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Sökning: L773:2153 7658 OR L773:2153 7933

  • Resultat 1-10 av 18
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1.
  • Erlinge, David, et al. (författare)
  • Therapeutic Hypothermia for the Treatment of Acute Myocardial Infarction-Combined Analysis of the RAPID MI-ICE and the CHILL-MI Trials.
  • 2015
  • Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert, Inc.. - 2153-7933 .- 2153-7658. ; 5:2, s. 77-84
  • Tidskriftsartikel (refereegranskat)abstract
    • In the randomized rapid intravascular cooling in myocardial infarction as adjunctive to percutaneous coronary intervention (RAPID MI-ICE) and rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction CHILL-MI studies, hypothermia was rapidly induced in conscious patients with ST-elevation myocardial infarction (STEMI) by a combination of cold saline and endovascular cooling. Twenty patients in RAPID MI-ICE and 120 in CHILL-MI with large STEMIs, scheduled for primary percutaneous coronary intervention (PCI) within <6 hours after symptom onset were randomized to hypothermia induced by rapid infusion of 600-2000 mL cold saline combined with endovascular cooling or standard of care. Hypothermia was initiated before PCI and continued for 1-3 hours after reperfusion aiming at a target temperature of 33°C. The primary endpoint was myocardial infarct size (IS) as a percentage of myocardium at risk (IS/MaR) assessed by cardiac magnetic resonance imaging at 4±2 days. Patients randomized to hypothermia treatment achieved a mean core body temperature of 34.7°C before reperfusion. Although significance was not achieved in CHILL-MI, in the pooled analysis IS/MaR was reduced in the hypothermia group, relative reduction (RR) 15% (40.5, 28.0-57.6 vs. 46.6, 36.8-63.8, p=0.046, median, interquartile range [IQR]). IS/MaR was predominantly reduced in early anterior STEMI (0-4h) in the hypothermia group, RR=31% (40.5, 28.8-51.9 vs. 59.0, 45.0-67.8, p=0.01, median, IQR). There was no mortality in either group. The incidence of heart failure was reduced in the hypothermia group (2 vs. 11, p=0.009). Patients with large MaR (>30% of the left ventricle) exhibited significantly reduced IS/MaR in the hypothermia group (40.5, 27.0-57.6 vs. 55.1, 41.1-64.4, median, IQR; hypothermia n=42 vs. control n=37, p=0.03), while patients with MaR<30% did not show effect of hypothermia (35.8, 28.3-57.5 vs. 38.4, 27.4-59.7, median, IQR; hypothermia n=15 vs. control n=19, p=0.50). The prespecified pooled analysis of RAPID MI-ICE and CHILL-MI indicates a reduction of myocardial IS and reduction in heart failure by 1-3 hours with endovascular cooling in association with primary PCI of acute STEMI predominantly in patients with large area of myocardium at risk. (ClinicalTrials.gov id NCT00417638 and NCT01379261).
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2.
  • Heinius, Göran, et al. (författare)
  • Effects of Different Fluid Regimes and Desmopressin on Uncontrolled Hemorrhage During Hypothermia in the Rat
  • 2012
  • Ingår i: Therapeutic Hypothermia and Temperature Management. - : Mary Ann Liebert. - 2153-7658 .- 2153-7933. ; 2:2, s. 53-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Resuscitation with large volumes of crystalloids during traumatic hemorrhagic shock might increase the mortality by inducing rebleeding. However, few studies have addressed this problem during hypothermic conditions. Sixty-eight Sprague-Dawley rats were exposed to a standardized femoral artery injury and resuscitated with low (LRe), medium (MRe), or high (HRe) intensity using lactated Ringer's solution after being cooled to 30°C. An additional MRe group was also given desmopressin since this drug might reverse hypothermic-induced impairment of the primary hemostasis. The rats were rewarmed after 90 minutes and observed for 3 hours. The incidence, on-set time, duration, and volume of bleedings and hemodynamic changes were recorded. Rebleedings occurred in 60% of all animals and were more voluminous in the HRe group than in the LRe group (p=0.01). The total rebleeding volume per animal increased with the rate of fluid administration (r=0.50, p=0.01) and the duration of each rebleeding episode was longer in the HRe group than in the LRe group (p<0.001). However, the mortality tended to be higher in the LRe group (LRe=6/15, MRe=1/15, HRe=2/15, p=0.07). Desmopressin did not change the bled volume or the mortality. Overall, the mortality increased if rebleeding occurred (10/35 rebleeders died vs. 1/25 nonrebleeders, p=0.015). Liberal fluid administration increased the rebleeding volume while a trend toward higher mortality was seen with the restrictive fluid program. Desmopressin had no effect on the studied parameters.
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3.
  • Rass, Verena, et al. (författare)
  • The Effect of Temperature Increases on Brain Tissue Oxygen Tension in Patients with Traumatic Brain Injury : A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Substudy
  • 2021
  • Ingår i: Therapeutic Hypothermia and Temperature Management. - : Mary Ann Liebert. - 2153-7658 .- 2153-7933. ; 11:2, s. 122-131
  • Tidskriftsartikel (refereegranskat)abstract
    • Fever may aggravate secondary brain injury after traumatic brain injury (TBI). The aim of this study was to identify episodes of temperature increases through visual plot analysis and algorithm supported detection, and to describe associated patterns of changes in on brain tissue oxygen tension (PbtO2). Data derive from the high-resolution cohort of the multicenter prospective Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) study. Temperature increases (≥0.5°C) were visually identified in 33 patients within the first 11 days of monitoring. Generalized estimating equations were used to detect significant changes of systemic and neuromonitoring parameters from baseline to the highest temperature. Patients were median 50 (interquartile range [IQR], 35–62) years old, and presented with a Glasgow Coma Scale (GCS) of 8 (IQR, 4–10). In 202 episodes of temperature increases, mean temperature rose by 1.0°C ± 0.5°C within 4 hours. Overall, PbtO2 slightly increased (ΔPbtO2 = 0.9 ± 6.1 mmHg, p = 0.022) during temperature increases. PbtO2 increased in 35% (p < 0.001), was stable in 49% (p = 0.852), and decreased in 16% (p < 0.001) of episodes. During episodes of temperature increases and simultaneous drops in PbtO2, cerebral perfusion pressure (CPP) decreased (ΔCPP −6.3 ± 11.5 mmHg; p < 0.001). Brain tissue hypoxia (PbtO2 <20 mmHg) developed during 27/164 (17%) episodes of effervescences, in the remaining 38/202 episodes baseline PbtO2 was already <20 mmHg. Comparable results were found when using algorithm-supported detection of temperature increases. In conclusion, during effervescences, PbtO2 was mostly stable or slightly increased. A decrease of PbtO2 was observed in every sixth episode, where it was associated with a decrease in CPP. Our data highlight the need for special attention to CPP monitoring and maintenance during episodes of fever.
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4.
  • Annborn, Martin, et al. (författare)
  • The Combination of Biomarkers for Prognostication of Long-Term Outcome in Patients Treated with Mild Hypothermia After Out-of-Hospital Cardiac Arrest-A Pilot Study
  • 2016
  • Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert, Inc.. - 2153-7933. ; 6:2, s. 85-90
  • Tidskriftsartikel (refereegranskat)abstract
    • To explore if the brain biomarker neuron-specific enolase (NSE) in combination with a biomarker for stress; CT-proAVP (copeptin), oxidation; peroxiredoxin 4 (Prx4), inflammation; procalcitonin (PCT), or with biomarkers from the heart; midregional proatrial natriuretic peptide (MR-proANP), or troponin T (TnT) can improve the prognostic accuracy of long-term outcome after out-of-hospital cardiac arrest (OHCA). Serum samples from cardiac arrest patients, treated at 33°C for 24 hours, were collected serially at 12, 24, and 48 hours after cardiac arrest. The concentration of the investigated biomarkers was measured using stored samples, and long-term outcome was evaluated by the cerebral performance category (CPC) at 6 months. Poor outcome was defined as CPC 3-5. Sixty-two patients with OHCA of presumed cardiac cause were included. NSE had best prognostic accuracy for poor outcome at 48 hours with a receiver operating characteristic area under curve (AUC) of 0.94 (95% confidence interval [CI] 0.87-1). The combination of NSE with TnT, both at 48 hours, increased the AUC to 0.98 (95% CI 0.95-1, likelihood ratio [LR] test p-value 0.07, net reclassification index [NRI] <0.001); NSE and MR-proANP, both at 12 hours, yielded an AUC of 0.91 (95% CI 0.80-1, LR test p-value 0.0014, NRI p-value 0.003); NSE at 48 hours with MR-proANP at 12 hours yielded an AUC of 0.97 (95% CI 0.92-1, LR test p-value 0.055, NRI p-value 0.04). This pilot study suggests that a combination of biomarkers with NSE could be beneficial for improving early prognostication of long-term outcome following OHCA.
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9.
  • Kander, Thomas, et al. (författare)
  • Bleeding complications after cardiac arrest and targeted temperature management, a post hoc study of the targeted temperature management trial
  • 2019
  • Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert, Inc.. - 2153-7933. ; 9:3, s. 177-183
  • Tidskriftsartikel (refereegranskat)abstract
    • Target Temperature Management (TTM) is standard care following out of hospital cardiac arrest (OHCA). The aim of the study was to evaluate if treatment temperature (33°C or 36°C) or other predefined variables were associated with the occurrence of bleeding in the TTM study. This study is a predefined, post hoc analysis of the TTM trial, a multinational randomized controlled trial comparing treatment at 33°C and 36°C for 24 hours after OHCA with return of spontaneous circulation. Bleeding events from several locations were registered daily. The main outcome measure was occurrence of any bleeding during the first 3 days of intensive care. Risk factors for bleeding, including temperature allocation, were evaluated. Complete data were available for 722/939 patients. Temperature allocation was not associated with bleeding either in the univariable (p = 0.95) or in the primary multivariable analysis (odds ratio [OR] 0.95; 95% confidence interval [CI] 0.64–1.41, p = 0.80). A multiple imputation model, including all patients, was used as a sensitivity analysis, rendering similar results (OR 0.98; 95% CI 0.69–1.38, p = 0.92). Factors associated with bleeding were increasing age, female sex, and angiography with percutaneous coronary intervention (PCI) within 36 hours of cardiac arrest (CA) in both the primary and the sensitivity analysis. TTM at 33°C, when compared to TTM at 36°C, was not associated with an increased incidence of bleeding during the first 3 days of intensive care after CA. Increasing age, female gender, and PCI were independently associated with any bleeding the first 3 days after CA.
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10.
  • Kander, Thomas, et al. (författare)
  • Wide Temperature Range Testing with ROTEM Coagulation Analyses.
  • 2014
  • Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert, Inc.. - 2153-7933. ; 4:3, s. 125-130
  • Tidskriftsartikel (refereegranskat)abstract
    • Mild induced hypothermia is used for neuroprotection in patients successfully resuscitated after cardiac arrest. Temperature-dependent effects on rotational thromboelastometry (ROTEM(®)) assays with EXTEM(®), FIBTEM(®), or APTEM(®) in cardiac arrest patients have not previously been studied. Ten patients with out-of-hospital cardiac arrest who underwent induced hypothermia were studied during stable hypothermia at 33°C. ROTEM temperature effects on EXTEM, FIBTEM, and APTEM assays were studied at temperatures set between 30°C and 42°C. Citrated whole blood test tubes were incubated in temperature-adjusted heating blocks and then investigated at respective temperature in the temperature-adjusted ROTEM. The following variables were determined: clotting time (CT), clot formation time (CFT), α-angle, and maximum clot firmness (MCF). The results from hypo- and hyperthermia samples were compared with the samples incubated at 37°C using the Wilcoxon matched-pairs signed-rank test. A p-value of <0.05 was considered significant. CT-EXTEM(®) and CT-APTEM(®) were prolonged by hypothermia at 30°C (p<0.01 for both) and 33°C (p<0.05 for both). Hyperthermia at 42°C shortened CT-EXTEM (p<0.05) and CT-APTEM (p<0.01). CFT-EXTEM(®) and CFT-APTEM(®) were markedly prolonged by hypothermia at 30°C, 33°C, and 35°C (p<0.01 for all except CFT-EXTEM, 35°C [p<0.05]). The α-angle-EXTEM was markedly decreased at 30°C, 33°C, and 35°C (p<0.01) but increased at 40°C (p<0.05) and 42°C (p<0.01); α-angle-APTEM showed similar results. MCF was unchanged at different temperatures for all tests. ROTEM (EXTEM, FIBTEM, and APTEM assays) revealed a hypocoagulative response to in vitro-applied hypothermia in the blood of cardiac arrest patients reflected in the prolonged clot initiation and decreased clot propagation. Hyperthermia showed the opposite effects. Clot firmness was not affected by temperature.
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