Response to Letter by Creutzfeldt et al
We thank Drs Creutzfeldt and colleagues for their thoughtful comments1 concerning our article.2 They review the literature on antiplatelet medication and outcome after intracerebral hemorrhage (ICH), including their own data,3 which were not yet published at the time of our submission.
Although we agree on more issues than not, we disagree that “it has yet to be determined whether measured platelet activity relates to APT [antiplatelet therapy] use, the dose of APT used, or some genetic or acquired cause of abnormal platelet function.” Dr Creutzfeldt cites the same paper as us on the different available assays for platelet activity in patients known to take aspirin; the assay we report on performed most closely to usually cited standard assay.4 Multiple platforms, including the platform we used, give results that are altered by the administration of aspirin to healthy control subjects.5 In patients with normal platelet activity while taking aspirin, such “aspirin resistance” can often be overcome by increasing the dose.6,7⇓ Although none of the patients in our cohort were known to have an inherited disorder of platelet function, platelet function assay results are helpful for the diagnosis of von Willebrand disease and may guide the response to therapy.8,9⇓
We agree that there is no consensus that known antiplatelet medication use impacts outcome after ICH; however, we feel this is the wrong question. The correlation between medication history and platelet activity in patients with ICH is suboptimal for a number of potential reasons.10 The important questions are whether platelet activity impacts outcome after ICH, if we can reliably improve platelet activity, and if that is enough to reduce ICH volume growth and improve outcomes. Going forward, we plan to examine the optimum method to improve platelet activity in patients with ICH and hope to build a case for prospective clinical trials of platelet-activating therapy in ICH. We think improving platelet activity after ICH is potentially safe and feasible, but proving it will require time and resources.
- ↵Creutzfeldt CJ, Becker KJ, Longstreth WT, Tirschwell DL, Weinstein JR. Platelet dysfunction in intraparenchymal hemorrhage [Letter]. Stroke. 2009; 40: e645.
- ↵Naidech AM, Jovanovic B, Liebling S, Garg RK, Bassin SL, Bendok BR, Bernstein RA, Alberts MJ, Batjer HH. Reduced platelet activity is associated with early clot growth and worse 3 month outcome after intracerebral hemorrhage. Stroke. 2009; 40: 2398–2401.
- ↵Lordkipanidze M, Pharand C, Schampaert E, Turgeon J, Palisaitis D, Diodati J. A comparision of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease. Eur Heart J. 2007; 28: 1702–1708.
- ↵Karon B, Wockenfus A, Scott R, Hartman S, McConnell J, Santrach P, Jaffe A. Aspirin responsiveness in healthy volunteers measured with multiple assay platforms. Clin Chem. 2008; 54: 1060–1065.
- ↵Gurbel P, Bliden K, DiChiara J, Newcomer J, Weng W, Neerchal N, Gesheff T, Chaganti S, Etherington A, Tantry U. Evaluation of dose-related effects of aspirin on platelet function: results from the Aspirin-Induced Platelet Effect (ASPECT) study. Circulation. 2007; 115: 3156–3164.
- ↵DiChiara J, Bliden K, Tantry U, Hamed M, Antonio M, Suarez T, Bailon O, Singla A, Gurbel P. The effect of aspirin dosing on platelet function in diabetic and nondiabetic patients: an analysis from the Aspirin-Induced Platelet Effect (ASPECT) study. Diabetes. 2007; 56: 3014–3019.
- ↵Naidech AM, Bassin SL, Bernstein RA, Batjer HH, Alberts MJ, Lindholm PF, Bleck TP. Reduced platelet activity is more common than anti-platelet medication use in patients in intracerebral hemorrhage. Neurocrit Care. 2009 Apr 21 [Epub ahead of print].