Anticoagulación tras una hemorragia cerebral

Abstract

Atrial fibrillation causes 50% of cardioembolic strokes and 20% of all strokes. Strokes produced by atrial fibrillation are larger, more disabling and more often fatal. Antivitamin K antagonists are able to prevent 64% of strokes, but increase the risk of intracranial haemorrhage. Direct oral anticoagulants have a 50% lower risk of producing intracranial haemorrhage than vitamin K antagonists. The number of patients receiving anticoagulation has increased markedly in the last decade and, consequently, so has the risk of anticoagulant-associated intracranial haemorrhage. Although the associated morbidity and mortality are very high, the need to resume anticoagulation must be considered among survivors at risk of stroke. Currently available data are drawn from observational studies. Based on these studies, the clinical practice guidelines have established general recommendations with low levels of evidence, which include avoiding anticoagulation in lobar intracranial haemorrhages and individualisation of anticoagulation in deep intracranial haemorrhages. Until new scientific evidence is available on the most effective preventive strategy, decisions should be individualised in each patient depending on certain factors such as age, the localisation and cause of the intracranial haemorrhage, the anticoagulant that produced the cerebral bleed, prior embolisms, and the presence or absence of multiple cerebral microhemorrhages. The treatments of choice are direct oral anticoagulants or percutaneous closure of the left atrial appendage.