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Marc R. Mayberg, MD; Anthony Furlan, MD

JAMA. 2000;283:2440-2442.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Elevated serum fibrinogen levels have been associated with poor outcome in patients with acute ischemic stroke.¹ Although the causality and specific mechanisms of the relationship between increased fibrinogen and stroke remain speculative, it has been proposed that lower fibrinogen levels after stroke may accelerate spontaneous fibrinolysis, inhibit thrombus propagation, promote the release of endogenous tissue-type plasminogen activator (tPA), or improve local cerebral blood flow through diminished viscosity.² Ancrod is a protease derived from Malaysian pit viper venom that produces rapid decreases in serum fibrinogen by accelerating cleavage of the fibrinogen A- chain.³ Ancrod has been shown to be effective in limiting infarction volume in animal models of acute stroke⁴ and in a randomized clinical trial.^5-6

In this issue of THE JOURNAL, Sherman and colleagues⁷ report the results of a multicenter, randomized clinical trial designed to test the efficacy of ancrod in reducing functional . . . [Full Text of this Article]

Author Affiliations: Cleveland Clinic Foundation, Cleveland, Ohio.

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