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Sökning: WFRF:(vanderPals Jesper)

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1.
  • Koul, Sasha, et al. (författare)
  • Delay From First Medical Contact to Primary PCI and All-Cause Mortality : A Nationwide Study of Patients With ST-Elevation Myocardial Infarction
  • 2014
  • Ingår i: Journal of the American Heart Association. - 2047-9980. ; 3:2, s. e000486-
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-Early reperfusion in the setting of an ST-elevation myocardial infarction (STEMI) is of utmost importance. However, the effects of early versus late reperfusion in this patient group undergoing primary percutaneous coronary intervention (PCI) have so far been inconsistent in previous studies. The purpose of this study was to evaluate in a nationwide cohort the effects of delay from first medical contact to PCI (first medical contact [FMC]-to-PCI) and secondarily delay from symptom-to-PCI on clinical outcomes. Methods and Results-Using the national Swedish Coronary Angiography and Angioplasty Register (SCAAR) registry, STEMI patients undergoing primary PCI between the years 2003 and 2008 were screened for. A total of 13 790 patients were included in the FMC-to-PCI analysis and 11 489 patients were included in the symptom-to-PCI analyses. Unadjusted as well as multivariable analyses showed an overall significant association between increasing FMC-to-PCI delay and 1-year mortality. A statistically significant increase in mortality was noted at FMC-to-PCI delays exceeding 1 hour in an incremental fashion. FMC-to-PCI delays in excess of 1 hour were also significantly associated with an increase in severe left ventricular dysfunction at discharge. An overall significant association between increasing symptom-to-PCI delays and 1-year mortality was noted. However, when stratified into time delay cohorts, no symptom-to-PCI delay except for the highest time delay showed a statistically significant association with increased mortality. Conclusions-Delays in FMC-to-PCI were strongly associated with increased mortality already at delays of more than 1 hour, possibly through an increase in severe heart failure. A goal of FMC-to-PCI of less than 1 hour might save patient lives.
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3.
  • Braun, Oscar, et al. (författare)
  • Concomitant use of warfarin and ticagrelor as an alternative to triple antithrombotic therapy after an acute coronary syndrome.
  • 2015
  • Ingår i: Thrombosis Research. - : Elsevier BV. - 1879-2472 .- 0049-3848. ; 135:1, s. 26-30
  • Tidskriftsartikel (refereegranskat)abstract
    • Treatment with warfarin in combination with clopidogrel has been shown to reduce the incidence of major bleeding as compared to triple antithrombotic therapy (TT; warfarin, clopidogrel and aspirin). However, there are uncertainties regarding the risk for thrombosis since poor-responsiveness to clopidogrel is common. Ticagrelor is a more potent platelet inhibitor, but data supporting concurrent use of ticagrelor and warfarin (dual antithrombotic therapy, DT) is limited. This study therefore sought to evaluate the risk of bleeding and thrombosis associated with DT after an acute coronary syndrome (ACS).
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4.
  • Demidova, Marina, et al. (författare)
  • ST-segment dynamics during reperfusion period and the size of myocardial injury in experimental myocardial infarction.
  • 2011
  • Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 1532-8430 .- 0022-0736. ; 44:1, s. 74-81
  • Tidskriftsartikel (refereegranskat)abstract
    • Exacerbation of ST elevation associated with reperfusion has been reported in patients with myocardial infarction. However, the cause of the "reperfusion peak" and relation of its magnitude to the size of myocardial damage has not been explored. The aim of our study was to assess the correlation between the ST-dynamics during reperfusion, the myocardium at risk (MaR), and the infarct size (IS).
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5.
  • Demidova, Marina, et al. (författare)
  • T wave alternans in experimental myocardial infarction: Time course and predictive value for the assessment of myocardial damage.
  • 2013
  • Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 1532-8430 .- 0022-0736. ; 46:3, s. 263-269
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: T-wave alternans (TWA) is associated with prognosis after myocardial infarction (MI), however its link to the extent of ischemic injury has not been clarified. We analyzed the course of TWA and its relation to myocardial damage in experimental myocardial infarction. METHODS: In 21 pigs, infarction was induced by 40-minute long balloon inflation in LAD under continuous 12-lead ECG monitoring. TWA was assessed in a 32-beat sliding window, using periodic component analysis and the Laplacian Likelihood Ratio method. Myocardium at risk (MaR) and infarct size (IS) were evaluated by SPECT and magnetic resonance imaging respectively. RESULTS: TWA appeared at 7.2±4.5minutes of occlusion, reached its maximum at 12.7±6.3 and lasted until 26.5±9.2minutes. The maximal level of TWA was associated with both MaR (r=0.499, p=0.035) and IS (r=0.65, p=0.004). CONCLUSION: TWA magnitude is associated with both MaR and IS in experiment, which encourages further studies in clinical settings.
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7.
  • Gidlöf, Olof, et al. (författare)
  • Cardiospecific microRNA Plasma Levels Correlate with Troponin and Cardiac Function in Patients with ST Elevation Myocardial Infarction, Are Selectively Dependent on Renal Elimination, and Can Be Detected in Urine Samples.
  • 2011
  • Ingår i: Cardiology. - : S. Karger AG. - 1421-9751 .- 0008-6312. ; 118:4, s. 217-226
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Circulating microRNAs (miRNAs) are promising as biomarkers for various diseases. We examined the release patterns of cardiospecific miRNAs in a closed-chest, large animal ischemia-reperfusion model and in patients with ST elevation myocardial infarction (STEMI). Methods: Six anesthetized pigs were subjected to coronary occlusion-reperfusion. Plasma, urine, and clinical parameters were collected from 25 STEMI patients undergoing primary percutaneous coronary intervention. miRNA was extracted and measured with qPCR. Results: In the pig reperfusion model miR-1, miR-133a, and miR-208b increased rapidly in plasma with a peak at 120 min, while miR-499-5p remained elevated longer. In patients with STEMI all 4 miRNAs increased abruptly from 70-fold to 3,000-fold in plasma, with a peak within 12 h (p < 0.01). miR-1 and miR-133a both correlated strongly with the glomerular filtration rate (GFR), indicating renal elimination. This was confirmed by detection of miR-1 and miR-133a, but not miR-208b or miR-499-5p, in urine. Peak values of miR-208b correlated with peak troponin and the ejection fraction. Conclusion: We demonstrate a distinct and rapid increase in levels of cardiospecific miRNA in the circulation after myocardial infarction. Release of miRNAs correlated with cardiomyocyte necrosis markers, the ejection fraction, and the GFR, indicating a possible role for these molecules as biomarkers for the diagnosis of STEMI as well as the prediction of long-term complications.
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8.
  • Gilje, Patrik, et al. (författare)
  • Plasma Levels of Liver-Specific miR-122 is Massively Increased in a Porcine Cardiogenic Shock Model and Attenuated by Hypothermia.
  • 2012
  • Ingår i: Shock. - 1540-0514. ; 37, s. 234-238
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS:: Tissue-specific circulating microRNAs are released into the blood after organ injury. In an ischemic porcine cardiogenic shock model we investigated the release pattern of cardiacspecific miR-208b and liver-specific miR-122 and assessed the effect of therapeutic hypothermia on their respective plasma levels. METHODS AND RESULTS:: Pigs were anesthetized and cardiogenic shock was induced by inflation of a PCI-balloon in the proximal LAD for 40 minutes followed by reperfusion. After fulfillment of the predefined shock criteria, the pigs were randomized to hypothermia (33°C, n=6) or normothermia (38°C, n=6). Circulating microRNAs were extracted from plasma and measured with quantitative real-time PCR. Tissue specificity was assessed by microRNA extraction from porcine tissues followed by quantitative real-time PCR. In vitro, the release of miR-122 from a cultured hepatocyte cell line exposed to either hypoxia or acidosis was assessed by real-time PCR. miR-122 was found to be highly liver specific whereas miR-208b was expressed exclusively in the heart. In the control group ischemic cardiogenic shock induced a 460.000-fold and a 63.000-fold increase in plasma levels of miR-122 (p<0.05) and miR-208b (p<0.05), respectively. Therapeutic hypothermia significantly diminished the increase of miR-122 compared to the normothermic group (p<0.005). In our model, hypothermia was initiated after coronary reperfusion and did neither affect myocardial damage as previously assessed by magnetic resonance imaging nor the plasma level of miR-208b. CONCLUSIONS:: Our results indicate that liver-specific miR-122 is released into the circulation in the setting of cardiogenic shock and that therapeutic hypothermia significantly reduces the levels of miR-122.
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9.
  • Götberg, Matthias, et al. (författare)
  • A Pilot Study of Rapid Cooling by Cold Saline and Endovascular Cooling Before Reperfusion in Patients With ST-Elevation Myocardial Infarction.
  • 2010
  • Ingår i: Circulation. Cardiovascular Interventions. - 1941-7632. ; 3, s. 400-407
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-Experimental studies have shown that induction of hypothermia before reperfusion of acute coronary occlusion reduces infarct size. Previous clinical studies, however, have not been able to show this effect, which is believed to be mainly because therapeutic temperature was not reached before reperfusion in the majority of the patients. We aimed to evaluate the safety and feasibility of rapidly induced hypothermia by infusion of cold saline and endovascular cooling catheter before reperfusion in patients with acute myocardial infarction. METHODS AND RESULTS: =0.12). Despite similar duration of ischemia (174+/-51 minutes versus 174+/-62 minutes, hypothermia versus control, P=1.00), infarct size normalized to myocardium at risk was reduced by 38% in the hypothermia group compared with the control group (29.8+/-12.6% versus 48.0+/-21.6%, P=0.041). This was supported by a significant decrease in both peak and cumulative release of Troponin T in the hypothermia group (P=0.01 and P=0.03, respectively). Conclusions-The protocol demonstrates the ability to reach a core body temperature of <35 degrees C before reperfusion in all patients without delaying primary percutaneous coronary intervention and that combination hypothermia as an adjunct therapy in acute myocardial infarction may reduce infarct size at 3 days as measured by MRI. Clinical Trial Registration-URL: http://clinicaltrials.gov. Unique identifier: NCT00417638.
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10.
  • Götberg, Matthias, et al. (författare)
  • Mild hypothermia reduces acute mortality and improves hemodynamic outcome in a cardiogenic shock pig model.
  • 2010
  • Ingår i: Resuscitation. - : Elsevier BV. - 1873-1570 .- 0300-9572. ; 81, s. 1190-1196
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: Cardiogenic shock is the main cause of death in patients hospitalized due to an acute myocardial infarction. Mild hypothermia reduces metabolism and could offer protective effects for this condition. The aim of our study was to investigate if mild therapeutic hypothermia would improve outcome and hemodynamic parameters in an ischemic cardiogenic shock pig model. METHODS: Twenty-five pigs (40-50kg) were anesthetized and a normothermic temperature of 38 degrees C was established utilising an endovascular cooling catheter in a closed-chest model. A Swan-Ganz catheter was placed in the pulmonary artery. Hemodynamic parameters were continuously monitored and blood gases were sampled every 30min. Ischemia was induced by inflation of a PCI balloon in proximal LAD for 40min. Sixteen pigs that have fulfilled predefined shock criteria were randomized to hypothermia (n=8), or normothermia (n=8). Hypothermia (33 degrees C) was induced after onset of reperfusion by using an endovascular temperature modulating catheter and was maintained until termination of the experiment. RESULTS: The pigs in the hypothermia group were cooled to <34 degrees C in approximately 45min. 5/8 pigs in the normothermia group died while all pigs in the hypothermia group survived (p<0.01). Stroke volume and blood pressure were significantly higher in the hypothermia group (p<0.05), whereas heart rate was significantly lower in the hypothermia group (p=0.01). Cardiac output did not differ among the groups (p=0.13). Blood gas analysis revealed higher mixed venous oxygen saturation, pH, and base excess in the hypothermia group indicating less development of metabolic acidosis (p<0.05). CONCLUSIONS: In this pig model, mild therapeutic hypothermia reduces acute mortality in cardiogenic shock, improves hemodynamic parameters and reduces metabolic acidosis. These findings suggest a possible clinical benefit of therapeutic hypothermia for patients with acute cardiogenic shock.
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