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see also:


  • atleplase is r-TPA and an intravenous thrombolytic agent used to dissolve blood clots within the vasculature


  • 1st clinical use of a tPA reported in 1984
  • tPA is a naturally occurring serine protease protein produced commercially via recombinant DNA techniques
  • it activates the fibrinolytic system under physiologic conditions by catalysing the conversion of plasminogen (preferentially that which is bound to fibrin) to plasmin
  • it is a clot specific agent because at low doses it tends to bind selectively at the site of new thrombus (eg. within the coronary artery lumen in AMI), resulting in more rapid coronary thrombolysis
  • the high doses needed for reperfusion result in higher intracranial bleeding than for SK
  • this risk is exacerbated by the need for heparin to avoid reocclusion as it has a short half life
  • initial dosing used was 60mg in 1st hr then 20mg/h for next 2hrs
  • accelerated dosing (see below) produced excellent coronary patency rates without increasing bleeding complications
  • approved in the US in 1996 for Mx of stroke with duration < 3hrs, this was later extended to 4.5hrs


clinical use and dose regimes

usage in AMI when emergent angioplasty is not available:

  • 2 x IV cannulae;
    • 5000IU IV stat then,
    • infusion 25000IU in 500ml NS @ 20ml/hr (<80kg) or 24ml/hr (>80kg) then as per protocol
    • continue for 48hrs after tPA started to prevent re-occlusion
  • accelerated TPA protocol:
    • 15mg over 2 minutes, then,
    • 0.75mg/kg (max. 50mg) over 30min, then,
    • 0.5mg/kg (max. 35mg) over 60min ⇒ Total dose NOT to exceed 100mg

usage in stroke:

usage in massive PE

adverse effects:

  • hypotension due to vasodilatation (7%)
  • major bleeding
    • risk of spontaneous intracranial haemorrhagic stroke (SICH):
      • 10% if given intra-arterially in acute stroke
      • intravenous use:
        • 6.4% in patients with acute stroke of < 3hrs duration (compared to 0.6% in placebo patients) 1)
        • 2.4% in patients with acute stroke of 3-4.5hrs duration (compared to 0.2% in placebo patients)2)
        • 3.5% if no acute stroke but PH CNS disease, TIAs or stroke
        • otherwise around 1%
        • risk factors for SICH:3)
          • CT hypodensity (early ischemic changes >1/3 of MCA territory)
          • Elevated serum glucose or history of diabetes mellitus
          • Symptom severity
          • Time to treatment (as above)
          • High systolic blood pressure
          • Low platelets
          • Advanced age
      • usually occurs at the site of ischaemic brain tissue
      • When compared to spontaneous ICH, postthrombolysis ICHs tend to be larger, more often multifocal, have less perihematomal oedema, and contain a blood fluid level 4)
    • risk of significant GIT bleed causing drop of haematocrit by 15% or more = 3%
  • minor bleeding ~19%
  • anaphylaxis (rare)
alteplase.txt · Last modified: 2019/11/20 16:25 (external edit)