Vitamin strategy may curb risk of second stroke
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A high-dose vitamin supplement may help reduce the risk of a second stroke, as well as death and cardiac events, according to a study published in the journal Stroke this month. The supplement consisted of vitamins B9 (folate), B6, and B12, which are known to reduce blood levels of homocysteine—an amino acid linked to heart disease.
In a previous report from the Vitamin Intervention for Stroke Prevention (VISP) study group, the combined vitamin therapy did not reduce recurrent stroke and cardiac events, but it turned out that the trial included patients who were not likely to benefit from the treatment.
“The VISP trial included patients with deficiency of vitamin B12 who were unlikely to respond to our treatment, as well as patients with renal failure, who would not respond as well to vitamin therapy,” Dr. David J. Spence of the Stroke Prevention and Atherosclerosis Research Centre in Ontario, Canada told Reuters Health.
When Spence and colleagues re-analyzed the results in a subgroup of 2,155 subjects deemed most likely to respond to treatment, the combined vitamin therapy did appear to have a beneficial effect on recurrence of stroke and cardiac events.
Specifically, the team compared results of low-dose vitamin versus high-dose vitamin therapy and found that high-dose vitamin supplements reduced recurrent stroke, death and heart disease by 21 percent. When they subdivided patients by baseline levels of vitamin B12, thus identifying those with difficulties absorbing the vitamin, the differences between the low-dose and high-dose groups became greater.
“It is too early to conclude that vitamin therapy to lower total homocysteine is ineffective in the prevention of cardiovascular events,” said Spence.
He and colleagues suggest that in the modern age in which grains are fortified with folate, the response to vitamin therapy for lowering homocysteine largely depends on B12 levels of the patients. Higher doses of B12, in addition to other therapies, will be required to reduce homocysteine, and thus to reduce stroke and the combined end point of stroke, death, and heart attack.
SOURCE: Stroke, November 2005.
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