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Effect of amlodipine on platelet inhibition by clopidogrel in patients with ischaemic heart disease: a randomised, controlled trial
  1. Andrew Y W Li1,
  2. Fook-Hong Ng1,
  3. Francis K L Chan2,
  4. Prabowo Tunggal1,
  5. Kit Chan1,
  6. Yuk-Kong Lau1
  1. 1Department of Medicine and Geriatrics, Ruttonjee Hospital, Hong Kong, China
  2. 2Department of Medicine & Therapeutics, the Chinese University of Hong Kong, Hong Kong, China
  1. Correspondence to Dr Andrew Y W Li, Department of Medicine and Geriatrics, Ruttonjee Hospital, 266 Queen's Road East, Wan Chai, Hong Kong, China; liyw{at}graduate.hku.hk

Abstract

Background Amlodipine inhibits cytochrome P450 (CYP) enzyme and has the potential to reduce clopidogrel bioactivation in vivo. Reports in previous retrospective studies described greater platelet reactivity in patients on amlodipine.

Objective To evaluate the treatment effect of clopidogrel in patients on amlodipine versus not on calcium-channel blockers (CCBs).

Design and setting Randomised, controlled, open-label trial conducted in a regional acute hospital.

Patients and interventions 98 patients on clopidogrel for ischaemic heart disease were recruited consecutively and randomised to take either amlodipine or drugs with inert CYP effects as controls. The P2Y12 reaction unit (PRU) was measured using whole blood obtained at baseline and on day 28.

Main outcome measures The primary analysis involved the PRU values on day 28. The secondary analyses were percentage of platelet inhibition and poor response to clopidogrel as defined by PRU>235.

Results Both groups experienced comparable day 28 PRUs (amlodipine 227±84 vs control 214±90; mean difference 12.7, 95% CI −22 to +47). Percentage of platelet inhibition (amlodipine 33% vs control 38%, mean difference −4.5%, 95% CI −14% to +5%) and those with poor response on day 28 (amlodipine 49% vs control 45%; p=0.76) did not differ significantly.

Conclusions Concomitant amlodipine has no negative impact on clopidogrel-mediated platelet inhibition in patients with ischaemic heart disease.

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Footnotes

  • Contributors All authors were solely responsible for the design, conduct and analyses of the study, drafting and editing of the paper and its final contents.

  • Funding This study was sponsored by the Cardiac Research Fund, Ruttonjee Hospital, which provided the expenditure for the platelet reactivity assay..

  • Competing interest FKLC has served as a consultant for Pfizer, Eisai, Takeda and Otsuka, and has received lecture fees from Pfizer, Astra Zeneca and Takeda.

  • Patient consent Obtained.

  • Ethics approval Ethics Committee of the Hong Kong East Cluster, Hospital Authority, Hong Kong Special Administrative Region.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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