Homocysteine as a Risk Factor for Ischemic Stroke: An Epidemiological Story in Evolution

Rl, Sacco; Jk, Roberts; Bs, Jacobs

doi:10.1159/000026169

Cited by 47 publications

(32 citation statements)

References 34 publications

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“…Several reports have reviewed the epidemiological evidence on elevated H(e) and stroke risk [1][2][3][22][23][24][25] and have come to the same conclusion: numerous case-control studies have consistently found an association between moderately elevated H(e) and stroke risk, but the results of the few prospective studies are not as consistent. Results of new studies since these reviews were conducted still support this conclusion.…”

Section: Discussionmentioning

confidence: 98%

Changes in Plasma Homocyst(e)ine in the Acute Phase After Stroke

Howard

Sides²,

Newman³

et al. 2002

Stroke

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Background and Purpose-Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period. Methods-A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke. Results-Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3Ϯ0.5 mol/L, which increased consistently to a mean of 12.0Ϯ0.05, 12.4Ϯ0.5, 13.3Ϯ0.5, and 13.7Ϯ0.7 mol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score. Conclusions-These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.

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Section: Discussionmentioning

confidence: 98%

Changes in Plasma Homocyst(e)ine in the Acute Phase After Stroke

Howard

Sides²,

Newman³

et al. 2002

Stroke

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“…HH is suggested to be an independent risk factor for atherosclerotic cerebrovascular diseases aside from classical vascular risk factors such as hypertension, smoking, hyperlipidemia, hyperglycemia and hyperfibrinogenemia (Brattstrom et al 1992;Giles et al 1998;Robinson et al 1998;Sacco et al 1998). HH exerts unfavorable effects on coagulation factors and platelets.…”

Section: Discussionmentioning

confidence: 99%

Serum Vitamin B12 and Folic Acid Levels in Acute Cerebral Atherothrombotic Infarction

Koçer

İnce

Canbulat³

et al. 2004

Tohoku J. Exp. Med.

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Hyperhomocysteinemia is an independent risk factor for atherothrombotic cerebral stroke. Vitamin B 12 and folic acid are important determinants of homocysteine metabolism. We aimed to evaluate the relationship, if present, between vitamin B 12 and folic acid levels and acute cerebral stroke in this study. Blood aliquots drawn within 24 hours after the stroke from hospitalized patients (n=66) with the diagnosis of acute ischemic cerebrovascular episode and also blood samples from 38 healthy controls without any vascular risk factor were analyzed. With a competitive, chemoluminescence assay, serum levels of vitamin B 12 and folic acid were measured in blood samples taken within 24 hours after the stroke.The differences and correlations were tested using frequency test, student-t test and multivariate analysis. Mean serum vitamin B 12 levels were significantly lower in the patients than in the control subjects, 245.40 (S.D.: 72.9) and 343.2 (S.D.: 113.0) pg/ml respectively (p=0.0001). This difference was independent from other risk factors. Likewise, mean serum folic acid levels were lower in the patients than in the control subjects, 4.62 (S.D.: 1.94) and 5.97 (S.D.: 1.19) ng/ml, respectively (p=0.003). Mean serum levels of vitamin B 12 and folate at the convalescence phase were 253.05 (S.D.: 68.78) pg/ml and 4.48 (S.D.: 2.08) ng/ml, respectively; the values obtained at the acute phase were not significantly different from the values obtained at the convalescence phase. We conclude that low vitamin B 12 and folic acid concentrations are associated with an increased risk of stroke, and the relationship for vitamin B 12 is independent from the other known modifiable stroke risk factors. For understanding the effects of B 12 and folate in stroke patients, more detailed follow-up studies with long period are needed.hyperhomocysteinemia; B 12 ; folate; atherotrombosis; stroke

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“…160,161 It is converted to cysteine by cystathionine B-synthase, a vitamin B 6 -dependent enzyme, or it can be remethylated by methionine synthase. The latter reaction is vitamin B 12 dependent and requires 5-methyl-tetrahydrofolate, a product of folic acid metabolism that uses methylene-tetrahydrofolate reductase (MTHFR).…”

Section: Homocysteinementioning

confidence: 99%

“…160 Alcohol, smoking, and physical inactivity also may alter homocysteine levels. 161 Reference ranges for total serum homocysteine concentrations in US residents have been established. 162 Overall, upper reference limits increase with age (eg, 95th percentile for men 60 years or olderϭ15.3 mol/L versus 11.4 mol/L for men 20 to 39 years), are higher for men than women (eg, 95th percentile for men 40 to 59 yearsϭ12.9 mol/L versus 10.2 mol/L for women 40 to 59 years), and are associated with low serum vitamin concentrations.…”

Section: Homocysteinementioning

confidence: 99%

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

Gorelick

2002

Stroke

196

115

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Background — It is estimated that about half of cardiovascular disease risk is explained by conventional risk factors. The realization that atherosclerosis is an inflammatory disease has led to a search for new stroke and cardiovascular disease risk factors and treatments. As such, the vulnerable atherosclerotic plaque has become the main focus for new medical strategies for plaque stabilization and stroke prevention. Summary of Review — In this invited review, I discuss inflammation as a possible risk factor for stroke, unifying mechanisms in ischemic stroke pathogenesis, and new avenues for stroke prevention—statin agents, angiotensin-converting enzyme inhibitors, and vitamins. These new stroke prevention therapies may help to reduce inflammation, serve to stabilize the atherosclerotic plaque, or act by other protective mechanisms. Conclusion — Beyond the traditional antithrombotic agents, statin agents, angiotensin-converting enzyme inhibitors, and vitamins may prove to be important additions to our armamentarium for stroke prevention.

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Homocysteine as a Risk Factor for Ischemic Stroke: An Epidemiological Story in Evolution

Cited by 47 publications

References 34 publications

Changes in Plasma Homocyst(e)ine in the Acute Phase After Stroke

Changes in Plasma Homocyst(e)ine in the Acute Phase After Stroke

Serum Vitamin B12 and Folic Acid Levels in Acute Cerebral Atherothrombotic Infarction

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

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