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Atherosclerosis 25건

  1. [해외논문]   Editorial board   SCI SCIE


    Atherosclerosis v.256 ,pp. iii , 2017 , 0021-9150 ,

    초록

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  2. [해외논문]   Inhibitory effect of PCSK9 on Abca1 protein expression and cholesterol efflux in macrophages   SCI SCIE

    Adorni, M.P. ; Cipollari, E. ; Favari, E. ; Zanotti, I. ; Zimetti, F. ; Corsini, A. ; Ricci, C. ; Bernini, F. ; Ferri, N.
    Atherosclerosis v.256 ,pp. 1 - 6 , 2017 , 0021-9150 ,

    초록

    Background and aims: Proprotein convertase subtilisin/kexin type 9 (PCSK9) may have extra-hepatic effects on cholesterol homeostasis of vascular macrophages. In this study, we aimed to investigate PCSK9 role on the anti-atherogenic process of ATP binding cassette transporter A1 (Abca1)-mediated cholesterol efflux. Methods: Abca1-mediated cholesterol efflux was evaluated by a radioisotopic technique in mouse peritoneal macrophages (MPM) from wild-type (WT) or LDL receptor knock-out (Ldlr -/- ) mice exposed to human recombinant PCSK9, in the presence of liver X receptor/retinoid X receptor (LXR/RXR) ligands or acetylated LDL (AcLDL) to stimulate Abca1 expression. Protein and gene expression was evaluated by Western blot and quantitative real time PCR, respectively. Results: PCSK9 inhibited Abca1-mediated cholesterol efflux induced by LXR/RXR agonists in WT MPM (-55%, p -/- MPM. This effect was fully abrogated by the co-incubation with an anti-PCSK9 antibody. The inhibition of Abca1-dependent efflux induced by PCSK9 was associated with a reduction of Abca1 protein expression only in WT cells. Abca1 gene expression was significantly downregulated by PCSK9 in WT macrophages (-64%, p

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  3. [해외논문]   Prevalence and severity of arterial calcifications in pseudoxanthoma elasticum (PXE) compared to hospital controls. Novel insights into the vascular phenotype of PXE   SCI SCIE

    Kranenburg, G. ; de Jong, P.A. ; Mali, W.P. ; Attrach, M. ; Visseren, F.L.J. ; Spiering, W.
    Atherosclerosis v.256 ,pp. 7 - 14 , 2017 , 0021-9150 ,

    초록

    Background and aims: Pseudoxanthoma elasticum (PXE) is a monogenetic disorder with progressive calcifications of the skin, the Bruch's membrane in the eyes and the arterial wall. Vascular disease is considered to be very prevalent, but the whole-body distribution of arterial calcifications in PXE is unknown. We aimed to systematically investigate arterial calcifications in PXE. Methods: We included 104 PXE patients from the Dutch PXE cohort and 93 hospital controls. All subjects underwent full-body low-dose CT scans without contrast. To investigate the prevalence and severity of arterial calcification per arterial location, CT scans were scored using a reproducible semi-quantitative scale with four calcification categories (interobserver kappa 0.54-0.99). Results: PXE patients (38/104 males) were 54 +/- 13 years and controls (45/93 males) 54 +/- 16 years old. Arterial calcifications were significantly more common in PXE patients in the intracranial internal carotid artery (75% vs. 44%), the arteries of the arms (20% vs. 3%), the femoral-popliteal arteries (74% vs. 44%) and the subpopliteal arteries (84% vs. 38%). In these arteries, calcification scores also indicated more severe calcification. No significant differences in prevalence of arterial calcification were observed in other arterial beds such as the coronary arteries (45% vs. 43%, p = 0.776), the carotid arteries (52% vs. 46%, p = 0.476) and the abdominal aorta (71% vs. 63%, p = 0.287). Analyses using patients younger than 55 years only, showed similar differences in prevalence of arterial calcifications between PXE patients and controls, with most pronounced calcifications in the arteries of the lower legs (67% vs. 8%). Similar patterns were observed in those without concomitant diabetes or renal dysfunction. Conclusions: In PXE, a vascular phenotype can be identified with a distribution of arterial calcifications that is clearly distinct from hospital controls and involves arterial calcifications in the legs, the intracranial internal carotid arteries and the arteries of the arms.

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  4. [해외논문]   Elevated 1-h post-load plasma glucose levels in subjects with normal glucose tolerance are associated with a pro-atherogenic lipid profile   SCI SCIE

    Andreozzi, F. ; Mannino, G.C. ; Perticone, M. ; Perticone, F. ; Sesti, G.
    Atherosclerosis v.256 ,pp. 15 - 20 , 2017 , 0021-9150 ,

    초록

    Background and aims: Evidence suggests that plasma glucose concentration ≥155 mg/dl at 1h during an oral glucose tolerance test (OGTT) (NGT 1 h-high) predicts both development of type 2 diabetes (T2DM) and cardiovascular events, among adults with normal glucose tolerance (NGT). An atherogenic lipid profile is detectable in subjects with impaired glucose tolerance (IGT) and T2DM. Whether individuals with NGT-1h-high also exhibit a pro-atherogenic lipid profile is still uncertain. Methods: The study cohort includes 1011 non-diabetic Caucasian adults participating in the CATAMERI study. All participants were submitted to anthropometrical evaluation before undergoing an OGTT. Subjects were categorized into NGT 1 h-low (1 h glucose

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  5. [해외논문]   Markers of sympathetic nervous system activity associate with complex plasma lipids in metabolic syndrome subjects   SCI SCIE

    Nestel, P.J. ; Khan, A.A. ; Straznicky, N.E. ; Mellett, N.A. ; Jayawardana, K. ; Mundra, P.A. ; Lambert, G.W. ; Meikle, P.J.
    Atherosclerosis v.256 ,pp. 21 - 28 , 2017 , 0021-9150 ,

    초록

    Background and aims: Plasma sphingolipids including ceramides, and gangliosides are associated with insulin resistance (IR) through effects on insulin signalling and glucose metabolism. Our studies of subjects with metabolic syndrome (MetS) showed close relationships between IR and sympathetic nervous system (SNS) activity including arterial norepinephrine (NE). We have therefore investigated possible associations of IR and SNS activity with complex lipids that are involved in both insulin sensitivity and neurotransmission. Methods: We performed a cross-sectional assessment of 23 lipid classes/subclasses (total 339 lipid species) by tandem mass spectrometry in 94 overweight untreated subjects with IR (quantified by HOMA-IR, Matsuda index and plasma insulin). Results: Independently of IR parameters, several circulating complex lipids associated significantly with arterial NE and NEFA (non-esterified fatty acids) and marginally with heart rate (HR). After accounting for BMI, HOMA-IR, systolic BP, age, gender, and correction for multiple comparisons, these associations were significant (p M3 ganglioside, sphingomyelin, phosphatidylcholine, alkyl- and alkenylphosphatidylcholine, phosphatidylinositol and free cholesterol; HR marginally (p = or 0.05) with ceramide, G M3 ganglioside, sphingomyelin, lysophosphatidylcholine, phosphatidylinositol, lysophosphatidylinositol and free cholesterol. Multiple subspecies of these lipids significantly associated with NE and NEFA. None of the IR biomarkers associated significantly with lipid classes/subclasses after correction for multiple comparisons. Conclusions: This is the first demonstration that arterial norepinephrine and NEFA, that reflect both SNS activity and IR, associate significantly with circulating complex lipids independently of IR, suggesting a role for such lipids in neural mechanisms operating in MetS.

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  6. [해외논문]   Plaque surface irregularity and calcification length within carotid plaque predict secondary events in patients with coronary artery disease   SCI SCIE

    Nonin, S. ; Iwata, S. ; Sugioka, K. ; Fujita, S. ; Norioka, N. ; Ito, A. ; Nakagawa, M. ; Yoshiyama, M.
    Atherosclerosis v.256 ,pp. 29 - 34 , 2017 , 0021-9150 ,

    초록

    Background and aims: Although comprehensive risk factor modification is recommended, a uniform management strategy does not necessarily prevent secondary events in patients with coronary artery disease (CAD). Therefore, identification of high-risk patients who may benefit from more intensive interventions may improve prognosis. Carotid ultrasound can reliably identify systemic atherosclerosis, and carotid plaque and intima-media thickness (IMT) are known independent risk factors for CAD. However, it is unclear whether findings on carotid ultrasound can improve prediction of secondary CAD events. Methods: The study population comprised 146 consecutive patients with CAD (mean age, 66 +/- 9 years; 126 with angina pectoris, 20 with acute myocardial infarction). IMT, plaque score, plaque area, plaque surface irregularity, and calcification length (calculated by summing the calcified lesions within each plaque accompanied by acoustic shadow) were measured at baseline. Patients were followed for 10 years to ascertain secondary CAD events defined as hard major adverse cardiovascular events (MACE; cardiac death and acute myocardial infarction) and as total MACE (hard MACE and angina pectoris with coronary revascularization). Results: Multiple regression analysis demonstrated that calcification length (p

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  7. [해외논문]   Hematopoietic arginase 1 deficiency results in decreased leukocytosis and increased foam cell formation but does not affect atherosclerosis   SCI SCIE

    Ren, B. ; Van Kampen, E. ; Van Berkel, T.J.C. ; Cruickshank, S.M. ; Van Eck, M.
    Atherosclerosis v.256 ,pp. 35 - 46 , 2017 , 0021-9150 ,

    초록

    Background and aims: Arginase1 (Arg1), an M2 macrophage marker, plays a critical role in a number of immunological functions in macrophages, which are the main cell type facilitating atherosclerotic lesion development. Arg1 uses the substrate l-arginine to create l-ornithine, a precursor molecule required for collagen formation and vascular smooth muscle cell differentiation. By reducing l-arginine availability, Arg1 limits the production of nitric oxide (NO), a pro-atherogenic factor in macrophages. In endothelial cells, conversely, NO is strongly anti-atherogenic. However, until now, the role of Arg1 in atherosclerosis is largely unknown. The aim of this study is to specifically investigate the effect of Arg1 deletion in hematopoietic cells on atherosclerosis susceptibility. Methods: Ldlr KO mice were transplanted with Arg1 flox/flox ;Tie2-Cre (Arg1 KO) bone marrow (BM) or wildtype (WT) BM. After 8 weeks of recovery on chow diet, recipients mice were fed a Western-Type Diet (WTD) for 10 weeks to induce atherosclerosis. Results: After 10-week WTD challenge, blood leukocyte counts were decreased by 25% (p

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  8. [해외논문]   Ideal cardiovascular health influences cardiovascular disease risk associated with high lipoprotein(a) levels and genotype: The EPIC-Norfolk prospective population study   SCI SCIE

    Perrot, N. ; Verbeek, R. ; Sandhu, M. ; Boekholdt, S.M. ; Hovingh, G.K. ; Wareham, N.J. ; Khaw, K.T. ; Arsenault, B.J.
    Atherosclerosis v.256 ,pp. 47 - 52 , 2017 , 0021-9150 ,

    초록

    Background and aims: Lipoprotein(a) (Lp[a]) is a strong genetic risk factor for cardiovascular disease (CVD). The American Heart Association has prioritised seven cardiovascular health metrics to reduce the burden of CVD: body mass index, healthy diet, physical activity, smoking status, blood pressure, diabetes and cholesterol levels (together also known as ideal cardiovascular health). Our objective was to determine if individuals with high Lp(a) levels could derive cardiovascular benefits if characterized by ideal cardiovascular health. Methods: A total of 14,051 participants of the EPIC-Norfolk study were stratified according to the cardiovascular health score (based on the number of health metrics with an ideal, intermediate or poor status). Of them, 1732 had a CVD event during a mean follow-up of 11.5 years. Cox proportional hazards models were used to describe the association between the cardiovascular health score and Lp(a) level or genotype (as estimated by the rs10455872 variant) with the risk of CVD. Results: We observed little or no differences in serum Lp(a) levels across the seven cardiovascular health metric categories. Among participants with high serum Lp(a) levels ≥50 mg/dl), those in the highest (i.e. healthiest) cardiovascular health score category (10-14) had an adjusted hazard ratio for cardiovascular disease of 0.33 (95% CI = 0.17-0.63, p = 0.001) compared to participants in the lowest (i.e. unhealthiest) cardiovascular health score category(0-4). Similar results were obtained when we replaced Lp(a) with rs10455872. Conclusions: Although Lp(a) levels are only slightly influenced by cardiovascular health metrics, an ideal cardiovascular health could substantially reduce CVD risk associated with high Lp(a) levels or genotype.

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  9. [해외논문]   Cellular subtype expression and activation of CaMKII regulate the fate of atherosclerotic plaque   SCI SCIE

    Maione, A.S. ; Cipolletta, E. ; Sorriento, D. ; Borriello, F. ; Soprano, M. ; Rusciano, M.R. ; D'Esposito, V. ; Markabaoui, A.K. ; De Palma, G.D. ; Martino, G. ; Maresca, L. ; Nobile, G. ; Campiglia, P. ; Formisano, P. ; Ciccarelli, M. ; Marone, G. ; Trimarco, B. ; Iaccarino, G. ; Illario, M.
    Atherosclerosis v.256 ,pp. 53 - 61 , 2017 , 0021-9150 ,

    초록

    Background and aims: Atherosclerosis is a degenerative process of the arterial wall implicating activation of macrophages and proliferation of vascular smooth muscle cells. Calcium-calmodulin dependent kinase type II (CaMKII) in vascular smooth muscle cells (VSMCs) regulates proliferation, while in macrophages, this kinase governs diapedesis, infiltration and release of extracellular matrix enzymes. We aimed at understanding the possible role of CaMKII in atherosclerosis plaques to regulate plaque evolution towards stability or instability. Methods: Clinically defined stable and unstable plaques obtained from patients undergoing carotid end arteriectomy were processed for evaluation of CaMKs protein expression, activity and localization. Results: The larger content of CaMKII was found in CD14 + myeloid cells that were more abundant in unstable rather than stable plaques. To test the biological effect of activated CD14 + myeloid cells, VSMCs were exposed to the conditioned medium (CM) of macrophages extracted from carotid plaques. CM induced attenuation of CaMKs expression and activity in VSMCs, leading to the reduction of VSMCs proliferation. This appears to be due to the CaMKII dependent release of cytokines. Conclusions: These results indicate a pivotal role of CaMKs in atherosclerosis by regulating activated myeloid cells on VSMCs activity. CaMKII could represent a possible target for therapeutic strategies based on macrophages specific inhibition for the stabilization of arteriosclerotic lesions.

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  10. [해외논문]   Carotid artery plaques and intima medial thickness in familial hypercholesteraemic patients on long-term statin therapy: A case control study   SCI SCIE

    Bos, S. ; Duvekot, M.H.C. ; ten Kate, G.J.R. ; Verhoeven, A.J.M. ; Mulder, M.T. ; Schinkel, A.F.L. ; Nieman, K. ; Watts, G.F. ; Sijbrands, E.J.G. ; Roeters van Lennep, J.E.
    Atherosclerosis v.256 ,pp. 62 - 66 , 2017 , 0021-9150 ,

    초록

    Background and aims: Statins reduce subclinical atherosclerosis and premature atherosclerotic cardiovascular disease (ASCVD) in patients with familial hypercholesterolemia (FH). However, some FH patients still develop ASCVD despite statin therapy. We compared subclinical atherosclerosis assessed by carotid plaque presence and intima media thickness (C-IMT), in long-term statin-treated FH patients and healthy controls. Furthermore, we analysed whether carotid ultrasonography findings associated with subclinical coronary atherosclerosis. Methods: We assessed the presence of carotid plaques and C-IMT in 221 asymptomatic heterozygous FH patients (48% men; 46 +/- 15 years) on long-term (10.0 +/- 7.8 years) statin treatment and 103 controls (32% men, 47 +/- 16 years). Results: The frequency of carotid plaques and C-IMT did not differ significantly between the FH patients and controls (69 (31%) versus 24 (23%), p = 0.1 and 0.58 +/- 0.13 versus 0.58 +/- 0.12 mm, p = 0.9, respectively). In a subgroup of 49 FH patients who underwent cardiac computed tomography, coronary artery calcification correlated with carotid plaque presence (R = 0.47; p = 0.001), but not with C-IMT (R = 0.20; p = 0.2). Conclusions: Carotid plaques and C-IMT did not differ between long-term statin-treated heterozygous FH patients and healthy controls. This shows that long-term statin treatment in these FH patients reduces carotid atherosclerosis to a degree of a healthy population. These findings strongly suggests that sonography of the carotid arteries during follow-up of statin-treated FH patients has limited value.

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