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Homocysteine-lowering therapy: a role in stroke prevention?
1Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute, London, ON, Canada. dspence@robarts.ca
Insights
Vitamin therapy to lower homocysteine may not prevent heart attacks but could reduce stroke risk. New approaches and higher doses of vitamin B12 show promise for stroke prevention.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Nutritional Science
Background:
- Previous trials suggest vitamin therapy lowering homocysteine is ineffective for cardiovascular events.
- Stroke pathogenesis is multifactorial, with thrombosis playing a key role, unlike myocardial infarction which is primarily plaque rupture.
- Elevated total homocysteine concentrations are linked to increased thrombosis risk.
Purpose of the Study:
- To investigate if vitamin therapy targeting homocysteine levels can differentially impact stroke versus myocardial infarction risk.
- To re-evaluate the efficacy of homocysteine-lowering vitamin therapy in preventing vascular events, particularly stroke.
Main Methods:
- Detailed assessment of the HOPE-2 clinical trial results.
- Reanalysis of the Vitamin Intervention for Stroke Prevention (VISP) trial, focusing on patients responsive to vitamin therapy.
Main Results:
- Findings suggest that higher doses of vitamin B12, alongside folate and vitamin B6, may reduce stroke risk.
- Routine vitamin therapy might not be effective, but specific approaches could still lower homocysteine and prevent stroke.
Conclusions:
- Homocysteine-lowering therapy may still be a viable strategy for stroke prevention, despite limited efficacy for myocardial infarction.
- Further research into higher-dose vitamin B12 and novel homocysteine-lowering methods is warranted for vascular event prevention.
Abstract:
On the basis of the results of several recent clinical trials, many researchers have concluded that vitamin therapy designed to lower total homocysteine concentrations is not effective in reducing the risk of cardiovascular events. However, whereas almost all myocardial infarctions are due to plaque rupture, stroke has many more pathophysiological mechanisms, and thrombosis-which is increased by raised total homocysteine concentrations-has an important role in many of these processes. Thus, stroke and myocardial infarction could respond differently to vitamin therapy. A detailed assessment of the results of the recent HOPE-2 trial and a reanalysis of the VISP trial restricted to patients capable of responding to vitamin therapy suggest that higher doses of vitamin B12 and perhaps new approaches to lowering total homocysteine besides routine vitamin therapy with folate, vitamin B6, and vitamin B12 could reduce the risk of stroke. Thus, therapy to lower homocysteine could still help to prevent stroke, if not other vascular outcomes.
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