2017 Cardiovascular Research Day Abstract Book

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43 Intracoronary Versus Intravenous Adenosine-Induced Maximal Hyperemia for Fractional Flow Reserve Measurement: A Systematic Review and Meta-Analysis Mohamed El-Helw, MD 1 • Mohamed Abo-Aly, MD 1 • Georges Lolay, MD 1 • Christopher Adams, MD 1 • Ahmed El-Sharaawy, MD 1 • Ahmed Abdel-Latif, MD, PhD 1 • Khaled Ziada, MD 1 1Division of <strong>Cardiovascular</strong> Medicine, Gill Heart Institute, University of Kentucky Postdoc Background: Measurement of fractional flow reserve (FFR) is considered the gold standard technique for the invasive hemodynamic assessment of borderline coronary artery stenosis. Currently, intravenous (IV) adenosine is the recommended approach; however intracoronary (IC) administration is widely used due to its convenience and lower cost. The correlation between IV and IC administration to assess coronary blood flow is not well studied. Objective: This systematic review and meta-analysis is conducted to review the available literature that compared FFR measurements using bolus IC vs. standard continuous IV of adenosine infusion for detection of significant coronary artery stenosis. Methods: We systematically searched MEDLINE, EMBASE, Google scholar and the Cochrane Central Register of Controlled Trials databases. We reviewed data pertaining to the used adenosine doses, side effects of each method of administration and FFR values. We performed statistical analyses examining the sensitivity, specificity, positive likelihood ratio, negative likelihood ratio and odds ratio in studies comparing bolus IC adenosine and continues IV adenosine infusion using random effects modelling. Results: We identified 8 studies addressing the primary review question. Compared to standard IV adenosine infusion, the overall sensitivity of IC adenosine is 0.843 (95% C.I. 0.701-0.925, P
44 Recapitulating In Vivo Fibroblast Differentiation Using a Hydrogel Cell Culture System Demetria Fischesser 1 • Onur Kanisicak, PhD 1 • Mario Perera 2 • Neil Ayres, PhD 2 • Jeff D Molkentin, PhD 1 1Molecular <strong>Cardiovascular</strong> Biology, Cincinnati Children's Hospital • 2 Chemistry, University of Cincinnati Graduate Student Cardiac fibroblasts are resident interstitial cells known to maintain the extracellular matrix (ECM) under normal physiological conditions through the secretion of collagens and other adherent proteins. During injury, these fibroblasts take on an activated, contractile state and deposit additional ECM proteins to contribute to scar formation. While this response is initially beneficial to prevent rupture and further injury, continuous scar development leads to fibrosis, pathological ventricular remodeling and dysfunction, and eventual organ failure. Though much has already been discovered about the importance of fibroblasts during development and injury response, there are still many aspects of their functions that remain unclear. In order to decipher these fibroblast functions, many in vitro systems have been used to easily manipulate fibroblasts while attempting to mimic in vivo conditions. However, most of these systems have used plastic or gelatin-coated plastic as the surface medium. These have proven to be much stiffer than physiological tissue and provide a static system inhospitable to the dynamic changes of the activating fibroblast. In order to mimic an adaptable in vivo environment for fibroblast culture, we have developed a new hydrogel technology to understand fibroblast behavior and differentiation. This technology utilizes gelatin norbornene and a thiol conjugated to a Reversible Addition-Fragmentation Chain Transfer (RAFT) polymer which can dynamically mimic the stiffness of both healthy and fibrotic tissue, thus allowing for seamless modeling of injury and disease in various tissues. Through morphology and differentiation studies, we have found that there is a significant difference between fibroblasts plated on plastic versus softer hydrogels which mimic in vivo conditions. Fibroblasts plated on plastic and stiffer surfaces become very large and flat, and express markers of differentiation, such as alpha-Smooth Muscle Actin (αSMA), within days of plating. On softer hydrogels, however, the fibroblasts remain small and eventually develop long stellate appendages. They produce αSMA much more slowly and at a much less robust level than on stiffer surfaces. The morphology and differentiation pattern seen on softer hydrogels is highly comparable to fibroblasts observed in vivo. We will use these initial findings to better understand the activation and differentiation of fibroblasts and how, in injury, they first inhibit tissue damage and later enhance it. In the future, we plan to manipulate this hydrogel system to intentionally change the stiffness of the surface on which fibroblasts have already been plated to determine if we can mimic disease states as well as reverse the fibroblast activation phenotype seen previously. 60
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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
Page 9 and 10: FEATURED SPEAKER Calum MacRae, M.D.
Page 11 and 12: SPECIAL PRESENTATION Mark Stoops He
Page 13 and 14: NOTES 12
Page 15 and 16: 2017 POSTER PARTICIPANTS 40 Mohamed
Page 17 and 18: 2017 ABSTRACTS 16
Page 19 and 20: 2 Inhibition of Megalin Reduces Ath
Page 21 and 22: 4 Identification of a Lipid Signatu
Page 23 and 24: 6 Serum Amyloid A Activates the NLR
Page 25 and 26: 8 Azithromycin Therapy Reduces Card
Page 27 and 28: 10 Evidence of Angiotensin II-depen
Page 29 and 30: 12 Auditory Entrainment of Respirat
Page 31 and 32: 14 Cardiac specific Rad knockout In
Page 33 and 34: 16 Hypercholesterolemia Induces Acu
Page 35 and 36: 18 A Novel Approach for Modifying I
Page 37 and 38: 20 Clinical Use of the Amplatzer Se
Page 39 and 40: 22 Regulation of Akt Signaling by N
Page 41 and 42: 24 Vascular Inflammatory Regulation
Page 43 and 44: 26 Vascular inflammation induced ex
Page 45 and 46: 28 Sexual Dimorphism of Angiotensin
Page 47 and 48: 30 Computational modeling of amylin
Page 49 and 50: 32 PCB 126 Exposure Increases Perip
Page 51 and 52: 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: 42 Lysophosphatidic Acid Receptor 4
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 and 104: 86 Pharmacological inhibition of Hu
Page 105 and 106: 88 The Effects of Hypercholesterole
Page 107 and 108: 90 Reduced HDL in mice overexpressi
Page 109 and 110: 92 Human Antigen R (HuR) Regulates
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94 Impact of miR-33 antagonism on c
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96 HB-EGF is a Key Positive Regulat
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98 HDL-miR-223 Communication Pathwa
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100 Short-Term Exercise Training Di
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102 The Ral-Exocyst Pathway Regulat
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NOTES 120
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2017 Cardiovascular Research Day Abstract Book

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