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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Aetiology and treatment of hyperhomocysteinaemia causing ischaemic stroke

P K Sarkar1, L A Lambert

  • 1Department of Medicine, Good Hope Hospital, Sutton Coldfield, W. Midlands, UK.

International Journal of Clinical Practice
|June 16, 2001
PubMed

Insights

High homocysteine levels are a significant risk factor for vascular diseases. Supplementation with folic acid, betaine, or vitamin B12 can lower homocysteine, potentially reducing stroke risk.

Area of Science:

  • Cardiovascular Medicine
  • Neurology
  • Clinical Biochemistry

Background:

  • Hyperhomocysteinemia is a prevalent, independent, and modifiable risk factor for atherosclerotic and thromboembolic diseases.
  • Elevated plasma homocysteine concentrations are associated with increased vascular risk, comparable to cholesterol and hypertension.

Purpose of the Study:

  • To review the etiology and treatment of hyperhomocysteinemia as a cause of ischemic stroke.
  • To highlight the importance of homocysteine in vascular risk assessment.

Main Methods:

  • Literature review of studies on hyperhomocysteinemia and vascular diseases.
  • Discussion of the role of homocysteine in cerebrovascular disease, coronary artery disease, and venous thrombosis.

Main Results:

  • Vascular risk increases progressively with higher plasma homocysteine levels.
  • Moderately elevated homocysteine is correctable with folic acid, betaine, or vitamin B12 supplementation.

Conclusions:

  • Hyperhomocysteinemia is a critical, modifiable risk factor for vascular and thromboembolic events.
  • While logical, direct proof linking homocysteine reduction to reduced ischemic stroke risk is pending.

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