Relationship of lipid oxidation with subclinical atherosclerosis and 10-year coronary events in general population

Gómez, Miquel; Vila, Joan; Elosúa, Roberto; Molina, Lluís; Bruguera, Jordi; Sala, Joan; Masiá, Rafel; Covas, María Isabel; Marrugat, Jaume; Fitó, Montserrat

doi:10.1016/j.atherosclerosis.2013.10.026

Cited by 52 publications

(49 citation statements)

References 28 publications

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“…Therefore, a causal link to the development of hypertension is a plausible explanation for the possible increased cardiovascular risk in patients with hyperuricemia [46]. Second, increased SUA levels may encourage lipid peroxidation and promote the oxidation of low-density lipoprotein (LDL) cholesterol [47], which may play a role in the development of atherosclerosis [48] and would also explain its association with CHD [49]. Interestingly, because human atherosclerosis plaques contain more UA than normal artery walls, researchers propose that SUA may have a direct role in the atherosclerosis process [50].…”

Section: Discussionmentioning

confidence: 99%

Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies

Zuo

Jiang

et al. 2016

BMC Cardiovasc Disord

117

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BackgroundHyperuricemia may be associated with an increased risk of coronary heart disease (CHD) mortality; however, the results from prospective studies are conflicting. The objective of this study was to assess the association between hyperuricemia and risk of CHD mortality by performing a meta-analysis.MethodsPubmed and Embase were searched for relevant prospective cohort studies published until July 2015. Studies were included only if they reported data on CHD mortality related to hyperuricemia in a general population. The pooled adjusted relative risk (RR) was calculated using a random-effects model.ResultsA total of 14 studies involving 341 389 adults were identified. Hyperuricemia was associated with an increased risk of CHD mortality (RR: 1.14; 95 % CI: 1.06–1.23) and all-cause mortality (RR: 1.20; 95 % CI: 1.13–1.28). For each increase of 1 mg/dl of serum uric acid (SUA), the overall risks of CHD and all-cause mortality increased by 20 and 9 %, respectively. According to the gender subgroup analyses, hyperuricemia increased the risk of CHD mortality in women (RR: 1.47; 95 % CI: 1.21–1.73) compared to men (RR: 1.10; 95 % CI: 1.00–1.19). The risk of all-cause mortality was greater in women.ConclusionsHyperuricemia may modestly increase the risk of CHD and all-cause mortality. Future research is needed to determine whether urate–lowering therapy has beneficial effects for reducing CHD mortality.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0379-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies

Zuo

Jiang

et al. 2016

BMC Cardiovasc Disord

117

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“…9 Recently, it has been shown that oxLDL is independently associated with 10-year risk of CAD events and improves the reclassification capacity of Framingham-derived risk functions. 10 Angiographic score (AngSc) provides information about the location and severity of atherosclerotic lesions 11 and is associated with AS 9 in patients with PAD. The AngSc is negatively correlated with maximum treadmill walking distance 12 and ankle-brachial pressure index (ABPI), 13 which is a functional measure of the severity of PAD.…”

Section: Introductionmentioning

confidence: 99%

Metabolomic signature of arterial stiffness in male patients with peripheral arterial disease

et al. 2015

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Arterial stiffness is an independent determinant of cardiovascular risk and a marker of subclinical organ damage. Metabolomics may facilitate identification of novel low-molecular cardiovascular risk factors. The aim of the present study was to compare metabolic signatures and functional-biochemical characteristics of patients with peripheral arterial disease (PAD) and clinically healthy subjects. We studied 42 men with symptomatic PAD (aged 66±7 years) and 46 healthy men (aged 66±8 years). Aortic pulse wave velocity (aPWV) was assessed by applanation tonometry using the Sphygmocor device. Metabolic profiling was performed with high-performance liquid chromatography and mass spectrometry. Serum oxidized low-density lipoprotein (oxLDL) level was measured by enzyme-linked immunosorbent assay. The aPWV as well as serum levels of lactate, free carnitine and 11 amino acids including tyrosine were higher among the patients with PAD. In contrast, serum levels of pyruvate, citrate, α-ketoglutarate, aconitate and cysteine were higher in the control group. In multiple regression models, aPWV was independently determined by log-tyrosine and log-oxLDL in the patients (R(2)=0.61; P<0.001) and by age, log-pyruvate and log-oxLDL in the controls (R(2)=0.52; P<0.001). Our study describes for the first time significant differences in metabolomic signature of patients with advanced atherosclerosis compared with clinically healthy controls. The aPWV is independently associated with serum levels of tyrosine and oxLDL in the patients with PAD and is related to pyruvate and oxLDL levels in the control group. The measurement of low-molecular metabolites, which are related to changes in vascular phenotypes, may lead to identification of novel vascular risk markers.

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“…We also demonstrated the relevance of traditional recipient risk factors, cv0 indicates no chronic vascular changes; cv1, vascular luminal narrowing of ≤25% via fibrointimal arterial thickening; cv2, vascular luminal narrowing of 26% to 50%; cv3, vascular narrowing of ≤50%; DSA, donor-specific antibodies; HLA, human leukocyte antigen; and MFI, mean fluorescence intensity. Among the 174 studies addressing an association between antibodies and arteriosclerosis in the current literature, only 3 were prospective population-based studies evaluating antiphosphorylcholine, 38 antioxidized low-density lipoprotein, 39 and antiphospholipid 40 antibodies. None of these studies integrated the simultaneous assessment of circulating antibodies, arteries, traditional cardiovascular risk factors, We defined a distinct disease entity, antibody-associated arteriosclerosis, which is characterized by circulating donor-specific anti-HLA antibodies, prominent arterial intimal thickening and hypercellularity associated with allograft endothelial activation (microcirculation inflammation), and complement fraction C4d deposition.…”

Section: Discussionmentioning

confidence: 99%

Determinants and Outcomes of Accelerated Arteriosclerosis

Loupy

Vernerey

Viglietti

et al. 2015

Circulation Research

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Rationale: The role of circulating antibodies in addition to traditional cardiovascular risk factors in the development of accelerated arteriosclerosis and their long-term clinical consequences have not been demonstrated. Objective: We investigated the role of circulating antibodies in accelerated arteriosclerosis and the role of immune-associated arteriosclerosis in graft and patient survival and the occurrence of major adverse cardiovascular events. Methods and Results: This was an observational prospective cohort study that included 1065 kidney transplant patients (principal cohort, n=744; validation cohort, n=321) between 2004 and 2010. Participants were assessed for traditional cardiovascular risk factors and circulating anti–human leukocyte antigen (HLA) antibodies. All patients underwent allograft biopsies to assess arteriosclerotic lesions and endothelial activation, endarteritis, and complement deposition. In the principal cohort, 250 (33.6%) patients had severe arteriosclerosis (luminal narrowing >25% via fibrointimal arterial thickening). Circulating donor-specific anti-HLA antibodies were significantly associated with severe allograft arteriosclerosis (hazard ratio, 2.9; P <0.0001), independently of traditional risk factors. Patients with severe arteriosclerosis and anti-HLA antibodies (n=91, 12.2%) demonstrated allograft endothelial activation, endarteritis, and complement deposition. High levels of anti-HLA antibodies and their complement binding capacity were associated with increased severity of arteriosclerosis. Patients with antibody-associated severe arteriosclerosis had decreased allograft survival and increased mortality ( P <0.0001); they exhibited a 2.5- and 4.1-fold increased risk of major adverse cardiovascular events compared with patients who had severe arteriosclerosis without antibodies and patients with minimal arteriosclerosis, respectively ( P <0.0005). Circulating donor-specific anti-HLA antibodies were significantly associated with occurrence of major adverse cardiovascular events (hazard ratio, 2.4; P =0.0004), independently of traditional risk factors. Conclusions: Circulating antibodies are major determinants of severe arteriosclerosis and major adverse cardiovascular events, independent of traditional cardiovascular risk factors.

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Relationship of lipid oxidation with subclinical atherosclerosis and 10-year coronary events in general population

Cited by 52 publications

References 28 publications

Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies

Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies

Metabolomic signature of arterial stiffness in male patients with peripheral arterial disease

Determinants and Outcomes of Accelerated Arteriosclerosis

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