Ever since the publication of the SPARCL trial (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) in 2006, neurologists became aware of the fact that statins may increase the risk for future intracerebral hemorrhage (ICH) in patients with previous ischemic stroke or ICH.1,2 At the same time, observational studies reported an increased risk for hemorrhagic transformation or even symptomatic bleeding in ischemic stroke patients undergoing thrombolysis who were pretreated with statins.3,4 As a consequence, many physicians were very careful to administer statins in patients with ICH and often stopped statin medication immediately after hospital admission in those who had been taking the medication before the event. In 2011, Westover et al5 provided a Markov decision model that came to the conclusion that statins should be avoided in patients with a history of ICH, particularly in those cases with a lobar location. In clinical practice, this often results in the somewhat counterintuitive situation that after an ICH, statins are often permanently discontinued, whereas platelet inhibitors or even oral anticoagulants are resumed depending on the underlying comorbidity.6
Statins exert many pleiotropic effects in addition to cholesterol lowering. These properties may contribute to both its protective effects and also some unwanted side effects, including an increased risk for bleeding.7,8 On the other hand, however, sudden discontinuation of statins may lead to rebound effects which may impair vascular function and induce adverse clinical effects in patients with acute vascular events.9–12 Some years ago, we formulated the recommendation that statins should not be paused and acutely discontinued in ischemic stroke patients undergoing thrombolysis and inferred—based on only sparse clinical data—that this probably also applies for patients after acute ICH.13
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