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CARDIOLOGY RESEARCH AND CLINICAL DEVELOPMENTS
AORTIC ANEURYSMS
RISK FACTORS, DIAGNOSIS,
SURGERY AND REPAIR
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CARDIOLOGY RESEARCH AND CLINICAL DEVELOPMENTS
AORTIC ANEURYSMS
RISK FACTORS, DIAGNOSIS,
SURGERY AND REPAIR
DANIEL FISCHHOF
AND
FRANZ HATIG
EDITORS
New York
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Copyright © 2013 by Nova Science Publishers, Inc.
All rights reserved. No part of this book may be reproduced, stored in a retrieval system or
transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical
photocopying, recording or otherwise without the written permission of the Publisher.
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Telephone 631-231-7269; Fax 631-231-8175
Web Site: http://www.novapublishers.com
NOTICE TO THE READER
The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or
implied warranty of any kind and assumes no responsibility for any errors or omissions. No
liability is assumed for incidental or consequential damages in connection with or arising out of
information contained in this book. The Publisher shall not be liable for any special,
consequential, or exemplary damages resulting, i
reliance upon, this material. Any parts of this book based on government reports are so indicated
and copyright is claimed for those parts to the extent applicable to compilations of such works.
Independent verification should be sought for any data, advice or recommendations contained in
this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage
to persons or property arising from any methods, products, instructions, ideas or otherwise
contained in this publication.
This publication is designed to provide accurate and authoritative information with regard to the
subject matter covered herein. It is sold with the clear understanding that the Publisher is not
engaged in rendering legal or any other professional services. If legal or any other expert
assistance is required, the services of a competent person should be sought. FROM A
DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE
AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS.
Additional color graphics may be available in the e-book version of this book.
Library of Congress Cataloging-in-Publication Data
Library of Congress Control Number: 2013935083
ISBN: (eBook)
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CONTENTS
Preface vii
Chapter 1 Genetic Risk Factors for Abdominal Aortic Aneurysms (AAA) 1
Helena Kuivaniemi, Evan J. Ryer, H. Richard Yoon
and James R. Elmore
Chapter 2 Assessment of Aortic Aneurysm Rupture Risk and Surgical Repair 31
Clement Kleinstreuer, Emily Childress and Mark Farber
Chapter 3 Pathogenesis of Abdominal Aortic Aneurysms 57
K. M. Mata, C. Tefé-Silva, C. R. Fernandes, E. M. Floriano,
P. S. Prudente and S. G. Ramos
Chapter 4 Morphometric Model of Abdominal Aortic Aneurysms and
the Significance of the Structural Changes in the Aortic Wall
for Rupture Risk Assessment 81
Radak,
-, Vera -,
D,
Chapter 5 Endovascular Aneurysm Repair in Challenging Anatomy 119
Pieter Broos, Rutger A. Stokmans, Bianca L. W. Bendermacher,
Philippe W. M. Cuypers, Marc van Sambeek
and Joep A.W. Teijink
Chapter 6 Abdominal Aortic Aneurysm Screening 139
Kevin C. Chun, Jacqulyne H. Sylvia, Kai Y. Teng,
Kiana M. Samadzadeh and Eugene S. Lee
Chapter 7 Aortic Hemodynamics and their Role in Aneurysm Location:
Can Mice Provide more Insight? 155
Bram Trachet, Stefaan Vandenberghe, Bart Loeys
and Patrick Segers
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Contents
vi
Chapter 8 Decision-Support System for Diagnosis of Abdominal Aortic
Aneurysm after Endovascular Repair 169
G. García, A. Tapia and M. De Blas
Chapter 9 Clinical, Hemodynamical and Mechanical Aspects of Aortic
Aneurisms and Endovascular Repair 181
Moshe Brand, Idit Avrahami, Asaph Nardi, Daniel Silverberg
and Moshe Halak
Index 193
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PREFACE
In this book, the authors present current research in the study of the risk factors,
diagnosis, surgery and repair of aortic aneurysms. Topics discussed in this compilation are the
genetic risk factors for abdominal aortic aneurysms (AAA); assessment of aortic aneurysm
rupture risk and surgical repair; morphometric model of abdominal aortic aneurysm and the
significance of the structural changes in the aortic wall for rupture risk assessment; the
pathogenesis of abdominal aortic aneurysms; endovascular aneurysm repair in challenging
anatomy; abdominal aortic aneurysm screening; aortic hemodynamics and their role in
aneurysm location; decision-support system for diagnosis of abdominal aortic aneurysm after
endovascular repair; and the clinical, hemodynamical and mechanical aspects of aortic
aneurysms and endovascular repair.
Chapter 1 Abdominal aortic aneurysm (AAA) is a complex, multifactorial disease with
a strong genetic component. About 20% of AAA patients have at least one relative with this
condition. Since the first candidate gene studies were published 20 years ago, nearly 100
genetic association studies using single nucleotide polymorphisms (SNPs) in biologically
relevant genes have been reported on AAA. The most significant results from candidate gene
studies are for sortilin-1 (SORT1), interleukin 6 receptor (IL6R), and apolipoprotein(a) (LPA).
Unbiased genome-wide approaches such as family-based DNA linkage studies and genome-
wide association studies have been carried out by international consortia to identify
susceptibility loci for AAA. The chromosomal regions in the human genome with the
strongest supporting evidence of contribution to the genetic risk for AAA are: 1) CDKN2BAS
gene (located on chromosome 9p21), also known as ANRIL, which encodes an antisense
RNA that regulates expression of the cyclin-dependent kinase inhibitors CDKN2A and
CDKN2B; 2) DAB2 interacting protein (DAB2IP; located on chromosome 9q33), which
encodes an inhibitor of cell growth and survival; 3) low density lipoprotein receptor-related
protein 1 (LRP1; located on chromosome 12q13.3), a plasma membrane receptor involved in
vascular smooth muscle and macrophage endocytosis, and 4) contactin-3 (CNTN3; located on
chromosome 3p12.3), which demonstrated the strongest association in smokers and yet its
function remains unclear. These four loci were identified in genome-wide association studies.
Using a different approach, DNA linkage analysis with affected relative-pairs, two additional
loci containing several plausible candidate genes, located on chromosomes 4q31 and 19q13,
were discovered. On-going and future studies to find additional risk loci include large meta-
analyses and whole genome sequencing. Furthermore, functional studies are needed to
establish the mechanisms by which these genes contribute to AAA pathogenesis. In the long-
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Daniel Fischhof and Franz Hatig
viii
term, these discoveries will result in important translational applications to the prevention,
diagnosis and management of AAAs.
Chapter 2 Contributions to rupture-risk assessment and surgical repair of abdominal
aortic aneurysms (AAAs) are reviewed. AAA-rupture occurs when the local wall stress
-wall strength. Such an event is quite unpredictable and rarely
foreshadowed by warning symptoms, but lethal in 80-90% of all cases. Typically, open
surgery or endovascular aneurysm repair (EVAR) by stent-graft insertion are recommended if
the maximum AAA-diameter exceeds 5.5cm. Still, a high degree of uncertainty regarding the
management of AAAs remains, especially for smaller AAAs. Hence, reliable rupture-risk
assessments as well as the development of criteria for well anchored and durable stent-graft
implantation are important ongoing research tasks. Clearly, predictive accurate and realistic
computer simulations of the transient three-dimensional blood flow and affected AAA-wall
dynamics can greatly contribute to the solution of these problems.
Through multiple studies aimed at AAA rupture risk assessment, the peak wall stress has
emerged as a widely accepted rupture predictor. These studies have focused on comparing
clinical/experimental findings with computational analyses of determining factors, such as
changes in maximum wall stress magnitude, wall stress distribution, and annual growth rate
of the maximum AAA-diameter. Most recently, modeling and simulation of two-way fluid-
structure interactions of anisotropic, patient-specific AAAs have improved the accuracy of
AAA rupture predictions. In addition, advanced EVAR techniques have successfully
expanded the target population.
Chapter 3 An abdominal aortic aneurysm (AAA) represents a complex
pathophysiological process of weakening and dilatation of the aortic wall, which is associated
with atherosclerosis, a chronic inflammatory response and hemodynamic alterations.
Degradation of the extracellular matrix by the matrix metalloproteinases (MMPs) and an
imbalance between MMPs and their tissue inhibitors (TIMPs), as well as the production of
reactive oxygen species, have fundamental roles in the development of AAA. The exact
pathogenetic mechanisms remain incompletely elucidated. In this study, the authors used an
experimental model that was developed in laboratory to induce AAA by
combining two potential causes of MMP secretion: inflammation and turbulent blood flow.
Male Wistar rats were divided into a control group (C) and an aneurysm group (A). The rats
in group A received both an injury and extrinsic stenosis of the wall of the abdominal aorta.
The rats in group C received a sham operation. The rats were euthanized at 3, 7 or 15 days
post-surgery (dps). Sections of the aorta including the aneurysm were collected for
morphological studies and MMP-2 and -9 and TIMP-1 and -2 assays. Dilatation to more than
300% of the normal aortic diameter was observed on 3 dps in 65% of the rats in group A and
was similar at 7 and 15 dps. The AAA wall underwent an intense remodeling process
characterized by a severe inflammatory response (neutrophils, macrophages and
lymphocytes), considerable destruction of elastin fibers and deposition of collagen as well as
an increase in the myofibroblast population and neovascularization. These alterations were
directly related to the dramatic increase of the levels of MMP-2 and -9 and TIMP-1 and -2
throughout the study period. Immunohistochemistry revealed an increase in the level of
inducible nitric oxide synthase (iNOS) in A group rats, suggesting that reactive oxygen
species (ROS) contribute to the degeneration of the aortic wall. AAA results from a cascade
of events that culminate in dilatation of the aortic wall. The inflammatory process associated
with turbulent intraluminal flow most likely causes endothelial dysfunction that creates a
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