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Hyperhomocysteinaemia as a cardiovascular risk factor: an update
R van der Griend1, D H Biesma, J D Banga
1Department of Internal Medicine, Sint Antonius Hospital, Nieuwegein, The Netherlands. r.griend@digd.azu.nl
The Netherlands Journal of Medicine
|April 12, 2000
Summary
High homocysteine levels are linked to cardiovascular disease, but a direct cause-effect link is unproven. Folic acid supplementation shows promise for lowering homocysteine, but ongoing trials are needed to confirm its cardiovascular benefits.
Area of Science:
- Cardiovascular Science
- Metabolic Disorders
- Nutritional Biochemistry
Background:
- Hyperhomocysteinaemia is an independent cardiovascular risk factor, supported by epidemiological data.
- Acquired causes include B-vitamin deficiencies and renal insufficiency; a common inherited cause (MTHFR gene mutation) doesn't increase cardiovascular risk.
- The precise mechanism of homocysteine-induced cardiovascular disease remains unclear, though endothelial dysfunction is implicated.
Purpose of the Study:
- To review the evidence linking hyperhomocysteinaemia to cardiovascular risk.
- To discuss diagnostic methods and reference values for homocysteine.
- To evaluate homocysteine-lowering therapies, particularly folic acid supplementation.
Main Methods:
- Epidemiological evidence review.
- Discussion of diagnostic approaches including fasting homocysteine and methionine loading tests.
- Analysis of pathophysiological mechanisms and therapeutic interventions.
Main Results:
- Epidemiological data strongly associate hyperhomocysteinaemia with cardiovascular risk.
- Methionine loading tests identify more cases than fasting tests; significant intra-individual variability necessitates repeated sampling.
- Folic acid (0.5 mg daily) is an effective homocysteine-lowering therapy, except in renal failure patients.
Conclusions:
- Hyperhomocysteinaemia is a significant cardiovascular risk factor, despite unproven causality.
- Folic acid supplementation is a primary therapeutic strategy for reducing homocysteine levels.
- Further large-scale clinical trials are essential to determine the impact of homocysteine-lowering therapy on cardiovascular outcomes.