Homocysteine as a predictor of early neurological deterioration in acute ischemic stroke.
OBJECTIVE
Hyperhomocysteinemia is a well-known risk factor for vascular disease. However, its action, mechanism, and role in the acute phase of stroke have not been determined. We tried to determine whether an association existed between elevated serum homocysteine levels and early neurological deterioration (END) in patients with acute ischemic stroke.


METHODS
We performed a secondary analysis from the Cilostazol in Acute Ischemic Stroke Treatment (CAIST) trial, which was a double-blinded, randomized, multicenter trial, assessing the noninferiority of cilostazol over aspirin within 48 hours of an acute ischemic stroke. END was defined as an increase of ≥1 point in motor power or an increase of ≥2 points in the total National Institute of Health Stroke Scale score within 7 days.


RESULTS
The mean (±SD) serum homocysteine level was 11.4±4.7 μmol/L. Of the 396 patients studied, 57 (14.4%) patients worsened during the 7 days after inclusion. Most (68%) of the END cases occurred within the first 24 hours after treatment. High levels (>10.3 μmol/L) of serum homocysteine were independent predictors for END (third quartile odds ratio, 3.45; 95% confidence intervals, 1.25-9.50; P=0.016; fourth quartile odds ratio, 3.36; 95% confidence intervals 1.18-9.52; P=0.023) in multivariate analysis.


CONCLUSIONS
Patients with acute stroke with elevated serum homocysteine levels are at an increased risk for END.
From the Department of Neurology, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul, South Korea (H.-M.K., Y.-S.L.); Department of Neurology, Seoul National University Bundang Hospital, Seongnam, South Korea (H.-J.B.); and Department of Neurology, Asan Medical Center, Seoul, South Korea (D.-W.K.).
Hyung-Min
HM
Kwon
Yong-Seok
YS
Lee
Hee-Joon
HJ
Bae
Dong-Wha
DW
Kang
D000368:Aged; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000473:pathology*; D002097:C-Reactive Protein / Q000032:analysis; D000077407:Cilostazol; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006711:Homocystine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood; D008297:Male; D008875:Middle Aged; D009420:Nervous System / Q000473:pathology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011237:Predictive Value of Tests; D011379:Prognosis; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012307:Risk Factors; D020521:Stroke / Q000473:pathology*; D013777:Tetrazoles / Q000627:therapeutic use
D001241:Aspirin; D015415:Biomarkers; D002097:C-Reactive Protein; D000077407:Cilostazol; D006442:Glycated Hemoglobin; D006711:Homocystine; D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles
cerebral infarction; homocysteine; stroke