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In reply

We thank Dr Pijak for his comments. Risk of stroke and recurrent stroke¹ is related to inflammatory markers. We agree that "rebound" inflammatory mechanisms may also play a role in the higher-than-expected increase of ischemic strokes² and coronary syndromes³ after discontinuation of aspirin. This hypothesis is supported by the increased efficacy of aspirin in patients with high C-reactive protein levels.⁴ Chiang et al⁵ have even found that low-dose aspirin in volunteers had anti-inflammatory but not antiplatelet action. It is likely that both mechanisms, and probably even others, play a role in the antithrombotic effect of aspirin.

AUTHOR INFORMATION

Correspondence: Dr Bogousslavsky, Department of Neurology, Centre Hospitalier Universitaire Vaudois, rue du Bugnon 46, 1011 Lausanne, Switzerland (julien.bogousslavsky@chuv.ch).

Alexandre B. Maulaz, MD; Daniel C. Bezerra, MD; Patrik Michel, MD; Julien Bogousslavsky, MD

1. Woodward M, Lowe GD, Campbell DJ, et al. Associations of inflammatory and hemostatic variables with the risk of recurrent stroke. Stroke. 2005;36:2143-2147. FREE FULL TEXT 2. Maulaz AB, Bezerra DC, Michel P, Bogousslavsky J. Effect of discontinuing aspirin therapy on the risk of brain ischemic stroke. Arch Neurol. 2005;62:1217-1220. FREE FULL TEXT 3. Ferrari E, Benhamou M, Cerboni P, Marcel B. Coronary syndromes following aspirin withdrawal: a special risk for late stent thrombosis. J Am Coll Cardiol. 2005;45:456-459. FREE FULL TEXT 4. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973-979. FREE FULL TEXT 5. Chiang N, Bermudez EA, Ridker PM, Hurwitz S, Serhan CN. Aspirin triggers antiinflammatory 15-epi-lipoxin A4 and inhibits thromboxane in a randomized human trial. Proc Natl Acad Sci U S A. 2004;101:15178-15183. FREE FULL TEXT

Arch Neurol. 2006;63:301.

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