Homocysteine and internal carotid artery occlusion in ischemic stroke.
ABSTRACT 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.
[Show abstract] [Hide abstract]
ABSTRACT: Background Leukoaraiosis (LA) is associated with structural and functional vascular changes that correlate with motor and gait disturbances, depressive symptoms, urinary disturbances, and dementia. The blood–brain barrier (BBB) plays a key role in development of lacunar stroke, leukoaraiosis, and other feature of cerebral small-vessel disease, and there are numerous studies examining changes in the BBB with normal aging and in dementia and LA. Aquaporin-4 (AQP-4), the primary water channel protein in the central nervous system, is involved in BBB development, function, and integrity, and its dysfunction induces several neurologic diseases. The aim of our study was to evaluate whether genetic variations in AQP-4 gene are associated with the development of LA. Methods DNA was amplified and the single-nucleotide polymorphisms in AQP-4 gene were investigated by melting curve analysis using real-time polymerase chain reaction. Results The frequency of both T allele and CT/TT genotypes of rs2075575 was significantly higher in LA group than in control group (C versus T, P = .0145; CC versus CT/TT, P = .038). However, no significant difference was observed between LA group and control group in rs9951307. Interestingly, the rs9951307 AG + GG genotype may confer a synergistic effect in odds ratio (OR) values when combined with the rs2075575 CT + TT genotypes (OR = 1.65 → 2.51). The C-A haplotype was significantly different between LA group and the control group (P = .005). By stratified analysis, rs2075575 and rs9951307 polymorphisms were statistically significant in the subjects with hypertension and hemoglobin A1c (P < .05), whereas the rs2075575 polymorphism was associated with high serum cholesterol (P < .05) and the rs9951307 polymorphism was associated with low serum homocysteine (P < .05). Conclusions Our results indicate that AQP-4 genetic variations and haplotypes might contribute to the risk factors for LA.Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association 05/2014; 23(5). DOI:10.1016/j.jstrokecerebrovasdis.2013.10.017 · 1.99 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 · 2.04 Impact Factor
[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. Methods 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. Results 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. Conclusions Cancer patients with ischemic stroke showed different risk factors, stroke biomarkers, and stroke etiology compared with noncancer patients with ischemic stroke.05/2014; 16(2):91-6. DOI:10.5853/jos.2014.16.2.91