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Archive for the ‘cerebral circualtion stroke’ Category

TPA is fibrin specific . . . still result in more stroke than streptokinase , why ?

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, cerebral circualtion stroke, STEMI-Primary PCI, Thrombolysis, tagged , , , , , , on March 30, 2014| Leave a Comment »

We know  streptokinase  is a non fibrin specific   agent that   results in systemic lytic state and hence more chance of bleeding.

TPA is fibrin specific  and it  will act only on fibrin  bound to clot , hence systemic bleeding risk should be less.

However , in real world , it is well  documented  stroke risk with TPA is consistently more than streptokinase .(It varies between .0.3-.5% with streptokinase , 0.7-to 1%  with TPA)

How do you explain this apparent  paradox ?

Possible explanations.

  1. The fibrin selectivity pf TPA is not absolute* .
  2. The lytic power of  TPA is more hence stroke is more likely.
  3. The FDP* released by TPA can trigger a systemic lytic state
  4. In the  post TPA protocol   heparin  is  mandatory and  this  contribute to stroke risk.

*What happens o fibrin degradation products (FDP) levels after TPA ?

FDP levels do increase after TPA  .This peaks at 1 hour after lysis.it Correlates well with risk of stroke.(Ho CH, Wang infarction.Thrombosis Research 1990, 58(3):331-341) ).

Reference

This is an excellent review with analysis from 14 studies with total of 142 907 patients with thrombolysis

A meta analysis of thrombolytic agents streptokinase vs tpa tnktpa stroke risk fibrin slectivity

Ho CH, Wang SP Serial thrombolysis-related changes after thrombolytic therapy with TPA in patients with acute myocardial infarction.Thrombosis Research 1990, 58(3):331-341

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Transient Ischemic attacks (TIA’s) of heart

Posted in Cardiology -unresolved questions, cerebral circualtion stroke, Infrequently asked questions in cardiology (iFAQs), My presentations, tagged , , on March 31, 2013| Leave a Comment »

Is Transient Ischemic attacks (TIAs)  belong to the  exclusive domain of cerebral circulation ?  Can it occur in the coroanry arteries ?  If so what situations ?

This is a presentation in one of the cardiological society of India annual scientific sessions . A pdf download is  provided

transient ischemic attacks attack of heart coronary tia

Download  a PDF presentation

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Why there is so much confusion regarding anti-coagulation following cardio-embolic stroke

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cerebral circualtion stroke, cerebral circulation stroke, general medicine, tagged , , , , , , on December 31, 2012| Leave a Comment »

The  major  issue of contention is fear of conversion of pure ischemic stroke into hemorrhagic stroke .

But here is a catch if you worry about that  . . . who will worry about recurrent emboli from heart ?

References

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678170/pdf/nihms104070.pdf


anti coagulation following cardio embolic stroke

aha stroke guidelines 2007

aha stroke guidelines

Recommendation for heparin

aha antiplatlet agent

Recommendation for anti-platelet drugs

I think  the 2007   stroke guidelines are the latest .Even after going  through the guidelines  I am not really clear about the answer for the question posed in this article.

One more thing   I  (mis) understood was  ,  In acute stroke thrombolysis seems to be safe  . . . Heparin seems to be dangerous ?  Is that true ?  It defies logic for  me !

One possible explanation is thromolysis is a emergency single shot salvaging  process . While prolonged heparin will ooze blood into Infarct ! This is exactly is the reason  in   tPA   should not be   followed up with heparin  in acute strokes.(unlike STEMI  where a follow up heparin is a must )

Regarding prevention of recurrent emboli , we need to bother about whether it is predominately platelet rich or RBC rich

Readers may contribute to find the exact answer !

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