Secondary prevention after cerebral ischaemia of presumed arterial origin: is aspirin still the touchstone?
- University Department of Neurology, University Hospital Utrecht, Utrecht, The Netherlands
- Julius Center for Patient Oriented Research, University Hospital Utrecht, Utrecht, The Netherlands
- University Department of Neurology, University Hospital Rotterdam Dijkzigt, Rotterdam, The Netherlands
- Dr Ale Algra, Julius Center for Patient Oriented Research, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Telephone: 0031 30 250 9350; fax 0031 30 250 5485; emailA.Algra{at}neuro.azu.nl
- University Department of Neurology, University Hospital Utrecht, Utrecht, The Netherlands
- Julius Center for Patient Oriented Research, University Hospital Utrecht, Utrecht, The Netherlands
- University Department of Neurology, University Hospital Rotterdam Dijkzigt, Rotterdam, The Netherlands
- Dr Ale Algra, Julius Center for Patient Oriented Research, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Telephone: 0031 30 250 9350; fax 0031 30 250 5485; emailA.Algra{at}neuro.azu.nl
- University Department of Neurology, University Hospital Utrecht, Utrecht, The Netherlands
- Julius Center for Patient Oriented Research, University Hospital Utrecht, Utrecht, The Netherlands
- University Department of Neurology, University Hospital Rotterdam Dijkzigt, Rotterdam, The Netherlands
- Dr Ale Algra, Julius Center for Patient Oriented Research, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Telephone: 0031 30 250 9350; fax 0031 30 250 5485; emailA.Algra{at}neuro.azu.nl
Patients who have had a transient ischaemic attack or non-disabling ischaemic stroke of presumed arterial origin have an annual risk of death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction that ranges between 4% and 11% without treatment.1 2 In the secondary prevention of these vascular complications the use of aspirin has been the standard treatment for the past two decades. Discussions about the dose of aspirin have dominated the issue for some time, although there is no convincing evidence for any difference in effectiveness in the dose range of 30-1300 mg/day.2 3 A far greater problem is the limited degree of protection offered by aspirin: the accumulative evidence from trials with aspirin alone and only for cerebrovascular disease of presumed arterial origin as qualifying event indicates that a dose of aspirin of at least 30 mg/day prevents only 13% of serious vascular complications.1 2 In this commentary we use the AntiPlatelet Trialists’ (APT) composite outcome event—death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction—unless otherwise stated. An outcome event that takes the entire vascular burden into account is most relevant from the perspective of a patient. In other words 87% of the major arterial complications are not avoided with aspirin. The question therefore is: Do we have something “stronger”?
Until recently the only alternative drug was ticlopidine. A direct comparison with aspirin was made in the Ticlopidine Aspirin Stroke Study (TASS).4 A total of 3069 patients with transient or non-disabling cerebral ischaemia were randomised between ticlopidine (250 mg twice daily) or aspirin (650 mg twice daily). The occurrence of non-fatal myocardial infarction was not reported in the original document,4 but data on the APT composite event were reported later.1 The relative risk reduction (RRR) was a 6% advantage in …
