Homocysteine and coronary heart disease risk in the PRIME study

Troughton, Judith A.; Woodside, Jayne V.; Arveiler, Dominique; Amouyel, Philippe; Ferrières, Jean; Ducimetière, Pierre; Patterson, Christopher; Kee, Frank; Yarnell, John; Evans, Alun

doi:10.1016/j.atherosclerosis.2006.05.014

Cited by 15 publications

(7 citation statements)

References 39 publications

(39 reference statements)

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“…It has been reported that 85.2% of Korean AP smoke 20 cigarettes/day or more, and 85.4% of AP smoked more than one pack of cigarettes/day for the last month 1. Since elevated Hcy strongly correlates with smoking and low blood folate levels were found in the PRIME case-control study, Hcy levels might be a secondary risk factor to low blood folate and smoking 22. Elevated Hcy may also be involved in hypertension because it is associated with impaired endothelial function due to the generation of oxidative stress, VCAM-1 and reduction of NO bioavailability 23,24.…”

Section: Discussionmentioning

confidence: 95%

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

Seo

Park

et al. 2010

Yonsei Med J

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PurposeElevated circulating oxidized low density lipoprotein (Ox-LDL) levels are associated with increased risk of atherosclerosis, which may be due to high plasma homocysteine (Hcy) and low intakes of antioxidants. We investigated the contribution of dietary intakes of antioxidants to Hcy-induced LDL oxidation in atherosclerotic patients (AP) and controls.Materials and MethodsMale AP (n = 101) who were confirmed by coronary angiography and 91 controls were evaluated by blood biochemistry and dietary intakes. To determine whether homocysteine is an independent risk factor for atherosclerosis, subjects were divided into three groups; low- (≤ 6.9 uM/L), normal- (7 uM-12 uM/L) and high- (≥ 12.1 uM/L) Hcy.ResultsPlasm levels of homocysteine and LDL were higher, but plasma apo A-I in HDL and folate were lower in the AP group. The odds ratio (OR) for the risk of atherosclerosis was 3.002 [95% confidence interval (CI), 1.27-7.09] for patients in the highest tertile with homocysteine ≥ 12.1 uM/L. AP having high homocysteine levels had low intakes of vitamin A, β-carotene and vitamin C. By logistic regression analysis, age, body mass index (BMI), plasma LDL, plasma folate, and low intakes of vitamin A and β-carotene were found to be risk factors for atherosclerosis in patients with high-Hcy, but dietary B vitamins including folate were not.ConclusionA high-Hcy level was a risk factor for atherosclerosis in patients with high Ox-LDL levels. High intakes of antioxidants appeared to be a protective factor for atherosclerosis, perhaps exerting a pro-oxidative effect on LDL when combined with high levels of Hcy and LDL. However, more evidence for the benefits of B vitamins as a homocysteine-lowering therapy is needed.

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Section: Discussionmentioning

confidence: 95%

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

Seo

Park

et al. 2010

Yonsei Med J

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“…A positive association was demonstrated between plasma homocysteine levels and extent of atherosclerosis [85, 86], as well as the risk of hypertension [87], stroke [85,86,87,88], carotid artery disease [89, 90], CHD [87, 91, 92], PAD [93, 94] as well as MI [95, 96]. …”

Section: Literature Search Resultsmentioning

confidence: 99%

Atherosclerotic Renal Artery Stenosis: Association with Emerging Vascular Risk Factors

Paraskevas¹,

Hamilton

Cross

et al. 2007

Nephron Clin Pract

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Background: The established risk factors for atherosclerotic renal artery stenosis (ARAS) include hypertension, diabetes mellitus, dyslipidemia, obesity,smoking, old age and family history. In the last few years, several emerging risk factors have been proposed as predictors of ARAS, namely homocysteine, fibrinogen, C-reactive protein, lipoprotein(a) and creatinine. Methods: We searched Pubmed/Medline for studies investigating the prognostic value of each of these emerging risk factors in ARAS. Results: Creatinine and C-reactive protein seem to be the most promising predictors of ARAS, whereas the prognostic value of homocysteine, lipoprotein(a) and fibrinogen is not yet fully determined. Conclusion: The establishment of a definite role for these emerging risk factors could result in earlier recognition and/or better management of ARAS with potential regression/slowing down of progression of stenosis. Modifying these markers may also improve the therapeutic approach of the associated systemic atherosclerosis in these high-risk patients. Future trials should focus on the effect of different classes of drugs (e.g. statins and fibrates) on the levels of the emerging risk factors and the association with ARAS progression.

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“…Despite previous meta‐analyses suggesting that homocysteine is an independent risk factor for atherosclerosis and other cardiovascular diseases (CVD) [1], recently there has been a debate regarding the role of homocysteine in the development of CVD [2]. However, evidence indicates that an elevated plasma homocysteine level is still considered as an important risk factor for CVD, at least in high‐risk patients [3,4]. It has been recently reported that total plasma homocysteine is a strong predictor of recurrence of unstable angina [5].…”

Section: Introductionmentioning

confidence: 99%

Homocysteine induces connective tissue growth factor expression in vascular smooth muscle cells

Liu

Luo

et al. 2008

Journal of Thrombosis and Haemostasis

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Summary. Background: Increased homocysteine levels in blood might be an important risk factor for the development of cardiovascular diseases. Connective tissue growth factor (CTGF) was found to be involved in atherosclerotic plaque progression. So far, the possible connection between homocysteine and CTGF has not been studied. Objective: This study was designed to test whether homocysteine could induce CTGF expression in vascular smooth muscle cells (VSMC). Methods and results: Hyperhomocysteinemia was induced in Sprague–Dawley rats after 4 weeks of a high‐methionine diet. CTGF mRNA and protein expression was detected in the aortas isolated from hyperhomocysteinemic rats, but not in the controls. The underlying mechanism of homocysteine‐induced CTGF expression was investigated in cultured human umbilical vein smooth muscle cells (HUVSMC). CTGF mRNA expression was induced after treatment with dl‐homocysteine (50 μmol L−1) for 1 h, which remained at the elevated level for up to 8 h. CTGF protein level increased after homocysteine treatment for 8 h, and the elevated status was maintained for up to 48 h. Several intracellular signals elicited by homocysteine are involved in CTGF synthesis, including protein kinase C (PKC) activation and reactive oxygen species (ROS). Transfection HUVSMCs with a CTGF small interference RNA (siRNA) plasmid, which specifically inhibited the expression of CTGF, decreased extracellular matrix (ECM) accumulation caused by homocysteine. Conclusion: Our results demonstrate that homocysteine could increase the expression of CTGF in VSMC both in vivo and in vitro. The novel findings suggest that homocysteine might contribute to accelerated progression of atherosclerotic lesions by inducing CTGF expression.

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Homocysteine and coronary heart disease risk in the PRIME study

Cited by 15 publications

References 39 publications

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

Atherosclerotic Renal Artery Stenosis: Association with Emerging Vascular Risk Factors

Homocysteine induces connective tissue growth factor expression in vascular smooth muscle cells

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