Factors Associated with the Steep Increase in Late Midlife Stroke Occurrence among US Men

Towfighi, Amytis; Saver, Jeffrey L.; Engelhardt, Rita; Ovbiagele, Bruce

doi:10.1016/j.jstrokecerebrovasdis.2007.12.007

Cited by 16 publications

(10 citation statements)

References 14 publications

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“…Most studies found an association between younger age and headache at stroke onset. 4,[22][23][24]26,39,43,47 In a prospective study of first ever ischemic stroke, 12.2% of those younger than 50 developed HAIS, compared with 8.5% of those older than 50 (p < 0.002). 31 In another population, 45.8% of younger patients (average age 42) developed HAIS vs 20.2% of older patients (average age 75, p < 0.05).…”

Section: Influence Of Age On Haismentioning

confidence: 99%

Headache after ischemic stroke

2020

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ObjectiveHeadache associated with ischemic stroke is poorly understood. To gain further insight, we systematically reviewed studies examining the prevalence and characteristics of new-onset poststroke headache.MethodsMedline and PubMed databases were queried. A total of 1,812 articles were identified. Of these, 50 were included in this systematic review. Twenty were included in a meta-analysis and meta-regression.ResultsHeadache occurred in 6%–44% of the ischemic stroke population. Most headaches had tension-type features, were moderate to severe, and became chronic in nature. Meta-analysis using an inverse-variance heterogeneity model revealed a pooled prevalence of 0.14 (95% confidence interval [CI] 0.07–0.23) with heterogeneity among studies. Metaregression revealed a significant association between prevalence and study location, the source population's national human development index (HDI), and study quality. We found higher prevalence in European (0.22, 95% CI 0.14–0.30) and North American (0.15, 95% CI 0.05–0.26) studies compared with Middle Eastern and Asian studies (0.08, 95% CI 0.01–0.18). However, within each region, populations from countries with higher HDI (p = 0.03) and studies with higher quality (p = 0.001) had lower prevalence. Calculated crude odds ratios (ORs) showed that posterior circulation stroke (pooled OR 1.92, 95% CI 1.4–2.64; n = 7 studies) and female sex (pooled OR 1.25, 95% CI 1.07–1.46; n = 11 studies) had greater odds of headache associated with ischemic stroke.ConclusionsTaken together, these data suggest that headache is common at the onset of or shortly following ischemic stroke and may contribute to poststroke morbidity. Better understanding of headache associated with ischemic stroke is needed to establish treatment guidelines and inform patient management.

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Section: Influence Of Age On Haismentioning

confidence: 99%

Headache after ischemic stroke

2020

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“…This condition frequently leads to premature coronary, cerebral or peripheral vascular impairments [16][17][18][19]. For that, this author firstly proposed the ''homocysteine hypothesis of atherosclerosis''.…”

Section: Cardiovascular Disordersmentioning

confidence: 99%

Hyper-homocysteinemia: a novel risk factor or a powerful marker for cardiovascular diseases? Pathogenetic and therapeutical uncertainties

Cacciapuoti

2011

J Thromb Thrombolysis

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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.

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“…Many clinical and epidemiological studies have demonstrated a positive correlation between homocysteine (Hcy) plasma levels and cardiovascular disorders (4,5), leading to the general conclusion that Hcy is a prothrombotic factor (6)(7)(8). However, the mechanism(s) through which elevated circulating levels of Hcy promote vascular disease and thrombosis is still unclear (9).…”

mentioning

confidence: 99%

Hydrogen sulphide pathway contributes to the enhanced human platelet aggregation in hyperhomocysteinemia

Bianca

Mitidieri

Minno

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Homocysteine is metabolized to methionine by the action of 5,10methylenetetrahydrofolate reductase (MTHFR). Alternatively, by thetransulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S),through multiple steps involving cystathionine beta-synthase and cystathioninegamma-lyase. Here we have evaluated the involvement of H2S in the thromboticevents associated with hyperhomocysteinemia. To this purpose we have usedplatelets harvested from healthy volunteers or patients newly diagnosed withhyperhomocysteinemia with a C677T polymorphism of the MTHFR gene (MTHFR++). NaHS(0.1-100 microM) or l-cysteine (0.1-100 microM) significantly increased plateletaggregation harvested from healthy volunteers induced by thrombin receptoractivator peptide-6 amide (2 microM) in a concentration-dependent manner. Thisincrease was significantly potentiated in platelets harvested from MTHFR++carriers, and it was reversed by the inhibition of either cystathioninebeta-synthase or cystathionine gamma-lyase. Similarly, in MTHFR++ carriers, thecontent of H2S was significantly higher in either platelets or plasma comparedwith healthy volunteers. Interestingly, thromboxane A2 production was markedlyincreased in response to both NaHS or l-cysteine in platelets of healthyvolunteers. The inhibition of phospholipase A2, cyclooxygenase, or blockade ofthe thromboxane receptor markedly reduced the effects of H2S. Finally,phosphorylated-phospholipase A2 expression was significantly higher in MTHFR++carriers compared with healthy volunteers. In conclusion, the H2S pathway isinvolved in the prothrombotic events occurring in hyperhomocysteinemic patients

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Factors Associated with the Steep Increase in Late Midlife Stroke Occurrence among US Men

Cited by 16 publications

References 14 publications

Headache after ischemic stroke

Headache after ischemic stroke

Hyper-homocysteinemia: a novel risk factor or a powerful marker for cardiovascular diseases? Pathogenetic and therapeutical uncertainties

Hydrogen sulphide pathway contributes to the enhanced human platelet aggregation in hyperhomocysteinemia

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