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  • ISSN: 2378-9344
    Volume 7, Issue 4
    Mini Review
    Takehiko Takayanagi*
    Atherosclerosis is a chronic vascular inflammatory disease characterized by oxidative stress and endothelial dysfunction. Oxidation of low-density lipoprotein (LDL), cholesterol is a key step in the development of atherosclerosis. Pathogenesis of atherosclerosis can begin with shear stress-induced endothelial dysfunction, which can lead to endothelial and platelet activation and adhesion of monocytes to the activated endothelium. These monocytes, upon differentiation into proinflammatory macrophages, can increase the uptake of oxidized LDL (oxLDL), and become foam cells, thereby exacerbating inflammatory signaling. Although the prolonged use of antioxidative components, such as polyphenols and supplemental vitamins C and E, has been proven effective in preventing atherosclerosis in animal models, this has not yet been demonstrated in human clinical trials. The use of multiple antioxidants with different mechanisms of action simultaneously has shown positive effects in the treatment of atherosclerosis. There is some indication that a diet rich in antioxidants may be beneficial in the prevention of cardiovascular events.
    Research Article
    Leah Gober, Allen Bui, and Jean Marie Ruddy*
    Best medical therapy for peripheral artery disease (PAD) includes statin and anti-platelet agents, a combination shown to decrease rates of major cardiovascular events. Despite these findings, many patients remain undertreated and the objective of this project was to investigate the rate of initiating anti-platelet and statin therapy for inpatients newly diagnosed with PAD with a focus on disparities by race and sex.
    A retrospective chart review of inpatients with newly diagnosed PAD was performed between January 1, 2016 to December 31, 2016 at a single institution. Demographics and comorbid conditions were collected. Primary outcomes included antiplatelet and statin prescription at discharge.
    The 44 patients included in this study were predominantly male (59% vs. 41%) and African American (61% vs. 39%). Between admission and discharge, prescriptions rose from 70% to 82% for statin and 82% to 91% for anti-platelet agents. Vascular specialists were more successful than non-vascular specialists at initiating medical therapy, with statin prescriptions increasing 22% and anti-platelet prescriptions climbing 23% for those admitted to a vascular specialist. Interestingly, when the ABI was reported in the normal range, rates of statin initiation were particularly compromised at only 40%. For the total patient sample, those discharged without a statin were more commonly African American (63%) and the majority were female (67%). All patients discharged without an antiplatelet were African American and 50% were females.
    Despite national guidelines, patients with PAD continue to be discharged without optimal medical therapy. This study suggests that obstacles to initiation may include race, sex, admitting service, or presence of a normal ABI. Further investigation is warranted to determine effective avenues for provider education and system-wide initiatives.
    Letter to the Editor
    Kamran A Gaba*, Charles Vincent and Prem Chana
    A novel coronavirus has caused a pandemic, resulting in the deaths of thousands of individuals worldwide. Health systems responded rapidly to this crisis and mobilised resources, maximising the effectiveness of interventions. Lessons can be applied from this experience to improve the safety of carotid interventions.
    Clinical Image
    João Miguel de Almeida Silva*, Guilherme Marcos Soares Dias and André Luiz Rezende
    A1 segment: Precommunicating Anterior Cerebral Artery; ACA: Anterior Cerebral Arteries; ACoA: Anterior Communicating Artery; DSA: Digital Subtraction Angiograph.
    Review Article
    Klas Norrby*
    Unfractionated heparin (UFH), made from very high-molecular mast cell proteoglycans, has the highest negative charge density of any known biological molecule. It binds to proteins, including many growth factors, facilitating the interaction between growth factors and their receptors. The degradation of native heparin includes continuous heparinase depolymerization. Low-molecular-weight heparins (LMWHs) used as anticoagulants are manufactured from UFH by diverse methods. Tinzaparin is the only LMWH that is produced enzymatically, by heparinase-depolymerization of UFH.
    Data show that Tinzaparin (6.5 kDa) injected s.c. significantly suppresses angiogenesis mediated by VEGF, a key regulator of physiological and pathological angiogenesis. Notably, a 5.0 kDa fraction of Tinzaparin exercises an even more potent angiogenesis-suppressive effect, while UFH (c. 15 kDa) tends to stimulate and 22 kDa heparins significantly stimulate VEGF-mediated angiogenesis, demonstrating fragment-mass-specific effects. The anti-angiogenic effect of the 5 kDa Tinzaparin fraction is shown also in angiogenesis mediated by basic fibroblast growth factor or endotoxin. There is a strong correlation between heparin fragment-mass and angiogenesis-modulating effect (r = 0.97 in the examined range of 2.6, 8, 15 and 22 kDa). Contrarily to Tinzaparin, the LMWH Dalteparin (6 kDa), produced by chemical depolymerization of UFH, stimulates VEGF-mediated angiogenesis demonstrating a non-equivalent angiogenesis-modulating effect among LMWHs.
    A novel hypothesis suggests that there is an in vivo ‘intrinsic heparin-depolymerization angiogenesis-modulating process’ due to continual heparinase depolymerization of angiogenic high-molecular weight heparins, including those in UFH, into anti-angiogenic low-molecular-weight heparins. Further depolymerization would produce inactive heparin species, as judged by the data.
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