scholarly journals Clinical analysis of lectin-like oxidized low-density lipoprotein receptor-1 in patients with in-stent restenosis after percutaneous coronary intervention

Medicine ◽  
2018 ◽  
Vol 97 (17) ◽  
pp. e0366 ◽  
Author(s):  
Junfeng Liu ◽  
Yunde Liu ◽  
Kegang Jia ◽  
Zhixiao Huo ◽  
Qianyu Huo ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Coronary Intervention ◽  
Clinical Analysis ◽  
Lipoprotein Receptor ◽  
Oxidized Low Density Lipoprotein ◽  
Stent Restenosis ◽  
Percutaneous Coronary ◽  
Density Lipoprotein Receptor ◽  
In Stent Restenosis

scholarly journals Soluble Lectin-Like Oxidized Low Density Lipoprotein Receptor-1 as a Biochemical Marker for Atherosclerosis-Related Diseases

2013 ◽  
Vol 35 ◽  
pp. 413-418 ◽  
Author(s):  
Angela Pirillo ◽  
Alberico Luigi Catapano
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Coronary Intervention ◽  
Soluble Form ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Oxidized Low Density Lipoprotein ◽  
Low Density Lipoprotein Receptor ◽  
Coronary Syndrome ◽  
Density Lipoprotein Receptor

Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), the main oxidized low-density lipoprotein (OxLDL) in endothelial cells, is upregulated in atherosclerotic lesions and is involved in several cellular processes that regulate the pathogenesis of atherosclerosis. The LOX-1 expressed on the cell surface can be proteolytically cleaved and released in a soluble form (sLOX-1) in the circulation under pathological conditions. Serum levels of sLOX-1, in fact, are elevated at the early stages of acute coronary syndrome and are associated with coronary plaque vulnerability and with the presence of multiple complex coronary lesions. Moreover, in subjects with stable CAD, levels of serum sLOX-1 are associated with the presence of lesions in the proximal and mid-segments of the left anterior descending artery that are the most prone to rupture; in subjects undergoing percutaneous coronary intervention, baseline preprocedural serum sLOX-1 levels are associated with the incidence of periprocedural myocardial infarction. Altogether, these findings suggest that circulating levels of sLOX-1 might be a diagnostic and prognostic marker for atherosclerotic-related events.

scholarly journals Impact of anemia on in-stent restenosis after percutaneous coronary intervention

2021 ◽  
Author(s):  
Huilin Hu ◽  
Shijun Wang ◽  
Guanmin Tang ◽  
Changlin Zhai ◽  
Liang Shen
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Low Density Lipoprotein ◽  
Multivariate Logistic Regression Analysis ◽  
Density Lipoprotein ◽  
Coronary Intervention ◽  
Logistic Analysis ◽  
Stent Restenosis ◽  
Percutaneous Coronary ◽  
Stent Diameter ◽  
In Stent Restenosis

Abstract Background Anemia is a well-recognized risk factor for adverse events after percutaneous coronary intervention (PCI), but data regarding the association between anemia and in-stent restenosis (ISR) remain limited.Methods A total of 538 patients who underwent PCI between January 2018 and September 2019 and performed follow-up angiography 9–12 months after the initial PCI was enrolled in the study. Baseline clinical and procedural characteristics were compared between ISR and non-ISR group. Multivariate logistic regression analysis was employed to determine the independent predictors of ISR.Results The incidence of anemia in patients with ISR was 53.5% and 19.0% in the non-ISR group, which was significantly different (P ༜0.001). The rate of diabetes, chronic kidney disease (CKD), bifurcation lesion and calcification was significantly higher in ISR group. In addition, low-density lipoprotein cholesterol (LDL-c), multiple stenting and stent diameter were also significantly related with ISR. After multivariate logistic analysis, anemia (odds ratio [OR], 2.786; 95% confidence interval [CI], 1.091 to 7.115; P = 0.032) together with LDL-c (OR, 1.682; 95% CI, 1.145 to 2.469; P = 0.008), diabetes (OR, 3.582; 95% CI, 1.406 to 9.125; P = 0.007), CKD (OR, 2.841; 95% CI, 1.006 to 8.027; P = 0.049), multiple stenting (OR, 2.823; 95% CI, 1.184 to 6.731; P = 0.019), and stent diameter (OR, 2.778; 95% CI, 1.069 to 7.194; P = 0.036) were closely associated with ISR.Conclusion Anemia is closely associated with ISR after PCI, patients with lower hemoglobin have a higher risk of ISR.

scholarly journals Impact of anemia on in-stent restenosis after percutaneous coronary intervention

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Huilin Hu ◽  
Shijun Wang ◽  
Guanmin Tang ◽  
Changlin Zhai ◽  
Liang Shen
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Propensity Score ◽  
Propensity Score Matching ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Coronary Intervention ◽  
Stent Restenosis ◽  
Percutaneous Coronary ◽  
Stent Diameter ◽  
In Stent Restenosis

Abstract Background Anemia is a common risk factor for post-percutaneous coronary intervention (PCI) adverse events; however, data on its association with in-stent restenosis (ISR) is limited. Methods 538 patients who underwent PCI between January 2017 and September 2019 and follow-up angiography 9–12 months after the initial PCI were enrolled in this study. Baseline clinical and procedural characteristics were compared between the ISR and non-ISR groups, and independent predictors of ISR were determined using propensity score matching. Results The incidence of anemia was 53.5% in patients with ISR and 19.0% in those without ISR. Univariable logistic regression analyses showed that anemia (OR, 4.283; 95% CI, 1.949–9.410; P < 0.001), diabetes mellitus (OR, 2.588; 95% CI, 1.176–5.696; P = 0.018), chronic kidney disease (OR, 3.058; 95% CI, 1.289–7.252; P = 0.011), multiple stenting (OR, 2.592; 95% CI, 1.205–5.573; P = 0.015), bifurcation lesion (OR, 2.669; 95% CI, 1.236–5.763; P = 0.012), and calcification (OR, 3.529; 95% CI, 1.131–11.014; P = 0.030) were closely associated with ISR. Low-density lipoprotein cholesterol (LDL-c) levels and stent diameter were also significantly linked to ISR, as was anemia (P = 0.009) after propensity score matching. Conclusion Anemia is closely associated with post-PCI ISR, and patients with lower hemoglobin levels are at a higher risk of ISR.

Alterations in vascular function by syncytiotrophoblast extracellular vesicles via lectin-like oxidized low-density lipoprotein receptor-1 in mouse uterine arteries

2018 ◽  
Vol 132 (21) ◽  
pp. 2369-2381 ◽  
Author(s):  
Floor Spaans ◽  
Anita Quon ◽  
Stewart R. Rowe ◽  
Jude S. Morton ◽  
Raven Kirschenman ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Extracellular Vesicles ◽  
Vascular Function ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Oxidized Low Density Lipoprotein ◽  
Uterine Arteries ◽  
Density Lipoprotein Receptor

Syncytiotrophoblast extracellular vesicles (STBEVs), released into the maternal circulation during pregnancy, have been shown to affect vascular function; however, the mechanism remains unknown. In rats, STBEVs were shown to reduce endothelium-mediated vasodilation via lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), a multi-ligand scavenger receptor that has been associated with vascular dysfunction. Recently, LOX-1 was shown to interact with the angiotensin II type 1 receptor (AT-1). We hypothesized that, in pregnant mice, STBEVs would impair vascular function via LOX-1 and would specifically affect angiotensin II responses. Uterine arteries from pregnant control (C57BL/6) and LOX-1 knockout (LOX-1KO) mice were isolated on gestational day (GD) 18.5. Endothelium-dependent (methylcholine (MCh); ± N(G)-Nitro-L-arginine methyl ester to assess nitric oxide (NO) contribution), and -independent (sodium nitroprusside) vasodilation, and vasoconstriction (angiotensin II; ± AT-1 [candesartan] or angiotensin II type 2 receptor (AT-2) [PD123.319] receptor antagonists; high potassium salt solution) responses were assessed using wire myography. AT-1 and AT-2 expression was analyzed using fluorescence microscopy. Human umbilical vein endothelial cells (HUVECs) were stimulated with STBEVs ± LOX-1 blocking antibody, and superoxide and peroxynitrite production were analyzed. Although MCh-induced vasodilation was decreased (P=0.0012), NO contribution to vasodilation was greater in LOX-1KO mice (P=0.0055). STBEVs delayed angiotensin II tachyphylaxis in arteries from control but not LOX-1KO mice (P<0.0001), while AT-1 and AT-2 expression was unchanged. STBEVs increased peroxynitrite production in HUVECs via LOX-1 (P=0.0091). In summary, LOX-1 deletion altered endothelium-mediated vasodilation, suggesting that LOX-1 contributes to vascular adaptations in pregnancy. STBEVs increased angiotensin II responsiveness and oxidative stress levels via LOX-1, suggesting that increased LOX-1 expression/activation or STBEVs could adversely affect vascular function and contribute to vascular complications of pregnancy.

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