P < 0.05) compared with patients who had an uneventful course. IL-6 levels above the median at admission were independently associated with a worse prognosis. No associations were found between IL-6 levels and the promoter polymorphisms. The -174 G > C polymorphism was not associated with cardiovascular death or a new myocardial infarction, whereas the -572 G > C polymorphism showed a borderline significant increase in risk (P = 0.05) in univariate analysis. In conclusion, the early IL-6 response during myocardial infarction is associated with prognosis in patients with Q-wave myocardial infarction, whereas no associations were found between IL-6 genotype and phenotype.

Aged↗
PubMed2004

Effect of Interleukin-6 promoter polymorphisms in survivors of myocardial infarction and matched controls in the North and South of Europe. The HIFMECH Study.

Elevated plasma IL-6 levels have been implicated in the pathogenesis of coronary heart disease. We have investigated the association of two polymorphisms in the promoter of IL-6 (-572G>C and -174G>C) with levels of inflammatory markers and risk of myocardial infarction (MI) in a European study of MI survivors and age-matched controls from two high-risk centres in the North of Europe, and two low risk centres in the South. IL-6 and CRP levels were similar in controls in both regions, but were higher in cases. For the -174G>C polymorphism the rare -174C allele showed a regional difference in allele frequency, being more common in the North European group (0.43 vs 0.28; p < 0.0005), where -174C allele carriers showed an apparent reduced risk of MI compared to -174GG homozygotes (OR 0.53, 95%CI 0.32, 0.86). No such effect was observed in the South or with the -572G>C in either group. Neither genotype was associated with a significant effect on plasma IL-6 levels in either cases or controls. Furthermore, no regional difference was observed in the frequency of the -572G>C SNP, suggesting that these polymorphisms are unlikely to be contributing to the observed increased risk of cardiovascular disease in Northern Europe.

Adult↗
PubMed2003

[C-reactive protein potential risk factor for cardiovascular disease].

C-reactive protein (CRP) is a protein produced mainly in the liver upon stimulation by interleukin-6. CRP is part of the acute phase response to inflammation and plasma concentrations rise 100-1000 times in patients with for example bacterial infections. High sensitive methods have made it possible to measure and compare low CRP levels in plasma. Prospective studies have shown that increased but comparatively low plasma CRP concentrations are associated with future coronary heart disease (CHD) in healthy individuals and in patients with known CHD. Further support for an important role for CRP comes from in vitro studies that have suggested that the CRP protein is intimately and actively involved in the atherosclerotic process. This has stimulated the interest for clinical evaluation and treatment of increased plasma CRP levels.

Biomarkers↗
PubMed2003

Comparison of effects of a thrombin-based femoral artery closure device with those of a mechanical compression device on serum C-reactive protein and amyloid A after percutaneous coronary intervention.

The present study evaluates whether the closing procedure of the femoral artery after percutaneous coronary intervention influences the degree of inflammation related to the procedure as measured by C-reactive protein (CRP) and serum amyloid A (SAA). A thrombin-based device (Duett sealing device) was compared with a mechanical compression device (FemoStop).

Aged↗
PubMed2003

Autoantibodies against modified low-density lipoproteins in coronary artery disease.

OBJECTIVES: To evaluate the importance of different autoantibodies against modified low-density lipoprotein (LDL) in patients with coronary artery disease (CAD). BACKGROUND: Previous studies of autoantibodies against LDL have shown that patients with CAD have increased titers of autoantibodies against LDL modified by copper and malondialdehyde (MDA), whereas there is a lack of information about autoantibody titers against LDL modified by hypochlorite (HOCl). Studies of autoantibodies in relation to severity of atherosclerosis are few and have reached divergent results. Furthermore, no data exist on the relationship between autoantibody titers and prognosis. METHODS: Titers of autoantibodies against copper-, MDA- and HOCl-modified LDL were determined in serum by ELISA. Autoantibody titers in young male survivors of a first myocardial infarction were compared with those of healthy controls and related to coronary angiographic findings and to prognosis during 11 years of follow-up. RESULTS: Patients had higher titers of autoantibodies against LDL modified by copper and MDA than controls. In contrast, no consistent associations were found between autoantibody titers and global severity of coronary atherosclerosis or number and severity of coronary stenoses and prognosis. CONCLUSIONS: The prognostic value of autoantibodies against modified LDL is limited in young postinfarction patients despite the fact that autoantibody titers against copper- and MDA-modified LDL are raised compared with healthy controls. Furthermore, the results indicate that autoantibodies against modified LDL are not protective in later stages of coronary atherosclerosis.

Adult↗
PubMed2003

Under utilisation of evidence-based treatment partially explains for the unfavourable prognosis in diabetic patients with acute myocardial infarction.

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 20440 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.

Adult↗
PubMed2003

No evidence that the PLA1/PLA2 polymorphism of platelet glycoprotein IIIa is implicated in angiographically characterized coronary atherosclerosis and premature myocardial infarction.

Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet aggregation. A polymorphism of the gene encoding the IIIa subunit, with the two allele forms PLA1 and PLA2, has been identified. Some, but not all, studies suggest that the PLA2 allele confers an increased risk of suffering a myocardial infarction. Conversely, a recent study suggests that the PLA1 allele may contribute to early atherosclerosis and more rapid progression of stable coronary artery disease. To test whether these associations could be reproduced in a well-characterized sample of survivors of premature myocardial infarction, we examined 369 patients admitted to coronary care units in the Stockholm area who suffered a first myocardial infarction before the age of 60 years. There were no significant differences in extent of coronary artery disease according to PLA genotype group (based on quantitative coronary angiography). In addition, the frequencies of PLA1 and PLA2 alleles did not differ from those of 388 well-matched control subjects without coronary artery disease. These results suggest that the PLA1/PLA2 polymorphism of the platelet glycoprotein IIIa gene does not substantially contribute to the development of coronary atherosclerosis or the genetic susceptibility to premature myocardial infarction.

Age Factors↗
PubMed2002

[Treatment of coronary artery stenosis. Considerable improvement of the catheter-based technique].

The technique to treat coronary artery stenoses by percutaneous coronary intervention (PCI) was introduced in 1977 and has since undergone considerable improvement. Important developments have been: 1. The use of stents, which minimize the risk of acute occlusions and reduce the incidence of restenosis. 2. Improvement in antiplatelet therapy, which decrease the risk of thromboembolic complications during and after PCI. 3. Specific treatment against restenosis by drug-eluting stents. PCI treatment with stents and reinforced antiplatelet therapy is well established today. If the initial encouraging results with PCI using drug-eluting stents without restenosis hold their promise, the vast majority of coronary revascularisations will be performed by PCI in the future.

Angioplasty, Balloon, Coronary↗
PubMed2002

Platelet function and myocardial injury during percutaneous coronary intervention.

BACKGROUND: Several studies have shown that inhibition of the glycoprotein IIb/IIIa receptor can reduce myocardial injury during percutaneous coronary intervention (PCI). The present study was performed to investigate platelet function, using a bedside diagnostic system, to test the hypothesis that patients with activated platelets have an increased risk for myocardial injury during PCI. Such information would be valuable to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor during and after the procedure. METHODS: 155 consecutive patients undergoing PCI were included in the study. 94 of the patients had stable angina pectoris and the remaining patients had unstable angina pectoris or ongoing myocardial infarction. Troponin T levels were measured in serum before PCI and at 6 am the day after PCI by an immunoassay. Platelet function was analyzed in arterial blood before PCI using the platelet function analyzer PFA-100(R) by Dade Behring. RESULTS: The platelet function analyzer PFA-100(R) could not discriminate between patients with or without myocardial injury during the procedure but between patients with or without acetyl salicylic acid. CONCLUSION: The platelet function analyzer PFA-100(R) cannot be used to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor but the results indicate that PFA-100(R) can be used to monitor platelet effects of ASA therapy.

Aged↗
PubMedDate not supplied

[PCI is now a refined method for treatment of coronary stenoses].

The technique of Percutaneous Coronary Intervention (PCI) has improved considerably over the last decades. Important developments have been the introduction of stents and better anticoagulation treatment. PCI is used most commonly in the treatment of unstable angina pectoris or non ST-elevation myocardial infarction. In Sweden today, more than half of the patients with ST-elevation myocardial infarction are treated primarily with PCI. Despite the high degree of opening of the infarct-related artery, the reduction in mortality is modest compared with treatment with thrombolysis indicating that there is room for considerable improvement. There is a need for randomised studies of adjunctive therapies but it can be speculated that thrombectomy devices and specific reperfusion injury therapy might reduce mortality in PCI treatment of ST-elevation myocardial infarction.

Angina Pectoris↗