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. Author manuscript; available in PMC: 2022 Mar 17.
Published in final edited form as: Stroke. 2009 Sep 24;40(11):e645–e646. doi: 10.1161/STROKEAHA.109.561191

Platelet Dysfunction in Intraparenchymal Hemorrhage

Claire J Creutzfeldt 1, Kyra J Becker 1, WT Longstreth Jr 1, David L Tirschwell 1, Jonathan R Weinstein 1
PMCID: PMC8930190  NIHMSID: NIHMS960675  PMID: 19797180

To the Editor

The Cerebral Hematoma And NXY Treatment (CHANT) investigators found no association between the use of antiplatelet therapy (APT) and intraparenchymal hemorrhage (IPH) volume, growth, or outcome. In the paper and accompanying editorial, authors concluded that acute reversal of antiplatelet medications was not justified.1,2 The literature on the topic yields conflicting results with some papers3–6 supporting an association between APT and outcome from IPH and others not.1,7–9 In the July issue of Stroke, Naidech et al10 suggest a possible explanation for the disparate results and an alternative strategy for determining which patients with IPH might benefit from either platelet infusion therapy or other therapies designed to achieve rapid hemostatic control. In their study of 68 patients with spontaneous IPH, reduced platelet activity was associated with early IPH growth and worse functional outcome. Platelets were infused in 24% of patients and improved platelet activity but not outcome. As the authors acknowledge, the lack of benefit may relate to the delay in treatment, which averaged 21 hours after symptom onset; alternatively, it may be related to their small sample size. An intriguing aspect of this study is that reduced platelet activity was measured, not assumed on the grounds of APT use. However, the reliability and validity of assays of platelet activity and their sensitivity to the effect of aspirin, let alone to that of clopidogrel, are not fully established.11

Before suggesting that platelet function be assessed routinely in patients with IPH, a few important questions need to be answered. It has yet to be determined whether measured platelet activity relates to APT use, the dose of APT used, or some genetic or acquired cause of abnormal platelet function. A consensus is still lacking on the association of platelet activity and outcome after IPH,3–9 and there is no convincing evidence that acting on reduced platelet activity can lead to improved outcomes.6

We commend Naidech et al for reviving this discussion. Both APT use and reduced platelet function are common in patients with IPH as is poor outcome. Given the inability of observational studies alone to resolve this issue, a rigorous evaluation of acute platelet infusion therapy in select patients with IPH seems warranted.

Footnotes

Disclosures

None.

References

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