Goal

A list of known failures that reasonably can be simulated through
pre-clinical testing.

Question

The following table lists failures that have been observed clinically,
focusing on implant failures and excluding delivery or delivery system
failures. The work assignment involved listing additional failure modes
that should be considered, noting whether the failure could be evaluated
or detected through pre-clinical testing, identifying potential causal
factors, rating the importance of the failure mode 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 3 Failure Modes**

<table>
<colgroup>
<col style="width: 6%" />
<col style="width: 12%" />
<col style="width: 5%" />
<col style="width: 5%" />
<col style="width: 22%" />
<col style="width: 2%" />
<col style="width: 2%" />
<col style="width: 2%" />
<col style="width: 2%" />
<col style="width: 3%" />
<col style="width: 24%" />
<col style="width: 10%" />
</colgroup>
<thead>
<tr class="header">
<th rowspan="2"></th>
<th rowspan="2"><span class="smallcaps">Failure</span></th>
<th colspan="2"><span class="smallcaps">Preclinical
Evaluation</span></th>
<th rowspan="2"><span class="smallcaps">Primary Causal
Factors</span></th>
<th colspan="5"><span class="smallcaps">Criticality</span></th>
<th rowspan="2"><span class="smallcaps">Comments</span></th>
<th rowspan="2"><span class="smallcaps">Reference</span></th>
</tr>
<tr class="odd">
<th>Yes</th>
<th>No</th>
<th>1</th>
<th>2</th>
<th>3</th>
<th>4</th>
<th>5</th>
</tr>
</thead>
<tbody>
<tr class="odd">
<td>3-1</td>
<td>Type I endoleak</td>
<td>8</td>
<td>3</td>
<td><ul>
<li><p>Anatomy</p></li>
</ul>
<ul>
<li><p>Poor seal.</p></li>
</ul>
<ul>
<li><p>Inadequate seal due to angulation, short neck, irregular
lumen.</p></li>
<li><p>Contact area complexity.</p></li>
<li><p>Inappropriate sizing, poor fixation, excessive neck angulation,
short neck length.</p></li>
<li><p>Inadequate anchoring, apposition, sealing.</p></li>
<li><p>Patient selection (Patient morphology changes, patient anatomy,
device sizing, device placement.)</p></li>
</ul></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
<td>12</td>
<td><ul>
<li><p>Eccentric tensile loads can cause loss of seal.</p></li>
<li><p>Accurate sizing and morphology assessment critical.</p></li>
<li><p>1 or 5, depends on closure. 1 if closes immediately.</p></li>
<li><p>Calcification, thrombus, angle, increase in size.</p></li>
<li><p>Can partially be assessed pre-clinically.</p></li>
<li><p>Can not duplicate clinical environment in vitro.</p></li>
<li><p>If patient selection issue, can't evaluate in vitro.</p></li>
<li><p>If device design issue, can evaluate in vitro.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-1</td>
<td>Type I endoleak, continued</td>
<td></td>
<td></td>
<td><ul>
<li><p>Poor/inappropriate imaging.</p></li>
<li><p>Design</p></li>
<li><p>Device design (Weak radial force, lack of conformability,
oversizing related ‘puckering’, poor angular engagement.)</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Radial Force; Improper Sizing</p></li>
<li><p>Short neck</p></li>
<li><p>Angle neck</p></li>
<li><p>Wrong diameter</p></li>
<li><p>Attachment Design</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td><p><strong><u>Workshop Comments:</u></strong></p>
<ul>
<li><p><strong>Is it necessary to model this for
testing?</strong></p></li>
<li><p><strong>What’s important is not the endoleak, per se, but why it
happens.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-2</td>
<td>Type II endoleak</td>
<td>1</td>
<td>9</td>
<td><ul>
<li><p>Patent Collaterals</p></li>
<li><p>Anatomy</p></li>
<li><p>Collaterals with flow paths.</p></li>
<li><p>Individual patient anatomy</p></li>
<li><p>Retrograde perfusion of branch vessels</p></li>
<li><p>This is normal anatomy, not fully impacted by graft</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Branch Vessels not ligated</p></li>
</ul></td>
<td>1</td>
<td></td>
<td>4</td>
<td>5</td>
<td>2</td>
<td><ul>
<li><p>Device independent.</p></li>
<li><p>Renals and IMAs.</p></li>
<li><p>Literature shows sac pressure diffs. with different size
vessels.</p></li>
<li><p>Current endografts are not designed to address type II leaks.
This is a patient management issue.</p></li>
<li><p>No, biological model likely required.</p></li>
<li><p>The effect of Type II endoleaks can be evaluated.</p></li>
<li><p>This failure mode has a strong relationship to patient
characteristics.</p></li>
<li><p>Can not duplicate clinical environment in vitro.</p></li>
<li><p>Property is not prosthesis related, it is procedure
related.</p></li>
<li><p>No, not controlled by device.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-3</td>
<td>Type III endoleak</td>
<td>10</td>
<td>3</td>
<td><ul>
<li><p>Cyclic loads, angulation, remodeling-induced loads</p></li>
<li><p>Design</p></li>
<li><p>Thin fabrics</p></li>
<li><p>Change in morphology.</p></li>
<li><p>Modular component separation or graft material holes</p></li>
<li><p>Poor graft material durability</p></li>
<li><p>An adequate design can fail because of a delivery issue</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Component separation</p></li>
<li><p>Porosity</p></li>
<li><p>Joint design</p></li>
<li><p>Durability-junction design</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>2</td>
<td>9</td>
<td><ul>
<li><p>Standard graft testing.</p></li>
<li><p>Deployment technique and dilatation after placement
critical.</p></li>
<li><p>Test dislocation forces and graft wear resilience.</p></li>
<li><p>Same as type I: Very critical, easy to test, must be evaluated
with extreme conditions of mating components.</p></li>
<li><p>The pull apart force can be quantified preclinically.</p></li>
<li><p>If this is a patient selection issue, it can't be evaluated
<em>in vitro</em>, but if this is a device design issue, it can be
evaluated <em>in vitro</em>.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-3</td>
<td>Type III endoleak, continued</td>
<td></td>
<td></td>
<td><ul>
<li><p>Patient selection (Patient morphology changes, patient anatomy,
device sizing, device placement.)</p></li>
<li><p>Device design (Weak radial force, lack of conformability,
oversizing related ‘puckering’, poor angular engagement.)</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-4</td>
<td>Type IV endoleak</td>
<td>10</td>
<td>1</td>
<td><ul>
<li><p>Excessive graft material permeability</p></li>
<li><p>Design</p></li>
<li><p>Thin fabrics</p></li>
<li><p>Covering design</p></li>
<li><p>Graft porosity.</p></li>
<li><p>Graft material porosity or permeability</p></li>
<li><p>Low porosity graft material</p></li>
<li><p>Graft wear, microholes, perforations, etc. chronically, ‘blush’
easily evaluated acutely</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Weave density, suture holes</p></li>
</ul></td>
<td></td>
<td>1</td>
<td>1</td>
<td>7</td>
<td>2</td>
<td><ul>
<li><p>Angle tests.</p></li>
<li><p>Standard test.</p></li>
<li><p>Mitigated through material selection.</p></li>
<li><p>Long term fatigue can assist in evaluating, short term
permeability testing is effective for acute blush prediction.</p></li>
<li><p>Can not duplicate clinical environment <em>in
vitro</em>.</p></li>
<li><p>The water permeability is easy to determine, however how that
relates to how/if the material will clot off in blood is the
challenge.</p></li>
<li><p>Difficult to evaluate pre-clinically.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-4</td>
<td>Type IV endoleak, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td><p><strong><u>Workshop Comments</u>:</strong></p>
<ul>
<li><p><strong>How is this defined? Graft porosity (blush) versus graft
holes (which can increase over time).</strong></p></li>
<li><p><strong>Perhaps this won’t be an issue in the future with tighter
weaves and smaller suture holes.</strong></p></li>
<li><p><strong>What is the clinical significance? If it doesn’t transmit
pressure or flow, is it a problem?</strong></p></li>
<li><p><strong>Water permeability of fabrics / leakage rates perhaps
cold be tied back to clinical situation.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-5</td>
<td>Endotension</td>
<td>2</td>
<td>5</td>
<td><ul>
<li><p>Really endoleak with very low flow-see endoleak causes
above</p></li>
<li><p>Gel phase of clotting.</p></li>
<li><p>Pressureized sac after exclusion</p></li>
<li><p>Endoleak of all four types</p></li>
<li><p>Unknown</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>N/A</p></li>
</ul></td>
<td>1</td>
<td>2</td>
<td>1</td>
<td>3</td>
<td>1</td>
<td><ul>
<li><p>Doesn't exist.</p></li>
<li><p>Imaging, device porosity.</p></li>
<li><p>May not exist; could be unseen Type I endoleak.</p></li>
<li><p>This is a patient management issue.</p></li>
<li><p>No, biological model likely required.</p></li>
<li><p>Whether or not can evaluate depends on source.</p></li>
<li><p>What is it?</p></li>
<li><p>Unknown, but important to understand.</p></li>
<li><p>Can not duplicate clinical environment in vitro.</p></li>
<li><p>Not in addition to above leaks.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-6</td>
<td>Graft wear holes</td>
<td>14</td>
<td></td>
<td><ul>
<li><p>Load concentration relative motion of metal-fabric interface in
angulated anatomy</p></li>
<li><p>Design</p></li>
<li><p>Angles</p></li>
<li><p>Relative movement between the stent and graft material</p></li>
<li><p>Relative motion and/or wear abrasion of graft and stent /
calcification</p></li>
<li><p>Micromotion, abrasion, weave deformation, specific design
etc.</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Graft/suture/ metal interaction</p></li>
<li><p>Metal to fabric interaction</p></li>
<li><p>Motion</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>4</td>
<td>8</td>
<td><ul>
<li><p>Cyclic testing with effects of angulation.</p></li>
<li><p>Metal-fabric interface is critical.</p></li>
<li><p>Difficulty is in defining the test parameters for each device
manufacturer.</p></li>
<li><p>Angle tests.</p></li>
<li><p>May be accentuated by angulations and endoleaks.</p></li>
<li><p>Typical of internally located stents (endoskeleton
design).</p></li>
<li><p>Testing in meaningful conditions can be completed.</p></li>
<li><p>With limited conditions.</p></li>
<li><p>Difficult to model the geometry accurately.</p></li>
<li><p>What are the conditions that lead to fabric wear holes? Test
should capture worst case conditions, which may be
graft-specific.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-6</td>
<td>Graft wear holes, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td><ul>
<li><p>Standard test methods for causing accelerated wear are useful for
comparative testing.</p></li>
<li><p>Breakages are due to axial compliance.</p></li>
<li><p>Measure permeability before and after durability
testing.</p></li>
<li><p>Is there a difference whether the stent is on the inside or the
outside?</p></li>
<li><p>Is there a need for pooling morphology data on explanted cases?
There should be standard imaging just prior to explant.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-7</td>
<td>Kinking of graft limbs</td>
<td>12</td>
<td>1</td>
<td><ul>
<li><p>Iliac tortuosity, remodeling-induced compressive loads may
produce buckling</p></li>
<li><p>Disease progression</p></li>
<li><p>Changes in morphology.</p></li>
<li><p>Vessel tortuosity</p></li>
<li><p>Migration, changes in aneurysmal morphology (e.g.,
length)</p></li>
<li><p>Remodeling, design and anatomy factors</p></li>
<li><p>Anatomy and device.</p></li>
<li><p>Tortuosity</p></li>
<li><p>Excessive angulation</p></li>
<li><p>Tight bifurcation</p></li>
<li><p>Leg cross-over</p></li>
<li><p>Remodeling?</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td>9</td>
<td>2</td>
<td><ul>
<li><p>Kink radius testing similar to graft testing guidance.</p></li>
<li><p>Angle and foreshortening tests.</p></li>
<li><p>Cannot test for all possibilities.</p></li>
<li><p>Occlusions may occur.</p></li>
<li><p>Can't really evaluate pre-clinically.</p></li>
<li><p>Easily tested/ evaluated; easily comparable to field
findings.</p></li>
<li><p>Can not duplicate clinical environment in vitro.</p></li>
<li><p>Stenting is a possible resolution.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-7</td>
<td>Kinking of graft limbs, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td><p><strong><u>Workshop Comments</u>:</strong></p>
<ul>
<li><p><strong>Quantify the radius of curvature before kinking occurs;
this can be used for comparative purposes.</strong></p></li>
<li><p><strong>What degree of kinking causes a clinical problem, or that
would change the degree of follow-up of the patient?</strong></p></li>
<li><p><strong>Kinking characteristics are likely to change over
time.</strong></p></li>
<li><p><strong>Kinking may have an effect on the long-term durability of
the graft.</strong></p></li>
<li><p><strong>Contained versus uncontained kink.</strong></p></li>
<li><p><strong>Definition: narrowing / buckling; discontinuity in
curvature.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-8</td>
<td>Loss of complete apposition (seal?) to vessel wall</td>
<td>9</td>
<td>4</td>
<td><ul>
<li><p>Device deformation or migration, potentially due to remodeling
induced loads. Disease progression</p></li>
<li><p>Design</p></li>
<li><p>Disease progression or change in neck geometry.</p></li>
<li><p>Change in size, shape, or composition at attachment site</p></li>
<li><p>Graft doesn’t expand with vessel or inappropriate sizing</p></li>
<li><p>Inadequate hoop strength, stent fracture, erosion of underlying
thrombus,</p></li>
<li><p>Dilatation of aneurysm</p></li>
<li><p>Remodeling + radial force</p></li>
<li><p>Can be studied as an evaluation for neck dilation</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Poor radial strength</p></li>
<li><p>Non-round vessel</p></li>
<li><p>Calcium / thrombus</p></li>
<li><p>Attachment design</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td>3</td>
<td>8</td>
<td><ul>
<li><p>Loss of seal assumed. Apposition does not ensure seal. Is this
unique failure mode?</p></li>
<li><p>If related to inappropriate sizing.</p></li>
<li><p>Cannot predict changes due to disease progression.</p></li>
<li><p>Evaluate different neck wall &amp; iliac wall
morphology.</p></li>
<li><p>Can evaluate. This is the “disease”, Types of leaks are the
‘symptom’.</p></li>
<li><p>Part of it can also be related to external parameters.</p></li>
<li><p>Fatigue, radial forces, healing, migration, etc. are all
related</p></li>
<li><p>Can not duplicate clinical environment in vitro.</p></li>
<li><p>We assume this refers to a growing aneurysm.</p></li>
<li><p>Materials for in-vitro evaluation are inadequate, animal models
are difficult and / or not representative of disease, cadavers are
difficult and represent that case only.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-9</td>
<td>Metallic component fracture</td>
<td>14</td>
<td></td>
<td><ul>
<li><p><em>In vivo</em> loads larger than estimated</p></li>
<li><p>Design</p></li>
<li><p>Anatomy</p></li>
<li><p>Angles, transitional forces</p></li>
<li><p>Design and progression of disease</p></li>
<li><p>Material fatigue.</p></li>
<li><p>Endograft fatigue</p></li>
<li><p>Inhospitable combination of mean and alternating mechanical
strains, stent material defect</p></li>
<li><p>Fatigue, exceeding UTS, surface finish, design, oversizing,
etc.</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Fatigue</p></li>
<li><p>Excessive strain</p></li>
<li><p>Metal to metal fretting</p></li>
<li><p>Corrosion</p></li>
<li><p>Stent design processing</p></li>
</ul></td>
<td></td>
<td>1</td>
<td>2</td>
<td>7</td>
<td>2</td>
<td><ul>
<li><p>Presumably via radial fatigue and bending. Maybe axial component
needs to be addressed.</p></li>
<li><p>Angle and transition zone testing.</p></li>
<li><p>Depends on location and effect on fixation and other device
components.</p></li>
<li><p>Importance depends on outcome and overall integrity of
assembly.</p></li>
<li><p>Depending on angulation and location then could be 5
criticality.</p></li>
<li><p>Criticality to endograft performance depends upon method of stent
attachment to graft material.</p></li>
<li><p>Highly device design dependant as to cause/effect and clinical
impact.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
<li><p>Criticality depends on location.</p></li>
<li><p>Fractures don’t appear to be critical unless they cause graft
erosion or prosthesis migration as well.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-10</td>
<td>Migration</td>
<td>11</td>
<td>1</td>
<td><ul>
<li><p>In vivo loads underestimated or device attachment strength
overestimated</p></li>
<li><p>Inadequate sizing or neck dilatation</p></li>
<li><p>Poor attachment</p></li>
<li><p>Axial forces against proximal or distal attachment
sites.</p></li>
<li><p>Inadequate fixation</p></li>
<li><p>Inadequate hoop strength, improper device selection, stent
fracture, anchor failure, host material erosion</p></li>
<li><p>Radial force loss, frictional/ engagement loss, neck dilation,
design issues, patient selection, remodeling</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Radial force; improper Sizing</p></li>
<li><p>Inadequate oversizing</p></li>
<li><p>Inadequate radial strength</p></li>
<li><p>Short / angled neck</p></li>
<li><p>Attachment design</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td>1</td>
<td>9</td>
<td><ul>
<li><p>Bifurcated device loads higher then tube device.</p></li>
<li><p>Angulation can increase anchorage loads.</p></li>
</ul>
<ul>
<li><p>Need to define the in vivo mechanism.</p></li>
<li><p>With difficulty.</p></li>
<li><p>Imaging.</p></li>
<li><p>Whole body and partial body migrations.</p></li>
<li><p>Yes, characterized as migration resistance or anchoring
force.</p></li>
<li><p>Yes, but only part of it can be evaluated. Others are not device
dependent.</p></li>
<li><p>This is critical as it leads to other loss of fixation issues
(acute and long term problems).</p></li>
<li><p>Can not duplicate all conditions.</p></li>
<li><p>Critical if it causes a type I endoleak.</p></li>
<li><p>Poor models: Silicone / latex tubing are not clinically relevant.
Animal and cadaver models are sub optimal (see above).</p></li>
</ul></td>
<td><p>Resch, 1999;</p>
<p>Malina, 1998</p></td>
</tr>
<tr class="even">
<td>3-11</td>
<td>Separation of modular components</td>
<td>10</td>
<td>1</td>
<td><ul>
<li><p>Inadequate expansion or sealing at joints. Loads underestimated.
Effects of angulation. Remodeling-induced loads or geometric
changes.</p></li>
<li><p>Design</p></li>
<li><p>Inadequate overlap and angulation</p></li>
<li><p>Inadequate insertion and post implant geometry changes</p></li>
<li><p>Change in morphology leads to change in loads.</p></li>
<li><p>Inadequate joint strength, aneurysm remodeling.</p></li>
<li><p>Poor overlapping (deployment error), inadequate hoop strength,
stent failure.</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>4</td>
<td>9</td>
<td><ul>
<li><p>With difficulty.</p></li>
<li><p>Angle and [friction] tests.</p></li>
<li><p>Difficult to model interface between device and vessel and
in-growth.</p></li>
<li><p>Can be life-threatening. Relationship between in vitro and in
situ difficult to model.</p></li>
<li><p>Standard test.</p></li>
<li><p>In-vitro tests are unable to account for remodeling of the
anatomy.</p></li>
<li><p>Yes, but only part of it can be evaluated. Others are not device
dependant.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-11</td>
<td>Separation of modular components, continued</td>
<td></td>
<td></td>
<td><ul>
<li><p>Remodeling of anatomy</p></li>
<li><p>Poor engagement, wrong size compatibility, design issues, loss of
radial forces, etc.</p></li>
<li><p>Morphology (remodeling)</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Insufficient fixation between components</p></li>
<li><p>Inadequate oversizing</p></li>
<li><p>Inadequate overlap</p></li>
<li><p>Inadequate radial strength</p></li>
<li><p>Junction design</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-12</td>
<td>Suture <strong>[or other attachment method]</strong> breaks causing
component separation</td>
<td>10</td>
<td>1</td>
<td><ul>
<li><p>Cyclic load-induced fatigue. Angulated anatomy focusing
load.</p></li>
<li><p>Design</p></li>
<li><p>Angles, transition forces, deployment techniques.</p></li>
<li><p>Post-implant stresses</p></li>
<li><p>Radial and axial forces at impedance mismatch.</p></li>
<li><p>Choice and method of suturing</p></li>
<li><p>Graft/stent cyclic wear</p></li>
<li><p>Abrasion of sutures, mechanical efforts on sutures (balloon
etc)</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Suture/metal interaction</p></li>
<li><p>Excessive metal to suture movement</p></li>
<li><p>Graft design</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td>3</td>
<td>8</td>
<td><ul>
<li><p>Can have adverse effect on implant integrity.</p></li>
<li><p>If causes are addressed in metallic component testing then the
same test would be appropriate.</p></li>
<li><p>Angle and transition zone testing.</p></li>
<li><p>Probably not desirable, but may not be important if decompress
forces and there is no injury to other graft components.</p></li>
<li><p>Difficult to model using existing durability since breaks are
caused by <em>in situ</em> geometry changes.</p></li>
<li><p>Actually a device migration; Need acceleration or clinical
evaluation.</p></li>
<li><p>Can't really evaluate pre-clinically.</p></li>
<li><p>Can evaluate pre-clinically, but very long process.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
<li><p>Most critical in anchor or seal zones.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="odd">
<td>3-12</td>
<td>Suture <strong>[or other attachment method]</strong> breaks causing
component separation, continued</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td><p><strong><u>Workshop Comments</u>:</strong></p>
<ul>
<li><p><strong>Balloon dilation should be done preclinically to
determine whether it has an effect on suture breaks.</strong></p></li>
<li><p><strong>Need to consider the primary function of the
suture.</strong></p></li>
<li><p><strong>Have the components separated?</strong></p></li>
<li><p><strong>Test the device with sutures intact and with sutures
broken.</strong></p></li>
<li><p><strong>For newer devices with different attachment systems and
non-textile fabrics, "device integrity” is the issue.</strong></p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-13</td>
<td>Sutured-fabric seam failure</td>
<td>11</td>
<td>1</td>
<td><ul>
<li><p>Cyclic load induced fatigue. Angulated anatomy focusing
load.</p></li>
<li><p>Design</p></li>
<li><p>Aortic pressure cycles.</p></li>
<li><p>Choice and method of suturing</p></li>
<li><p>Graft/stent cyclic wear, pulsatile pressure loading
(creep)</p></li>
<li><p>Mechanical efforts including ballooning</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Inadequate design or process to make seam</p></li>
<li><p>Inadequate suture strength or numbers</p></li>
<li><p>Graft-material design</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td>2</td>
<td>8</td>
<td><ul>
<li><p>Same as 3-12 second comment.</p></li>
<li><p>Same as graft wear hole.</p></li>
<li><p>Yes, but only part of it can be evaluated. Others are not device
dependent.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
</ul></td>
<td>Norgren, 1998</td>
</tr>
<tr class="odd">
<td>3-14</td>
<td>Suture breaks – other</td>
<td>11</td>
<td>1</td>
<td><ul>
<li><p>Cyclic load induced fatigue. Angulated anatomy, focusing
load.</p></li>
<li><p>Design</p></li>
<li><p>Radial and axial forces.</p></li>
<li><p>Choice and method of suturing</p></li>
<li><p>Abrasion of sutures, mechanical efforts on sutures (balloon
etc)</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Suture/metal interaction</p></li>
<li><p>Inadequate suture strength or numbers</p></li>
</ul></td>
<td>1</td>
<td>3</td>
<td>4</td>
<td>3</td>
<td>1</td>
<td><ul>
<li><p>Same as 3-12 second comment.</p></li>
<li><p>Angle and transition testing.</p></li>
<li><p>Some suture breaks may not effect integrity of stent
graft.</p></li>
<li><p>Not as important as 3-12.</p></li>
<li><p>Criticality to endograft performance depends upon redundancy of
suture attachments.</p></li>
<li><p>Can sort of evaluate pre-clinically.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
</ul></td>
<td></td>
</tr>
<tr class="even">
<td>3-15</td>
<td><p>Twisting of graft limbs</p>
<p>[resulting in compromised patency]</p></td>
<td>9</td>
<td>1</td>
<td><ul>
<li><p>Deployment manipulation, inadequate radiopacity.</p></li>
<li><p>Design</p></li>
<li><p>Deployment errors and complex devices</p></li>
<li><p>Change in post-implant geometry.</p></li>
<li><p>Change in morphology.</p></li>
<li><p>Deployment technique and aneurysm remodeling</p></li>
<li><p>Migration, inadequate device selection, morphological changes in
the aneurysm.</p></li>
<li><p>Remodeling, delivery misplacement or inappropriate
maneuver</p></li>
<li><p>Change of anatomy over time.</p></li>
<li><p>Tortuosity, implant design, deployment technique</p></li>
<li><p>Technique</p></li>
<li><p>Delivery system design, graft design</p></li>
</ul></td>
<td>1</td>
<td>3</td>
<td>6</td>
<td>6</td>
<td>1</td>
<td><ul>
<li><p>Twisting only significant if leads to limb thrombosis or other
adverse event.</p></li>
<li><p>Twist and angle stress test.</p></li>
<li><p>Important if effects long-term function i.e., angles and
thrombosis.</p></li>
<li><p>Serious if limb occlusion occurs.</p></li>
<li><p>Could lead to occlusion/thrombosis.</p></li>
<li><p>Yes, biological model may be required to assess physiological
significance.</p></li>
<li><p>Can sort of evaluate pre-clinically.</p></li>
<li><p>Yes, but only part of it can be evaluated. Others are not device
dependent.</p></li>
<li><p>Can not duplicate all conditions.</p></li>
<li><p>Stenting is a possible resolution.</p></li>
<li><p>Criticality depends on design.</p></li>
<li><p>Same philosophy as for kinking.</p></li>
</ul></td>
<td><p>Carpenter, 2001;</p>
<p>Kalliafas, 2000;</p>
<p>Resch, 2000;</p>
<p>Holzenbein, 2001</p></td>
</tr>
<tr class="odd">
<td>3-15a</td>
<td>Aorto-duodenal fistulation due to stent failure or anchor
penetration</td>
<td></td>
<td>1</td>
<td><ul>
<li><p>Mechanical stent failure or excessive anchor penetration</p></li>
</ul></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
<td><ul>
<li><p>Incidence is rare, however, if/when it occurs, can have major
deleterious patient consequences.</p></li>
</ul></td>
<td>Parry, 2001</td>
</tr>
<tr class="even">
<td>3-15b</td>
<td>Renal Artery Obstruction</td>
<td>1</td>
<td></td>
<td><ul>
<li><p>Inadequate deployment accuracy</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td><ul>
<li><p>Yes, characterized as deployment accuracy.</p></li>
<li><p>5/176 (2.8%) incidence rate in an aorto-uni-iliac design.
(Kalliafas, 2000)</p></li>
<li><p>Approximately 6% of patients with normal preoperative renal
function who undergo endovascular AAA repair develop renal dysfunction.
For patients with preoperative renal impairment, the perioperative
mortality rate is high, 27%, following endovascular aortic aneurysm
repair. (Walker, 1998)</p></li>
</ul>
<p><strong><u>Workshop Comment</u>:</strong></p>
<ul>
<li><p><strong>This is a clinical failure that could be related to
device performance (e.g., radiopacity, deployment
sequence).</strong></p></li>
</ul></td>
<td><p>Kalliafas, 2000;</p>
<p>Walker, 1998</p></td>
</tr>
<tr class="odd">
<td>3-15c</td>
<td>Iliac tortuosity or access site complica-tions, such as rupture</td>
<td></td>
<td>1</td>
<td><ul>
<li><p>Dimensional incompatibility of host anatomy and delivery
system.</p></li>
<li><p>Delivery system flexibility/pushability</p></li>
</ul></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td><ul>
<li><p>17/266 (6.4%) of patient required conversion to open surgery due
to inability to deploy the endoprosthesis [presumably due to access and
delivery problems per May et al., Eur J Vasc Endovasc Surg 2000 Jun;
19(6): 648-655.</p></li>
</ul></td>
<td>May, 2000</td>
</tr>
<tr class="even">
<td>3-15d</td>
<td>Dissimilar metal corrosion</td>
<td>1</td>
<td></td>
<td><ul>
<li><p>Design</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15e</td>
<td>Excessive deployment force</td>
<td>1</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-15f</td>
<td>Poor deployment accuracy</td>
<td>1</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15g</td>
<td>Tip unable to retract through prosthesis</td>
<td>1</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-15h</td>
<td>Corrosion</td>
<td>1</td>
<td></td>
<td><ul>
<li><p>Material selection, processing</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15i</td>
<td>Renal insufficiency</td>
<td>1</td>
<td></td>
<td><ul>
<li><p>Renal flow disturbance</p></li>
</ul></td>
<td></td>
<td></td>
<td></td>
<td>1</td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-15j</td>
<td>Graft stretch</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15k</td>
<td>Host response</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-15l</td>
<td>Vessel trauma</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15m</td>
<td>Radial creep</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="even">
<td>3-15n</td>
<td>Longitudinal creep</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr class="odd">
<td>3-15o</td>
<td>Graft material rupture</td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
</tbody>
</table>

***Additional Comments***

A general comment from the point of view of test system manufacturers is
that simulating *in vivo* mechanisms of the failure modes is one of the
most important considerations for pre-clinical mechanical testing.
Furthermore, an understanding of the *in vivo* mechanisms related to
each failure mode is important from a testing standpoint. Test designers
can comment on the feasibility of a test. We can comment on the best
approach for testing given the technology available to us. However, we
require guidance in defining the *in vivo* mechanisms that we attempt to
simulate. Our comments regarding feasibility of pre-clinical testing are
based upon our strong knowledge of available leading edge testing
technology while restricted by currently limited knowledge of the *in
vivo* mechanisms.

# **Comments on Question 3:12, 3:13, 3:14**

Failure of suture material, either at a seam line or as a means of
securing the metallic component(s) to the fabric, arises from the
combination of two principal failure mechanisms; creep, and abrasive
loss of cross-section. The cyclic loading of the aortic application
means that a third mechanism could be involved as well, that of
fatigue-related material changes.

Creep is the time-dependent, plastic deformation of a material under
load. Susceptibility of a given material and configuration is largely a
function of load magnitude as a fraction of break force as well as the
load duration.

The pressure differential acting across the device fabric wall acts to
move the fabric into the wire frame if the wire frame is located on the
outer surface. Conversely, if the frame is located internal to the
fabric, the fabric is forced away from the frame; this load must be
borne by the members that attach the fabric to the frame.

# **Metallic component fracture, failure modes, (also relevent to section IV)**

##### [Fracture/Failure in self-deploying stent grafts]{.underline} Fracture of stent frame components is a product of the strains induced by the loading conditions. A spectrum of loading conditions must be considered; from a single load of a magnitude sufficient to produce tensile failure to repetitive loads small enough to be tolerated infinitely. Between these two extremes are a range of conditions that will produce fatigue fracture under cyclic loading.

Under cyclic loading conditions, two components of the strains induced
in the frame member must be considered to predict lifetime under those
conditions; the mean strain under which the device components are
operating and the cyclic strains induced by the cardiac cycle.

*Nominal loading conditions*

For a self-expanding stent frame, the conditions that produce the mean
and alternating strains arise from the manner in which the devices are
deployed in-situ. The end of a device is placed in the neck of the aorta
adjacent to the aneurysm. The retention of the device in the aortic neck
depends on the interference fit afforded by the "oversizing" of the
device relative to the neck diameter. If, for example, the oversizing
employed is 20%, the graft proximal diameter (enclosed within the
artery) will be only about 80% of the relaxed diameter (neglecting
elastic recoil of the vessel). Thus, the greatest mean cyclic strains in
the device will occur within the compressed segment of the artery and
the blood pressure will be acting to decompress that segment so that the
greatest strains will be at diastole. In contrast, systole places the
greatest tensile loading on the graft segment within the aneurysm,
though with a very low mean strain, particularly since some of the load
is transferred to the polymeric portion of the device.

The strains generated by the diameter excursion of the device during the
cardiac cycle can be modeled using the methods of finite element
analysis; this provides the relationship of device compression to
induced strain for each apex of the device. The high strain zones can be
identified and modeled using S/N testing of the frame; fatigue life
estimations under the anticipated in-vivo loading conditions can thus be
developed. Device performance is generally verified with a pulsatile
loading test of the entire device out to the specified design life.

Many metals, including the nitinol wire from which the excluder frame is
constructed, exhibit what is termed an endurance limit under flexural
fatigue conditions. That is, some conditions of mean and alternating
strains exist that will not produce fatigue failure even when the
material is subjected to an infinite number of cycles. Ideally, the
device is designed such that the strains induced in-vivo are less than
those of the endurance limit.

#### *In Vivo loading conditions*

Actual loading conditions are far more complex than the ideal described
above. Device loading conditions fall into one of three categories:
within design parameters, excessive strain but within design loading
mode, and bending.

[Within design parameters]{.underline}

If a graft is loaded within design parameters, the engineering life
model projections should provide a reasonable estimate of device
performance.

[Within design loading mode, but excessive strain]{.underline}

Wire fracture can result when the design levels for either the mean or
alternating components are exceeded. The mean strain can be excessive
due to oversizing. Large alternating strains can result from excessive
diameter excursion of the aorta, particularly in the thoracic segment.
Limited review of AAA cases suggests that excessive oversizing is a
frequent occurrence on the proximal end, but that the alternating
strains are lower than would be anticipated based on literature review
of aortic compliance.

[Bending]{.underline}

In some unknown fraction of the patients, conditions exist that produce
unanticipated bending. This bending appears to result from the
translation of the aorta and is not necessarily distributed along the
length of the device. In the case of thoracic devices, the bending is
about the longitudinal axis. Stiffness mismatches, such as at the device
end(s), or in overlap locations, provide a site at which the bending can
be particularly concentrated. Thus far, this same bending phenomena has
not been observed in AAA. The wire excursions produced in this bending
mode are entirely outside of the design parameters and the induction of
large strains is possible.

Large wire excursions have been observed in application of devices to
thoracic dissections. This has been particularly true in cases of
inadequately-treated dissection in which the wall of the
aorta/dissection undergoes large excursions with each cardiac cycle; the
device also undergoes large excursions, inducing large alternating
strains far beyond design parameters.

*Device type and wire failure*

The sequela of strut breakage is entirely dependent upon the design of
the device. Three general cases exist for stent grafts: stent frame on
the inside of the polymeric component, stent frame on the outside, and
the case in which the frame is between more than one polymeric layer.

One ameliorating factor of wire breakage in general is that it is far
more likely to occur in the section contained within the aneurysm neck
than the segment contained within the aneurysm; thus if the frame is on
the outside of the polymer segment, the broken segment is trapped
against the aortic wall and cannot embolize. This, of course, is not an
ameliorating feature if the frame is on the inside of the device. In any
event however, the likelihood of multiple breaks allowing the release of
a wire segment appears low since the strain in adjacent apices goes down
when a break in a given apex occurs.

In the case in which the wire is entirely contained in a polymer
"sandwich", the consequences of breakage appear to be low, since the
wire cannot escape. Enough breaks would need to occur so that the
frictional force holding the device in place was overcome by the fluid
flow related forces causing device movement.

In both cases in which the frame and fabric represent separate
components (frame on the inside or the outside) wire breakage at the
sites of frame attachment can lead to relative displacement of the
components. Discontinuous frames can provide a hinge-point so that the
metallic component can be spared large strains induced by unintended
bending (see above) but, this can allow abrasive contact of the fabric
with the frame

# 

## References 

Carpenter JP; Neschis DG; Fairman RM; Barker CF; Golden MA; Velazquez
OC; Mitchell ME; Baum RA. **J Vasc Surg**. 2001 Feb; 33(2): 296-302;
discussion 302-3

Holzenbein TJ; Kretschmer G; Thurnher S; Schoder M; Aslim E; Lammer J;
Polterauer P. **J Vasc Surg**. 2001 Feb; 33(2 Suppl): S46-54

Kalliafas S; Albertini JN; Macierewicz J; Yusuf SW; Whitaker SC;
Macsweeney ST; Wenham PW; Hopkinson BR. **J Vasc Surg**. 2000 Jun;
31(6): 1185-92

Malina M; Lindblad B; Ivancev K; Lindh M; Malina J; Brunkwall J. **J
Endovasc Surg**. 1998 Nov; 5(4): 310-7

May et al., **Eur J Vasc Endovasc Surg** 2000 Jun; 19(6): 648-655.

Norgren L; Jernby B; Engellau L **J Endovasc Surg**. 1998 Aug; 5(3):
269-72

Parry DJ; Waterworth A; Kessel D; Robertson I; Berridge DC; Scott DJ.
**J Vasc Surg**. 2001 Apr; 33(4): 874-9

## Resch T; Ivancev K; Brunkwall J; Nyman U; Malina M; Lindblad B. J Vasc Interv Radiol. 1999 Mar; 10(3): 257-64; discussion 265-6

## Resch T; Lindblad B; Lindh M; Brunkwall J; Ivancev K. J Endovasc Ther. 2000 Dec; 7(6): 446-50

Walker, 1998

## Abstracts of Selected References (from above)

Carpenter JP; Neschis DG; Fairman RM; Barker CF; Golden MA; Velazquez
OC; Mitchell ME; Baum RA, Failure of endovascular abdominal aortic
aneurysm graft limbs**. J Vasc Surg**. 2001 Feb; 33(2): 296-302;
discussion 302-3.

> OBJECTIVE: Endovascular abdominal aortic aneurysm (AAA) grafts are
> subject to subsequent failure of endograft limbs. We sought to
> determine what device-related factors could be identified that might
> contribute to limb failure. METHODS: We reviewed the records of
> patients who had undergone endovascular AAA repair and femorofemoral
> bypass grafting at a single institution. RESULTS: Endovascular AAA
> repair was performed in 173 patients. There were 137 bifurcated
> endografts and 36 aortomonoiliac grafts combined with femorofemoral
> bypass grafts, yielding a total population of 310 aortic graft limbs
> and 36 femorofemoral grafts. Thirty-nine additional patients underwent
> femorofemoral bypass grafting for occlusive disease. The cumulative
> primary patency of all endografts performed for AAA was 92% at 21
> months. Secondary patency was achieved for all failed endograft limbs.
> There were 24 aortic graft limb \"failures\" that required
> intervention: seven limbs underwent thrombosis requiring revision;
> kinked limbs requiring stenting either at the time of graft placement
> (17) or subsequently (7) were identified. Fully supported endograft
> limbs had better primary patency (97% at 18 months) than unsupported
> limbs (69% at 18 months, P \<.001). The aortomonoiliac grafts with
> femorofemoral bypass grafts tended to have better patency (97% at 18
> months) than bifurcated endografts (90% at 18 months), but this did
> not reach statistical significance (P =.28, not significant).
> Femorofemoral grafts performed for occlusive disease were found to
> have somewhat lower patency than those performed for AAA (83% vs 92%
> at 18 months of follow-up, P =.37, not significant). CONCLUSIONS:
> Fully supported AAA endografts provide superior endograft limb patency
> compared with unsupported designs. Consideration should be given to
> routine stenting of all unsupported endograft limbs. Aortomonoiliac
> grafts and bifurcated grafts provide similar results for endograft
> limb patency. Femorofemoral bypass grafts performed in conjunction
> with aortomonoiliac grafts for AAA disease provide excellent
> short-term patency.

Holzenbein TJ; Kretschmer G; Thurnher S; Schoder M; Aslim E; Lammer J;
Polterauer P. Midterm durability of abdominal aortic aneurysm endograft
repair: a word of caution. **J Vasc Surg**. 2001 Feb; 33(2 Suppl):
S46-54

> PURPOSE: Endograft technology for abdominal aortic aneurysm (AAA)
> repair is being applied more liberally. There is little information
> about the midterm performance of these grafts. This study is focused
> on follow-up interventions after endograft repair for AAA. METHODS:
> Prospective follow-up analysis of a consecutive patient series (n =
> 173 patients) at a single center who underwent endovascular AAA repair
> up to 50 months after operation. Seventeen percent of the patients
> were regarded unfit for open surgery. Four types of commercially
> available grafts were used. The Society for Vascular
> Surgery/International Society for Cardiovascular Surgery guidelines
> were applied for endograft implantation and data preparation. RESULTS:
> In two patients, the procedure was converted to open surgery. In one
> procedure, emergency repair for iliac artery rupture was performed.
> The 30-day mortality rate was 2.8% (n = 5 patients). An early second
> procedure to correct type I endoleaks was necessary in 8 cases (4.6%;
> 3-10 days). The following midterm results were obtained: median
> follow-up of the 166 remaining patients was 18 months (range, 1-50
> months); 50 additional procedures were necessary in 37 patients
> (22.3%) for the treatment of leaks (n = 45 interventions) or to
> maintain graft patency (n = 5 grafts; four patients with concomitant
> graft segment disconnection); and 46% of the reinterventions were
> performed within the first year of follow-up and 74% of the
> reinterventions were performed within the second year of follow-up.
> One patient died after emergency surgery for rupture as the result of
> a secondary endoleak at 1 year. Although seven interventions (14%)
> were performed for type II endoleak, no serious complications were
> related to patent sidebranches. There was no statistically significant
> difference between the need for maintenance in different graft
> configurations (tubular, bifurcated, aorto-uniiliac), or number of
> graft segments (1, 2, 3-4, \> or = 5 segments). New generation grafts
> (after 1996) performed better than early generation grafts (P = 0.04,
> chi-squared test) with regard to endoleak development. CONCLUSION:
> Endograft repair for AAA is safe but, with current technology, not as
> durable as open repair. Our data suggest that the use of endograft
> repair for AAA is becoming safer as endograft design improves.
> Nevertheless in 26.6% of the patients, there is need for
> reintervention within midterm follow-up. Close follow-up is crucial
> because late leaks may develop after more than 2 years after the
> initial procedure. Endoluminal repair should therefore be applied with
> caution, strict indication, and only if a tight follow-up is
> warranted. These findings may also affect health care reimbursement
> policies.

Kalliafas S; Albertini J-N; Macierewicz J; Yusuf S-W; Whitaker S-C;
Macsweeney S-T; Wenham P-W; Hopkinson B-R. Incidence and treatment of
intraoperative technical problems during endovascular repair of complex
abdominal aortic aneurysms. **J Vasc Surg**. 2000 Jun; 31(6): 1185-92

> PURPOSE: The purpose of this study was to assess the incidence and
> management of intraoperative technical problems during endovascular
> repair (EVR) of complex abdominal aortic aneurysms (AAA). METHODS:
> From February 1995 to March 1999, 204 EVRs of nonruptured AAA were
> performed at our institution. One hundred seventy-six patients had an
> in-house custom-made graft; 172 were aorto-uni-iliac grafts, and four
> were aortoaortic grafts. Twenty- eight patients had a bifurcated
> graft. One hundred fourteen patients (56%) were high risk for
> conventional open repair. One hundred nine patients (53%) were not
> suitable for most commercially available devices. RESULTS:
> Intraoperative technical problems occurred in 81 patients (40%). There
> were 37 endoleaks (27 proximal, 10 distal), 15 graft stenoses, one
> failure of graft deployment, two graft thromboses, three aortoiliac
> ruptures, five renal artery occlusions (one bilateral, four
> unilateral), and 18 internal iliac occlusions (five bilateral, 13
> unilateral). Endovascular management of these problems was successful
> in 37 of the 81 patients (46%) and included 15 balloon dilatations, 21
> additional stent placements, and one graft thrombectomy. Fifteen of
> the 81 patients (19%) had open procedures (four periaortic ligature
> placements, six open aneurysm repairs, three common iliac ligations,
> and two extra-anatomic bypass grafts). In the remaining 29 patients,
> the on-table problem was managed expectantly. During follow-up, two of
> 37 patients (5%) who were treated successfully with endovascular
> procedures experienced recurrence. There were five deaths (33%) among
> the 15 patients who underwent open procedures. CONCLUSION:
> Intraoperative problems occur frequently during the endovascular
> management of complex aneurysms. Many of these problems can be managed
> with additional endovascular techniques without an increased risk of
> recurrence or procedure-related complications. Open procedures in
> high-risk patients carry a high mortality rate. The team performing
> EVR of AAA should be skillful in advanced endovascular and open
> surgical procedures.

Malina M; Lindblad B; Ivancev K; Lindh M; Malina J; Brunkwall J.
Endovascular AAA exclusion: will stents with hooks and barbs prevent
stent-graft migration? **J Endovasc Surg**. 1998 Nov; 5(4): 310-7

> PURPOSE: To investigate if stents with hooks and barbs will improve
> stent-graft fixation in the abdominal aorta. METHODS: Sixteen- to
> 24-mm-diameter Dacron grafts were deployed inside cadaveric aortas.
> The grafts were anchored by stents as in endovascular abdominal aortic
> aneurysm repair. One hundred thirty-seven stent-graft deployments were
> carried out with modified self-expanding Z-stents with (A) no hooks
> and barbs (n = 75), (B) 4 5-mm-long hooks and barbs (n = 39), (C) 8
> 10-mm-long, strengthened hooks and barbs (n = 19), or (D) hooks only
> (n = 4). Increasing longitudinal traction was applied to determine the
> displacement force needed to extract the stent-grafts. The radial
> force of the stents was measured and correlated to the displacement
> force. RESULTS: The median (interquartile range) displacement force
> needed to extract grafts anchored by stent A was 2.5 N (2.0 to 3.4),
> stent B 7.8 N (7.4 to 10.8), and stent C 22.5 N (17.1 to 27.9), p \<
> 0.001. Both hooks and barbs added anchoring strength. During traction,
> the weaker barbs were distorted or caused intimal tears. The stronger
> barbs engaged the entire aortic wall. The radial force of the stents
> had no impact on fixation, while aortic calcification and graft
> oversizing had marginal effects. CONCLUSIONS: Stent barbs and hooks
> increased the fixation of stent-grafts tenfold, while the radial force
> of stents had no impact. These data may prove important in future
> endograft development to prevent stent-graft migration after aneurysm
> exclusion.

Norgren L; Jernby B; Engellau L. Aortoenteric fistula caused by a
ruptured stent-graft: a case report. **J Endovasc Surg**. 1998 Aug;
5(3): 269-72

> PURPOSE: To report a case of aortoenteric fistula secondary to
> endovascular abdominal aortic aneurysm (AAA) exclusion using the
> Stentor bifurcated endovascular graft. METHODS AND RESULTS: Seventeen
> months after a successful endovascular AAA procedure, a male patient
> developed upper gastrointestinal bleeding. An aortoenteric fistula was
> diagnosed. At operation, the endograft fabric was found to be ruptured
> in an area of suture disruption between the nitinol stents.
> Coincidentally, a pre-existing inflammatory process might have caused
> adhesions between the bowel and the aortic wall, predisposing to
> fistula formation. The patient recovered after placement of a
> conventional aortic graft. CONCLUSIONS: Suture disruption between the
> internal support stents is a recognized complication in the
> first-generation Stentor device. Although the case described here is
> probably not typical of the consequences of this sequela, it does
> reinforce the need for continual periodic imaging to check for signs
> of graft disruption in Stentor endografts.

Parry DJ; Waterworth A; Kessel D; Robertson I; Berridge DC; Scott DJ.
Endovascular repair of an inflammatory abdominal aortic aneurysm
complicated by aortoduodenal fistulation with an unusual presentation.
**J Vasc Surg**. 2001 Apr; 33(4): 874-9

> Aortoenteric fistulation (AEF) is a well-documented late complication
> of open abdominal aortic aneurysm (AAA) repair, occurring in between
> 0.4% and 4% of cases. In the absence of an anastomosis, AEF is likely
> to be rare after endovascular aneurysm repair (EVAR) and has only
> recently been described in the literature as a result of mechanical
> stent failure or migration. We present the case of a 61-year-old man
> who underwent EVAR for an AAA with a \"nonspecific\" periaortic
> inflammatory mass. Six months postoperatively, an AEF developed,
> presenting with metastatic sepsis followed by septic infective
> thromboembolization to his right leg, and amputation was necessary.
> His stent was well positioned and mechanically intact. We emphasize
> the need for vigilance about the risk of AEF when adopting an
> endovascular approach to repair the AAA with a nonspecific periaortic
> inflammatory mass and highlight the need for awareness about the
> unusual septic manifestations of AEF.

Resch T; Ivancev K; Brunkwall J; Nyman U; Malina M; Lindblad B. Distal
migration of stent-grafts after endovascular repair of abdominal aortic
aneurysms. **J Vasc Interv Radiol**. 1999 Mar; 10(3): 257-64; discussion
265-6

> PURPOSE: To analyze patients after endovascular repair of abdominal
> aortic aneurysm (AAA) with respect to distal migration of stent-grafts
> and its underlying causes. MATERIALS AND METHODS: Sixty-five patients
> underwent endovascular repair between January 1994 and February 1997.
> There were seven women and 58 men, with a mean age of 71 years (range,
> 51-84 years). Three patients died in the perioperative period (one of
> myocardial infarction and two of multiorgan failure) and two patients
> died within 4 months of the procedure of non-procedure-related causes.
> In addition, two patients were followed at another hospital. The
> remaining 58 patients were followed up with spiral computed tomography
> scans at 1, 3, and 6 months, and biannually thereafter. Angiography
> was performed at 1 month and 1 year after the procedure and
> additionally when deemed clinically necessary. Mean follow-up was 29
> months (range, 1-49). Migration more than 5 mm was considered
> significant. RESULTS: Twenty-six patients (45%) showed distal
> migration of stent-grafts during follow-up. Mean follow-up time at
> detection of migration was 13 months (range, 1-36 months). Thirteen
> cases of migration were ascribed to dilatation of the proximal
> aneurysmal neck during follow-up. Ten cases of migration were ascribed
> to causes other than neck dilatation or poor patient selection. In
> three cases, no obvious cause for the migration was found. The
> migration was complete in eight cases, leading to late conversion to
> open surgical repair. On two of these occasions, complete migration
> lead to aneurysm rupture. In addition, four patients received
> additional stent-grafts as proximal extensions. CONCLUSIONS: Distal
> migration of stent-grafts after endovascular AAA repair occurred
> frequently in this series. Dilatation of the proximal aneurysmal neck
> is a major cause of distal migration of stent-grafts. Improved
> proximal fixation is needed to secure long-term durability.

Resch T; Lindblad B; Lindh M; Brunkwall J; Ivancev K. Aneurysm expansion
and retroperitoneal hematoma after thrombolysis for stent-graft limb
occlusion caused by distal endograft migration. **J Endovasc Ther**.
2000 Dec; 7(6): 446-50

> PURPOSE: To describe a complication of thrombolytic therapy used to
> treat graft limb occlusion precipitated by distal migration and
> kinking of an abdominal aortic stent-graft. CASE REPORT: A 5.5-cm
> abdominal aortic aneurysm (AAA) in a 66-year-old woman was treated
> with Vanguard bifurcated stent-graft. At the 1-year follow-up, she
> complained of left leg claudication. Computed tomography (CT) showed a
> 36% reduction in maximum AAA diameter, but the stent-graft had
> migrated distally approximately 5 mm, and the left graft limb was
> occluded. Thrombolysis was initiated, but after approximately 8 hours,
> abdominal pain began. Emergent CT scanning revealed rapid aneurysm
> expansion and a retroperitoneal hematoma. Thrombolytic treatment was
> stopped; transfusions and thrombogenic drugs were given to restore
> hemodynamic stability. The aneurysm began to decrease in size. The
> occluded graft limb had been reopened by the lytic therapy, uncovering
> a stenosis in the native artery distal to the graft limb. Stent
> placement restored outflow. The retroperitoneal hematoma resolved over
> time, and the aneurysm sac shrank to its prelytic diameter. The
> patient is well with a functioning endograft 18 months after the
> occlusion (30 months after stent-grafting). CONCLUSIONS: Caution must
> be taken when using thrombolysis in patients with endovascular aortic
> grafts because unexpected bleeding complications might arise.
> Thrombectomy, femorofemoral bypass, or stent or stent-graft extensions
> might be safer alternatives for treating occluded stent-graft limbs.