Intracranial hemorrage is the most malignant form of stroke, always one of the top mortality causes in statistics anywhere. Low dose aspirin is widely used for the prevention of cerebral ischemic disease, both for secondary and primary prevention, that is, in people who have or have not had an initial ischemia. But frequently it is blamed for intracranial hemorrage, even when other anticoagulant medication is involved. Until now there has been no statistically proved increase in intracranial hemorrage in people taking aspirin long term at a lower dose, 75-300mg daily. In a study of 400000 people in the UK carried out by a multinational European team of epidemiologists, people of 40-84 years and matched controls were followed by a mean of 5,4 years, with a maximum follow up of 14,9 years.

Of all the cases of intracranial hemorrage there were 1611 cases of intracerebral hemorrage, 483 subdural hematomas, 385 subarachnoid hemorrages. There was no difference between controls and those who took aspirin, except that those who received aspirin had lower incidence of subarachnoid hemorrage.

Approximately one quarter of all hemorrages were related to trauma, and 2/3 of these were subdural hematomas. Approximately 1/4 of the hemmorages were fatal, the majority of which were intracerebral bleeds.

The protective effect of aspirin in subarachnoid hemorrage may be related to an effect on inhibition of cyclo-oxigenase isozymes which contribute to aneurysm rupture and formation. Other protective effects of aspirin coming out of similar studies include primary prevention in cardiovascular disease and colorectal cancer.

This study suggests strongly that aspirin is the least important factor in the generation of intracranial hemorrage, such as alcohol and the use of concomittant anticoagulants. The major risk factors identified in this study were a previous intracranial hemorrage, hemodyalisis, severe renal dysfunction and use of warfarin.

LC Soriano et al. Neurology 2017, 89:2280-2287

Dr Paulo Bittencourt

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