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Chapter 14
https://t.me/med1917
The Impact of Thrombus as a Cause and
as a Result of Complicated Percutaneous
Coronary Intervention
Judit Karacsonyi
1
VA North Texas Health Care System and UT Southwestern Medical Center, Dallas, TX, United States;2University of Szeged, Szeged, Hungary;
3
Minneapolis Heart Institute, Minneapolis, MN, United States;4Cedars Sinai Heart Institute, Los Angeles, CA, United States
1,2
, Timothy He nry
3,4
, Imre Ungi2, Subhash Banerjee1and Emmanouil S. Brilakis
1,3
INTRODUCTION
Intracoronary thrombus can be challenging to treat and increases the risk of percutaneous coronary intervention (PCI).
Coronary thrombus may cause ischemia leading to PCI (primary thrombus), but can also sometimes be the result of PCI
(secondary thrombus), formed initially in the sheath and delivered through the guide catheter into the coronary artery or
formed on coronary guidewires or device s. Moreover, intracoronary thrombus can form at areas of dissection or in the
setting of other periprocedural complications resulting in slow or no flow. We present a practical approach to the
management of primary and secondary coronary thrombotic lesions.
THROMBUS AS THE CAUSE OF COMPLICATIONS
Intracoronary thrombus is an important cause of acute coronary syndromes, both with and without ST-segment elevation.
Management of thrombotic lesions can be hindered by difficulty in wiring through a thrombotic occlusion, challenges in
restoring antegrade flow, and distal embolization.
Wiring Through the Thrombotic Occlusion: Risk of Perforation
Similar to wiring through chronically occluded vessels, wiring through an acutely formed thrombotic complete occlusion
can be challenging, in part because the distal vessel may be poorly or not at all visible, since collaterals may not have had
enough time to form. Moreover, it may be impossible to determine whether there is angulation within the occluded
segment or whether the guidewire has entered into side branches. In the case of guidewire exit from the vessel, subsequent
advancement of a balloon can result in perforation, further complicating an already high-risk clinical presentation.
To minimize the risk for perforation, initial wiring through an acute complete thrombotic occlusion is usually attempted
with soft workhorse guidewires. Occasionally advancement of the guidewire alone will result in restoration of some
antegrade flow that could facilitate subsequent wiring attempts and management of intracoronary thrombus. If a soft
guidewire fails to advance through the occlusion, then a soft, polymer-jacketed guidewire, such as the Whisper (Abbott
Vascular, Santa Clara, CA, USA) or Fielder FC (Asahi Intecc, Nagoya, Japan), is a common next choice. Escalation to
stiffer polymer-jacketed guidewires (such as the Pilot 200) should be avoided, if possible, as it increases the risk for
perforation, but may be needed in some challenging lesions. Guidewire advancement over a microcatheter or a low profile
balloon (1.0 x 20 mm or1.2 20 mm) can also be useful for crossing by increasing support and allowing guidewire
exchanges without losing wire position. Occasionally, advancing a knuckled guidewire may help advance through areas of
tortuosity with low (although not zero) risk of perforation, but may require strong guide catheter support, that can
sometimes be achieved by using a guide catheter extension.
Cardiovascular Thrombus. https://doi.org/10.1016/B978-0-12-812615-8.00014-4
Copyright © 2018 Elsevier Inc. All rights reserved.
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If the location of the guidewire tip is uncertain after advancing it through an occlusion, it may be best not to advance a
balloon but attempt to clarify the wire position first. If there is absolutely no antegrade flow after wiring, obtaining a second
arterial access and performing contralateral injection may help clarify the wire position. Alternatively, one could inject
contrast through an over-the-wire balloon or microcatheter. The use of intravascular ultrasound can often aid in confirming
intraluminal placement of the guidewire. Careful “dottering” of the thrombotic lesion with a low-profile short balloon may
also be performed; however, it is not a reliable strategy to confirm true lumen guidewire position.
Sometimes, wiring may fail because the lesion being crossed is not the culprit lesion for the acute event (it may be a
chronic total occlusion). Alternatively, some patients may have more than one culprit lesion. Repeat review of the
angiogram (and of prior angiograms if available) and correlation of the electrocardiographic and angiographic findings may
be helpful in such cases. Intravascular imaging (especially with optical coherence tomography, which is the best imaging
modality for detecting intracoronary thrombus) can be especially helpful in cases with unclear or multiple potential culprit
lesions, as the presence of a thrombus within a lesion strongly suggests it is a culprit (Fig. 14.1).
In the case of wire perforation during attempts to cross a thrombotic lesion, the first step is to inflate a balloon proximal
to the perforation site to stop bleeding into the pericardium and minimize the risk for tamponade. Anticoagulation should
not be reversed, as it may lead to additional thrombus formation given the presence of intracoronary equipment. Prolonged
balloon inflation may sometimes lead to hemostasis. If not, large-vessel perforations are usually treated by implanting a
covered stent over the perforation site, whereas distal perforations are treated with embolization (most commonly with
autologous fat or with a coil) [1]. This is best achieved by using the “block and deliver” technique [2,3], during which
balloon inflation is maintained for as long as possible during attempts to achieve hemostasis. If a large (8 Fr) guide catheter
is being used, balloon inflation and delivery of a covered stent or fat/coil can be achieved in most cases through the same
guide catheter. If a smaller guide catheter is being used, a second guide catheter may be needed to allow delivery of a
covered stent or coils (“ping-pong” guide technique) [4].
Restoring Antegrade Flow (Fig. 14.2)
Sometimes guidewire crossing alone restores some antegrade flow. If not, inflation of a small balloon (usually 2 mm in
diameter) at low pressure (6e8 atm) may rest ore at least partial antegrade flow and allow planning of subsequent treatment
steps.
Failure to restore antegrade flow after ballooning could be due to large residual thrombus, severe distal vessel disease,
or failure to cross into the distal vessel segment with the wire. If large thrombus burden is suspected, aspiration thrombectomy or laser may be beneficial. If wiring into a small branch is suspected, it may be best to leave the original wire in
place and attempt wiring with another wire, followed by balloon angioplasty. Wire perforation may have occurred if wiring
is very challenging.
Potent antithrombotic medication administration (both antithrombin and antiplatelet) is critical for treating thrombotic lesions, to minimize the risk fo r thrombus expansion or new thrombus formation. Antiplatelet treatment may be
best achieved with more potent and rapidly acting oral P2Y12 inhibitors (such as prasugrel and ticagrelor) in combination w ith an intravenous antiplatelet agent, such a glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitor or cangrelor. Anticoagulation is most commonly achieved with unfractionated heparin. If the patient has received pretreatment with a
P2Y12 inhibitor, bivalirudin could also be used. If GP IIb/IIIa receptor antagonists are being used, heparin is given at a
dose of 50e70 U/kg intravenous bolus to achieve an activated clotting time (ACT) of 200e250 s. When no GP IIb/IIIa
receptor antagonis ts are being used, a 7 0e 100 U/kg bolus of unfractionated heparin is recommended with an ACT goal
of 250e300 s [5].
If antegrade flow is restored yet a large thrombus remains, one treatment option is to defer further intervention by
allowing 24e48 h of intense antithrombotic therapy (including aspirin, P2Y12 inhibitor, intravenous platelet inhibitor, and
antithrombin therapy). Subsequent angiography frequently shows reduced thrombus burden, allowing balloon angioplasty
and stenting with significantly lower risk for distal embolization and no reflow [6,7]. Echavarría-Pinto et al. showed
significant reduction in thrombus burden with intensive antithrombotic therapy (consisting of GP IIb/IIIa inhibitors,
enoxaparin, aspirin, and clopidogrel) and lower incidence of distal embolization among 89 patients [6]. In some cases an
excellent angiographic result may be obtained after thrombus aspiration alone; in such cases observation without stent
implantation has been advocated. Escaned et al. reported outcomes on 28 ST-segment elevation myocardial infarction
(STEMI) patients in whom thrombus aspiration resulted in: (1) restoration of thrombolysis in myocardial infarction (TIMI)
flow grade 3; (2) residual TIMI thrombus grade 3; (3) absence of a residual significant stenosis; and (4) absence of
significant distal thrombus embolization. Despite stenting not being performed, the culprit vessel was patent when repeat
angiography was performed after 6 2 days [8].
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FIGURE 14.1 Optical coherence tomography for identifying the culprit lesion in a patient with acute myocardial infarction. A patient presented
with anterior ST-segment elevation acute myocardial infarction. Diagnostic angiography revealed (A) a severe proximal left anterior descending artery
(LAD) lesion (yellow arrow) and (B) moderate lesions on the LAD and left circumflex (Cx) coronary arteries. (C) After stenting of the LAD lesion the
ST-segment elevation continued, as did the patient’s angina despite antegrade TIMI 3 flow. (D) After repeat angiographic review, an intermediate Cx
lesion was detected (yellow arrow). (E) Optical coherence tomography revealed a thrombus within the mid-Cx lesion, suggesting it was an active culprit
lesion. (F) After successful stent deployment in the Cx lesion, the ST-segment elevation and the patient’s angina resolved. TIMI, thrombolysis in
myocardial infarction.
In lesions with large thrombus, if a decision is made to proceed with PCI because of ongoing symptoms or high-risk
plaque features, consideration should be given to thrombectomy before further balloon angioplasty and stenting. Although
thrombectomy in this setting is logical in selected cases, routine use is not supported by randomized controlled trial data, as
discussed in detail under Thrombectomy for Primary Percutaneous Coronary Intervention: Clinical Trials and Guidelines.
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FIGURE 14.2 Overview of the management of the thrombotic coronary lesion. The two mainstays of treatment are preventing thrombus propagation
and restoring coronary flow.
If thrombectomy is chosen, it is usually performed with an aspiration thrombectomy catheter (such as the Export,
Pronto, etc.). Larger (such as 7 Fr) aspiration thrombectomy catheters are more effective than smaller ones (such as 6 Fr).
Delivery of the aspiration catheter can be difficult but can be facilitated by inserting a 0.035-in. guidewire into the
aspiration lumen (“armored aspiration catheter”) [9]. Alternatively, especially for large thrombi, thrombectomy can be
performed by using a guide catheter extension and aspirating through the manifold [10]. However, use of a guide catheter
extension, such as the GuideLiner catheter (Vascula r Solutions, Minneapolis, MN, USA) and the Guidezilla (Boston
Scientific, Natick, MA, USA), carries increased risk for complications, such as distal dissection, air embolization, and stent
deformation during delivery attempts.
To minimize the risk of embolization (both distally and in the aorta) suction should be maintained until the thrombectomy catheter is removed from the guide catheter, followed by aspiration of the guide catheter. This minimizes the risk
of thrombi remaining within the guide catheter and being reinjected into the coronary artery or into the aorta. Occasionally
there is limited blood return from the aspiration catheter, which may be due to a large thrombus obstructing the tip of the
catheter [11] (Fig. 14.3).
Multiple runs of aspiration thrombectomy may be needed in cases with large thrombus burden. The over-the-wire
lumen of the aspiration catheter could then be used to administer vasodilators or antiplatelet agents directly within the
thrombotic coronary artery [11].
Excimer laser coronary atherectomy (ELCA) is another option for reducing the size of coronary thrombus. ELCA can
be performed in addition to or instead of aspiration thrombectomy, although the 5-min warmup time of the current system
is a limitation when urgent treatment is needed, such as in patients with STEMI. ELCA induces shock waves that can
separate thrombi from the vessel wall, potentially facilitating adjunctive thrombectomy [12]. As a result of the laser,
explosive gas bubbles can form within the hemoglobin, potentially serving to dissolve the clot by forming acoustic waves
in the thrombus structure [13,14]. Laser has an inhibitory effect on platelet aggregation, as a result of the interaction
between the 308-nm ultraviolet beam and the platelets, a phenomenon that has been called the “stunned platelet phenomenon” [15]. The 0.9-mm laser catheter (Spectranetics, Colorado Springs, CO, USA) is most commonly used in native
coronary arteries, with the larger size catheters reserved for treating saphenous vein grafts or very large native coronary
arteries. The LaserAMI (Laser Angioplasty in AMI [acute myocardial infarction]) trial randomized 27 STEMI patients to
ELCA and adjunct PCI with stent implantation versus PCI with stent implantation. The two study groups had similar
improvement in myocardial blush and final corrected TIMI frame count; however, the corrected TIMI frame count gain
was higher in the laser group [16].
Another method for restoring flow in the presence of large thrombus is stenting over the thrombus, effectively
“trapping” the thrombus behind the stent struts. However, stenting can still cause distal embolization, in part due to a
“cheese grater” effect of the stent struts. Moreover, thrombus can lead to stent undersizing and malapposition.
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FIGURE 14.3 Thrombus (black arrow) attached to the end of the aspiration catheter. There is poor blood return in the aspiration syringe.
Reproduced with permission from Stys A, Stys T, Khan M, Rajpurohit N. What to do when your aspiration thrombectomy catheter gets overwhelmed. Cath
Lab Digest March 2015;23(3):54e5. Copyright HMP Communications.
Preventing Embolization
Treating coronary lesions with large thrombus may lead to embolization, distally or sometimes even proximally. For
example, during attempts to remove a thrombus, it may embolize into a more proximal coronary branch or into the aorta,
causing systemic embolism, such as stroke.
Thrombus removal before balloon angioplasty and stenting can help decrease the risk for distal embolization. Another
approach is to use an embolic protection device, either a balloon occlusion device, such as the GuardWire (Medtronic,
Minneapolis, MN, USA), or a filter. However, insertion of the embolic protection device may by itself lead to embolization, and routine use of an embolic protection device in primary PCI was not associated with improved clinical outcomes
in the EMERALD (Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris) [17] and PRIDE
(Protection During Saphenous Vein Graft Intervention to Prevent Distal Embolization) [18] trials. An innovative technique
for distal protection (called “forward and backward” aspiration) involves ne gative aspiration through a deep-seated
GuideLiner catheter during balloon angioplasty and stenting. This technique was associated with no distal embolization
and no reflow among 30 patients with intracoronary thrombus undergoing primary PCI in one study [19].
If a large thrombus is located close to an important bifurcation with large branches, protecting both branches with wires
may help prevent branch occlusion and facilitate treatment if those branches become obstructed by thrombus. If distal
embolization occurs, aspiration thrombectomy may help remove some of the embolized thrombi and restore antegrade
flow. Moreover, administration of vasodilators (such as adenosine [20], nicardipine [21], nitroprusside [22], and verapamil
[23]) may help improve antegrade flow, which in turn may reduce the risk for additional thrombus formation.
Thrombectomy for Primary Percutaneous Coronary Intervention: Clinical Trials
and Guidelines
Rheolytic thrombectomy is not recommended in STEMI patients because of a higher incidence of major adverse cardiac
events in the AIMI (AngioJet Rheolytic Thrombectomy in Patients Undergoing Primary Angioplasty for Acute Myocardial
Infarction) trial; in this trial the 30-day major adverse cardiac event rate was higher in the rheolytic thrombectomy
compared with the PCI-alone group (6.7% vs. 1.7%, P ¼ .01), a difference primarily driven by higher mortality (4.6% with
rheolytic thrombectomy vs. 0.8% without, P ¼ .02) [24]. On the other hand, Parodi et al. found that rheolytic
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thrombectomy might be beneficial in cases with large thrombus burden, resulting in better stent apposition and lower
target-vessel revascularization rate than manual thrombus aspiration [25]. Similarly, a retrospective study showed that
rheolytic thrombectomy was associated with lower 2-year incidence of major adverse cardiac events in patients in large
thrombus burden and acute myocardial infarction complicated by cardiogenic shock [26]. Nevertheless, rheolytic
thrombectomy is currently used very infrequently for treating coronary thrombus.
Routine use of aspiration thrombectomy for primary PCI was examined in three large randomized controlled trials
(Table 14.1). The first one was the Thrombus Aspiration during Percutaneous Coronary Intervention in Acute Myocardial
Infarction Study (TAPAS), a single-center study that randomized 1071 STEMI patients to aspiration thrombectomy followed by stenting versus stenting alone. The aspiration thrombectomy group had a higher frequency of myocardial blush
grade 3 and ST-segment elevation resolution, which translated to lower 12-month incidence of cardiac death (3.6% vs.
6.7%, P ¼ .02) and cardiac death or myocardial infarction (5.6% vs. 9.9%, P ¼ .008) [27,28]. As a result of TAPAS the
rates of aspiration throm bectomy significantly increased.
The second large trial was the Thrombus Aspiration in ST- Elevation Myocardial Infarction in Scandinavia (TASTE)
trial, which enrolled 7012 patients and did not show any difference in all-cause mortality at 30 days (2.8% in the thrombus
aspiration group vs. 3.0% in PCI-only group, P ¼ .63). The neutral outcome was consistent in all patient subgroups,
regardless of baseline clinical or angiographic characteristics. Furthermore, there was no significant effect of thrombus
aspiration on any of the prespecified secondary end points (30-day rates of hospitalization for recurrent myocardial
infarction, stent thrombosis, target-vessel revascularization, target-lesion revascularization, and the composite of all-cause
TABLE 14.1 Randomized Clinical Trials Examining Aspiration Thrombectomy
Trial Author Year n Primary End Point
TOTAL [31] Jolly et al. 2015 10,732 Composite of cardiovascular
TASTE [36] Lagerqvist
TASTE [29] Frobert
INFUSE-AMI
[37]
EXPIRA [38] Sardella
TAPAS [28] Vlaar
TAPAS [27] Svilaas
et al.
et al.
Stone
et al.
et al.
et al.
et al.
2014 7,244 All-cause mortality at 30 days;
2013 7,244 All-cause mortality at 30 days 2.8% 3.0 .63
2012 452 Infarct size (percentage of
2009 175 Occurrence of myocardial
2008 1,060 Cardiac death or nonfatal
2008 1,071 Myocardial blush grade of
death, recurrent MI, cardiogenic shock, or NYHA class
IV heart failure within
180 days
secondary end point, all-cause
mortality at 1 year
total left-ventricular mass)
at 30 days assessed by
cardiac MRI
blush grade 2 and the
rate of 90-min ST-segment
resolution >70%.
reinfarction after 1 year
0 or 1 (defined as absent
or minimal myocardial
reperfusion)
Aspiration
Thrombectomy
Event Rate
6.9% 7.0 .86
5.3% 5.6 .57
Infarct size: 17% 17.3 .51
Myocardial blush
grade 2: 88%
ST-segment
resolution >70%:
64%
3.6% 6.7 .020
Myocardial blush
grade of 0 or 1
occurred in
17.1%
PCI-Only
Event Rate
(%) P
60 .001
39 .001
26.30 <.001
EXPIRA, Thrombectomy with Export Catheter in Infarct-Related Artery During Primary Percutaneous Coronary Intervention; INFUSE-AMI, Intracoronary
Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction; MI, myocardial infarction; MRI, magnetic resonance imaging; NYHA, New York Heart Association; PCI, percutaneous coronary intervention; TAPAS, Thrombus Aspiration During Percutaneous Coronary Intervention in Acute Myocardial Infarction Study; TASTE, Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia; TOTAL, Trial of Routine
Aspiration Thrombectomy with PCI versus PCI Alone in Patients with STEMI.
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mortality or recurrent myocardial infarction) [29]. In post hoc analyses of the 180-day follow-up, the composite end point
of cardiovascular death, rehospitalization with new myocardial infarction, cardiogenic shock, or new hospitalization for
heart failure was similar in the aspiration and no-aspiration groups, as was the incidence of stroke [30]. TASTE was limited
by the open-label design of the trial and lack of blinded event adjudication, but raised questions about the effectiveness of
aspiration thrombectomy.
The third and largest randomized trial was the Trial of Routine Aspiration Thrombectomy with PCI versus PCI Alone
in Patients with STEMI (TOTAL) trial, which enrolled 10,732 patients. Similar to TASTE, in STEMI patients undergoing
primary PCI, routine manual thrombectomy did not reduce the risk of cardiovascular death, recurrent myocardial
infarction, cardiogenic shock, or New York Heart Association (NYHA) class IV heart failure within 180 days (composite
end point: thrombectomy, 6.9%, vs. PCI alone, 7.0%; P ¼ .86). Moreover, thrombectomy was associ ated with an increased
risk of stroke at 30 days (0.7% vs. 0.3%, P ¼ .02) [31]. The 1-year follow-up results wer e similar [32].
A 2017 patient-level meta-analysis of the above three trials showed that manual thrombectomy was associated with a
strong trend for lower incidence of cardiovascular death at 30 days (2.4% vs. 2.9%, hazard ratio 0.84; 95% CI 0.70e1.01;
P ¼ .06), but also a strong trend for higher incidence of stroke or transient ische mic attack (0.8% vs. 0.5%, odds ratio 1.43;
95% CI 0.98e2.10; P ¼ .06) [33]. In patients with large thrombus (TIMI thrombus grade 3 or higher) cardiovascular death
was decreased (2.5% vs. 3.1%, hazard ratio 0.80; 95% CI 0.65e0.98; P ¼ .03 ), at the cost of increased incidence of stroke
or transient ischemic attack (0.9% vs. 0.5%, odds ratio 1.56; 95% CI 1.02e2.42, P ¼ .04) [33].
As a result of these studies the 2015 ACC/AHA/SCAI (American College of Cardiology/American Heart Association/
Society for Cardiovascular Angiography and Interventions) focused update on primary PCI for patients with STEMI gave a
class III recommendation for routine aspiration thrombectomy before primary PCI (level of evidence A) [34] and a class IIb
recommendation for selective and bailout aspiration thrombectomy in patients undergoing primary PCI (level of evidence
C, limited data). Similarly, the 2015 guidelines of the European Society of Cardiology for the management of acute
coronary syndromes in patients presenting with ST-segment elevation suggested that aspiration thrombectomy cannot be
recommended considering the lack of benefit observed in STEMI, while this treatment modality has not been established
by adequately sized, randomized clinical trials in non-ST-segment elevation acute myocardial infarction [35].
THROMBUS AS THE RESULT OF COMPLICATED PERCUTANEOUS CORONARY
INTERVENTION
Coronary thrombus may form during PCI by a variety of mechanisms (Fig. 14.4), including thrombus formation within the
guide catheter or at the tip of the arterial sheath that is injected into the coronary artery, inadequate antithrombotic therapy,
and any complication that reduces coronary flow.
Thrombus Embolization From the Sheath or Guide Catheter
Although infrequent, thrombus can form at the tip of arterial sheaths; when a catheter is subsequently advanced through the
sheath the thrombus may be carried into the coronary artery causing acute occlusion. Prevention of this complication is key
and can be achieved with aspiration of the sheath before insertion of a guide catheter. Also, if there is no arterial pressure
waveform or there is a dampened pressure waveform after insertion of the catheter and it cannot be corrected with catheter
repositioning, then the catheter should be removed WITHOUT injecting.
Suboptimal Antithrombotic Treatment
Anticoagulation and antiplatelet therapies are important for preventing coronary thrombus formation. Pretreatment with a
P2Y12 inhibitor should be done whenever possible and an intravenous antiplatelet agent, such as GP IIb/IIIa inhibitors or
cangrelor, may be administered in patients who are not pretreated. If unfractionated heparin is used the ACT should be
250e300 s if no GP IIb/IIIa inhibitors are used, or 200e250 s if GP IIb/IIIa inhibitors are used.
In some patients the venous line may malfunction and the patient may not receive the anticoagulant despite “intravenous administration.” That is why some operators do not start PCI until after they confirm that the ACT is above a
certain threshold, such as 200 or 250 s.
During long complex cases, such as chronic total occlusion interventions, the ACT may decrease. To prevent this, the
ACT should be periodically checked (every 20e30 min) and additional doses of unfractionated heparin administered, if
needed. This can be facilitated by inserting a small (usually 4 Fr) sheath in a large vein, such as the common femoral vein,
or sometimes through the arterial sheath side port.
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FIGURE 14.4 Potential causes of thrombus formation during PCI. ACT, activated clotting time; GP, glycoprotein; PCI, percutaneous coronary
intervention.
If despite precautions thrombus is formed and causes embolization, subsequent management of the intracoronary
thrombus is performed as described under Thrombus as the Cause of Complications. Thrombus formation compromising
flow during PCI can cause acute hemodynamic compromise, occasionally requiring hemodynamic support.
Despite traditional teaching about reversing heparin anticoagulation if a perforation occurs, most operators currently do
not administer protamine until after removal of all coronary equipment (guidewires, balloon, etc.). Coronary thrombosis
occurring after coronary perforation can be extremely challenging to treat (Fig. 14.5).
FIGURE 14.5 “A Perfect Storm”: Coronary thrombosis following coronary perforation. (A) Coronary angiography demonstrating a left anterior
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descending coronary artery (LAD) chronic total occlusion (yellow arrow). (B) Antegrade wire escalation resulted in successful “true-to-true” crossing with
a Fielder XT guidewire (yellow arrow), as confirmed by contralateral injection. (C) Because of severe calcification orbital atherectomy was performed
(yellow arrow). (D) Despite atherectomy the mid-LAD lesion could not be dilated with a balloon (“balloon undilatable”- yellow arrow). (E) Repeat orbital
atherectomy was performed followed by repeat balloon inflation. Balloon rupture occurred (yellow arrow), resulting in LAD perforation. (F) A balloon
was immediately inflated in the proximal LAD to stop the bleeding (yellow arrows) through a second guide in a “ping-pong guide” fashion. (G) Delivery
of a covered stent (yellow arrows) was difficult because of the severe calcification. Using an 8-Fr GuideLiner, a Graftmaster stent was deployed and
(H) the perforation sealed. Two drug-eluting stents were deployed, (I) one to cover the mid-LAD distal to the covered stent (yellow arrows) and (J) a
second one to cover the proximal LAD (yellow arrows). (K) Repeat angiography revealed stent thrombosis (yellow arrow). No protamine had been
administered and the activated clotting time was 227 s. (L) Aspiration thrombectomy with an Export catheter (yellow arrow) was successful. (M) A third
drug-eluting stent was deployed in the proximal LAD (yellow arrows). (N) Final angiography revealed TIMI 3 flow without further complications and
well-expanded stents. (O) Control transthoracic echocardiography revealed a small pericardial effusion without signs of tamponade.
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Complications Causing Decreased Coronary Flow
Any complication causing decreased coronary flow may result in coronary thrombus formation (Fig. 14.4). Acute
thrombus formation can also occur during stenting of acute (Fig. 14.6), complex (Fig. 14.7), and/or lipid-rich lesions, as
detected by near-infrared spectroscopy or optical coherence tomography. That is why the use of an embolic protection
device in association with an intensive antithrombotic strategy has been advocated for the treatment of lipid-rich lesions.
FIGURE 14.6 Acute stent thrombosis after primary percutaneous coronary intervention (PCI). A patient presented with anterior ST-segment
elevation myocardial infarction. (A) Diagnostic angiography revealed occluded left anterior descending coronary artery (LAD-yellow arrow). (B) The
lesion was treated with a drug-eluting stent, achieving TIMI 3 flow without any complications. Eight hours later the patient returned to the catheterization
laboratory due to recurrent anterior ST-segment elevation. (C) Repeat coronary angiography showed a patent stent with TIMI 3 antegrade flow with a
possible area of repeat stenosis (yellow arrow). (D) Optical coherence tomography (OCT) showed acute stent thrombosis with nonocclusive thrombus. (E)
After aspiration thrombectomy and administration of glycoprotein IIb/IIIa inhibitors, OCT demonstrated decreased thrombus size. (F) No further PCI was
performed, and the patient had no recurrent symptoms but was given an additional 12-h infusion of a glycoprotein IIb/IIIa inhibitor.
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