title: Discontinuation of statin treatment in stroke patients.
abstract: OBJECTIVE
  Statins reduce the risk for myocardial infarctions and stroke which may in part depend on cholesterol-independent (pleiotropic) vasoprotective effects. Here, we review evidence to suggest that the abrupt discontinuation of statin medication exerts negative vascular effects in patients with acute vascular events.
  
  
  RESULTS
  It is increasingly recognized that statins (HMG-CoA reductase inhibitors) exert rapid cholesterol-independent effects. Cessation of statin treatment confers overshoot activation of heterotrimeric G-proteins Rho and Rac causing production of reactive oxygen species and suppression of NO bioavailability. In humans, discontinuation of statin therapy leads to a proinflammatory, prothrombotic state with impaired endothelium function. In patients with acute coronary syndromes, abrupt discontinuation of statin therapy significantly increases morbidity and mortality, whereas in stable vascular patients discontinuation may be safe. Recent prospective data indicated that the cessation of statin medication in acute ischemic stroke patients confers a significantly higher likelihood of early neurological deterioration and poor outcome.
  
  
  CONCLUSIONS
  We propose that in all acute ischemic stroke patients chronically treated with statins before the event, treatment should be continued and the patient should receive medication at the day of the stroke.
authors.affiliation: Klinik und Polikinik für Neurologie, Charité Universitätsmedizin Berlin, Charité Campus Mitte, D-10117 Berlin, Germany. matthias.endres@charite.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Endres
authors.forename: Ulrich
authors.initials: U
authors.lastname: Laufs
mesh_terms: D000208:Acute Disease; D000818:Animals; D002097:C-Reactive Protein / Q000032:analysis; D004730:Endothelium, Vascular / Q000503:physiopathology; D004789:Enzyme Activation; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D007249:Inflammation / Q000139:chemically induced; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D017382:Reactive Oxygen Species; D012189:Retrospective Studies; D020521:Stroke / Q000188:drug therapy*; D013375:Substance Withdrawal Syndrome / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D019851:Thrombophilia / Q000139:chemically induced; D016896:Treatment Outcome; D020830:rac1 GTP-Binding Protein / Q000378:metabolism; D020741:rho GTP-Binding Proteins / Q000378:metabolism
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D002097:C-Reactive Protein; D052250:Nitric Oxide Synthase Type III; D020830:rac1 GTP-Binding Protein; D020741:rho GTP-Binding Proteins