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BRIEF COMMUNICATIONS: Bruce Ovbiagele and Jeffrey L. Saver The smoking–thrombolysis paradox and acute ischemic stroke Neurology 2005; 65: 293-295 [Abstract] [Full text] [PDF]

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The smoking/thrombolysis paradox and acute ischemic stroke

Mark Fisher   (31 August 2005)

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Bruce Ovbiagele, Jeffrey L. Saver   (31 August 2005)

The smoking/thrombolysis paradox and acute ischemic stroke 31 August 2005
Mark Fisher, Department of Neurology, UC Irvine UCI Medical Center, 101 The City Dr. South, Bldg 55, Rm 121, Orange, CA 92868 Send Correspondence to journal: Re: The smoking/thrombolysis paradox and acute ischemic stroke mfisher{at}uci.edu Mark Fisher	I read with interest the article by Ovbiagele and Saver. [1] A relationship between cigarette smoking and outcome following tPA treatment for stroke was previously reported [2], with evidence of significant decreased risk of intracranial hemorrhage in smokers treated with tPA. The smoking-reduced hemorrhage relationship is still unclear, although it is notable that nicotine treatment depletes brain microvascular tPA and enhances focal brain ischemia in a rat experimental stroke model. [3] References 1) Ovbiagele B, Saver JL. The smoking-thrombolysis paradox and acute ischemic stroke. Neurology 2005;65:293-295. 2) The NINDS t-PA Stroke Study Group. Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. Stroke 1997;28:2109-2118. 3) Wang L, Kittaka M, Sun N, Schreiber SS, Zlokovic BV. Chronic nicotine treatment enhances focal ischemic brain injury and depletes free pool of brain microvascular tissue plasminogen activator in rats. J Cereb Blood Flow Metab 1997;17:136-146. The author reports no conflicts of interest.
Reply to Fisher 31 August 2005
Bruce Ovbiagele, Stroke Center and Department of Neurology 710 Westwood Blvd., Rm 1-240, Los Angeles, CA 90095, Jeffrey L. Saver Send Correspondence to journal: Re: Reply to Fisher ovibes{at}mednet.ucla.edu Bruce Ovbiagele, et al.	We thank Dr. Fisher for his interest in our article. Dr Fisher is correct in pointing out that a previous analysis of the NINDS-TPA trials found evidence of significant decreased risk of intracerebral hemorrhage (ICH) in smokers treated with tPA. [1] However, this result was found only for the overall ICH rate that comprised both symptomatic and asymptomatic intracerebral hemorrhages. Smoking was not independently associated with a decreased risk for symptomatic intracerebral hemorrhage.[1] In the NINDS-TPA trials analysis of ICH after thrombolysis for acute ischemic stroke, "symptomatic ICH was defined as a CT-documented hemorrhage that was temporally related to deterioration in the patient's clinical condition." [1] On the other hand, "asymptomatic ICH was defined as CT-documented hemorrhage that was not associated with deterioration in the patient's neurological condition." As such, the lower National Institute for Health Stroke Scale (NIHSS) score at 24 hours post-treatment among smokers who received thrombolysis, as noted in our analysis of the NINDS-TPA trials, [2] cannot be explained by a "smoking-reduced hemorrhage relationship." References 1. Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. The NINDS t-PA Stroke Study Group. Stroke, 1997;28:2109-2118. 2. Ovbiagele B, Saver JL. The smoking-thrombolysis paradox and acute ischemic stroke. Neurology. 2005;65:293-295. The authors report no conflicts of interest.