Homocysteine is associated with increased arterial resistance and eventually causes luminal reduction. The purpose of the present study was to evaluate an association between the plasma concentration of total homocysteine (tHcy) and stenosis or occlusion of the internal carotid artery (ICA) in patients with ischemic stroke.
In total, 391 patients with ischemic stroke were evaluated from March 2007 to February 2008. The criterion for ICA stenosis or occlusion was set at greater than 50% luminal narrowing or complete obstruction in at least one ICA. Patients were assigned to one of three groups: normal ICA, ICA stenosis, and ICA occlusion.
ICA stenosis was found in 71 patients, whereas ICA occlusion in 22 patients (18.2% and 5.6%, respectively). Plasma tHcy was significantly higher in groups with ICA stenosis/occlusion with the highest value of ICA occlusion (14.6 ± 1.0 µmol/L, p = 0.025). A 1 µmol/L increase of tHcy showed an adjusted odds ratio of 1.12 (95% confidence intervals, 1.03-1.24, p=0.008) for ICA occlusion in a multivariate logistic model adjusted for all possible confounders, including age, sex, vascular risk factors, and stroke classifications.
Elevated levels of tHcy were significantly associated with the ICA occlusion, independent of vascular risk factors and stroke subtypes.
"Homocysteine is an aminoacid byproduct of methionine metabolism, which aggravates artherosclerosis by damaging hemangioendothelial cells, increasing platelet aggregation through changing arachidonic acid metabolism, and decreasing anticoagulation factor activity.25 Increased homocysteine levels correlate with stenosis and occlusion of intracranial vessels in patients with ischemic stroke, and it also increases stroke risk.26,27 In the current study, no differences in homocysteine concentrations were found between cancer and noncancer patients with ischemic stroke. "
[Show abstract][Hide abstract] ABSTRACT: Background and Purpose
Stroke is common among cancer patients. However, risk factors and biomarkers of stroke in cancer patients are not well established. This study aimed to investigate risk factors and biomarkers as well as etiology of ischemic stroke in cancer patients.
A retrospective review was conducted in cancer patients with ischemic stroke who were admitted to a general hospital in Busan, Korea, between January 2003 and December 2012. The risk factors and biomarkers for stroke and stroke subtypes in cancer patients were compared with age- and sex-matched noncancer patients with ischemic stroke who were admitted to the same hospital during the same period.
One hundred fifty-six cancer patients with ischemic stroke were identified. Cancer patients with ischemic stroke were found to have a significantly lower proportion of hypertension, atrial fibrillation, hyperlipidemia, and ischemic heart disease than noncancer patients with ischemic stroke. However, stroke biomarkers, such as erythrocyte sedimentation rate and high-sensitivity C-reactive protein, fibrinogen, pro-brain natriuretic peptide, and D-dimer levels, were significantly increased in cancer patients with ischemic stroke than in noncancer patients. Large-artery atherosclerosis and stroke of undetermined cause were more common in cancer patients with ischemic stroke than in noncancer patients with ischemic stroke.
Cancer patients with ischemic stroke showed different risk factors, stroke biomarkers, and stroke etiology compared with noncancer patients with ischemic stroke.
[Show abstract][Hide abstract] ABSTRACT: Nutritional parameters, such as B-vitamins, have not been studied for an association with low-density lipoprotein (LDL) particle size. The present study explored whether serum vitamin levels, including folate and vitamin B-12, could be associated with LDL particle size.
Using a randomly selected population of 255 hospital workers, we collected detailed lipid profiles, including triglyceride (TG), high-density lipoprotein (HDL) cholesterol, and LDL particle sizes. The peak particle size of LDL was measured by density gradient ultracentrifugation and a pore gradient lipoprotein system. Serum folate and vitamin B-12 levels were measured about 1 year later and analyzed. Carotid intima-media thickness (IMT) and hepatic steatosis were diagnosed ultrasonographically, and metabolic syndrome was diagnosed using ATP III criteria.
LDL peak particle size was significantly correlated with carotid mean IMT (r=-0.16, p=0.010). Serum folate levels were significantly and positively correlated with HDL cholesterol and negatively with TG, although the latter showed borderline significance. With increasing serum folate levels, the LDL peak particle size showed a gradual independent increase, even when adjusted for age, sex, hepatic steatosis, metabolic syndrome, and the TG/HDL cholesterol ratio.
Folate may act to enhance LDL particle size. Future clinical and research work should include a study of the safe application and manipulation of folate levels in order to control LDL particle size.
Journal of atherosclerosis and thrombosis 12/2010; 17(12):1218-25. DOI:10.5551/jat.5629 · 2.73 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Increased homocysteine levels can be responsible for arterial ischemic events, such as MI, stroke or peripheral vascular disease. Homocysteine is metabolized by two pathways: re-methylation and trans-sulfuration. Both involve folic acid, and vitamins B(6-12.) Several studies assumed that the folates and vitamins B supplementation or dietary source to normalize plasma homocysteine. But, even if tends to normalize homocysteine levels, lowering homocysteine by B-group vitamins and/or folates does not reduce cardiovascular risk. In fact, recent reports confirmed that hyper-homocysteinemia is not directly responsible for cardiovascular disease, but is merely present in individuals suffering for acute and/or chronic cardiovascular events, as a collateral finding. Reduced methylation potential (MP) [due to decreased S-adenosyl-methionine (AdoMet)/S-adenosyl-homocysteine (AdoHcy) ratio] induced by the elevated plasma homocysteine levels seems to be the true responsible for cardiovascular diseases (CVD). The pathogenic mechanisms responsible for CVD appear to be dependent of DNA hypomethylation inducing an inhibition of cyclin A transcription and a reduction of endothelial cells growth. But, other human studies performed in a wide range are requested.
Journal of Thrombosis and Thrombolysis 07/2011; 32(1):82-8. DOI:10.1007/s11239-011-0550-4 · 2.17 Impact Factor
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