The relationship between statin use and intracerebral hemorrhage (ICH) has not been definitively established. Studies show both benefit and detriment. Statins may decrease the level of platelet aggregation and thrombogenesis and thus worsen an ICH, but they also modulate the immune system, inhibit the inflammatory process, and improve cerebral blood flow, promoting neuroprotection and tissue recovery. Despite physiological and clinical evidence on both sides of the argument, the idea that statins should be avoided whenever brain hemorrhage is involved has permeated stroke practice. Indeed, early and more recent epidemiological studies have shown a convincing inverse association between low levels of low-density lipoprotein cholesterol and the risk of hemorrhagic stroke.1 Whether this association can be applied to patients treated with statins is less clear. Is the fear of statin use for ICH justified? What is the basis on which clinicians have come to avoid statins for their hemorrhage risk, and how should this information guide our practice in light of newer evidence? Part of the confusion arises from a lack of clarity of the association between statin use and hemorrhage under different ICH etiologies. The pathophysiology may be quite different if the brain hemorrhage occurs in the setting of ischemic stroke vs after thrombolytic therapy, in hypertensive ICH, or in other conditions such as amyloid angiopathy.
Gonzalez-Castellon MA, Marshall RS. Statin Use and Brain Hemorrhage: Real Risk or Unfounded Fear? JAMA Neurol. 2014;71(11):1353–1354. doi:10.1001/jamaneurol.2014.2463
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