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Sökning: WFRF:(Frostfeldt Gunnar)

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1.
  • Frostfeldt, Gunnar, et al. (författare)
  • Low molecular weight heparin (Dalteparin) as adjuvant treatment to thrombolysis in acute myocardial infarction-a pilot study : BIOchemical markers in acute coronary syndromes (BIOMACS II)
  • 1999
  • Ingår i: Journal of the American College of Cardiology. - 0735-1097 .- 1558-3597. ; 33:3, s. 627-633
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: This randomized, double blind, placebo-controlled pilot trial evaluated the effect of dalteparin as an adjuvant to thrombolysis in patients with acute myocardial infarction regarding early reperfusion, recurrent ischemia and patency at 24 h. BACKGROUND: Low-molecular-weight heparin, given subcutaneously twice daily without monitoring, might be an attractive alternative to conventional intravenous heparin in the treatment of acute myocardial infarction. METHODS: In 101 patients dalteparin/placebo 100 IU/kg was given just before streptokinase and a second injection 120 IU/kg after 12 h. Monitoring with continuous vector-ECG was done to obtain signs of early reperfusion and later ischemic episodes. Blood samples for myoglobin were obtained at start and after 90 min to evaluate signs of reperfusion. Coronary angiography was performed after 20-28 h to evaluate TIMI-flow in the infarct-related artery. RESULTS: Dalteparin added to streptokinase tended to provide a higher rate of TIMI grade 3 flow in infarct-related artery compared to placebo, 68% versus 51% (p = 0.10). Dalteparin had no effects on noninvasive signs of early reperfusion. In patients with signs of early reperfusion, there seemed to be a higher rate of TIMI grade 3 flow, 74% versus 46% (myoglobin) (p = 0.04) and 73% versus 52% (vector-ECG) (p = 0.11). Ischemic episodes 6-24 h. after start of treatment were fewer in the dalteparin group, 16% versus 38% (p = 0.04). CONCLUSIONS: When dalteparin was added as an adjuvant to streptokinase and aspirin, there were tendencies for less ECG monitoring evidence of recurrent ischemia and better patency at 24 h, warranting further study.
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  • Frostfeldt, Gunnar, et al. (författare)
  • Possible reasons for the prognostic value of troponin-T on admission in patients with ST-elevation myocardial infarction
  • 2001
  • Ingår i: Coronary Artery Disease. - 0954-6928 .- 1473-5830. ; 12:3, s. 227-237
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: In patients with acute myocardial infarction and ST-segment elevation, increased troponin-T (TnT) on admission implies an increased mortality. OBJECTIVE: To elucidate the underlying mechanisms of the prognostic value of TnT. METHODS AND RESULTS: One hundred and one patients were included and all received thrombolytic treatment. The patients were compared according to TnT level on admission (cut-off 0.1 microg/l). Elevation of TnT was associated with long-term mortality and also with longer delay, more episodes of chest pain during the last 24 h and fewer noninvasive signs of reperfusion at 90 min. In the group with elevated TnT, the coronary angiography at 24 h showed a strong trend towards lower patency in the infarct-related artery. TnT was also associated with increased infarct size if a higher cut-off level (0.43 microg/l) was used. In univariate analysis, elevated TnT, longer delay, repeated chest pain, Q-waves on admission and reduced left ventricular (LV) function were significantly associated with long-term mortality. In multivariate models, only reduced LV function and less than TIMI (thrombolysis in myocardial infarction) grade 3 flow turned out to be significant independent risk factors. CONCLUSIONS: The prognostic value of TnT level on admission regarding long-term mortality was confirmed and seems mainly to be explained by its association with longer delay and recent myocardial damage, but its association with reduced effect of thrombolytic treatment, larger infarct size and impaired LV function might also be of importance.
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  • Diderholm, Erik, et al. (författare)
  • The prognostic and therapeutic implications of increased troponin T levels and ST depression in unstable coronary artery disease : the FRISC II invasive troponin T electrocardiogram substudy
  • 2002
  • Ingår i: American Heart Journal. - : Elsevier BV. - 0002-8703 .- 1097-6744. ; 143:5, s. 760-767
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: In unstable coronary artery disease, both increased troponin T level and occurrence of ST-segment depression are associated with a worse prognosis. In the Fast Revascularisation in InStability in Coronary disease trial II invasive study, we evaluated whether the troponin T level, alone and combined with ST depression, identified more severe coronary artery disease or a greater efficacy of an early invasive strategy. METHODS: In the study, 2457 patients with unstable coronary artery disease were randomized to early invasive or noninvasive strategy. Troponin T value and admission electrocardiogram results were available in 2286 patients. RESULTS: In the noninvasive cohort, death or myocardial infarction occurred in 16.6% with troponin T level > or =0.03 microg/L versus 8.5% with troponin T level < 0.03 microg/L (P <.001). In the invasive group, 49% of patients with both ST depression and troponin T level > or =0.03 microg/L had 3-vessel or left main disease compared with 17% if neither finding was present (P <.001). The invasive strategy reduced death/myocardial infarction at 12 months in the cohort with both ST depression and troponin T level > or =0.03 microg/L from 22.1% to 13.2% (risk ratio, 0.60; 95% confidence interval, 0.43 to 0.82; P =.001). In the cohort with either ST depression or troponin T level > or =0.03 microg/L or neither of these findings, the absolute gain of the invasive strategy was smaller and more uncertain. CONCLUSION: Patients with unstable coronary artery disease with the combination of troponin T level > or =0.03 microg/L and ST depression have a poor prognosis and, in half of the cases, 3-vessel or left main disease. In these patients, an early invasive strategy will substantially reduce death/myocardial infarction.
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  • Frostfeldt, Gunnar, 1956- (författare)
  • Coagulation Inhibition and Development of Myocardial Damage in ST-Elevation Myocardial Infarction
  • 2002
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • In 101 patients with ST-elevation myocardial infarction treated with streptokinase the additional effects of lmw-heparin (dalteparin) were investigated. The prognostic value of troponin-T (TnT) was elucidated and the development of myocardial damage was investigated with Positron Emission Tomography (PET).Dalteparin tended to provide a higher rate of TIMI grade 3 flow in the infarct-related artery at 24 h compared to placebo. In patients with signs of early reperfusion there was a higher rate of TIMI grade 3 flow in the dalteparin group compared to placebo. There were significantly fewer patients with ischemic episodes at 6-24 h in the dalteparin compared to placebo group.The increase in coagulation activity was attenuated in the dalteparin group. There was a tendency to more ischemic episodes and lower frequency of TIMI grade 3 flow in patients with persistent elevation of coagulation activity at 18 h. Among deceased patients the coagulation activity was significantly higher than in survivors. The association between elevated TnT on admission and long-term mortality might be explained by longer delay, episodes of chest pain during the last 24 h, less non-invasive signs of reperfusion at 90 minutes, and lower patency in the infarct-related artery at 24 h. Eight patients were investigated with PET at 3h, 24 h and after 3 weeks. PET outlines the infarct region with reduced perfusion and metabolism. The oxidative metabolism in the infarct region at 3 h correlated with the water-Perfusable Tissue Fraction (PTF) and its improvement over time.Dalteparin seems to improve maintenance of coronary patency, which can be explained by attenuation of the increased coagulation activity. Elevated TnT level on admission is associated with a worse outcome, which can partly be explained by less successful fibrinolytic treatment. PET investigations might to be a useful method in future trials evaluating new agents in the treatment of acute myocardial infarction.
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8.
  • Frostfeldt, Gunnar, et al. (författare)
  • Development of myocardial microcirculation and metabolism in acute ST-elevation myocardial infarction evaluated with positron emission tomography
  • 2005
  • Ingår i: Journal of Nuclear Cardiology. - : Springer Science and Business Media LLC. - 1071-3581 .- 1532-6551. ; 12:1, s. 43-54
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Early reperfusion is an established therapeutic objective in acute myocardial infarction (MI). The relationship of regional myocardial microcirculation and metabolism toward outcome in acute human MI is not well known.METHODS AND RESULTS: In 8 patients, positron emission tomography (PET) was performed with oxygen 15-labeled water at 3 hours, 24 hours, and 3 weeks after the start of fibrinolytic treatment, with carbon 11 acetate at 3 hours and with fluorine 18 fluorodeoxyglucose at 24 hours and 3 weeks. Absolute quantification of perfusion and water-perfusable tissue fraction (PTF), metabolic activity, and substrate extraction in 4 regions of interest was performed. Coronary angiography was performed at 24 hours. Short-term outcome at 3 weeks was evaluated by contractile reserve with dobutamine stress echocardiography and lung water measurements with PET. Early regional perfusion, PTF, and extraction and utilization of oxygen and glucose decreased closer to the infarct region ( P < .001 for all). Infarct-related oxygen utilization and extraction of oxygen and glucose were closely related to outcome ( P < .01 for all). PTF improved significantly in the infarct-related regions over time in proportion to early oxygen extraction and utilization.CONCLUSIONS: This pilot study indicates that PET might be useful in the evaluation of treatment efficacy and that restoration of oxidative metabolism is more closely related to myocardial damage recovery than perfusion in the early phase after MI.
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  • Jernberg, Tomas, et al. (författare)
  • Reply.
  • 2004
  • Annan publikation (övrigt vetenskapligt/konstnärligt)
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