Neurological Sciences

, Volume 39, Issue 4, pp 745–748 | Cite as

Prior antiplatelet therapy is not associated with larger hematoma volume or hematoma growth in intracerebral hemorrhage

  • Verena van Ginneken
  • Patricia Engel
  • Jochen B. Fiebach
  • Heinrich J. Audebert
  • Christian H. Nolte
  • Andrea Rocco
Original Article


Hematoma volume (HV) and hematoma growth (HG) predict mortality and poor outcome in intracerebral hemorrhage (ICH). While the influence of oral anticoagulation on HV, HG and outcome is well established, the effect of prior antiplatelet therapy (APT) remains uncertain. We retrospectively examined data from all patients with acute, primary ICH, and baseline head CT admitted to our department between January 2005 and February 2014. HV were calculated by ABC/2 method. HG was defined as present if HV increased between baseline and follow-up CT ≥ 30% or ≥ 6 mL. We analyzed the influence of APT on HV, HG, and in-hospital mortality using univariate and multivariate analyses. In addition, we used propensity score matching to assess differences in in-hospital mortality rates. From 668 screened patients, 343 had primary ICH and fulfilled all inclusion criteria. APT was present in 99 patients (29%). Baseline median HV was 16 mL (IQR 6–46). HG occurred in 44 of 160 patients with follow-up CT (28%). In-hospital mortality was 10% (n = 36). APT was associated with older age, a mRS score before admission (pre-mRS) of > 2, and presence of cardiovascular comorbidities. We did not find an association between APT and larger baseline HV (p = 0.32), or HG (OR 0.8, 95% CI 0.4–1.9). After propensity score matching for age, pre-mRS, gender, and cardiovascular comorbidities, APT was not associated with higher in-hospital mortality (OR 1.90, 95% CI 0.85–4.24, p = 0.117). This study did not show a higher risk for larger HV, HG, or in-hospital mortality in primary ICH patients with APT.


Intracerebral hemorrhage ICH Antiplatelet therapy Aspirin 



V. van Ginneken was responsible for the concept, data analysis, and writing of the article. P. Engel was responsible for data analysis and revision of the article. H.J. Audebert, J.B. Fiebach, and C.H. Nolte were responsible for the critical revision of the article. A. Rocco was responsible for the concept, experimental design, and co-writing. We thank all colleagues from the Department of Neurology, Charité CBF for their support and contribution in data acquisition.

Compliance with ethical standards

Conflict of interest

A. Rocco has received honoraria for lectures from Bayer and Ever pharma. C.H. Nolte has received honoraria and/or consultancies from Pfizer, Bayer, BMS, Boehringer Ingelheim, and Sanofi. J. B. Fiebach has received consulting, lecture, and advisory board fees from Perceptive, BioClinica, Boehringer Ingelheim, Cerevast, Brainomix, and Lundbeck as well as a grant from the German Federal Ministry of Education and Research (01EO0801 and 01EO01301). H.J. Audebert has received research grants from Berlin Innovation Fund and German Federal Ministry for Education and Research. H.J. Audebert reports receiving speaker honoraria from Boehringer Ingelheim, EVER Neuropharma, Pfizer, BMS, Strehlows GmbH, and speaker and consultancy honoraria from Lundbeck A/S, Pfizer, Sanofi, and Roche Diagnostics. All remaining authors report no conflicts of interest.


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Copyright information

© Springer-Verlag Italia S.r.l., part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of NeurologyCharité—Universitätsmedizin BerlinBerlinGermany
  2. 2.Center for Stroke Research Berlin (CSB)BerlinGermany

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