The authors of the present study investigated the influence of previous antiplatelet (AP) or anticoagulant (AC) therapy on subsequent stroke mortality at different time points up to one year post stroke. The authors found that prior antiplatelet or anticoagulant use was associated with increased mortality following haemorrhagic stoke but not ischaemic stroke after adjustment for common factors associated with a poor prognosis.
Today there is widespread use of antiplatelet or anticoagulant medication for primary prevention of cardiovascular events. Having in mind the associated hemorrhagic side-effects of these medications, there is a potential harmful effect, especially in patients experiencing a stroke.
Conflicting evidence exists regarding the influence of the previous use of medications such as anti-platelets or anticoagulants on outcomes in patients presenting with ischemic or hemorrhagic stroke.
Aim of the Study
The present study examined the influence of previous antiplatelet (AP) or anticoagulant (AC) therapy on subsequent stroke mortality at different time points up to one year post stroke.
The present study was designed in a retrospective, single university hospital registry fashion that included all consecutive stroke patients admitted to a single large university hospital between January 2004 and November 2008. The main outcome measures were mortality risks at 7, 30, 60,90 and 365 days. Measures were assessed following ischaemic and haemorrhagic stroke, adjusting for age, gender, premorbid Rankin and stroke severity.
Among 3308 patients with first or recurrent stroke (53% women, mean age 77.7 ± 11.5 years, 86% ischaemic stroke) the one-year mortality was 35.2% (999) for ischaemic stroke and 48.3% (227) for haemorrhagic stroke. Compared with no previous therapy, the mortality following ischaemic stroke for those already receiving AP or AC was not associated with increased mortality at any time points up to one year after presentation in the fully adjusted model. However, patients with haemorrhagic stroke had a worse prognosis at all time points after standard risk factor adjustment. For patients who used aspirin or warfarin prior to haemorrhagic stroke compared with no use, ORs (95% CIs) were 1.31 (0.64 to 2.68) and 2.91 (1.23 to 6.89) for 7 days, 2.36 (1.18 to 4.71) and 2.37 (1.00 to 5.61) for 30 days, 2.18 (1.10 to 4.29) and 2.86 (1.20 to 6.84) for 60 days, 2.56 (1.27 to 5.13) and 2.82 (1.16 to 6.86) for 90 days and 1.67 (0.89 to 3.12) and 2.44 (1.06 to 5.62) for 365 days.
This study showed no evidence that short, medium or longer term mortality (up to one year) post stroke was influenced by prior AP/AC therapy in patients who had ischaemic stroke. In contrast, in patients with haemorrhagic stroke prior use of warfarin was associated with a significantly increased risk of mortality at all time points examined. Prior use of aspirin therapy also appeared to carry a higher risk compared with no therapy at 30, 60 and 90 days in this group.
Prior antiplatelet or anticoagulant use was associated with increased mortality following haemorrhagic stoke but not ischaemic stroke after adjustment for common factors associated with a poor prognosis.
Although the present study was based on a large sample size there are certain limitations, such as not capturing dose, duration or indication of antiplatelet use, not quantifying the anticoagulant effect (by measuring international normalized ratio (INR)), not investigating cause-specific mortality and finally, not reporting specific co-morbidities that could affect survival.
These findings raise the hypothesis that in patients with hemorrhagic stroke, early determination of antiplatelet or anti-coagulant activity via measuring platelet reactivity or INR could have an impact on acute treatment.
Corresponding author from original paper
Dr Phyo Kyaw Myint, Norwich Medical School, Chancellors Drive, University of East Anglia, Norwich, Norfolk NR4 7TJ, UK; email@example.com.