Platelet aggregation inhibitors, vitamin K antagonists and risk of subarachnoid hemorrhage

Background: Use of platelet aggregation inhibitors and vitamin K antagonists has been associated with an increased risk of intracranial hemorrhage (ICH). Whether the use of these antithrombotic drugs is associated with an increased risk of subarachnoid hemorrhage (SAH) remains unclear, especially as...

Full description

Saved in:
Bibliographic Details
Published in:Journal of thrombosis and haemostasis 2011-03, Vol.9 (3), p.517-523
Main Authors: RISSELADA, R., STRAATMAN, H., VAN KOOTEN, F., DIPPEL, D. W. J., VAN DER LUGT, A., NIESSEN, W. J., FIROUZIAN, A., HERINGS, R. M. C., STURKENBOOM, M. C. J. M.
Format: Article
Language:English
Subjects:
Adult
Aged
anticoagulants
Anticoagulants - adverse effects
Case-Control Studies
Cross-Over Studies
Databases, Factual
Female
Humans
Male
Medical Record Linkage
Middle Aged
Netherlands
Odds Ratio
platelet aggregation inhibitor
Platelet Aggregation Inhibitors - adverse effects
Risk Factors
subarachnoid hemorrhage
Subarachnoid Hemorrhage - etiology
thromboembolism
Vitamin K - antagonists & inhibitors
vitamin K antagonists
vitamins
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background: Use of platelet aggregation inhibitors and vitamin K antagonists has been associated with an increased risk of intracranial hemorrhage (ICH). Whether the use of these antithrombotic drugs is associated with an increased risk of subarachnoid hemorrhage (SAH) remains unclear, especially as confounding by indication might play a role. Objective: The aim of the present study was to investigate whether use of platelet aggregation inhibitors or vitamin K antagonists increase the risk of SAH. Methods: We applied population‐based case–control, case–crossover and case–time–control designs to estimate the risk of SAH while addressing issues both of confounding by indication and time varying exposure within the PHARMO Record Linkage System database. This system includes drug dispensing records from community pharmacies and hospital discharge records of more than 3 million community‐dwelling inhabitants in the Netherlands. Patients were considered a case if they were hospitalized for a first SAH (ICD‐9‐CM code 430) in the period between 1st January 1998 and 31st December 2006. Controls were selected from the source population, matched on age, gender and date of hospitalization. Conditional logistic regression was used to estimate multivariable adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of SAH during use of platelet aggregation inhibitors or vitamin K antagonists. In the case–crossover and case–time–control designs we selected 11 control periods preceding the index date in successive steps of 1 month in the past. Results: In all, 1004 cases of SAH were identified. In the case–control analysis the adjusted OR for the risk of SAH in current use of platelet aggregation inhibitors was 1.32 (95% CI: 1.02–1.70) and in current use of vitamin K antagonists 1.29 (95% CI: 0.89–1.87) compared with no use. In the case–crossover analysis the ORs for the risk of SAH in current use of platelet aggregation inhibitors and vitamin K antagonists were 1.04 (95% CI: 0.56–1.94) and 2.46 (95% CI: 1.04–5.82), respectively. In the case–time–control analysis the OR for platelet aggregation inhibitors was 0.50 (95% CI: 0.26–0.98) and for vitamin K antagonists 1.98 (95% CI: 0.82–4.76). Conclusion: The use of platelet aggregation inhibitors was not associated with an increased SAH risk; the modest increase observed in the case–control analysis could be as a result of confounding. The use of vitamin K antagonists seemed to be associated with an increased
ISSN:1538-7933
1538-7836
1538-7836
DOI:10.1111/j.1538-7836.2010.04170.x