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(Stroke. 2002;33:473.)
© 2002 American Heart Association, Inc.

Original Contributions

Changes in Plasma Homocyst(e)ine in the Acute Phase After Stroke

Virginia J. Howard, MSPH; Elizabeth G. Sides, MEd; George C. Newman, MD, PhD; Stanley N. Cohen, MD; George Howard, DrPH; M. Rene Malinow, MD James F. Toole, MD for the Stability of Plasma Homocyst(e)ine in Acute Stroke Patients (SHASP) Study Investigators

From the Department of Epidemiology and International Health (V.J.H.) and the Department of Biostatistics (G.H.), University of Alabama at Birmingham, Birmingham, Ala; Department of Neurology (E.G.S.) and Stroke Research Center, Department of Neurology (J.F.T.), Wake Forest University School of Medicine, Winston Salem, NC; Department of Neurology (G.C.N.), State University of New York at Stony Brook, Stony Brook, NY; Division of Neurology, Cedars-Sinai Medical Center and Department of Neurology, West Los Angeles Veterans Affairs Healthcare Center (S.N.C.), Los Angeles, Calif; and Oregon Regional Primate Research Center (M.R.M.), Beaverton, Ore.

Correspondence to Virginia J. Howard, MSPH, Department of Epidemiology and International Health, University of Alabama at Birmingham, 1530 3rd Ave S, RPHB 210F, Birmingham, AL 35294-0022. E-mail vjhoward{at}uab.edu

Background and Purpose—; Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period.

Methods—; A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke.

Results—; Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3±0.5 µmol/L, which increased consistently to a mean of 12.0±0.05, 12.4±0.5, 13.3±0.5, and 13.7±0.7 µmol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score.

Conclusions—; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.

Key Words: homocyst(e)ine • stroke, acute • stroke, ischemic

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