### Goal

A Common Understanding of the Environment and the Limitations of

Our Understanding of this Environment.

Table 1

The following table lists some of the morphologic and physiologic
characteristics of an aorta where an endovascular graft is intended to
be placed for treatment of AAA. The work assignment involved suggesting
characteristics that could affect the function or performance of an
endovascular graft, identifying the range of the values, rating the
importance of the characteristics from a clinical standpoint and
providing comments. The discussion at the workshop centered on the
compiled work assignment. Both the compiled work assignment and workshop
comments are included in the table.

**Table 1 Morphologic and Physiologic Characteristics Pre-Implant**

<table>
<colgroup>
<col style="width: 6%" />
<col style="width: 13%" />
<col style="width: 17%" />
<col style="width: 3%" />
<col style="width: 3%" />
<col style="width: 3%" />
<col style="width: 0%" />
<col style="width: 3%" />
<col style="width: 3%" />
<col style="width: 34%" />
<col style="width: 0%" />
<col style="width: 10%" />
</colgroup>
<thead>
<tr class="header">
<th colspan="2" rowspan="2"><strong><span
class="smallcaps">Characteristics</span></strong></th>
<th rowspan="2"><strong><span class="smallcaps">Range of probable
Values</span></strong></th>
<th colspan="6"><strong><span
class="smallcaps">Criticality</span></strong></th>
<th colspan="2" rowspan="2"><strong><span
class="smallcaps">Comments</span></strong></th>
<th rowspan="2"><strong><span
class="smallcaps">References</span></strong></th>
</tr>
<tr class="odd">
<th>1</th>
<th>2</th>
<th>3</th>
<th colspan="2">4</th>
<th>5</th>
</tr>
</thead>
<tbody>
<tr class="odd">
<td colspan="12"><h4 id="aneurysm-characteristics">Aneurysm
Characteristics</h4></td>
</tr>
<tr class="even">
<td>1-1</td>
<td>Branch vessels</td>
<td><p><u>Prevalence estimates:</u></p>
<ul>
<li><p>Majority of patients</p></li>
<li><p>80% of cases involve branch vessels</p></li>
</ul>
<p><u>Number:</u></p>
<ul>
<li><p>0 to 8</p></li>
<li><p>IMA, lumbar arteries, artery of Drummond</p></li>
<li><p>Highly variable</p></li>
</ul></td>
<td>1</td>
<td>1</td>
<td>2</td>
<td colspan="2">4</td>
<td>2</td>
<td><ul>
<li><p>Device independent.</p></li>
<li><p>IMA and accessory renals are important</p></li>
<li><p>Potential Type II endoleaks.</p></li>
<li><p>Prolonged patency of branch vessels have been implicated as a
primary source of Type II endoleak in patients having endovascular AAA
repair (Fan, 2001; Baum, 2000). Persistent retrograde perfusion of
branch vessels can have adverse consequences. In some centers proactive
embolization of branch vessels is a preferred approach. (Walker,
1999)</p></li>
<li><p>If renals could be addressed, &gt; 5mm proximal neck population
could be treated, and TAA as well. Hypogastrics important for those
patients where 2 must be occluded.</p></li>
</ul></td>
<td colspan="2"><p>Fan, 2001;</p>
<p>Baum, 2000;</p>
<p>Walker, 1999;</p>
<p>Eurostar Progress Report, “angio-graphy side branches”</p></td>
</tr>
<tr class="odd">
<td>1-1</td>
<td>Branch vessels, continued</td>
<td><p><strong><u>Workshop comments:</u></strong></p>
<p><strong>Delete Artery of Drummond (“meandering
artery”)</strong></p></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td><p><strong><u>Workshop comments:</u></strong></p>
<p>Things to consider in case selection:</p>
<ul>
<li><p><strong>Accessory renal or misposition;</strong></p></li>
<li><p><strong>Hypogastric close to aorta; and</strong></p></li>
<li><p><strong>Size of biggest patent lumbar or IMA.</strong></p></li>
</ul>
<p><strong>Things to consider with device testing:</strong></p>
<ul>
<li><p><strong>Branch vessels not important/critical;</strong></p></li>
<li><p><strong>Is relevant because dealing with pressure gradient –
either big or not; and</strong></p></li>
<li><p><strong>Worst case for durability is no patent branch vessels
because larger gradient.</strong></p></li>
</ul>
<p><strong>No consensus on criticality.</strong></p></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-2</td>
<td><p>Iliac involvement</p>
<p><strong>Aneurysm of iliac arteries</strong></p></td>
<td><p><u>Prevalence estimates:</u></p>
<ul>
<li><p>~ 25% of cases</p></li>
<li><p>20-30%</p></li>
<li><p>32%</p></li>
<li><p>40% (Eurostar)</p></li>
<li><p>40-70%</p></li>
<li><p>60% of cases involve iliac arteries</p></li>
<li><p>Type II AAAs and its subgroups comprised (72.3%) of AAA
morphologies. In these cases, a sufficient proximal neck was present,
but the aneurysm extended into the iliac arteries; 56% of these were
eligible for a bifurcated endograft. (Schumacher, 1997).</p></li>
</ul></td>
<td></td>
<td>1</td>
<td>4</td>
<td colspan="2">3</td>
<td>2</td>
<td><ul>
<li><p>Landing zone length proximal to internal iliac artery. CIA
involvement may provide a volume into which device can buckle/kink. IIA
involvement is a separate issue.</p></li>
<li><p>Iliac extension of aneurysmal disease is commonly observed, and
poses one of the key factors dictating device design (tubular vs.
bifurcated) and distal type II endoleak (Schumacher, 1997; Schurink,
1999). In turn, distal Type II endoleak has been implicated as a risk
factor for surgical conversion (Harris, 2000).</p></li>
<li><p>Potential Type I endoleaks.</p></li>
<li><p>Leaves little healthy tissue to seal, also requires large iliac
sizes for ectatic conditions where treatable.</p></li>
<li><p>Patient population dependent. Graft type selection.</p></li>
</ul></td>
<td colspan="2"><p>Schumacher 1997;</p>
<p>Schurink, 1999;</p>
<p>Harris, 2000;</p>
<p>Eurostar Progress Report, “classification of AAA”</p></td>
</tr>
<tr class="odd">
<td>1-2</td>
<td><p>Iliac involvement,</p>
<p>continued</p>
<p><strong>Aneurysm of iliac arteries</strong></p></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>More important than branch vessels.</strong></p></li>
<li><p><strong>Related to fixation.</strong></p></li>
<li><p><strong>With iIiac involvement/aneurysms there is more tortuosity
and more changes over time.</strong></p></li>
<li><p><strong>Iliac involvement affects the length of the device and
the diameters the attachment sites will accommodate. Longer devices are
more prone to problems.</strong></p></li>
<li><p><strong>Columnar strength is important for treating aneurysms
with iliac involvement.</strong></p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-3</td>
<td>Multiple lesions</td>
<td><p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>Multiple aneurysms of the infrarenal abdominal aorta are not
widely reported.</p></li>
<li><p>10-25% will have iliac stenosis to some degree; estimated 15%
rate (Eurostar Progress Report, “additional procedures, PTA and
endarterectomy”)</p></li>
<li><p>5% of cases involve multiple lesions.</p></li>
<li><p>5-10%</p></li>
<li><p>Minority of patients.</p></li>
</ul></td>
<td>1</td>
<td>4</td>
<td>3</td>
<td colspan="2">1</td>
<td></td>
<td><ul>
<li><p>Multiple lesions are rare and are, generally, not amenable to
treatment by current stent-graft technologies.</p></li>
<li><p>“Lesion” too broad a term in AAA. Clarify between stenosis,
multiple sacs, etc.</p></li>
<li><p>Need to cover all lesions, hence the graft length.</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Not very prevalent or important for pre-clinical
testing.</strong></p></li>
</ul></td>
<td colspan="2">Eurostar Progress Report</td>
</tr>
<tr class="odd">
<td>1-4</td>
<td>Shape <strong>of the aneurysm</strong></td>
<td><p><u>Shape classifications</u>:</p>
<ul>
<li><p>Concentric; eccentric; saccular; fusiform; false</p></li>
<li><p>Class I-V</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>95% fusiform, 5% saccular</p></li>
</ul></td>
<td></td>
<td>3</td>
<td>4</td>
<td colspan="2">1</td>
<td></td>
<td><ul>
<li><p>Although the shape of an aneurysm may dictate its rupture
probability (Elger, 1996), the initial shape of a treated AAA probably
has little influence on endoprosthesis performance.</p></li>
<li><p>“Shape” of a seal zone is also important. Proximal neck shape is
critical, however, saccular requires additional case planning and
immediate treatment.</p></li>
<li><p>Disease etiology related and hence the type of graft and design
of procedure.</p></li>
</ul></td>
<td colspan="2">Elger, 1996</td>
</tr>
<tr class="even">
<td>1-4</td>
<td>Shape <strong>of the aneurysm</strong>, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>If there is more potential for lateral movement, the
shape makes a big difference.</strong></p></li>
<li><p><strong>Forces are different if lining thrombus as compared to
excluding an empty aneurysm.</strong></p></li>
<li><p><strong>For pre-clinincal testing, need to address which type of
aneurysm is more challenging (i.e., empty or not) for the particular
device design.</strong></p></li>
<li><p><strong>Wall characteristics may possibly be more
important.</strong></p></li>
<li><p><strong>It is not known why some have thrombus and some do
not.</strong></p></li>
<li><p><strong>Angulation and shape of sack should be considered in
testing.</strong></p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-5</td>
<td>Size<strong>/diameter</strong></td>
<td><p><u>Diameters</u>:</p>
<ul>
<li><p>20-80 mm</p></li>
<li><p>30-100+ mm</p></li>
<li><p>40-120 mm</p></li>
<li><p>40-90 mm</p></li>
<li><p>45 –100 mm</p></li>
<li><p>Those typically treated are &gt; 40 – 45 mm.</p></li>
<li><p>Careful follow up or treatment of those between 35-150 mm.
Eurostar reports 22-150 mm. Commonly 50-100 mm.</p></li>
<li><p>2X baseline aorta defines aneurysmal; diameter at rupture varies,
usually greater than 5 cm</p></li>
</ul>
<p><strong><u>Workshop comment:</u></strong></p>
<p><strong>Take out 20-30</strong></p></td>
<td>1</td>
<td>2</td>
<td>4</td>
<td colspan="2">1</td>
<td>2</td>
<td><ul>
<li><p>Large proximal necks may be prone to continued dilatation. Larger
aneurysms may have potential for greater remodeling when
excluded.</p></li>
<li><p>Increased rupture risk.</p></li>
<li><p>AAA size is important particularly in patient screening and
selection. Armon (1997) showed significantly more short (&lt; 1.5 cm),
wide (&gt; 3 cm), and hence, unsuitable proximal necks were found in
patients with aneurysms &gt; 7 cm in diameter. AAA Diameter &gt; 60 mm
and the need for adjuvant procedures represent the most important risk
factors for failure to complete the procedure (Buth and Laheij,
2000).</p></li>
<li><p>More an issue as to whether to intervene or not.</p></li>
<li><p>Larger sacs are likely to have longer disease
extensions.</p></li>
</ul></td>
<td colspan="2"><p>Buth and Laheij, 2000;</p>
<p>Armon, 1997</p></td>
</tr>
<tr class="even">
<td>1-6</td>
<td>Tortuosity / angulation <strong>of aorta – curve of the
sack</strong></td>
<td><p><u>Range</u>:</p>
<ul>
<li><p>120-180°</p></li>
<li><p>0-120°</p></li>
<li><p>0-100</p></li>
<li><p>0-60°</p></li>
<li><p>Highly variable.</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>Variable morphology of the AAA sac is commonplace.</p></li>
</ul></td>
<td></td>
<td>1</td>
<td>1</td>
<td colspan="2">5</td>
<td>3</td>
<td><ul>
<li><p>Can produce concentrated loads on device and/or device interface
with vessel, depending on implant design. Can increase loads at vessel
attachment and modular component interfaces. Can provide volume into
which device can kink/buckle, possibly with proximal migration of distal
end. Can complicate prosthesis sizing.</p></li>
<li><p>At neck or iliacs, potential Type I endoleaks; in iliacs,
potential occlusions or dissections.</p></li>
<li><p>Not a major concern for the AAA sac, provided delivery can be
accomplished.</p></li>
<li><p>Severe angles are very important and require additional case
planning and skill.</p></li>
<li><p>Considering neck to sac angulation here.</p></li>
<li><p>Access difficulties. Risk of dislodging mural thrombus.</p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-6</td>
<td>Tortuosity / angulation <strong>of aorta – curve of the
sack</strong>, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td><strong>x</strong></td>
<td><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>The importance of this parameter is device
related.</strong></p></li>
<li><p><strong>Must consider calcification with this as it affects the
ability of the device to conform to the vessel and the tendency for the
aorta to straighten.</strong></p></li>
<li><p><strong>It is critical to consider the graft
path.</strong></p></li>
<li><p><strong>Affects fixation.</strong></p></li>
<li><p><strong>Must change the concept of angulation. Need a method to
describe in 3D.</strong></p></li>
<li><p><strong>Important, but not easily defined, measured, described,
or quantified.</strong></p></li>
<li><p><strong>This parameter relates to rotational stresses and should
be considered in that context.</strong></p></li>
<li><p><strong>Optimally, need multiple tortuosity models for
pre-clinical testing.</strong></p></li>
<li><p><strong>The bifurcation angle is important to
consider.</strong></p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-6a</td>
<td><p>OTHER</p>
<p>Mural thrombus in aneurysm sac</p></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td colspan="2">1</td>
<td></td>
<td><ul>
<li><p>If present, may provide external support to implant.</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Full versus empty, as described above.</strong></p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-6b</td>
<td>Fixation sites</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td><ul>
<li><p>Length and diameter of fixation sites, and vessel wall
characteristics are critical.</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Need to consider portions of graft
crossing.</strong></p></li>
<li><p><strong>May be related to tears in the fabric due to interaction
of limbs. There is disagreement as to whether this presents a clinical
problem since it has not been seen in explants.</strong></p></li>
<li><p><strong>Can affect flow through legs due to compression of the
legs.</strong></p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-6c</td>
<td>Distal aortic neck diameter</td>
<td><ul>
<li><p>18-30 mm, if present</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-6d</td>
<td>Distal aortic neck length</td>
<td><ul>
<li><p>15-54 mm, if present</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-6e</td>
<td>Aneurysm length</td>
<td><ul>
<li><p>42-140 mm</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-6f</td>
<td>Diameter of lumen in sac</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td>1-6g</td>
<td>Bifurcation diameter</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td><ul>
<li><p>Small bifurcation diameter can constrict lumens.</p></li>
</ul></td>
<td colspan="2"></td>
</tr>
<tr class="odd">
<td>1-6h</td>
<td>Hypogastric artery involvement</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
</tr>
<tr class="even">
<td colspan="12"><strong>Neck Characteristics</strong></td>
</tr>
<tr class="odd">
<td>1-7</td>
<td>Neck Angles</td>
<td><p><u>Pre-deployment neck angulation estimates</u>:</p>
<ul>
<li><p>70-110°</p></li>
<li><p>0-100°</p></li>
<li><p>0-90°</p></li>
<li><p>0-90+°</p></li>
<li><p>0-60°</p></li>
<li><p>Mean: 64</p></li>
<li><p>Range: 5-180 (Eurostar)</p></li>
<li><p>0 to 60</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>20% of the cases involve angle &gt; 30</p></li>
</ul>
<ul>
<li><p>25% of cases &gt;60</p></li>
<li><p>75% of the population has some angulation (Eurostar Progress
Report)</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>5</td>
<td>6</td>
<td colspan="2"><ul>
<li><p>Pre-deployment neck angulation is a predictor of adverse
outcomes. Albertini (2000) has shown that neck angulation was
significantly greater in patients who had proximal perigraft endoleak
(50 16, p=0. 0005) or graft migration (54 20, p=0.003), compared to
patients who had neither of these two complications (37 18).</p></li>
<li><p>Challenge to seal, concentrates loads, difficult to
anchor.</p></li>
<li><p>Potential Type I endoleaks and stent-against-graft
motion.</p></li>
<li><p>Considering neck to patient body centerline. Combinations of
short necks with angulation can cause endoleaks.</p></li>
<li><p>Affect the quality of graft anchorage and seal.</p></li>
</ul></td>
<td><p>Fillinger et al;</p>
<p>Albertini, 2000;</p>
<p>Eurostar Progress Report, “significant angulation”</p></td>
</tr>
<tr class="even">
<td>1-7</td>
<td>Neck Angles, continued</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td><strong>x</strong></td>
<td><strong>x</strong></td>
<td colspan="2"><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Angles are important because they affect fixation and
sealing.</strong></p></li>
<li><p><strong>The difficulty is how to measure and define angulation.
An option is to measure minimum bend angle/radius of curvature.
Centerline angulation can be measured, however, it is not just the angle
that is important. Fixation points along graft length are also important
[conformity to vessel wall].</strong></p></li>
<li><p><strong>Stress distribution is different, depending on where the
bend is.</strong></p></li>
<li><p><strong>Need accurate geometric descriptions of
necks.</strong></p></li>
<li><p><strong>Fixation points distally are also important, that is,
where the stress points are on the angle of the curve.</strong></p></li>
<li><p><strong>There is an interesting model by the Nottingham
group/Brian Hopkinson</strong></p></li>
<li><p><strong>The neck angles will affect material failure and the
relationship between components</strong></p></li>
<li><p><strong>The importance of neck angles is device
specific.</strong></p></li>
<li><p><strong>There may be some inertial forces on the graft related to
neck angle.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-8</td>
<td>Neck Lengths</td>
<td><ul>
<li><p>10-15 mm</p></li>
<li><p>0-40 mm</p></li>
<li><p>0-50 mm</p></li>
<li><p>0-80 mm</p></li>
<li><p>0-30+ mm ,</p></li>
<li><p>10 – 15 mm.</p></li>
<li><p>Mean length is 27 mm, range 5-101 (Eurostar)</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>30% of the cases involve lengths &lt; 15 mm</p></li>
<li><p>&gt;20% are &lt;10 mm</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td><p>10</p>
<p><strong>!</strong></p></td>
<td colspan="2"><ul>
<li><p>Short neck reduces tolerance for angulation, provides shorter
seal zone (and attachment zone for infrarenal attachment
devices).</p></li>
<li><p>Short necks are a large part of the population, especially high
surgical risk patients.</p></li>
<li><p>Pre-deployment neck length is a key factor in patient selection
(Armon, 1997) and is essential to ensure good fixation and minimization
of endoleak. The criticality of neck length is compounded by its dynamic
natural history (Lipski, 1998).</p></li>
<li><p>Because clinical / market pressures exist to expand the
applicability of the stent-graft technology, it can be anticipated that
attempts to place devices in neck lengths below 15 mm are routinely
made.</p></li>
<li><p>Increases the potential for Type I endoleaks.</p></li>
<li><p>Affect the quality of graft anchorage and seal.</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>The comments from the compiled work assignment were
reviewed and accepted.</strong></p></li>
<li><p><strong>It is critical to measure neck lengths accurately and
sometimes difficult to do. Need to measure centerline length and length
of potential wall contact. The mean fixation/contact length is the most
important.</strong></p></li>
<li><p><strong>Neck length is not clearly defined, that is, when the
neck ends.</strong></p></li>
</ul></td>
<td><p>Greenberg et al;</p>
<p>Armon, 1997;</p>
<p>Lipski, 1998;</p>
<p>Wain, 1998;</p>
<p>Eurostar Progress Report, “pre-operative measure-ments”</p></td>
</tr>
<tr class="even">
<td>1-9</td>
<td>Neck Shapes</td>
<td><p><u>Nomenclature</u>:</p>
<ul>
<li><p>Conical /\ (reverse taper)</p></li>
<li><p>Concentric; ellipse; irregular; beveled; tapered; flared</p></li>
<li><p>Parallel, hour-glass, funnel, irregular, inverted-funnel</p></li>
<li><p>Forward taper, reverse taper, parallel, bubbles</p></li>
<li><p>Straight, conic (standard or reversed)</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>20% of the cases involve reverse tapered necks</p></li>
<li><p>&gt;10% conic, reverse conic</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>How often are conical necks seen?</strong></p></li>
<li><p><strong>Need a definition of conical necks, e.g., &gt;10%
dilatation.</strong></p></li>
<li><p><strong>Is it important to include length in the
definition?</strong></p></li>
</ul></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td>5</td>
<td>5</td>
<td colspan="2"><ul>
<li><p>Challenge to infrarenal anchorage.</p></li>
<li><p>Because the conical neck configuration can influence anchoring
and sealing, it needs to be taken into account. Although not
demonstrated by Albertini (2000), conical neck configurations have been
associated with graft migration (Ivancev, 1997). Also, device oversizing
relative to the neck diameter dictates mean strain conditions for
fatigue life estimation.</p></li>
<li><p>Increases the potential for Type I endoleaks.</p></li>
<li><p>Criticality depends on device design and ability to conform and
seal.</p></li>
<li><p>Affect the quality of graft anchorage and seal.</p></li>
</ul>
<p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Bigger at the bottom is the most challenging neck to
treat. Either evaluation of the graft must include modeling conical
necks, or patients with conical necks should be excluded from being
treated with the device.</strong></p></li>
<li><p><strong>There was disagreement as to whether devices should be
tested for all potential anatomies or whether they only need to be
evaluated for the anatomies intended to be treated with that specific
device. In other words, is it appropriate to specify the patient
population to be treated in the labeling and not collect any data
relevant for patients who may be treated with the device, regardless of
what the label says?</strong></p></li>
</ul></td>
<td><p>Albertini, 2000;</p>
<p>Ivancev, 1997</p></td>
</tr>
<tr class="odd">
<td>1-9a</td>
<td><p><u>OTHER</u>:</p>
<p>Irregular neck lumen profile</p></td>
<td><ul>
<li><p>Calcified</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td>1</td>
<td></td>
<td colspan="2"><ul>
<li><p>Can be challenge to seal.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-9b</td>
<td>Thrombus, calcification in neck</td>
<td><ul>
<li><p>20-50% depending on severity</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2">2</td>
<td></td>
<td>2</td>
<td colspan="2"><ul>
<li><p>Potential Type I endoleaks.</p></li>
<li><p>Extent of disease and effect on seal.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-9c</td>
<td>Extra renal arteries in neck</td>
<td><ul>
<li><p>0-3</p></li>
</ul></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-9d</td>
<td>Neck diameter</td>
<td><ul>
<li><p>14-30 mm</p></li>
<li><p>14-36 mm</p></li>
<li><p>18-33 mm</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td>3</td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="odd">
<td>1-9e</td>
<td>Iliac artery take off angle</td>
<td><ul>
<li><p>0-90</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-9f</td>
<td>Renal Artery Configura-tion</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Potentially important for the design and evaluation of devices
incorporating supra-renal anchoring. Ability to accurately deliver and
deploy devices in the region of the renal arteries is important to avoid
occlusion.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-9g</td>
<td>Ectatic tissue in neck</td>
<td><p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>&gt; 25% of population</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td>1</td>
<td colspan="2"><ul>
<li><p>Do these dilate more? Mid-term data is controversial.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td colspan="12"><strong>Hemodynamic Related
Characteristics</strong></td>
</tr>
<tr class="odd">
<td>1-10</td>
<td>Blood flow pathway (e.g., presence of channels, branches and
anatomical pathway)</td>
<td><h1 id="sources">Sources</h1>
<ul>
<li><p>Accessory renals or large critical IMA’s.</p></li>
<li><p>Flow paths from collateral branch to another or to central
lumen.</p></li>
<li><p>Variable.</p></li>
</ul></td>
<td>3</td>
<td>2</td>
<td colspan="2">2</td>
<td>2</td>
<td></td>
<td colspan="2"><ul>
<li><p>Important to identify and embolize or follow.</p></li>
<li><p>Potential Type II endoleaks.</p></li>
<li><p>Because the presence of an implanted endoprosthesis will alter
flow patterns, the pre-implant blood flow patterns through the aneurysm
are anticipated to have little practical significance on endoprosthesis
performance.</p></li>
<li><p>The anatomical pathway for bloodflow through an AAA is as varied
as AAA morphology. Nevertheless, three different flow regimens may be
identified as described by Egelhoff (1999).</p></li>
</ul></td>
<td>Egelhoff, 1999</td>
</tr>
<tr class="even">
<td>1-11</td>
<td>Blood flow rate</td>
<td><ul>
<li><p>2.0 – 3.0 L/min or less</p></li>
<li><p>2.0 – 4.0 L/min</p></li>
<li><p>2.2 – 5.0 L/min</p></li>
<li><p>2.5 – 5.5 L/min</p></li>
<li><p>3.0 – 6.0 L/min</p></li>
<li><p>Elderly population is not pumping at max rates, however some
(very few) are free of coronary co-morbidities</p></li>
</ul>
<p><u>Rest</u>:</p>
<ul>
<li><p>3.0 – 4.0 L/min</p></li>
</ul>
<p><u>Exercise</u>:</p>
<ul>
<li><p>5.0 – 6.0 L/min</p></li>
</ul></td>
<td>2</td>
<td>3</td>
<td colspan="2">5</td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Minor importance to loads on device.</p></li>
<li><p>Blood flow rate is important for shear/drag effects and impact
loading, both of which affect anchoring and device integrity. Rest and
exercise conditions should be considered, and a suitable worst case
condition identified.</p></li>
<li><p>Distal outflow is a major predictor of success.</p></li>
<li><p>Effect would relate to the degree of PP.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-11</td>
<td>Blood flow rate, continued</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>Flow rate is very important in the context of
seal/calcification/thrombus.</strong></p></li>
<li><p><strong>There was disagreement as to the importance of flow rate
on the forces applied to the implant. There were basically three
camps:</strong></p></li>
</ul>
<ol type="1">
<li><p><strong>those who weren’t sure of the
importance;</strong></p></li>
</ol>
<ul>
<li><p><strong>Do we know flow rate?</strong></p></li>
<li><p><strong>Has anyone looked at flow rate and its
effects?</strong></p></li>
<li><p><strong>Should the range be evaluated?</strong></p></li>
</ul>
<ol start="2" type="1">
<li><p><strong>those who thought it very important;
and</strong></p></li>
</ol>
<ul>
<li><p><strong>The forces on the device depends on the amount of blood
pushing through a set diameter.</strong></p></li>
<li><p><strong>Pressure <em>and</em> flow are related to
resistance.</strong></p></li>
</ul>
<ol start="3" type="1">
<li><p><strong>those who thought it not important because its effects
are insignificant compared to the effects of pressure.</strong></p></li>
</ol>
<ul>
<li><p><strong>Flow rate is much less important than
pressure.</strong></p></li>
<li><p><strong>Forces due to flow are negligible. They are only
important if it causes leg motion.</strong></p></li>
</ul>
<ul>
<li><p><strong>Measuring flow in an isolated manner is
meaningless.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-12</td>
<td>Pulse pressure (systolic / diastolic)</td>
<td><ul>
<li><p>Extreme exercise systolic pressure was 242 mm Hg in AAA patients
(Best, 1998); Peak exercise systolic pressure 95<sup>th</sup> percentile
in healthy 70-79 y.o. men/women was 243/222 mm Hg. Mean resting systolic
pressure in men/women was ~144/~133 mm Hg (Daida, 1996).</p></li>
<li><p>This type of patient population is with multiple other vascular
co-morbidities, so pulse pressure profile is already modified.</p></li>
</ul>
<h1 id="differential">Differential</h1>
<ul>
<li><p>30-100 mm Hg</p></li>
<li><p>40-60 mm Hg</p></li>
<li><p>Systolic 110-200</p></li>
<li><p>Diastolic 60-10</p></li>
</ul>
<p><u>Normotensive</u>:</p>
<ul>
<li><p>120 / 80 mm Hg</p></li>
</ul>
<p><u>Hypertensive</u>:</p>
<ul>
<li><p>180 / 120 mm Hg</p></li>
</ul></td>
<td>2</td>
<td></td>
<td colspan="2">6</td>
<td>1</td>
<td>1</td>
<td colspan="2"><ul>
<li><p>A major determinant of loads on implant</p></li>
<li><p>Increased rupture potential with increased pulse pressure;
Increased pulse pressure may lead to increased relative movement
stent-graft, with or without endoleak.</p></li>
<li><p>Pulse pressures can influence compliance and radial loading, both
of which contribute to fatigue life estimation. Normotensive and
hypertensive should be considered, and a suitable worst-case condition
identified.</p></li>
<li><p>Equate to the dynamic forces applied to the graft.</p></li>
</ul></td>
<td><p>Best, et al, 1998;</p>
<p>Daida, et al, 1996;</p>
<p>Sonesson et al;</p>
<p>Ivancell et al</p></td>
</tr>
<tr class="odd">
<td>1-13</td>
<td>Temperature</td>
<td><ul>
<li><p>Body temp</p></li>
<li><p>36-40°C</p></li>
<li><p>96-103 F</p></li>
<li><p>37C</p></li>
<li><p>37 +/- 2 C</p></li>
</ul></td>
<td>7</td>
<td>2</td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Reasonable to expect temperature to be constant.</p></li>
<li><p>No direct correlation known at this point.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-13a</td>
<td><p><u>OTHER</u>:</p>
<p>Viscosity</p></td>
<td></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>May result in increased chance of thrombus formation, but rare
incidence.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-13b</td>
<td>Thrombo-genicity</td>
<td></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>May result in increased chance of thrombus formation, but rare
incidence.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-13c</td>
<td>Medication (e.g., blood thinner)</td>
<td></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Do patients on blood thinners (e.g., Coumadin) clot and heal as
do the animal studies or ‘normal’ patients.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-13d</td>
<td>Activated clotting times</td>
<td><ul>
<li><p>Baseline to 300+ seconds</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Determines rate of perigraft leakage.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td colspan="12"><strong>Vessel Wall Characteristics</strong></td>
</tr>
<tr class="odd">
<td>1-14</td>
<td>Atheroma-tous material</td>
<td><ul>
<li><p>0-100% circumference</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>Atherosclerotic lesions are commonplace in AAA disease.</p></li>
<li><p>Seen in severe disease</p></li>
<li><p>&gt;20%</p></li>
<li><p>10% of the cases involve atheromatous material</p></li>
</ul></td>
<td></td>
<td>2</td>
<td colspan="2">3</td>
<td>4</td>
<td>1</td>
<td colspan="2"><ul>
<li><p>Embolization &amp; fixation risk.</p></li>
<li><p>Criticality when seen in neck=4; iliacs=4; aneurysm=2.</p></li>
<li><p>Atheroscelerotic plaques can cause stress concentration in the
AAA wall, and up to a 200% increase in risk of rupture
(Inzoli).</p></li>
<li><p>Nodules / disease may still present challenge to circumferential
sealing.</p></li>
<li><p>In landing zones.</p></li>
<li><p>Disease extension.</p></li>
</ul></td>
<td>Inzoli, 1993</td>
</tr>
<tr class="even">
<td>1-15</td>
<td><p>Compliance/ elasticity</p>
<p>(axial and circumferential)</p></td>
<td><p><u>Percent compliance estimates</u>:</p>
<ul>
<li><p>1-2% in the diseased aorta containing an endograft</p></li>
<li><p>Unknown at implant but a diseased wall has reduced elasticity and
compliance.</p></li>
<li><p>Variable.</p></li>
<li><p>5-7% circumferential, for healthy tissue (lower for
disease)</p></li>
<li><p>? axial</p></li>
</ul>
<p><u>Cyclic Variability</u>:</p>
<ul>
<li><p>Diseased Human AAA: 1.6 – 3.7 (Wilson, 1998; Wilson
2000)</p></li>
<li><p>Normal Human Abdominal Aorta: 3.0% - 13.1% (Sonesson, 1994;
Lanne, 1994)</p></li>
</ul></td>
<td></td>
<td>2</td>
<td colspan="2">4</td>
<td>3</td>
<td>1</td>
<td colspan="2"><ul>
<li><p>Implant must anchor and seal over range. Affects cardiac cycle
dilatiation for stent fatigue.</p></li>
<li><p>Accurate sizing needed.</p></li>
<li><p>Important for sizing / oversizing study, ballooning, hook/barb
design, and frictional performance.</p></li>
<li><p>Circumferential compliance is a critical deteminant of the cyclic
strain conditions experienced by the device <em>in-situ</em>. This is
particularly the case for the attachment regions (e.g., infrarenal
aortic neck); and less of an issue for the aneurysmal sac itself.
Effects on rupture are contested (Wilson, 1998; Sonesson,
1999).</p></li>
<li><p>Ease of access and graft attachment.</p></li>
</ul></td>
<td><p>Wilson K, 1998;</p>
<p>Wilson, 2000;</p>
<p>Sonesson, 1994;</p>
<p>Sonesson, 1999;</p>
<p>Lanne, 1994</p></td>
</tr>
<tr class="odd">
<td>1-15</td>
<td><p>Compliance/ elasticity</p>
<p>(axial and circumferential), continued</p></td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><p><strong><u>Workshop comments:</u></strong></p>
<ul>
<li><p><strong>There was much discussion and little consensus on the
relevance of aortic compliance on the durability of the implant; the
presence or absence of compliance in the diseased aorta; the presence or
absence of compliance in the aorta treated with an endograft; and the
need to measure compliance or to attempt to simulate physiologic
compliance in whole device durability testing.</strong></p></li>
<li><p><strong>Specific comments were:</strong></p></li>
<li><p><strong>Compliance ranges from 3-13% .</strong></p></li>
<li><p><strong>The compliance at fixation points is not
known.</strong></p></li>
<li><p><strong>Compliance is not just important at the fixation points.
The transition areas are also important.</strong></p></li>
<li><p><strong>Compliance is not important over time as it is eliminated
or at least influenced with implantation of the
endograft.</strong></p></li>
<li><p><strong>It is most important to have relevant amounts of device
movement/excursion in durability testing than to maintain a specified
compliance.</strong></p></li>
<li><p><strong>Compliance can be important and will impart
strain.</strong></p></li>
<li><p><strong>Compliance has lead to failure.</strong></p></li>
<li><p><strong>Can use compliance to figure out what devices can
tolerate.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-16</td>
<td>Degree of calcification</td>
<td><ul>
<li><p>Heavy Ca++</p></li>
<li><p>None, present, or extreme.</p></li>
<li><p>None to severe.</p></li>
<li><p>Variable. Segmental to circumferential.</p></li>
<li><p>0-100% circumference</p></li>
<li><p>Mural calcification is a frequent companion of AAA disease, both
within the neck region and the aneurysmal wall.</p></li>
<li><p>&gt;20% to some degree, &lt;10% with severe calcification in the
neck</p></li>
</ul></td>
<td></td>
<td>1</td>
<td colspan="2">3</td>
<td>5</td>
<td>1</td>
<td colspan="2"><ul>
<li><p>Can affect anchorage and sealing surface.</p></li>
<li><p>Criticality when seen in neck=5; iliacs=5; aneurysm=3.</p></li>
<li><p>Calcification of the neck region can influence anchoring and barb
penetration. Additionally, focal calcifications may contribute to graft
material erosion.</p></li>
<li><p>Device circumferential conformance is important; hook/barb
penetration challenge as well.</p></li>
<li><p>Criticality depends on method of fixation. If hooks, more
critical.</p></li>
<li><p>Graft sizing and anchorage.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17</td>
<td>Presence of thrombus</td>
<td><ul>
<li><p>Diffuse, friable.</p></li>
<li><p>None, present, or extreme.</p></li>
<li><p>None to severe.</p></li>
<li><p>Variable.</p></li>
<li><p>Spherical, cylindrical, or pleomorphic in shape. 0-100% in
circumference.</p></li>
<li><p>Mural thrombosis is a frequent companion of AAA disease, both
within the neck region and the aneurysmal sac.</p></li>
</ul>
<p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>10% of the cases involve thrombus.</p></li>
</ul></td>
<td></td>
<td>2</td>
<td colspan="2">4</td>
<td>3</td>
<td>1</td>
<td colspan="2"><ul>
<li><p>Can affect sealing surface.</p></li>
<li><p>Embolization risk.</p></li>
<li><p>Criticality when seen in neck=5; iliacs=4; aneurysm=2.</p></li>
<li><p>Inzoli (1993) and Di Martino (1998) both assert that the presence
of mural thrombus provides a shielding function to the aneurysmal wall,
effectively decreasing wall stress. Matsumura and Pearce (1999) showed
that the amount of pre-exisiting thrombus bears no important
relationship to the response of the aneurysm following endovascular
repair. Potential for embolization.</p></li>
<li><p>A real-world challenge that must be designed for; testing,
however, is difficult as thrombus is altered by graft (i.e., may
organize, lyse, etc.).</p></li>
<li><p>Disease extension. Not differentiable to atheroma on CT.</p></li>
</ul></td>
<td><p>Marin et al in JVS;</p>
<p>Inzoli, 1993;</p>
<p>Di Martino 1998;</p>
<p>Matsumura and Pearce, 1999</p></td>
</tr>
<tr class="even">
<td>1-17a</td>
<td>Iliac tortuosity</td>
<td></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>Significant effect on implant kinking or buckling and distal
anchorage loads.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17b</td>
<td>Collagen enzyme disorder</td>
<td></td>
<td></td>
<td></td>
<td colspan="2">1</td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>COPD correlation?</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>1-17c</td>
<td>Oblong / non-circular cross-section</td>
<td><p><u>Prevalence estimates</u>:</p>
<ul>
<li><p>&gt;15%</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"><ul>
<li><p>Conformability, seal-ability, critical. Sizing and oversizing
needs to be evaluated as well.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17c</td>
<td>Common iliac diameter</td>
<td><ul>
<li><p>5-41 mm</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-17d</td>
<td>Common iliac length</td>
<td><ul>
<li><p>10-204 mm</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17e</td>
<td>Iliac landing site</td>
<td><ul>
<li><p>Common or external iliac</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td>1</td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-17f</td>
<td>Distal seal site diameter</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17g</td>
<td>Distal seal site length</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td>1</td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-17h</td>
<td>Hypogastric artery location</td>
<td><ul>
<li><p>Involved or not involved in iliac aneurysm</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17I</td>
<td>Access angle of entry</td>
<td><ul>
<li><p>30-45</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-17j</td>
<td>Ilio-femoral tortuosity</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17k</td>
<td>Method of access</td>
<td><ul>
<li><p>Arterial puncture, use of conduits</p></li>
</ul></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
</tr>
<tr class="even">
<td>1-17l</td>
<td>Vascular access considerations</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>e.g., suitability of the ilio-femoral vasculature to allow
delivery of the endoprosthesis, also methods of access and closure,
etc.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>1-17m</td>
<td>Iliac morphology considerations</td>
<td></td>
<td></td>
<td></td>
<td colspan="2"></td>
<td></td>
<td></td>
<td colspan="2"><ul>
<li><p>e.g., diameter, length from bifurcation to hypogastrics,
tortuosity, disease state, etc. (Basically all the considerations that
apply to proximal neck anchoring also apply to the iliac anchoring
sites.)</p></li>
</ul></td>
<td></td>
</tr>
</tbody>
</table>

**[General comments from the workshop]{.underline}:**

-   **There needs to be a balance between robustness or the ideal and
    what is feasible.**

-   **There need to be relative comparisons between devices and their
    attributes.**

-   **It is critically important that the community share explant
    information.**

##  

## References

Albertini J; Kalliafas S; Travis S; Yusuf SW; Macierewicz JA; Whitaker
SC; Elmarasy NM; Hopkinson **BR Eur J Vasc Endovasc Surg**. 2000 Mar;
19(3): 308-12

Armon MP; Yusuf SW; Whitaker SC; Gregson RH; Wenham PW; Hopkinson BR **J
Endovasc Surg**. 1997 Aug; 4(3): 279-83

Baum RA; Carpenter JP; Tuite CM; Velazquez OC; Soulen MC; Barker CF;
Golden MA; Pyeron AM; Fairman RM **Radiology**. 2000 May; 215(2): 409-13

Best, Tajik, Gibbons, and Pellikka, **Annals of Internal Medicine**,
Vol. 129, No. 8, October, 1998, pp. 628-631.

Buth J; Laheij RJ. **J Vasc Surg**. 2000 Jan; 31(1 Pt 1): 134-46.

Daida, Allison, Squires, Miller, and Gau, **Mayo Clinic Proceedings**,
Vol. 71, 1996, pp. 445-452.

Di-Martino E; Mantero S; Inzoli F; Melissano G; Astore D; Chiesa R;
Fumero R. **Eur J Vasc Endovasc Surg**. 1998 Apr; 15(4): 290-9

Egelhoff CJ; Budwig RS; Elger DF; Khraishi TA; Johansen KH. **J
Biomech**. 1999 Dec; 32(12): 1319-29

Elger DF; Blackketter DM; Budwig RS; Johansen KH. **J Biomech Eng**.
1996 Aug; 118(3): 326-32

Eurostar Progress Report.

Fan CM; Rafferty EA; Geller SC; Kaufman JA; Brewster DC; Cambria RP;
Waltman AC **Radiology**. 2001 Jan; 218(1): 176-82

Filinger, et al.

Greenberg, et al.

Harris PL; Vallabhaneni SR; Desgranges P; Becquemin JP; van-Marrewijk C;
Laheij RJ. J Vasc Surg. 2000 Oct; 32(4): 739-49

Inzoli F; Boschetti F; Zappa M; Longo T; Fumero R. **Eur J Vasc Surg**.
1993 Nov; 7(6): 667-74

Ivancev K; Malina M; Lindblad B; Chuter TA; Brunkwall J; Lindh M; Nyman
U; Risberg B. **J Endovasc Surg**. 1997 Aug; 4(3): 242-51

Lipski DA; Ernst CB. **J Vasc Surg**. 1998 May; 27(5): 805-11;
discussion 811-2

Marin et al. **J Vasc Surg**

Matsumura JS; Pearce WH. **J Surg Res**. 1999 Jan; 81(1): 11-4

Schumacher H; Eckstein HH; Kallinowski F; Allenberg JR. **J Endovasc
Surg**. 1997 Feb; 4(1): 39-44

Schurink GW; Aarts NJ; van-Bockel JH. **Br J Surg**. 1999 May; 86(5):
581-7

Sonesson B; Sandgren T; Lanne T. **Eur J Vasc Endovasc Surg**. 1999 Dec;
18(6): 487-93

Sonesson B; et al. **J Vasc Surg**. 1994 20:959-69.

Wain RA; Marin ML; Ohki T; Sanchez LA; Lyon RT; Rozenblit A; Suggs WD;
Yuan JG; Veith FJ. **J Vasc Surg**. 1998 Jan; 27(1): 69-78; discussion
78-80

Walker SR; Macierewicz J; Hopkinson BR. **J Endovasc Surg**. 1999 Nov;
6(4): 350-3

Wilson K; Bradbury A; Whyman M; Hoskins P; Lee A; Fowkes G; McCollum P;
Ruckley CV. **Eur J Vasc Endovasc Surg**. 1998 Jun; 15(6): 472-7

## Abstracts of Selected References (from above)

Albertini J; Kalliafas S; Travis S; Yusuf SW; Macierewicz JA; Whitaker
SC; Elmarasy NM; Hopkinson BR. Anatomical risk factors for proximal
perigraft endoleak and graft migration following endovascular repair of
abdominal aortic aneurysms. **Eur J Vasc Endovasc Surg**. 2000 Mar;
19(3): 308-12

INTRODUCTION: proximal perigraft endoleak (PPE) and graft migration are
associated with significant morbidity and mortality. Objective data
establishing correlation between neck anatomy and these complications
are lacking. The aim of this study was to analyse the anatomy of the
neck in order to find which variables were significantly associated with
PPE and graft migration. METHODS: one hundred and eighty-four patients
underwent endovascular repair (EVR) of infrarenal AAA using an in-house
custom-made stent graft (Gianturco stents plus Dacron). Thirty-one
patients had PPE and fifteen had graft migration. Neck diameter was
measured at the level of renal arteries and lower limit of the neck.
Necks were classified according to shape. Neck angulation was measured
from spiral computed tomography (CT) or magnetic resonance imaging (MRI)
reconstructions, or angiograms. Thrombus or atheroma lining and presence
of calcifications were recorded. RESULTS: neck angulation was
significantly greater in patients who had PPE (50+/-16, p=0. 0005) or
graft migration (54+/-20, p=0.003), compared to patients who had none of
these two complications (37+/-18). Neck diameter was significantly
greater in patients with PPE (p=0.05). Incidence of PPE or graft
migration was not significantly higher in the presence of a conical
shape, thrombus or atheroma lining and calcifications. CONCLUSION: neck
angulation was the risk factor most significantly related to PPE and
graft migration.

Armon MP; Yusuf SW; Whitaker SC; Gregson RH; Wenham PW; Hopkinson RB.
**J Endovasc Surg**. 1997 Aug; 4(3): 279-83

> PURPOSE: To assess the effect of abdominal aortic aneurysm (AAA) size
> on overall aneurysm morphology with special attention to possible
> relationships among various anatomic variables that determine the
> feasibility of endovascular repair. METHODS: One hundred sixty-eight
> patients were assessed with spiral computed tomographic angiography to
> measure the length and diameter of the AAA, the proximal neck, and the
> common iliac arteries. Anatomic variables were correlated with
> aneurysm size using Spearman\'s rank order correlation coefficients
> (rS); comparisons among small, intermediate, and large aneurysms were
> made using the Chi-square test. RESULTS: Correlations between aneurysm
> size and the anatomic variables above were weak. The strongest
> association was between aneurysm size and aortic length (rS = 0.41, p
> \< 0.001). Subgroup analysis showed no difference in proximal neck
> length, neck diameter, or overall suitability for endovascular repair
> between aneurysms greater or smaller than 5.5-cm diameter. However,
> significantly more short (\< 1.5 cm), wide (\> 3 cm), and hence,
> unsuitable proximal necks were found in patients with aneurysms \> 7
> cm in diameter (chi 2 = 7.8, p \< 0.01). CONCLUSIONS: Shortening and
> widening of the proximal neck seems to increase with aneurysm size but
> only after the aneurysm expands beyond 7 cm in diameter. Aneurysms
> with diameters in the 4.5- to 5.5-cm range are no more suitable for
> endovascular repair than those between 5.5 and 7 cm. The lack of any
> significant correlation between anatomic variables emphasizes the need
> for accurate preoperative assessment of the anatomy of each individual
> patient before endovascular repair.

Baum RA; Carpenter JP; Tuite CM; Velazquez OC; Soulen MC; Barker CF;
Golden MA; Pyeron AM; Fairman RM. Diagnosis and treatment of inferior
mesenteric arterial endoleaks after endovascular repair of abdominal
aortic aneurysms. **Radiology.** 2000 May; 215(2): 409-13

PURPOSE: To review the incidence and repair of inferior mesenteric
arterial (IMA) type II endoleaks after endovascular repair of abdominal
aortic aneurysms. MATERIALS AND METHODS: Fifty patients who underwent
endovascular repair of abdominal aortic aneurysms were examined. If an
endoleak was identified at 30-day postoperative computed tomography,
conventional arteriography was performed to identify and eliminate its
source. After the exclusion of attachment site leaks, a catheter was
placed selectively in the superior mesenteric artery (SMA). If
retrograde filling of the IMA and aneurysm was identified, coil
embolization was attempted through the SMA and middle colic artery.
Intrasac pressures were measured at embolization. RESULTS: Eight of 50
patients (16%) had type II endoleaks that were attributed to retrograde
flow in the IMA. Intrasac measurements demonstrated systemic pressure in
six patients and one-half systemic pressure in two patients. The IMA was
embolized through the SMA and left colic artery in seven patients and
through the translumbar aorta in one patient. CONCLUSION: Retrograde
flow in the IMA is responsible for many type II endoleaks. Systemic
pressures are transmitted into the aneurysm sac from the IMA. The IMA
can be embolized successfully with an SMA approach in most patients.

Buth J; Laheij RJ. Early complications and endoleaks after endovascular
abdominal aortic aneurysm repair: report of a multicenter study. **J
Vasc Surg**. 2000 Jan; 31(1 Pt 1): 134-46.

> OBJECTIVE: The aim of this study was the identification of risk
> factors for adverse events and the assessment of the early success
> rate in 1554 patients with abdominal aortic aneurysms (AAAs) who
> underwent treatment with endovascular technique between January 1994
> and March 1999. For this purpose, the clinical and procedural data
> were correlated with observed complications and endoleaks. METHODS:
> The data were collected from 56 European centers and submitted to a
> central registry. Patient characteristics, aortoiliac anatomic
> features, operative technical details, types of devices used, and
> experience of the teams of physicians were correlated with the
> occurrence of complications and endoleaks. The technical success rate
> was assessed according to the Society for Vascular
> Surgery/International Society for Cardiovascular Surgery, North
> American Chapter, guidelines. For the assessment of correlations
> between risk factors and adverse events, a multivariate logistic
> regression analysis was used. RESULTS: The operative complications
> were grouped into three categories: failure to complete the procedure
> (39 patients, of which 27 underwent a conversion to an open AAA
> repair; 2.5%); device-related or procedure-related complications (149
> patients; 10%); and arterial complications (51 patients; 3%). The most
> important risk factors for failure to complete the procedure included
> an aneurysm diameter of 60 mm or more and the need for adjuvant
> procedures. The factors that predicted device-related and arterial
> complications were the experience of the team with endovascular AAA
> treatment and the need for adjuvant procedures. Forty patients (2.6%)
> died within 30 days after operation. American Society of
> Anesthesiologists III and IV operative risk classification results
> predicted higher mortality rates than did American Society of
> Anesthesiologists operative risk classification I and II results. The
> patients who underwent operation in 1994, the first year documented in
> this registry, and those who required adjuvant procedures also had an
> increased risk of perioperative death. The incidence rate of systemic
> complications within the first 30 days (279 patients; 18%) was higher
> in patients aged 75 years or more, in patients with an impaired
> cardiac status, and in patients considered unfit for an open
> procedure. An endoleak was detected at the completion of the procedure
> in 16% of the cases and was still present after 1 month in 9%. The
> risk factors for primary endoleaks were female gender and age of 75
> years and older. The observed technical success rate in this patient
> series was 72%. CONCLUSION: The learning curve of the doctors and the
> need for adjuvant procedures were independent risk factors of
> operative device-related and arterial complications. The importance of
> proper instruction during an institution\'s initial phase with this
> treatment is emphasized by these observations. Although the
> endovascular management of AAAs is less stressful than open surgery,
> systemic complications were still the most common adverse events
> during the first postoperative month. These complications were
> associated with several patient-related factors, including advanced
> age, impaired cardiac status, and poor general medical condition.
> These observations may be a guide for improved patient selection for
> endovascular AAA repair.

Di-Martino E; Mantero S; Inzoli F; Melissano G; Astore D; Chiesa R;
Fumero R. Biomechanics of abdominal aortic aneurysm in the presence of
endoluminal thrombus: experimental characterisation and structural
static computational analysis. **Eur J Vasc Endovasc Surg**. 1998 Apr;
15(4): 290-9

> OBJECTIVES: To evaluate the role played by biomechanical and
> geometrical parameters of endoluminal thrombus and of aortic wall on
> abdominal aortic aneurysm (AAA) behaviour. MATERIALS AND METHODS:
> Tensile tests on 21 AAA thrombus specimens from six patients
> undergoing AAA repair and numerical evaluation of aneurysmal aortic
> wall stress and strain distribution. Parameters of the analysis were
> lumen eccentricity, thrombus Young\'s Modulus and the aortic wall
> constitutive equation. RESULTS: There was a linear stress/strain for
> all the thrombus specimens. The numerical analyses show the mechanical
> behaviour of AAA as a function of lumen eccentricity and biomechanical
> parameters. CONCLUSIONS: Well organised thrombus reduces the effect of
> the pressure load on the aneurysmal aortic wall.

Egelhoff CJ; Budwig RS; Elger DF; Khraishi TA; Johansen KH. Model
studies of the flow in abdominal aortic aneurysms during resting and
exercise conditions. **J-Biomech**. 1999 Dec; 32(12): 1319-29

Pulsatile flow in abdominal aortic aneurysm (AAA) models has been
examined in order to understand the hemodynamics that may contribute to
growth of an AAA. The model studies were conducted by experiments (flow
visualization and laser Doppler velocimetry) and by numerical simulation
using physiologically realistic resting and exercise flow conditions. We
characterize the flow for two AAA model shapes and sizes emulating early
AAA development through moderate AAA growth (mean and peak Reynolds
numbers of 362 \< Re(mean) \< 1053 and 3308 \< Re(peak) \< 5696 with
Womersley parameter 16.4 \< alpha \< 21.2). The results of our
investigation indicate that AAA flow can be divided into three flow
regimes: (i) Attached flow over the entire cycle in small AAAs at
resting conditions, (ii) vortex formation and translation in moderate
size AAAs at resting conditions, and (iii) vortex formation, translation
and turbulence in moderate size AAAs under exercise conditions. The
second two regimes are classified in the medical literature as disturbed
flow conditions that have been correlated with atherogenesis as well as
thrombogenesis. Thus, AAA disturbed hemodynamics may be a contributing
factor to AAA growth by accelerating the degeneration of the arterial
wall. Our investigation also concluded that vortex development is
considerably weaker in an asymmetric AAA. Furthermore, turbulence was
not observed in the asymmetric model. Finally, our investigation
suggests a new mode of transition to turbulence: vortex ring instability
and bursting to turbulence. The transition process depends on a
combination of the pulsatile flow conditions and the tube
cross-sectional area change.

Elger DF; Blackketter DM; Budwig RS; Johansen KH. The influence of shape
on the stresses in model abdominal aortic aneurysms. **J Biomech Eng**.
1996 Aug; 118(3): 326-32

> Presence of a small abdominal aortic aneurysm (AAA) often presents a
> difficult clinical dilemma\--a reparative operation with its inherent
> risks versus monitoring the growth of the aneurysm, with the
> accompanying risk of rupture. The risk of rupture is conventionally
> believed to be a function of the AAA bulge diameter. In this work, we
> hypothesized that the risk of rupture depends on AAA shape. Because
> rupture is inevitably linked to stress, membrane theory was used to
> predict the stresses in the walls of an idealized AAA, using a model
> which was axisymmetric and fusiform, with the ends merged into
> straight opened-ended tubes. When the stresses for many different
> shapes of model AAAs were examined, a number of conclusions became
> evident: (i) maximum hoop stress typically exceeded maximum meridional
> stress by a factor of 2 to 3 (ii) the shape of an AAA had a small
> effect on the meridional stresses and a rather dramatic effect on the
> hoop stresses, (iii) maximum stress typically occurred near the
> inflection point of a curve drawn coincident with the AAA wall, and
> (iv) the maximum stress was a function\--not of the bulge
> diameter\-\--but of the curvatures (i.e. shape) of the AAA wall. This
> last result suggested that rupture probability should be based on wall
> curvatures, not on AAA bulge diameter. Because curvatures are not much
> harder to measure than bulge diameter, this concept may be useful in a
> clinical setting in order to improve prediction of the likelihood of
> AAA rupture.

Fan CM; Rafferty EA; Geller SC; Kaufman JA; Brewster DC; Cambria RP;
Waltman AC. Endovascular Stent-Graft in Abdominal Aortic Aneurysms: The
Relationship between Patent Vessels that Arise from the Aneurysmal Sac
and Early Endoleak. **Radiology.** 2001 Jan; 218(1): 176-82

> PURPOSE: To determine the association of patent sac branch vessels
> (lumbar and inferior mesenteric arteries \[IMAs\] with early endoleak
> rate after stent-graft repair of abdominal aortic aneurysm (AAA).
> CONCLUSION: Sac branch vessel patency is associated with significantly
> hight early and type 2 endoleak rates after stent-graft repair of
> AAAs; thus patent sac branches play an important role in the
> pathogenesis of endoleaks.

Harris PL; Vallabhaneni SR; Desgranges P; Becquemin JP; van-Marrewijk C;
Laheij RJ. European Collaborators on Stent/graft techniques for aortic
aneurysm repair. Incidence and risk factors of late rupture, conversion,
and death after endovascular repair of infrarenal aortic aneurysms: the
EUROSTAR experience. **J Vasc Surg.** 2000 Oct; 32(4): 739-49

OBJECTIVE: The EUROSTAR (European Collaborators on Stent/graft
techniques for aortic aneurysm repair) Registry was established in 1996
to collect data on the outcome of treatment of patients with infrarenal
aortic aneurysms with endovascular repair. To date, 88 European centers
of vascular surgery have contributed. The purpose of the study was to
evaluate the results of this treatment in the medium term (up to 4
years) according to the analysis of \"hard\" or primary end points of
rupture, late conversion, and death. PATIENTS AND METHODS: Patients with
aortic aneurysms suitable for endovascular aneurysm repair were notified
to the EUROSTAR Data Registry Centre before treatment to eliminate bias
due to selective reporting. The following information was collected on
all patients: (1) demographic details and the anatomic characteristics
of their aneurysms, (2) details of the endovascular device used, (3)
complications encountered during the procedure and the immediate
outcome, (4) results of contrast enhanced computed tomographic imaging
at 3, 6, 12, and 18 months after operation and at yearly intervals
thereafter, and (5) all adverse events. Life table analysis was
performed to determine the cumulative rates of (1) death from all
causes, (2) rupture, and (3) late conversion to open repair. Risk
factors for rupture and late conversion were identified through
regression analysis. RESULTS: By March 2000, 2464 patients had been
registered, and their mean duration of follow-up was 12.19 months (SD,
12.3 months). There were 14 patients with confirmed rupture of their
aneurysms. The cumulative rate (risk) of rupture was approximately 1%
per year. Emergency surgery was undertaken in 12 (86%) patients, of whom
five (41.6%) survived. Two patients who were not treated surgically also
died, which resulted in an overall death rate of 64.5% (9/14) of the
patients. Significant risk factors for rupture were proximal type I
endoleak (P =.001), midgraft (type III) endoleak (P =.001), graft
migration (P =.001), and postoperative kinking of the endograft (P
=.001). Forty-one patients underwent late conversion to open repair with
a perioperative mortality rate of 24.4% (10/41). The cumulative rate
(risk) of late conversion was approximately 2.1% per year. Risk factors
(indications) for late conversion were proximal type I endoleak (P =.
001), midgraft (type III) endoleak (P =.001), type II endoleak (P =.
003), graft migration (P =.001), graft kinking (P =.001), and distal
type I endoleak (P =.001). CONCLUSIONS: Endovascular repair of
infrarenal aortic aneurysms with the first- and second-generation
devices that predominated in this study was associated with a risk of
late failure, according to an analysis of observed hard end points of 3%
per year. Action taken to address the risk factors identified by the
study may improve results in the future.

Inzoli F; Boschetti F; Zappa M; Longo t; Fumero R. Biomechanical factors
in abdominal aortic aneurysm rupture. **Eur J Vasc Surg**. 1993 Nov;
7(6): 667-74

> Hitherto the size of abdominal aortic aneurysms (AAA) has been
> considered the most important factor in determining the risk of
> rupture. For this reason most interest has been devoted to physical,
> echographic and tomographic analyses of the shape of AAA. However, it
> is known that rupture can also occur in small AAA. Other factors must
> be considered to have an important role in the natural history of
> aneurysms. The aim of this study was to characterise the mechanical
> stress in the wall of an AAA due to pressure in the presence of
> atherosclerosis, intraluminal thrombus and anatomical restraints. The
> Finite Elements Method (FEM) was used to determine wall stress
> distribution. Due to the simplicity of the AAA structure an
> axisymmetric model has been built. The results of the structural
> analysis confirms that maximum stress increases with diameter. These
> effects may be reduced by the presence of intraluminal thrombus, which
> in the models reduces maximum stress by up to 30%; however this is not
> the case for dissecting thrombus. On the other hand atherosclerotic
> plaques cause stress concentration and a significant increase in
> maximum wall stress. The risk of rupture can increase by about 200%.
> Finally the investigation shows the FEM is a versatile tool for
> studying the mechanics of vascular structures. It enables the
> influence of various parameters on wall stress to be quantified in
> diagnostic settings, and so could be useful for predicting the rupture
> of AAA, although at present such predictions are limited by data
> leakage and by the approximations used in the model.

Ivancev K; Malina M; Lindblad B; Chuter TA; Brunkwall J; Lindh M; Nyman
U; Risberg B. Abdominal aortic aneurysms: experience with the
Ivancev-Malmo endovascular system for aortomonoiliac stent-grafts. **J
Endovasc Surg**. 1997 Aug; 4(3): 242-51

PURPOSE: To describe a component-based aortomonoiliac stent-graft system
and the first clinical results achieved with this device in endovascular
abdominal aortic aneurysm (AAA) repair. METHODS: From November 1993 to
October 1996, 45 patients aged 60 to 86 years underwent endoluminal
exclusion of true AAAs (median diameter 60 mm) involving the common
iliac arteries (median diameter 16 mm right and 15 mm left) using
unilimb stent-grafts deployed with the Iancev-Malmo system. RESULTS: Six
immediate conversions occurred in the beginning of the series due to
endografts that were too short. Complications, including 2 inadvertent
renal artery occlusions, 7 kinked grafts, 6 iliac artery dissections,
and 3 perioccluder leaks, were prominent features in the first 15
patients. Five patients died in the postoperative period, four of whom
were nonsurgical candidates. There were five significant stent-graft
migrations: one 3 weeks after surgery due to mechanical injury of the
proximal stent and four after 1 year owing to continuous dilation of a
wide proximal neck, stent-graft placement in a conical, thrombus-lined
proximal neck, and two instances of proximal extension separation from
the main graft. Translumbar aneurysm perfusion required embolization in
3 patients. CONCLUSIONS: Despite early complications associated with a
learning curve, exclusion of large AAAs using unilimb stent-grafts is
feasible. Strict inclusion criteria are necessary in order to improve
mortality among nonsurgical candidates and minimize the risk for late
migration.

Lipski DA; Ernst CB. Natural history of the residual infrarenal aorta
after infrarenal abdominal aortic aneurysm repair. **J Vasc Surg**. 1998
May; 27(5): 805-11; discussion 811-2

PURPOSE: We determined the natural history of the residual native
infrarenal aortic segment after conventional abdominal aortic aneurysm
(AAA) repair. METHODS: For the retrospective arteriographic case series,
800 hundred translumbar aortograms (TLAs) were obtained for 272
patients, before and after conventional AAA repair. The main outcome
measures were changes in the aortographic diameter and the length of the
infrarenal aortic segment, corrected and uncorrected for magnification
by normalization to the first lumbar vertebral body height. RESULTS: The
mean follow-up time from the preoperative TLA to the most recent
postoperative TLA was 42 months (range, 1 to 257 months). Vertebral body
height did not change (p = 0.35). The length of the native infrarenal
aorta cephalad to the proximal anastomosis increased a mean of 3 mm,
from 23 to 26 mm (p = 0.001). However, in 115 patients (43%), this
aortic segment elongated more than 5 mm, and in 63 patients (24%), it
elongated more than 10 mm. The native residual infrarenal aorta above
the proximal anastomosis dilated a mean of 1 mm, from 23 to 24 mm (p =
0.001), but in 21 patients (8%), it dilated more than 5 mm. There was a
weak positive correlation between the increase in residual native aortic
diameter and duration of follow-up. There was a negative correlation
between this increase and the initial size. The diameters of the
proximal anastomosis and proximal graft did not change. Marked
variability in the changes in aortic dimensions was observed.
CONCLUSIONS: A mean period of 42 months after conventional AAA repair,
the native infrarenal aortic segment elongates and dilates. Although
such enlargement is statistically significant, the average increase
appears to be small. However, residual aortic cuff diameter increased
more than 5 mm and neck length more than 10 mm in a significant number
of patients, with potentially serious implications for endovascular
treatment of AAA.

Matsumura JS; Pearce WH. Preexisting thrombus and aortic aneurysm size
change after endovascular repair. **J Surg Res**. 1999 Jan; 81(1): 11-4

> BACKGROUND: Recent studies have demonstrated the effectiveness of
> endovascular grafting with aneurysm shrinkage following total
> exclusion of the abdominal aortic aneurysm (AAA). However, little is
> known about the effect of the preexisting thrombus (PT) on changes in
> aneurysm size following endovascular grafting. Therefore, this study
> is designed to determine the effect of PT on aneurysm size following
> endovascular grafting. METHODS: Blinded measurements of preoperative,
> postoperative, and 1-year computed tomographic scans of 44 patients
> undergoing endovascular grafting for AAA were performed. PT fraction
> was determined by the formula This was normalized for preoperative AAA
> growth. Pearson correlations were performed with AAA minor diameter
> change over the first year. RESULTS: There was no statistically
> significant relationship between PT fraction and rate of aneurysm size
> change (all patients, r = 0. 196 and P = 0.207). When patients with
> persistent leaks were excluded, the r = 0.234 and P = 0.170 also were
> not statistically significant. CONCLUSIONS: The amount of PT bears no
> important relationship to the response of the aneurysm following
> endovascular repair. Failure of aneurysms to shrink after endovascular
> treatment should not be attributed to large PT, but should prompt a
> thorough investigation for incomplete exclusion of the AAA. Long-term
> studies are needed to validate the efficacy of this new form of
> treatment.

Schumacher H; Eckstein HH; Kallinowski F; Allenberg JR. Morphometry and
classification in abdominal aortic aneurysms: patient selection for
endovascular and open surgery. **J Endovasc Surg.** 1997 Feb; 4(1):
39-44

PURPOSE: To evaluate the anatomic morphology of abdominal aortic
aneurysms (AAAs) and compose a classification system to facilitate
patient selection for endovascular graft (EVG) repair. METHODS: Data on
242 consecutive AAA patients evaluated on a nonemergent basis in a
3.5-year period to July 1996 were prospectively entered into a registry.
Patients were examined using sequential intravenous spiral computed
tomographic angiography and intraarterial digital subtraction
angiography. The data collected and analyzed included: diameters of the
supra- and infrarenal aorta, aneurysm, aortoiliac bifurcation, and iliac
arteries; lengths of the proximal neck, distal cuff, and aneurysm;
degrees of iliac artery tortuosity; and occlusion of the visceral,
renal, or iliac arteries. RESULTS: The 242 aneurysms could be easily
grouped into three distinctive categories related to the extent of the
aneurysmal disease. Type I AAAs (11.2%) had nondilated, thrombus-free
infrarenal (15 mm) necks and distal (10 mm) cuffs appropriate for EVG
anchoring. In type II and its subgroups (72.3%), a sufficient proximal
neck was present, but the aneurysm extended into the iliac arteries; 56%
of these were eligible for a bifurcated endograft. In type III (16.5%),
a sufficient proximal neck was missing, independent of distal
involvement. In all, 51.7% were good EVG candidates based on AAA
morphology. Taking into consideration relevant concomitant vascular
diseases, proximal iliac kinking, and iliac, renal, or visceral
occlusive disease, only 30.2% of the population were potential
candidates for an efficient and secure EVG repair using the devices
currently available. CONCLUSIONS: In contrast to classical open repair,
detailed preoperative measurements are recommended for EVG planning. The
use of liberal EVG indications may lead to a higher incidence of
complications, whereas restrictive morphology-based selection criteria
may offer excellent results.

Schurink GW; Aarts NJ; van-Bockel JH. Endoleak after stent-graft
treatment of abdominal aortic aneurysm: a meta-analysis of clinical
studies. **Br J Surg.** 1999 May; 86(5): 581-7

> BACKGROUND: Endoleak is the major complication after endovascular
> treatment of abdominal aortic aneurysm (AAA) and its incidence seems
> to remain significant. Little is known about the association of device
> type and configuration with respect to the incidence, location, time
> of onset and fate of endoleakage. METHODS: A meta-analysis was
> performed via a Medline search of clinical studies after 1995 dealing
> with the endovascular treatment of AAA. Details of number of patients
> treated, configuration and type of endovascular device were collected.
> Data concerning site of origin, time of occurrence and fate of the
> endoleak were retrieved, along with information on change in diameter
> of the aneurysm with time. RESULTS: The 23 publications included
> reported on 1189 patients. The 1118 patients with successfully
> inserted transfemoral endovascular grafts experienced 270 endoleaks
> (24 per cent). The majority arose from the distal stent attachment
> site (36 per cent), were present immediately after stent-graft
> placement (66 per cent) and were persistent in time (37 per cent).
> Tube grafts were more frequently affected by endoleakage (35 per cent;
> P \< 0.0001), especially at the distal stent attachment site (51 per
> cent), than bifurcated grafts (18 per cent; P = 0.004) and
> aortounilateral devices (20 per cent; P = 0.70). Self- expandable
> stent-grafts were more frequently associated with endoleaks (25 per
> cent) than balloon-expandable stent-grafts (17 per cent) (P = 0.037).
> CONCLUSION: Endovascular treatment of AAA is an evolving field. Even
> after the initial learning curve and attention to device-related
> problems, it is still accompanied by a significant number of
> endoleaks. Uniform presentation of results of treatment is necessary
> for analysing the effect of differences between patients, aneurysm
> morphology and device type.

Sonesson B; Sandgren T; Lanne T. Abdominal aortic aneurysm wall
mechanics and their relation to risk of rupture. **Eur J Vasc Endovasc
Surg**. 1999 Dec; 18(6): 487-93

PURPOSE: to see whether aneurysmal aortic wall mechanics can be used as
a predictor of abdominal aortic aneurysm (AAA) rupture. METHOD: among
285 individuals, followed conservatively for AAA and monitored for
aneurysm growth and wall mechanics on at least one occasion at our
institution between January 1991 and January 1998, eleven subsequently
ruptured. Wall mechanics were estimated as stiffness (beta). This was
calculated from diameter and pulsatile diameter change, determined
non-invasively by an ultrasonic echo-tracking system and blood pressure
obtained by the auscultatory method. The results were compared with
those of 121 individuals electively operated on for AAA. RESULTS: no
difference in aortic stiffness was found between those that subsequently
ruptured (beta=35, median) compared to those non-ruptured (beta=38,
median) AAAs (p=0.855). There was no difference in diameter in ruptured
(58.8 mm) compared with non-ruptured (54.1 mm) AAAs (p=0.129). All
ruptured AAAs showed an expansion of diameter over time. CONCLUSION:
this study shows no difference in aneurysmal aortic wall mechanics in
those AAAs that subsequently ruptured compared with electively operated
AAAs. The results indicate that it is not possible to use aneurysmal
aortic wall stiffness as a predictor of rupture.

Wain RA; Marin ML; Ohki T; Sanchez LA; Lyon RT; Rozenblit A; Suggs WD;
Yuan JG; Veith FJ. Endoleaks after endovascular graft treatment of
aortic aneurysms: classification, risk factors, and outcome. **J Vasc
Surg**. 1998 Jan; 27(1): 69-78; discussion 78-80

PURPOSE: Incomplete endovascular graft exclusion of an abdominal aortic
aneurysm results in an endoleak. To better understand the pathogenesis,
significance, and fate of endoleaks, we analyzed our experience with
endovascular aneurysm repair. METHODS: Between November 1992 and May
1997, 47 aneurysms were treated. In a phase I study, patients received
either an endovascular aortoaortic graft (11) or an aortoiliac,
femorofemoral graft (8). In phase II, procedures and grafts were
modified to include aortofemoral, femorofemoral grafts (28) that were
inserted with juxtarenal proximal stents, sutured endovascular distal
anastomoses within the femoral artery, and hypogastric artery coil
embolization. Endoleaks were detected by arteriogram, computed
tomographic scan, or duplex ultrasound. Classification systems to
describe anatomic, chronologic, and physiologic endoleak features were
developed, and aortic characteristics were correlated with endoleak
incidence. RESULTS: Endoleaks were discovered in 11 phase I patients
(58%) and only six phase II patients (21%; p \< 0.05). Aneurysm neck
lengths 2 cm or less increased the incidence of endoleaks (p \< 0.05).
Although not significant, aneurysms with patent side branches or severe
neck calcification had a higher rate of endoleaks than those without
these features (47% vs 29% and 57% vs 33%, respectively), and patients
with iliac artery occlusive disease had a lower rate of endoleaks than
those without occlusive disease (18% vs 42%). Endoleak classifications
revealed that most endoleaks were immediate, without outflow, and
persistent (71% each), proximal (59%), and had aortic inflow (88%). One
patient with a persistent endoleak had aneurysm rupture and died.
CONCLUSIONS: Endoleaks complicate a significant number of endovascular
abdominal aortic aneurysm repairs and may permit aneurysm growth and
rupture. The type of graft used, the technique of graft insertion, and
aortic anatomic features all affect the rate of endoleaks. Anatomic,
chronologic, and physiologic classifications can facilitate endoleak
reporting and improve understanding of their pathogenesis, significance,
and fate.

Walker SR; Macierewicz J; Hopkinson BR. Endovascular AAA repair:
prevention of side branch endoleaks with thrombogenic sponge. **J
Endovasc Surg.** 1999 Nov; 6(4): 350-3

PURPOSE: To report a technique that might decrease the incidence of
lumbar artery endoleaks following endovascular repair (EVR) of abdominal
aortic aneurysms (AAAs). METHODS: Ninety-three patients (86 males,
median age 72 years, range 56 to 88) undergoing EVR with the
aortomonoiliac technique were entered into a study to detect and then
occlude patent side branches before completion of the endografting
procedure. Prior to deploying the iliac occluder, an aneurysmogram was
performed to detect patent aortic side branches. If these side branches
were found, an absorbable gelatin sponge was inserted into the aneurysm
sac via the occluder introducer sheath. The patients were followed with
contrast-enhanced spiral computed tomography (CT) at 1 week and 3, 6,
and 12 months to detect the presence of endoleaks. RESULTS: Forty-eight
(52%) patients demonstrated patent side branches that were occluded by
the insertion of gelatin sponges into the aneurysm sac. The remaining 45
patients without evidence of side branch flow were untreated. Ten
(10.7%) patients died in the perioperative period, and 15 (16.1%)
primary endoleaks (13 proximal, 2 distal) were detected. This left 68
(73.1%) patients for follow-up, 33 (48.5%) of whom had patent branch
vessels treated with the thrombogenic sponge. The median follow-up was 4
months (range 1 to 17), during which time no side branch endoleak was
detected on surveillance CT scans in any of the 68 patients, which
included all patients treated with the thrombogenic sponge technique and
those in whom no patent side branches had been identified. CONCLUSIONS:
We have demonstrated a safe and reliable method of preventing lumbar
artery endoleaks following endovascular AAA repair.

Wilson K; Bradbury A; Whyman M; Hoskins P; Lee A; Fowkes G; McCollum P;
Ruckley CV. Relationship between abdominal aortic aneurysm wall
compliance and clinical outcome: a preliminary analysis. **Eur J Vasc
Endovasc Surg**. 1998 Jun; 15(6): 472-7

> BACKGROUND: Aortic compliance, as measured by the pressure-strain
> elastic modulus (Ep) and stiffness (B), may allow a more precise
> estimate of abdominal aortic aneurysm rupture risk than size alone.
> AIM: To determine the relationships between AAA compliance, size,
> growth, and clinical outcome. METHODS: One-hundred and twelve patients
> with initially non-operated AAA (86 men, 26 women, mean age 73 years),
> recruited from five centres, underwent baseline compliance
> measurements and were then followed for a median of 7 (range 2-18)
> months; 85 patients underwent repeated measurements (median 3, range
> 2-5) 3-6-monthly over a median of 12 (range 3-18 months). RESULTS:
> Seven patients have ruptured and 16 have undergone repair of
> non-ruptured AAA. AAA that ruptured had significantly lower Ep and B
> (more compliant). In AAA that ruptured or required repair there was an
> inverse relationship between diameter and Ep and B. In those
> undergoing repeated measurements AAA expansion was only associated
> with a significant increase in Ep and B in non-operated patients.
> CONCLUSIONS: Baseline AAA compliance was significantly related to
> rupture and the future requirement for operative repair. Failure of
> compliance to increase with size may be a marker for rapid growth,
> developmental symptoms and rupture.