What is the primary time window for the administration of fibrinolytic therapy?

1. Albers GW. Expanding the window for thrombolytic therapy in acute stroke. The potential role of acute MRI for patient selection. Stroke 1999;30:2230-2237.


2. Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008;359:1317-1329.

3. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Blaha MJ, et al. Heart disease and stroke statistics—2014 update: a report from the American Heart Association. Circulation 2014;129:e28-e292.

4. NINDS rt-PA Stroke Study Group. Intracerebral hemorrhage after intravenous tPA therapy for ischemic stroke. Stroke 1997;28:2109-2118.

5. Greenberg DA. Neurogenesis and stroke. CNS Neurol Disord Drug Targets 2007;6:321-325.

6. Adams HP Jr, Adams RJ, Brott T, del Zoppo GJ, Furlan A, Goldstein LB, et al. Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association. Stroke 2003;34:1056-1083.

7. Wang X, Tsuji K, Lee SR, Ning M, Furie KL, Buchan AM, et al. Mechanisms of hemorrhagic transformation after tissue plasminogen activator reperfusion therapy for ischemic stroke. Stroke 2004;35:2726-2730.

8. Wang W, Li M, Chen Q, Wang J. Hemorrhagic transformation after tissue plasminogen activator reperfusion therapy for ischemic stroke: mechanisms, models, and biomarkers. Mol Neurobiol 2015;52:1572.

9. Jickling GC, Liu DZ, Stamova B, Ander BP, Zhan X, Lu A, et al. Hemorrhagic transformation after ischemic stroke in animals and humans. J Cereb Blood Flow Metab 2014;34:185-199.

10. Lapchak PA. Hemorrhagic transformation following ischemic stroke: significance, causes, and relationship to therapy and treatment. Curr Neurol Neurosci Rep 2002;2:38-43.

11. Won S, Lee JH, Wali B, Stein DG, Sayeed I. Progesterone attenuates hemorrhagic transformation after delayed tPA treatment in an experimental model of stroke in rats: involvement of the VEGF-MMP pathway. J Cereb Blood Flow Metab 2014;34:72-80.

12. Ballabh P, Braun A, Nedergaard M. The blood-brain barrier: an overview: structure, regulation, and clinical implications. Neurobiol Dis 2004;16:1-13.

13. Ishiguro M, Kawasaki K, Suzuki Y, Ishizuka F, Mishiro K, Egashira Y, et al. A Rho kinase (ROCK) inhibitor, fasudil, prevents matrix metalloproteinase-9-related hemorrhagic transformation in mice treated with tissue plasminogen activator. Neuroscience 2012;220:302-312.

14. Ishiguro M, Mishiro K, Fujiwara Y, Chen H, Izuta H, Tsuruma K, et al. Phosphodiesterase-III inhibitor prevents hemorrhagic transformation induced by focal cerebral ischemia in mice treated with tPA. PLoS One 2010;5:e15178.

15. Machado LS, Kozak A, Ergul A, Hess D, Borlongan CV, Fagan SC. Delayed minocycline inhibits ischemia-activated matrix metalloproteinases 2 and 9 after experimental stroke. BMC Neurosci 2006;7:56.

16. Murata Y, Rosell A, Scannevin RH, Rhodes KJ, Wang X, Lo EH. Extension of the thrombolytic time window with minocycline in experimental stroke. Stroke 2008;39:3372-3377.

17. Fagan SC, Waller JL, Nichols FT, Edwards DJ, Pettigrew LC, Clark WM, et al. Minocycline to improve neurologic outcome in stroke (MINOS): a dose-finding study. Stroke 2010;41:2283-2287.

18. Switzer JA, Hess DC, Ergul A, Waller JL, Machado LS, Portik-Dobos V, et al. Matrix metalloproteinase-9 in an exploratory trial of intravenous minocycline for acute ischemic stroke. Stroke 2011;42:2633-2635.

19. Blacker DJ, Prentice D, Alvaro A, Bates TR, Bynevelt M, Kelly A, et al. Reducing haemorrhagic transformation after thrombolysis for stroke: a strategy utilising minocycline. Stroke Res Treat 2013;2013:362961.

20. Matsumoto M. Cilostazol in secondary prevention of stroke: impact of the cilostazol stroke prevention study. Atheroscler Suppl 2005;6:33-40.

21. Koto T, Takubo K, Ishida S, Shinoda H, Inoue M, Tsubota K, et al. Hypoxia disrupts the barrier function of neural blood vessels through changes in the expression of claudin-5 in endothelial cells. Am J Pathol 2007;170:1389-1397.

22. Hao JL, Nagano T, Nakamura M, Kumagai N, Mishima H, Nishida T. Galardin inhibits collagen degradation by rabbit keratocytes by inhibiting the activation of pro-matrix metalloproteinases. Exp Eye Res 1999;68:565-572.

23. Mishiro K, Ishiguro M, Suzuki Y, Tsuruma K, Shimazawa M, Hara H. A broad-spectrum matrix metalloproteinase inhibitor prevents hemorrhagic complications induced by tissue plasminogen activator in mice. Neuroscience 2012;205:39-48.

24. Mayne M, Ni W, Yan HJ, Xue M, Johnston JB, Del Bigio MR, et al. Antisense oligodeoxynucleotide inhibition of tumor necrosis factor-alpha expression is neuroprotective after intracerebral hemorrhage. Stroke 2001;32:240-248.

25. Shibuya M, Suzuki Y, Sugita K, Saito I, Sasaki T, Takakura K, et al. Effect of AT877 on cerebral vasospasm after aneurismal subarachnoid hemorrhage. J Neurosurg 1992;76:571-577.

26. Fu H, Hosomi N, Pelisch N, Nakano D, Liu G, Ueno M, et al. Therapeutic effects of postischemic treatment with hypotensive doses of an angiotensin II receptor blocker on transient focal cerebral ischemia. J Hypertens 2011;29:2210-2219.

27. Ishrat T, Pillai B, Ergul A, Hafez S, Fagan SC. Candesartan reduces the hemorrhage associated with delayed tissue plasminogen activator treatment in rat embolic stroke. Neurochem Res 2013;38:2668-2677.

28. Suzuki Y, Nagai N, Umemura K, Collen D, Lijnen HR. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice. J Thromb Haemost 2007;5:1732-1739.

29. Huang Z, Huang PL, Ma J, Meng W, Ayata C, Fishman MC, et al. Enlarged infarcts in endothelial nitric oxide synthase knockout mice are attenuated by nitro-L-arginine. J Cereb Blood Flow Metab 1996;16:981-987.

30. Tan Z, Turner RC, Leon RL, Li X, Hongpaisan J, Zheng W, et al. Bryostatin improves survival and reduces ischemic brain injury in aged rats after acute ischemic stroke. Stroke 2013;44:3490-3497.

31. Tan Z, Lucke-Wold BP, Logsdon AF, Turner RC, Tan C, Li X, et al. Bryostatin extends tPA time window to 6 h following middle cerebral artery occlusion in aged female rats. Eur J Pharmacol 2015;764:404-412.

32. Ding Q, Chai H, Mahmood N, Tsao J, Mochly-Rosen D, Zhou W. Matrix metalloproteinases modulated by protein kinase Cepsilon mediate resistin-induced migration of human coronary artery smooth muscle cells. J Vasc Surg 2011;53:1044-1051.

33. Keep RF, Zhou N, Xiang J, Andjelkovic AV, Hua Y, Xi G. Vascular disruption and blood-brain barrier dysfunction in intracerebral hemorrhage. Fluids Barriers CNS 2014;11:18.

34. Meenakshisundaram T, Jose AF, Steven ML, John HG, Berislav VZ. Activated protein C promotes neovascularization and neuro-genesis in post-ischemic brain via protease activated receptor 1. J Neurosci 2008;28:12788-12797.

35. Fylaktakidou KC, Hadjipaclou-Litina DJ, Litinas KE, Nicolaides DN. Natural and synthetic coumarin deriv58atives with antiinflammatory/antioxidant activities. Curr Pharm Design 2004;30:3813-3833.

36. Zuo W, Chen J, Zhang S, Tang J, Liu H, Zhang D, et al. IMMH004 prevents toxicity induced by delayed treatment of tPA in a rat model of focal cerebral ischemia involving PKA-and PI3K-dependent Akt activation. Eur J Neurosci 2014;39:2107-2118.

37. Hartung T. Anti-inflammatory effects of granulocyte colony-stimulating factor. Curr Opin Hematol 1998;5:221-225.

38. dela Peña IC, Yoo A, Tajiri N, Acosta SA, Ji X, Kaneko Y, et al. Granulocyte colony-stimulating factor attenuates delayed tPA-induced hemorrhagic transformation in ischemic stroke rats by enhancing angiogenesis and vasculogenesis. J Cereb Blood Flow Metab 2015;35:338-346.

39. Sobrino T, Millán M, Castellanos M, Blanco M, Brea D, Dorado L, et al. Association of growth factors with arterial recanalization and clinical outcome in patients with ischemic stroke treated with tPA. J Thromb Haemost 2010;8:1567-1574.

40. Ullegaddi R, Powers HJ, Gariballa SE. Antioxidant supplementation with or without B-group vitamins after acute ischemic stroke: a randomized controlled trial. JPEN J Parenter Enteral Nutr 2006;30:108-114.

41. Allahtavakoli M, Amin F, Esmaeeli-Nadimi A, Shamsizadeh A, Kazemi-Arababadi M, Kennedy D. Ascorbic acid reduces the adverse effects of delayed administration of tissue plasminogen activator in a rat stroke model. Basic Clin Pharmacol Toxicol 2015;117:335-339.

42. Culp WC, Brown AT, Lowery JD, Arthur MC, Roberson PK, Skinner RD. Dodecafluoropentane emulsion extends window for tPA therapy in a rabbit stroke model. Mol Neurobiol 2015;52:979-984.

43. Albers GW, Goldstein LB, Hess DC, Wechsler LR, Furie KL, Gorelick PB, et al. Stroke Treatment Academic Industry Roundtable (STAIR) recommendations for maximizing the use of intravenous thrombolytics and expanding treatment options with intra-arterial and neuroprotective therapies. Stroke 2011;42:2645-2650.

44. Lapchak PA, Zhang JH, Noble-Haeusslein LJ. RIGOR guidelines: escalating STAIR and STEPS for effective translational research. Transl Stroke Res 2013;4:279-285.

45. Korninger C, Collen D. Studies on the specific fibrinolytic effect of human extrinsic (tissue-type) plasminogen activator in human blood and in various animal species in vitro. Thromb Haemost 1981;46:561-565.

46. Haelewyn B, Risso JJ, Abraini JH. Human recombinant tissueplasminogen activator (alteplase): why not use the ‘human’ dose for stroke studies in rats? J Cereb Blood Flow Metab 2010;30:900-903.

47. Jiang Y, Fan X, Yu Z, Cheng C, Wang XS, Lo EH, et al. Low dose tPA plus annexin A2 combination attenuates tPA delayed treatment-associated hemorrhage and improves recovery in rat embolic focal stroke. Neurosci Lett 2015;602:73-78.

48. Zhu H, Fan X, Yu Z, Liu J, Murata Y, Lu J, et al. Annexin A2 combined with low-dose tPA improves thrombolytic therapy in a rat model of focal embolic stroke. J Cereb Blood Flow Metab 2010;30:1137-1146.

49. Borlongan CV. Bone marrow stem cell mobilization in stroke: a ‘bonehead’ may be good after all! Leukemia 2011;25:1674-1686.

50. dela Peña I, Antoine A, Reyes S, Hernandez D, Acosta S, Pabon M, et al. Stem cell-based neuroprotective strategies in stroke. In : Shetty AK, editor. Neural Stem Cells in Health and Disease Singapore: World Scientific Publishing Co.; 2015. p. 371-408.

51. Bentley P, Ganesalingam J, Carlton Jones AL, Mahady K, Epton S, Rinne P, et al. Prediction of stroke thrombolysis outcome using CT brain machine learning. Neuroimage Clin 2014;4:635-640.

52. Berkhemer OA, Fransen PSS, Beumer D, van den Berg LA, Lingsma HF, Yoo AJ, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med 2014;372:1009-1018.

53. Minnerup J, Wersching H, Teuber A, Wellmann J, Eyding J, Weber R, et al. Outcome after thrombectomy and intravenous thrombolysis in patients with acute ischemic stroke: a prospective observational study. Stroke 2016;47:1584-1592.

54. Rubin MN, Barrett KM. What to do with wake-up stroke. Neurohospitalist 2015;5:161-172.

55. Whiteley WN, Emberson J, Lees KR, Blackwell L, Albers G, Bluhmki E, et al. Risk of intracerebral haemorrhage with alteplase after acute ischaemic stroke: a secondary analysis of an individual patient data meta-analysis. Lancet Neurol 2016;15:925-933.

56. Amaro S, Laredo C, Renú A, Llull L, Rudilosso S, Obach V, et al. Uric acid therapy prevents early ischemic stroke progression: a tertiary analysis of the URICO-ICTUS trial (efficacy study of combined treatment with uric acid and r-tPA in acute ischemic stroke). Stroke 2016;47:2874-2876.

57. Toni D, Fiorelli M, Gentile M, Bastianello S, Sacchetti ML, Argentino C, et al. Progressing neurological deficit secondary to acute ischemic stroke. A study on predictability, pathogenesis, and prognosis. Arch Neurol 1995;52:670-675.

58. Parsons M, Spratt N, Bivard A, Campbell B, Chung K, Miteff F, et al. A randomized trial of tenecteplase versus alteplase for acute ischemic stroke. N Engl J Med 2012;366:1099-1107.

59. Henninger N, Fisher M. Extending the time window for endovascular and pharmacological reperfusion. Transl Stroke Res 2016;7:284-293.

60. Ehrenreich H, Weissenborn K, Prange H, Schneider D, Weimar C, Wartenberg K, et al. Recombinant human erythropoietin in the treatment of acute ischemic stroke. Stroke 2009;40:e647-e656.

61. Ishrat T, Soliman S, Guan W, Saler M, Fagan SC. Vascular protection to increase the safety of tissue plasminogen activator for stroke. Curr Pharm Des 2012;18:3677-3684.

What is the time window for fibrinolytic therapy?

Efficacy. For optimal results, fibrinolytic therapy should be administered as early as possible, preferably within the first 3 to 6 hours and potentially up to 12 hours after the onset of symptoms (Figure I in the Data Supplement). After 3 hours of symptom onset the clinical benefit of fibrinolysis markedly decreases.

What is the primary time window for the administration of fibrinolytic therapy timed from the onset of systems quizlet?

Fibrinolytic therapy should be provided to eligible patients within 3 hours of symptom onset and 1 hour of hospital arrival. Door-to-admission time should be 3 hours.

When should fibrinolytic therapy be administered in STEMI ACLS?

Fibrinolytic therapy is the treatment of choice for STEMI patients who meet specific criteria: Patient has been symptomatic (Chest pain) for longer than 15 minutes but less than 12 hours. ECG is diagnostic for ST elevation indicating an MI or a new Left Bundle Branch Block.

Why is there a 3 hour window for tPA?

The timing of treatment is important, because giving a strong blood thinner like tPA during a stroke can cause bleeding inside the brain. The longer a patient waits to get treatment, the more likely it is that the risks of treatment will outweigh the benefits.

Toplist

Neuester Beitrag

Stichworte