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10]

Review Article

Stent Fracture: How Frequently Is It Recognized?

Mohammed Khalil Mohsen, Awad Alqahtani, Jassim Al suwaidi
Heart Hospital, Hamad Medical Corporation, Doha, Qatar

ABSTRACT

In spite of there being several case reports, coronary stent fracture is not a well‑recognized entity and incidence rates are
likely to be underestimated. In this article, we review different aspects of stent fracture, including incidence, classification,
predictors, outcome, diagnosis, and management.

Key words: Complication of percutaneous coronary intervention (PCI), instent restenosis, stent fracture, stent thrombosis
How to cite this article: Mohsen MK, Alqahtani A, suwaidi JA. Stent fracture: How frequently is it recognized?. Heart Views 2013;14:72-81.
© Gulf Heart Association 2013.

INTRODUCTION in daily practice, ranging from conventional BMS and

old-generation DES to newer generations of DES:

A
dramatic revolution in the field of intervention
cardiology has been heralded by the use drug-
eluting stents (DES) replacing bare metal stents
(BMS), and thereby significantly reducing the restenosis
rates and the need for repeat revascularization. [1‑4]
However, the occurrence of late‑onset complications,
such as stent thrombosis, has raised concern over the
use of DES. In addition, there has been an increasing
awareness of stent fracture (SF) as a potential
complication following DES implantation.
Review of the literature shows there is increasing
concern about SF as a potential cause of stent
restenosis and thrombosis, which can lead to adverse
clinical outcomes such as recurrent angina, myocardial
infarction (MI), and even sudden death.
The objective of this article is to analyze controversial
issues about the incidence, diagnostic tools, and clinical
implications of SF.
BACKGROUND
In 1964, Charles Theodore Dotter and Melvin P. Judkins
described the first angioplasty. [5] In 1977, Andreas
Grüntzig, a German radiologist, successfully performed
the first balloon coronary angioplasty,[6] a revolutionary
treatment that led to the birth of interventional cardiology.
Coronary stents were first developed in the
mid‑1980s, [7] and have ultimately replaced plain
balloon angioplasty after the observed improvements
in angiographic and clinical outcomes seen with their
use.[8,9] Nowadays, different types of stents are used
Address for correspondence: Dr. Awad Alqahtani,
Heart Hospital, Hamad Medical Corporation, P. O. Box 3050, Doha, Qatar.
E‑mail: aalqahtani7@hmc.org.qa
DES with novel coatings, dedicated bifurcation stents,
self‑expanding stents, and biodegradable stents.
Coronary SF was first reported in 2002 after a BMS
implantation in a venous bypass graft.[10] The first case of
coronary DES fracture appeared in 2004,[11] after which
several cases of SFs were reported.
INCIDENCE
The reported incidence of SF varies widely between
different studies. These variations are related to many
different factors including definition of SF among these
studies, the methods used to detect SF, type of stent
used, and the population studied.
The majority of studies report the incidence of SF
between 1 and 8% [Table 1].[12] The incidence also varies
depending on the percentage of patients who undergo
follow‑up with the available imaging modalities with
variable sensitivity of detection of SF.
Generally speaking, the overall incidence of SF
is most likely underestimated due to different reasons
given below:
1. Patients with SF might be asymptomatic, particularly
in case of minor fractures, and therefore, if the
angiographic or any other imaging modality
follow‑up were clinically driven, then many cases
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Mohsen, et al.: Stent fracture: How frequently is it recognized?

of SF were not reported. On the other hand, the
incidence of SF is expected to be higher in studies
where repeat procedure and the use of imagining
modalities were clinically driven secondary to
selection potential bias
2. Not all SFs can be detected with conventional
angiography; therefore, many patients might be
treated as stent thrombosis or stenosis without the
detection of SF, especially if other more sensitive
diagnostic imaging modalities were not used
3. As SF might lead to stent thrombosis, several
patients might present with sudden cardiac death
before diagnosis.
Although most SFs occurred in sirolimus stents,
several cases of SF were also reported in other
types of stents, including BMS, [10,13‑16] Taxus, [17‑19]
Xience (everolimus‑eluting stent),[20] and zatrolimus.[21,22]
In a series of 530 patients (of a total 2728 patients
treated with DES) who underwent repeat angiography
during follow‑up, SF was identified in 10 patients (a

Table 1: The incidence of SF, adverse clinical outcome, and percentage of TLR in patients with SF
Study Incidence Adverse clinical outcome TLR (%)
Lee et al.,[16] 1.9% 60% ISR and 10% ST 70
Lee[17] 1.5% 53.3% ISR 53.3
Ino et al.,[9] 4.9% 33% ISR 28
Chung[30] 0.84% 65% ISR 30
Aoki et al.,[24] 3.1% 37.5% ISR 50
Umeda et al.,[25] 7.7% 15.2% ISR 9
Park et al.,[48] 0.89% for SES 41.7% 33.3
0.09% PES
Chakravarty et al.,[39] meta‑analysis of eight studies Mean incidence 4% 38% 17
TLR: Target lesion revascularization; SES: Serolimus-eluting stent; PES: paclitaxel-eluting stents; ISR: Instent restenosis

b
Figure 1: Shows (a) types of stent fracture,(b) classification of calcification. Nakazawa G, Finn AV, Vorpahl M, Ladich E, Kutys R,
Balazs I, Kolodgie FD, Virmani R. Incidence and predictors of drugeluting stent fracture in human coronary artery a pathologic
analysis. J Am Coll Cardiol. 2009 Nov 17;54(21):1924-31. PubMed PMID: 19909872. (Figure added with permission from author)

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Mohsen, et al.: Stent fracture: How frequently is it recognized?

prevalence of 1.9%). All occurred with sirolimus‑eluting
stents.[23]
Aoki et al., reported an incidence of SF of 2.6%
when they studied 256 patients who underwent
angioplasty with SES.[24]
Umeda et al., studied 422 patients treated with
Cypher stents and found a 7.7% incidence of SF during
follow‑up.[25]
In an autopsy study, the incidence of SF was 29%,
which is much higher than clinically reported. A high
rate of adverse pathologic findings was observed
in lesions with grade V SF, whereas fracture with
grade I–IV did not have a significant impact on the
pathological outcome [Figure 1].[26] Autopsy studies
could be expected to have a higher incidence of SF
compared to living patients as the studied population
might have had a higher incidence of stent thrombosis
and restenosis in which SF might be the cause, leading
to a higher reported incidence of SF.
DEFINITION AND CLASSIFICATION
The definition of SF varies from study to study and various
morphologic classification schemes have been used.
Some studies discriminate between isolated strut fractures
and SF.[27] Some include both complete and partial types
of fractures,[28] while others only include severe fractures
with complete separation of stent segments [Table 2,
Figure 1].[1,24]
PREDICTORS OF SF
Stents are more likely to fracture in the presence of the
following factors:
1. Technical factors:
• Balloon or stent overexpansion, as it may
theoretically weaken the stent struts[32]
• Stent overlap, which results in localized rigidity
creating hinge points that deform the stent
leading to fracture[33]
• Stent length: Longer stents may be subjected
to higher radial forces[32]
• Inappropriate handling of stent[34]
• Stenting technique: An example of stenting
technique that might cause SF is crush
technique. A case has been reported of stent
strut fracture in a bifurcation lesion treated with
crush stenting, resulting in restenosis.[35]
2. Stent type and stent conformability:
Stent conformability is defined as the degree to
which a stent can bend around its longitudinal axis
after deployment.[36] Decreased stent conformability
can lead to longitudinal straightening of the vessel
after stent deployment, which subjects the stent
to the countervailing force of the vessel wall. This
tends to revert the vessel axis to its original shape,
leading to SF.[36]
Most cases of SF were reported with the use of
sirolimus‑eluting stent (SES). Several theories have
been proposed to explain this association.
The first was attributed to the design of the SES,
with its rigid, closed‑cell structure that results in greater
straightening of the vessel, which subjects the stent to
greater forces during the cardiac cycle.[1] Secondly, it is
easier to detect SF in SES as it is a more radio‑opaque
structure.[37] On the other hand, Taxus and BMS have
greater neointimal coverage, which could mask the
fractured struts, as well as it may strengthen and
stabilize the struts to withstand mechanical forces.[38]
Despite the higher incidence of SF in SES, it does
not necessarily translate into a clinically significant
difference, as it has been shown by different studies that

Table 2: Classification of SF according to different studies

Lee et al.,[23] Minor: Single‑strut fracture
Shaikh et al.,[1] Moderate: Fracture >1 strut
Kim et al.,[29] Major: Complete separation of stent segments
Umeda et al.,[25] Complete fracture: Complete separation of stent segments
Partial fracture: Single or multiple stent strut fracture
Chung et al.,[30] Disruption: Inner and outer stent struts separated without displacement; linear or curvilinear alignment of
stent maintained
Avulsion: Outer struts separated; connection of inner struts maintained
Displacement: Proximal and distal pats of fractured stents completely separated; linear or curvilinear of
the stent lost
Lee et al.,[31] Avulsion: Fractured stent segments separated completely (fluoroscopy) or stent struts absent from stent
fracture site (IVUS)
Partial: Stent struts absent in ≥⅓ of the vessel wall on IVUS
Collapse: Folded and compacted inner and outer walls of the stent found in a bended segment with ≥45°
on fluoroscopy
Nakazawa et al.,[26] Type 1: Single‑strut fracture
[Figure 1] Type 2: ≥2 strut fractures without deformation
Type 3: ≥2 strut fractures with deformation
Type 4: Multiple strut fracture with acquired transection but without gap
Type 5: Multiple strut fractures with acquired transection with gap in the stent body
SF: Stent fracture; IVUS: Intravascular ultrasound

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Mohsen, et al.: Stent fracture: How frequently is it recognized?
Table 3: Incidence of SF in different coronary arteries
Vessel stent location Incidence of SF (%)
RCA
LAD
Circumflex
Saphenous vein grafts
LM
SF: Stent fracture; RCA: Right coronary artery; LM: left main; LAD: Left anterior
descending
SES are associated with lower rates of stent restenosis
and late luminal loss compared to paclitaxel‑eluting
stents (PES).[36,39‑41]
3. Anatomic and pathologic factors which include the
following:
• Tortuous and highly angulated vessel[37]
• Long lesions
• C  hange in vessel angulation after stent
implantation, which can create a significant
distortion force[25]
• C  omplex lesions: In the ACROSS/TOSCA 4
study, SF was more frequent in the complex
lesion subset of chronic total occlusion.[42]
• S  tent location: [Table 3] SF is more common
in right coronary artery (RCA) and saphenous
graft locations as these vessels are dynamic
during cardiac contractions. Stents in these
locations may be subjected to repetitive
distorting forces, as some segments of these
vessels have more flexion points during the
cardiac cycle.[1,11] Repetitive cardiac contraction
exposes the stent to compression, torsion,
kinking, elongation, bending, and shear
stress, [11,43] which can cause fracture from
mechanical fatigue.[44] The points of SFs are
usually located at hinges[24] subjected to either
medial or shear forces created by non‑uniform
vessel anatomy.
Table 2 shows the incidence of SF according
to the vessel stent location in a meta‑analysis
of eight studies with 108 SFs in 5321 patients,
where the incidence of SF in RCA was the
highest while left main (LM) stents were less
likely to fracture.[39]
4. Other possible causes:
There are other possible causes that may lead
to SF. Sanchez et al., [45] reported a case of
biventricular pacing leading to LAD coronary
SF where the chief risk for SF was the vascular
angulation; however, this risk was increased by
abnormal myocardial contraction patterns that
were induced by the ventricular pacing. Hoshi
et al., reported a case of fatal ostial right coronary
artery SF, aneurysm formation, and coronary artery
perforation caused by mechanical stress between
the sternum and dilated aortic root.[46] SF was also
75
reported following stenting of myocardial bridge.[47]
In one study, chronic kidney disease was found as
56.4 an independent predictor of DES fracture.[48]
30.4 It is important to mention that clinical characteristics
10.9 such as CAD risk factors and previous MI or CABG do
1.7 not determine the risk of SF.[39]
<0.01
CLINICAL PRESENTATION AND
OUTCOME
In spite of its low reported incidence, SF represents
an important clinical entity as it may present with serious
clinical sequelae [Table 3].
It is important to mention that not all SFs are
associated with clinical sequelae as it can be an
incidental finding in asymptomatic patients, particularly
with mild forms of SF (isolated strut fractures).
SF can present as recurrent angina, MI,[49,50] and
even sudden death.[51] So, it is possible that some cases
of sudden cardiac death in patients with previous stent
implantation might be secondary to SF, leading to stent
thrombosis.
Usually severe forms of SF have more adverse
clinical outcomes, as reported by Nakazawa et al.,[26]
The most likely explanation for the development of
in‑stent restenosis in case of SF is the poor distribution
or interruption of drug delivery as a result of strut
fracture, which will suppress the inhibition of neointimal
formation, leading to neointimal overgrowth and
stenosis.[48]
In a study by Lee et al.,[23] 530 patients with DES
underwent repeat angiography. SF was identified in
10 patients. None of these fractures were detectable at
the time of stent placement. The median time interval
from stent implantation to detection of fracture at repeat
angiography was 226 days (ranging from 7 to 620 days).
Six patients had binary restenosis and one patient had
stent thrombosis, all necessitating repeat intervention.
On routine follow‑up coronary angiography
6-9 months after SES implantation, Ino et al.,[28] reported
33% in‑stent binary restenosis, 28% target lesion
revascularization (TLR), and 0% stent thrombosis rates
in SF lesions. All patients with SF had an additional
follow‑up for 24 months, but no major adverse coronary
events were observed.
In a literature review by Chhatriwalla et al.,[52] a total
of 289 SFs, with available information about patient
presentation, were found. 10.4% of cases presented
with ST segment elevation myocardial infarction [STEMI]
or stent thrombosis and 26.3% presented with Non ST
segment elevation myocardial infarction [NSTEMI] or
Unstable angina [UA]. The review also highlighted the
difference in clinical presentation between patients
with DES fracture and patients with BMS fractures,
and it was noticed that STEMI occurred more often in
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Mohsen, et al.: Stent fracture: How frequently is it recognized?
patients in the first group, indicating that the latter has
more benign presentation. This might be explained by
the thicker neointimal layer that develops around the
BMS, which limits the contact of stent material with the
arterial lumen inhibiting thrombus formation. In case of
DES, because of the absence of this thick neointimal
layer, fractures allow the stent’s metal structure to come
into contact with the vessel lumen, leading to thrombus
formation.
Several studies showed that SFs, particularly
severe forms, were associated with high rate of TLRs
[Table 3].[23,27]
In a study by Park et al.,[48] the clinical presentation
of patients with SF did not differ from those without
SF, including the severity of angina, the incidence
of Acute coronary syndrome [ACS], and event silent
ischemia. Despite that, it is important to mention that
in this study, 50% of SFs were of type 1, and overall,
types 1, 2, and 3 represented 96.1% of all cases,
while type 4 represented only 3.9% and there were no
type 5 fractures. It is expected that the majority of these
patients will have similar outcomes compared to patients
without fracture, as the adverse clinical outcome in SF
is associated with severe forms. It is worth mentioning
that the rate of binary stenosis, as well as target lesion
revascularization, was significantly higher in the SF
group compared to the control group (41.7% vs. 11.4%
and 33.3% vs. 8.1%, respectively).
It is also important to recognize that while the
probability of ISR and TLR is increased in patients with
SF, the opposite is also true. That is to say the probability
of SFs is increased in patients with ISR and in patients
requiring TLR.[39]
It is worth mentioning that the time of occurrence of
SF, the time between SF and the development of stent
stenosis or thrombosis, and the occurrence of symptoms
are still not well recognized. Some patients presented
as early as 3 days after stent implantation (Xience)[20]
and others presented after several years.[53,54]
In the study by Lee et al., mentioned previously, the
median time interval from stent implantation to detection
of fracture at repeat angiography was 226 days (ranging
from 7 to 620 days).[23]
An interesting finding in a study by Ino et al.,[55] is
that late stenosis was not observed in SF sites without
early restenosis during the midterm follow‑up after SES
implantation.
SF AND CORONARY ANEURYSM
There are several reported cases of coronary
artery aneurysms associated with DES SF. [56,57]
Previous reports suggested several potential causes
for aneurysmal formation:[11,58‑60]
1. The use of oversized balloon and high‑pressure
balloon dilatation, which result in intima media tearing
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2. SF which may also tear the arterial wall
3. The drug and/or polymer of the DES might cause
some sort of inflammation or hypersensitivity reaction
causing adventitial inflammation, weakening of the
media, excessive dilatation and, consequently,
aneurysmal formation and marked malapposition of
the stent.[59] The FDA reports and autopsy findings
suggest that DES may be a cause of systemic and
intrastent hypersensitivity reactions that, in some
cases, have been associated with late thrombosis
and death.[60]
Jindal et al.,[61] reported a case of giant coronary
aneurysm after Cypher implantation in a patient
who presented with fever of unknown origin.
Histopathology revealed a predominantly
lymphocytic and eosinophilic infiltrate with an
absence of giant cells, suggesting that local
hypersensitivity reactions caused the aneurysm.
4. It was also suggested that the coating drug of
DES might inhibit the process of healing, leading
to aneurysmal dilatation. Kim et al., reported a
case of simultaneous occurrence of coronary
aneurysm at both the DES‑implanted sites without
high‑pressure ballooning, which suggests that an
aneurysmal dilatation may have preceded SF,
rather than the fracture of the stent leading to
aneurysmal formation. Kim et al., attributed the
unique property of the DES as the potential cause
of coronary aneurysm.[58]
T here might also be association between SF,
pseudoaneurysm, and infection. Kelvin S. H. Loke[62]
reported a case of pseudoaneurysm and coronary
abscess secondary to coronary SF identified with
Tc‑99m hexamethylpropyleneamine oxime‑labeled
white blood cell SPECT/CT scintigraphy.
W. Kyle Stribling reported a case of giant
aortocoronary saphenous vein graft
pseudoaneurysm caused by SF in an 80‑year‑old
patient who presented with fever and was found to
have positive blood culture for methicillin‑sensitive
Staphylococcus aureus.[63]
In an intravascular ultrasound (IVUS) study which
was done to identify SF as a cause of stent failure,
17 patients were evaluated by IVUS where 20
SFs were found. Five SFs occurred in a coronary
aneurysm (accompanied by malapposition in
three patients) despite the absence of aneurysm
at index stenting. Comparing the SFs associated
with aneurysm (5/20) with those that occurred
without association with aneurysm (15/20),
complete SF was more frequent (100% vs. 27%).
All fractures were after Cypher stent implantation
and all presented more than 1 year after index
stenting.[38]
To the best of our knowledge, there are no cases
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Mohsen, et al.: Stent fracture: How frequently is it recognized?
of Taxus SF associated with coronary aneurysm,
despite several reports of cases of acquired
coronary aneurysm after Taxus implantation.[61‑66]
It is worth mentioning that it is possible that the
association between coronary aneurysm and SF
is a reciprocal one. In other words, as SF might
cause aneurysm, aneurysmal formation and
malapposition might precede SF. This would lead
to excessive motion of the stent, leading to SF.[38]
DIAGNOSTIC MODALITIES
Conventional fluoroscopy
Stent visibility is limited on conventional fluoroscopy.
There are several factors that contribute to stent
visibility, including the patient’s build, a stent platform,
and stent thickness.[34] Earlier generation stainless steel
stents are more visible than the newer cobalt‑chromium
stents (such as Xience), as the first have a strut thickness
of 0.0055 inches compared to the latter that have a strut
thickness 0.0032 inches.[34]
IVUS
In several studies, IVUS was used to confirm the
diagnosis of SF that was suggested by angiography.
In other studies, IVUS detected several cases of SF
that were missed by angiography. So, the use of IVUS
increased the rate of SF detection in multiple studies.
Yamada et al., [67] in a prospective study of 102
Cypher stents with 100% angiographic and IVUS
follow‑up, observed three SFs (3%), all detected with
IVUS but not observed on angiography.
Another advantage of IVUS over conventional
angiogram is the ability of IVUS to identify mechanisms
of stent failure by providing information regarding
neointima formation, vessel remodeling, perivascular
tissue, stent expansion, stent strut distribution, and
malapposition.[38] A limitation of IVUS is that the resolution
is only approximately 150 micrometer and the echoes
frequently cause artifacts.[38]
Another limitation of IVUS is the occasional
difficulty in passing the IVUS across the lesion when
there is SF, especially with stent displacement.
Stent boost
This technology has improved the visibility of stent
struts.[68] It involves the automated detection of proximal
and distal markers of balloon catheters in each cine
frame. [69] This automated marker detection is done
through the identification of blob‑like structures.[70] This
technology can be also used to position a stent precisely
over a previously stented segment.[34] Another advantage
of stent boost over IVUS is that it does not add to the
procedural costs. A limitation of stent boost technology is
that a balloon catheter needs to be placed in the vicinity of
77
Figure 2: A Fractured right coronary stent by MDCT. The
RCA stents became two pieces. Li P, Gai L. Coronary stent
fracture detected by multidetector computed tomography. Int J
Cardiovasc Imaging. 2010 Oct;26(7):729-30. Epub 2010 Mar
28. PubMed PMID: 20349340 (Figure added with permission
from author)
a stent or stented segment in order to acquire images.[34]
Multi‑detector computed tomography (MDCT)
Several cases of SF detected by MDCT have been
reported [Figure 2].[71‑73] In a retrospective study, 18 SFs
were detected by MDCT in 371 patients with 545
stents. Six SFs were not detected by initial conventional
angiograms in this study.[74] Pang et al.,[75] evaluated
the ability of 64‑slice computed tomography (CT),
conventional cine‑angiography, and IVUS to detect
SFs under ideal conditions. They concluded that under
ideal in vitro conditions, CT has a high accuracy when
used to evaluate coronary SFs. The overall accuracy,
sensitivity, and specificity of detecting SFs are lower
with conventional cine‑angiography. SFs were not
detected using IVUS in this study, which was attributed
to the limitations of acoustic window inherent to in vitro
procedures and the longitudinal orientation of the
fractures.
Hecht et al., [76] evaluated stent gaps in 292
consecutive patients with 613 stents. Correlations with
catheter coronary angiography (CCA) were available
in 143 patients with 384 stents. The authors concluded
that stent gap by CT angiography [CTA] is associated
with 28% of ISR, and ISR is found in 46% of stent gaps.
They also noted that stent gap is infrequently seen on
catheter angiography, and most likely represents SF in
the setting of a single stent and may represent SF or
overlap failure in overlapping stents.
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Mohsen, et al.: Stent fracture: How frequently is it recognized?

c h

f
a
d i

b e g j
Figure 3: An Exactly Matching Set among Angiography, Fluoroscopy, and OCT A nonfractured stent shows (a) no restenosis in
angiography, (b) no distorted stent in fluoroscopy, (c) preserved coronary lumen (white circle), and (d) well-covered stent struts
(yellow circle) in optical coherence tomography (OCT). (c–e) Neointima grows evenly. A fractured stent shows (f) focal restenosis in
angiography, (g) distorted and fractured stent in fluoroscopy, and (i) excessive neointimal hyperplasia with absence of stent struts
(white line) at fractured site in OCT. (h, j)

Optical coherence tomography (OCT)
This imaging modality can also be used to detect
SF [Figure 3]. In a study by Kashiwagi et al.,[77] it was
found that the absence of stent strut was the most
common morphological feature of SF in OCT. It was
also noticed that both the mean and maximal neointimal
area were larger in the SF group and the distribution of
neointimal area showed a peak at the fracture site in
the fractured stent group.
The advantage of OCT over IVUS is that it has
better resolution (10 times the resolution of IVUS) and
fewer artifacts.[38]
MANAGEMENT
There is no consensus about the ideal management
of SFs. The decision should depend on the type of
fracture, presence of ischemia, and the presence of
factors that predict possible recurrence. If the reason
of SF was stent overexpansion, then restenting
the lesion again is possible with avoidance of stent
overexpansion. On the other hand, when SF is caused by
a non‑modifiable factor like excessive vessel tortuosity,
then referring the patient for CABG is more reasonable
when there is a clear need for revascularization.
Khanna et al., reported a case of acute STEMI
6 years after implantation of a sirolimus‑eluting stent,
secondary to complete SF, which was treated with
CABG because of the expected recurrence of SF.[53]
In a study by Lee, [17] 1009 patients with DES
underwent a follow‑up coronary angiography irrespective
of symptoms. Seventeen SFs were detected in
15 patients (1.5%). All SF patients were continued
on medication with combination antiplatelet therapy,
regardless of angina symptoms. If in‑stent restenosis at the
fractured site was significant, coronary interventions were
performed even in patients without ischemic symptoms.
Some patients were treated with heterogeneous DES
for restenosis lesions (5/8 patients) and the rest were
treated with either homogenous DES (2 patients), or
plain balloon angioplasty (1 patient) or medical treatment
only (7 patients). The authors concluded that if patients
with SF were continued on combination antiplatelet

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Mohsen, et al.: Stent fracture: How frequently is it recognized?
therapy irrespective of ischemic symptoms, there would
be a low rate of major adverse cardiac events, especially
cardiac death associated with SF. In case of SES fracture,
we are not sure whether restenting with other types of
stents – like BMS or other type of DES – might prevent
or decrease recurrence of SF, as the higher incidence of
SF in SES might be due to higher visibility of SES, rather
than the design of the stent. However, some cases of
SES fractures have been treated with reimplantation of
BMS.[54] In one study, among 24 patients with fractured
stents, 8 patients required TLR, where 3 patients were
treated with balloon angioplasty only, 3 with PES, and 2
with zotarolimus‑eluting stent (ZES).[48]
An important tip in the management of SF by
restenting, when there is difficulty in passing the wire or
balloon across the lesion, is to use stent boost guidance
to manipulate the wire and balloon across the lesion.[34]
CONCLUSION
SF represents an important clinical entity which
is most likely underestimated. Clinical presentation
ranges from an incidental finding in an asymptomatic
patient to a presentation of recurrent angina, MI, and
even sudden death. Factors such as right coronary
artery and saphenous graft stenting, lesion angulations,
long stents, and the use of DES are all associated with
increased prevalence of SF.
There is no consensus on the best diagnostic
imaging modality for detection of SFs, but it is well
recognized that conventional angiography is not
sufficiently sensitive for this purpose. Multiple imaging
modalities can be used, including IVUS, stent boost,
MDCT, and OCT.
Management of SF should be individualized
depending on the presence of ischemic signs and
symptoms, the presence of predictors of recurrence, the
type of stent and the type of fracture, and the available
techniques. Further studies with frequent clinical
follow‑up and using different imaging modalities are
needed for a better understanding of this entity.
In the future, with better understanding of this
condition, we might be able to create a scoring index
depending on the presence of the predictors mentioned,
in order to estimate the risk of SF before stenting or
restenting. In addition, understanding this entity will
also influence the future of stent design, intended to
minimize the risk of SF in the future.
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Source of Support: Nil, Conflict of Interest: None declared.

Al-Aqsa Mosque, Jerusalem,

Palestine
Al-Aqsa Mosque is the second oldest
mosque in Islam after the Ka'ba in Mecca,
and is third in holiness and importance after
the mosques in Mecca and Medina.
Its name in Arabic is Al-Masjid El-Aqsa,
meaning Tha Farthest Mosque.
The rectangular Al-Aqsa Mosque is 144,000
square meters, 35 acres, or 1/6 of the entire
area within the walls of the Old City of
Jerusalem as it stands today. It is also called
Al-Haram El-Sharif (the Nobel Sanctuary).
Al-Aqsa Mosque holds up to 400,000
worshippers at one time.
Al – Aqsa Mosque was originally built nearly
1300 years ago by Muslim Caliph Al-Walid the son of AbdulMalek bin Marwan in 709 AD.
Throughout its history, Al-Aqsa was subject to successive restoration work due to damages caused by earthquakes,
etc. The outer dome was covered with Lead in 1985 replacing the Aluminum dome of 1964, in order to restore
it to its original cover. The inner dome, decorated with stucco work, dates back to the 13th century.
Source: http://www.atlastours.net/holyland/al_aqsa_mosque
Submitted by: Dr. Mohamed K. Mohsen
Heart Hospital, Doha, Qatar

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