2017 Cardiovascular Research Day Abstract Book

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87 Perioperative high density lipoprotein particle changes and the risk of acute kidney injury after cardiac surgery Loren Smith, MD, PhD 1 • Derek Smith, PhD 2 • Alan Remaley, MD, PhD 3 • MacRae Linton, MD 4 • Frederic Billings IV, MD 5 1Anesthesiology, Vanderbilt University Medical Center • 2 Biostatistics, Vanderbilt University Medical Center • 3 National Heart, Lung, and Blood Institute, National Institutes of Health • 4Medicine and Pharmacology, Vanderbilt University Medical Center • 5 Anesthesiology and Medicine, Vanderbilt University Medical Center Faculty Acute kidney injury (AKI) after cardiac surgery occurs in up to 30% of patients and increases the risk of postoperative myocardial infarction and death. No effective treatments exist. Increased intraoperative oxidative stress independently predicts AKI after cardiac surgery. High density lipoproteins (HDL) have anti-oxidant capacity. We hypothesize that perioperative HDL cholesterol concentration (HDL-C), HDL particle concentration (HDL-P) and HDL composition are associated with the risk of postoperative AKI. We analyzed data from a prospective, 393-subject trial of perioperative atorvastatin to prevent AKI after cardiac surgery. Statin-using patients were randomized to placebo or 80mg atorvastatin the morning of surgery and 40mg on postoperative day 1. Stain-naïve patients were randomized to placebo or 80mg the day prior to surgery and 40mg daily thereafter during hospitalization. The associations between 1) HDL-C, 2) small HDL particle concentration, and 3) the change in HDL-P from anesthetic induction to postoperative day two with maximum serum creatinine change from baseline in the first 48 postoperative hours were assessed using two-component latent variable mixture models adjusted for known AKI risk factors. Regression analyses assessed interactions of chronic statin use, perioperative atorvastatin treatment, and HDL-C on AKI risk. We quantified HDL particle size by NMR Lipoprofile test in 90 subjects. HDL-C and HDL-P change over time were assessed with mixed effects models adjusted for AKI risk factors. We quantified myeloperoxidase (MPO) activity of apolipoprotein B-depleted serum in 30 subjects using a bioluminescence assay. A higher preoperative HDL-C was independently associated with a decreased postoperative serum creatinine change (p=0.02). The association between a high HDL-C and an attenuated increase in serum creatinine was strongest in chronic statin-using patients (p=0.008) and was enhanced with perioperative atorvastatin treatment (p=0.004) and increasing chronic statin dose (p=0.003). HDL- C did not change during the perioperative period (p=0.60), however, HDL-P decreased (p
88 The Effects of Hypercholesterolemia on Wound Healing and Endothelial Angiogenic Properties Yedida Bogachkov 1 • Lin Chen, MD, PhD 2 • Myung-Jin Oh, PhD 3 • Luisa A. DiPietro, PhD 2 • Irena Levitan, PhD 4 1Pharmacology, University of Illinois at Chicago • 2 Periodontics, University of Illinois at Chicago • 3Medicine, University of Chicago • 4 Pulmonary, Critical Care, Sleep and Allergy, University of Illinois at Chicago Graduate Student Nearly 31 million adults in the US have elevated total cholesterol levels over 240 mg/dL, and almost 32% of US adults have LDL cholesterol levels of 200mg/dL or above. Our study focuses on the impact of dyslipidemia on wound healing and wound angiogenesis. Using ApoE-/- mice, a known dyslipidemic model and a skin punch biopsy wound healing assay, we show that ApoE -/- mice show significantly delayed wound closure on days 2-7 post-wounding compared to control mice. These same ApoE-/- also display significantly decreased angiogenesis on days 10 and 14 post wounding, based on PECAM staining for endothelial cells, indicative of endothelial cell infiltration of the wound bed and new blood vessel growth. Furthermore, macrophage infiltration is also reduced. This significant suppression of wound angiogenesis is also seen when LDL is directly applied to the wounds via subcutaneous injections on C57BL6 mice. Additionally, using a matrigel plug assay, we show significantly suppressed angiogenesis in C57BL6 mice fed a Western Diet for 40 weeks. These results utilize an Isolectin B4 probe, which is indicative of endothelial cell infiltration into the matrigel plug and new blood vessel growth. Finally, in vitro studies on human aortic endothelial cells were pursued showing LDL significantly decreases endothelial cell proliferation, whereas its oxidized form, oxLDL, shows an increase in proliferation. In sum, we have shown in vivo that hypercholesterolemic mice have a decreased angiogenic potential, and in vitro, excess LDL leads to a decrease in angiogenic potential of aortic endothelial cells. 104
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Cardiovascular Research Day ABSTRAC
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SCHEDULE FOR THE DAY Friday, Novemb
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SCHEDULE FOR THE DAY continued Frid
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2017 GILL HEART INSTITUTE YOUNG INV
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FEATURED SPEAKER Calum MacRae, M.D.
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SPECIAL PRESENTATION Mark Stoops He
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NOTES 12
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2017 POSTER PARTICIPANTS 40 Mohamed
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2017 ABSTRACTS 16
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2 Inhibition of Megalin Reduces Ath
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4 Identification of a Lipid Signatu
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6 Serum Amyloid A Activates the NLR
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8 Azithromycin Therapy Reduces Card
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10 Evidence of Angiotensin II-depen
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12 Auditory Entrainment of Respirat
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14 Cardiac specific Rad knockout In
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16 Hypercholesterolemia Induces Acu
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18 A Novel Approach for Modifying I
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20 Clinical Use of the Amplatzer Se
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22 Regulation of Akt Signaling by N
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24 Vascular Inflammatory Regulation
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26 Vascular inflammation induced ex
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28 Sexual Dimorphism of Angiotensin
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30 Computational modeling of amylin
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32 PCB 126 Exposure Increases Perip
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34 Endothelial Mineralocorticoid Re
Page 53 and 54: 36 Optimization of immunomagnetic s
Page 55 and 56: 38 Gestational Diabetes Provokes Po
Page 57 and 58: 40 The Prognostic Role of Elevated
Page 59 and 60: 42 Lysophosphatidic Acid Receptor 4
Page 61 and 62: 44 Recapitulating In Vivo Fibroblas
Page 63 and 64: 46 Sex-Specific Differences in Card
Page 65 and 66: 48 Ticagrelor Reduces Inflammation
Page 67 and 68: 50 Association between Plasma Chole
Page 69 and 70: 52 Does Light Pollution Affect the
Page 71 and 72: 54 Impact of miR-33 antagonism on m
Page 73 and 74: 56 Isolation and characterization o
Page 75 and 76: 58 The XY sex chromosome complement
Page 77 and 78: 60 CHROME: a Long Non-coding RNA th
Page 79 and 80: 62 Making Good: Secretory Quality C
Page 81 and 82: 64 Thrombospondin 1 (TSP1) Deficien
Page 83 and 84: 66 Serum Amyloid A3 is a High Densi
Page 85 and 86: 68 Adipocyte deficiency of ACE2 inc
Page 87 and 88: 70 Hypercholesterolemia-induced end
Page 89 and 90: 72 Increased Circulating Trimethyla
Page 91 and 92: 74 Circulating Bacterial Small RNA
Page 93 and 94: 76 Pancreatic Beta Cell Export of m
Page 95 and 96: 78 Understanding inhibition of lipo
Page 97 and 98: 80 Insulin signaling regulates apol
Page 99 and 100: 82 Protease-activated Receptor 2 De
Page 101 and 102: 84 Reduced Low-Density Lipoprotein
Page 103: 86 Pharmacological inhibition of Hu
Page 107 and 108: 90 Reduced HDL in mice overexpressi
Page 109 and 110: 92 Human Antigen R (HuR) Regulates
Page 111 and 112: 94 Impact of miR-33 antagonism on c
Page 113 and 114: 96 HB-EGF is a Key Positive Regulat
Page 115 and 116: 98 HDL-miR-223 Communication Pathwa
Page 117 and 118: 100 Short-Term Exercise Training Di
Page 119 and 120: 102 The Ral-Exocyst Pathway Regulat
Page 121 and 122: NOTES 120
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2017 Cardiovascular Research Day Abstract Book

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