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(Stroke. 2006;37:2455.)
© 2006 American Heart Association, Inc.

Letters to the Editor

Response to Letter by Topakian et al

Neurovascular Research Laboratory, Stroke Unit, Neurology Department, Vall d’Hebron Hospital, Barcelona, Spain

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Response:

I am pleased with the interest shown by Topakian et al on our recent study,¹ and I am also sure they are very interested in the field of biomarkers and the possibility of using those to guide stroke thrombolysis and not just in setting up "a relationship" with Vall d’Hebron Stroke Unit by exchanging monthly letters through Stroke.^2,3

Affairs apart, they raise some very interesting points. They suggest that some treatments such as statins might be influencing C-reactive protein (CRP) level. However, we did this analysis and no differences in CRP level existed regarding pretreatment with statins. In fact, around 20% of our patients were on statins before stroke and those had similar CRP levels than the ones who were not taking statins (0.57 mg/dL [0.22 to 0.88] versus 0.59 mg/dL [0.22 to 0.91], P=0.99).

It is possible that the anti-inflammatory effect reported for several statins is abrogated in the acute phase of a vascular event. In fact, in a pilot study conducted by our group using statins in the acute phase of ischemic stroke, we were not able to show a decrease in CRP levels measured at several time-points after simvastatin treatment.⁴ Alternatively, it is also possible to think about the fact that stroke patients on statins having similar CRP levels than those not on statins might reflect a lack of effect of statins to control the activity of the vascular disease in those patients. Might that be the reason why they had a stroke? Perhaps . . . [Full Text of this Article]