J Neurocrit Care.  2020 Dec;13(2):93-100. 10.18700/jnc.200023.

The good genotype for clopidogrel metabolism is associated with decreased blood viscosity in clopidogrel-treated ischemic stroke patients

  • 1Department of Neurology, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Republic of Korea
  • 2Department of Neurology, Bundang Jesaeng General Hospital, Seongnam, Republic of Korea


Blood viscosity (BV) is a measurement of the intrinsic resistance of blood to flow, and high BV increases thromboembolic risk. Although laboratory documentation of clopidogrel resistance has been shown to predict an increased risk of cardiovascular events in patients with ischemic stroke, there is no evidence that cytochrome P450 2C19 (CYP2C19) polymorphisms in clopidogrel-treated patients influence BV after ischemic stroke.
Patients with ischemic stroke or transient ischemic attack within 7 days of symptom onset from April 2018 to October 2019 were included. Patients were classified into the good genotype group for clopidogrel metabolism (ultrarapid or extensive metabolizer) and poor genotype group (intermediate/unknown or poor metabolizer) based on their CYP2C19 genotype status. A scanning capillary-tube viscometer was used to assess whole BV, and patients were divided into decreased BV and increased BV groups.
The final analyses included 174 patients (109 men and 65 women) with a mean age of 66.4±11.24 years. The good genotype was found in 44% of patients with decreased systolic BV (SBV) and 27% of those with increased SBV (P=0.029), suggesting that BV changes were related to the CYP2C19 genotype for clopidogrel metabolism. Binary logistic regression analysis showed that CYP2C19 genotype status (P=0.024) and baseline SBV (P<0.0001) were significantly associated with decreased BV. The good genotype for clopidogrel metabolism was associated with decreased BV in patients with ischemic stroke treated with clopidogrel.
The present results indicate that the effect of clopidogrel treatment on ischemic stroke prevention could be modulated not only by inhibition of platelet function but also by changes in the hemorheological profile.


Blood viscosity; Hematocrit; Stroke
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