Anti-platelet therapy for stroke, what’s a ED Doc to do?

As a follow up to one of my esteemed colleague’s recent quick hit on the basics of strokes, I present some findings from time spent on the stroke unit these last few weeks.  Stroke is fairly popular here in the great state of Kentucky—we supremely enjoy our fried food, cigarettes, and lack of exercise (‘Merica!).  Therefore, stroke alerts are a fairly common occurrence in the ED and we keep our neurology friends busy (aka stroke team rounded for 10 hours a day).  But not everywhere is lucky enough to have an on call neurologist present for all stroke alerts.

So you’re the ED doc and they might have a stroke. Qu’est-ce que tu vas faire*!?!

Firstly, a head CT.  This is the first branch of the decision tree.  As previously mentioned, strokes are either hemorrhagic or ischemic, and the management of each is entirely different (ie do they get tPa or not). Without regards to whether to use tPa or not, this will focus on the ischemic subtype.

And within this subtype of ischemic stroke patients who cannot receive tPa, one comes to another branch in the decision tree.  Is the patient in atrial fibrillation (afib)?  Usually this can be evident from physical exam (ie irregularly irregular pulse) and telemetry, but an EKG can be confirmatory.  The management of an ischemic stroke in afib (aka cardioembolic ischemic stroke) differs greatly from one that isn’t (aka noncardioembolic ischemic stroke).  Cardioembolic strokes requires anticoagulants (eg warfarin) while a non-cardioembolic stroke only requires anti-platelets (eg aspirin).  Once again, the following will only focus on non-cardioembolic stroke and choice of anti-platelet.

*That’s French speak for ‘What ya gonna do’

Aspirin is dece*

There is some controversy in the stroke world as to the initial choice of anti-platelet for secondary prophylaxis of non-cardioembolic ischemic strokes.  One thing most everyone can agree on though is the utility of aspirin.  Aspirin within 48 hours has shown to decrease stroke reoccurrence and improve long term outcomes in multiple trials and meta-analyses 1,2,8.

*Dece= decent in Caucasian phrasin’

So what about the other fancy anti-platelets? 

There have been a multitude of trials that one is welcome to read by following the references below but I present my personal summary for secondary prophylaxis based on what I’ve read in the trials:

– Aspirin is more effective than placebo1,2

-Aggrenox (dipyramidole+aspirin) is better than placebo3

-Plavix is better than aspirin in composite vascular endpoint (you can decide for yourself whether that’s truly better for stroke or not)7

-Aggrenox may be better than aspirin3,5

-Plavix and Aggrenox are equivalent4

– ASA+ Plavix is equivalent to plavix alone but increases risks of bad side effects (eg bleeding)6

– Ticlopidine is better than placebo9

-Ticlopidine may be better than aspirin but with increased costs, lab f/u (i.e. biweekly CBC’s the first 3 months due to risk of neutropenia), and worse side effects may decrease the cost/benefit ratio10

Blah blah too many words—Break it down, C Belch

So a patient comes in with signs of stroke.  Their CT is negative for bleed and they’re outside of the tPa window.  They’re not in afib.  What are you gonna do?  My personal guidelines based on the evidence:

–          Aggrenox or Plavix monotherapy are good initial choices for non-cardioembolic ischemic strokes and better than aspirin alone

–          Do NOT use aspirin + Plavix dual therapy for these types of strokes due to the increased risks of bleeding. Leave that combo for cardiologists.

–          Aspirin and ticlopidine are also good initial choices.  But aspirin may be less effective than Aggrenox or Plavix monotherapy and ticlopidine has a poor side effect profile and increased costs

Public Service announcement:  As always, each patient is different and requires a personalized and evidence based approach to medication choices based on side effect profile and individual patient preference.  I also reference below the American College of Chest physician’s recommendations11 —they set forth their own guidelines based on the evidence which are very similar to what is proposed above.  And if all else fails, ask your friendly neighborhood pharmacist.

 

Sources:

  1. The International Stroke Trial (IST). Lancet. 1997 May 31; 349 (9065): 1569-81
  2. Chinese Acute Stroke Trial (CAST). Lancet 1997 Jun 7; 349 (9066): 1641-9
  3. European Stroke Prevention Study 2 (ESPS 2).  J Neurol Sci. 1996; 143(1-2): 1-13
  4. PRoFESS trial.  NEJM. 2008; 359 (12): 1238-1251
  5. European/Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT).  Lancet. 2006; 367 (9534):  1665-1673
  6. MATCH trial.  Lancet. 2004. Jul 24-30; 364(9431):  331-7
  7. CAPRIE trial.  Lancet.  1996 Nov 16; 348(9038):  1329-39
  8. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, MI, and stroke in high risk pts.  (Antithrombotic Trialists’ Collaboration).  BMJ.  2002 Jan 12; 324 (7329):  71-86
  9. Canadian American Ticlopidine Study (CATS).  Lancet.  1989 Jun 3; 1(8649):  1215-20
  10. A randomized trial comparing ticlopidine HCL w/ asa for prevention of stroke in high risk pts.  (TASS).  NEJM.  1989 Aug 24; 321 (8):  501-7
  11. Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence based clinical practice guidelines.  Feb 2012; 141 (2_suppl)

Compiled by: Chris Belcher

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