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Plasma homocysteine is a risk factor for recurrent vascular events in young patients with an ischaemic stroke or TIA

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Abstract

Objectives

Young patients with an ischaemic stroke or transient ischaemic attack (TIA) often have no vascular risk factors. Hyperhomocysteinaemia is an established risk factor for stroke in elderly patients but it is uncertain whether it is also important for the prognosis of young ischaemic stroke and TIA patients. We examined the possible effect of the plasma homocysteine level on the risk of recurrent vascular events in patients between 18 and 45 years of age.

Methods

The study population consisted of 161 consecutive patients with a recent cerebral infarction or TIA. Data on the primary event and the homocysteine level were collected retrospectively from hospital records. General practitioners and patients were contacted by telephone to record vascular events and the type of medication used during the follow–up period. Vascular events included cerebral infarction, TIA, pulmonary embolism, venous thrombosis, myocardial infarction and peripheral arterial disease.

Results

A Kaplan- Meier curve showed a dose effect relationship between event-free survival time and tertiles of the homocysteine level (Log rank statistic 5.91; p = 0.05). The Cox hazard ratio, after adjustment for homocysteine lowering treatment, was 1.7 (95 % CI, 1.1 to 2.8) for any vascular outcome event, 1.9 (95% CI, 1.1 to 3.0) for arterial outcome events and 1.8 (95 % CI, 1.1 to 2.9) for cerebral outcome events.

Conclusions

In spite of our small number of outcome events we found a significant association at the 95% confidence level between homocysteine level and the risk of recurrent vascular events in young patients with an ischaemic stroke or TIA. The association is of the same magnitude as in elderly people.

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Correspondence to Diederik W. J. Dippel MD.

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Bos, M.J., van Goor, ML.P.J., Koudstaal, P.J. et al. Plasma homocysteine is a risk factor for recurrent vascular events in young patients with an ischaemic stroke or TIA. J Neurol 252, 332–337 (2005). https://doi.org/10.1007/s00415-005-0647-9

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  • DOI: https://doi.org/10.1007/s00415-005-0647-9

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