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The Impact of Thrombus as a Cause and as a Result of Complicated Percutaneous Coronary Intervention
Chapter 14
The Impact of Thrombus as a Cause and as a Result of Complicated Percutaneous Coronary Intervention Judit Karacsonyi1, 2, Timothy Henry3, 4, Imre Ungi2, Subhash Banerjee1 and Emmanouil S. Brilakis1, 3 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
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 devices. 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.
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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 restore 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 for 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 with 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 antagonists are being used, a 70e100 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 (Vascular 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 negative 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 thrombectomy 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 Aspiration Thrombectomy Event Rate
PCI-Only Event Rate (%)
Trial
Author
Year
n
Primary End Point
TOTAL [31]
Jolly et al.
2015
10,732
Composite of cardiovascular death, recurrent MI, cardiogenic shock, or NYHA class IV heart failure within 180 days
6.9%
7.0
.86
TASTE [36]
Lagerqvist et al.
2014
7,244
All-cause mortality at 30 days; secondary end point, all-cause mortality at 1 year
5.3%
5.6
.57
TASTE [29]
Frobert et al.
2013
7,244
All-cause mortality at 30 days
2.8%
3.0
.63
INFUSE-AMI [37]
Stone et al.
2012
452
Infarct size (percentage of total left-ventricular mass) at 30 days assessed by cardiac MRI
Infarct size: 17%
17.3
.51
EXPIRA [38]
Sardella et al.
2009
175
Occurrence of myocardial blush grade 2 and the rate of 90-min ST-segment resolution >70%.
Myocardial blush grade 2: 88%
60
.001
ST-segment resolution >70%: 64%
39
.001
.020
TAPAS [28]
Vlaar et al.
2008
1,060
Cardiac death or nonfatal reinfarction after 1 year
3.6%
6.7
TAPAS [27]
Svilaas et al.
2008
1,071
Myocardial blush grade of 0 or 1 (defined as absent or minimal myocardial reperfusion)
Myocardial blush grade of 0 or 1 occurred in 17.1%
26.30
P
<.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 associated with an increased risk of stroke at 30 days (0.7% vs. 0.3%, P ¼ .02) [31]. The 1-year follow-up results were 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 ischemic 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 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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FIGURE 14.7 Thrombus embolization during percutaneous coronary intervention of a right coronary artery chronic total occlusion (RCA CTO). A 64-year-old man presented with stable angina and newly diagnosed decreased left-ventricular systolic function. (A) Angiography revealed an RCA CTO (yellow arrow) with a clear proximal cap, length 50 mm, septal and epicardial collaterals. (B and C) The RCA ostium was engaged with an 8-Fr Amplatz Left 1 and the left coronary ostium was engaged with an 8-Fr EBU 3.75 guide catheter. The CTO was successfully crossed using the CrossBoss catheter (yellow arrow) and the “fast spin” technique (“true to true” crossing), as confirmed on orthogonal projections (yellow arrow). (D) The lesion was predilated with a 2.5 30-mm balloon and intravascular ultrasound revealed underexpanded stents and neointimal hyperplasia. (E) The lesion was predilated multiple times with a 3.5 15-mm Angiosculpt balloon followed by implantation of a 3.5 38-mm drug-eluting stent (DES) in the mid-RCA and a 4.0 28-mm DES in the proximal RCA, covering the ostium. Postdilation was performed with a 3.5 25-mm noncompliant balloon and a 4.0 8-mm Ostial flash balloon (yellow arrow). (F and H) Final angiography revealed a lesion at the distal RCA bifurcation (yellow arrow), followed by occlusion of the right posterolateral branch (yellow arrow). Activated clotting time was 259 s. Aspiration thrombectomy with an Export catheter (Medtronic) retrieved a large thrombus (as confirmed by histologic examination [G]), (I) followed by restoration of antegrade TIMI 3 flow in all distal branches.
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Treatment of coronary complications leading to coronary thrombus formation should consist of (1) general treatment measures for coronary thrombus (Fig. 14.2) and (2) specific treatment of the underlying coronary complication (Fig. 14.4). For example, coronary dissection is treated with stent implantation (ensuring that guidewire position is not lost), stent underexpansion is treated with high-pressure balloon inflations, and equipment loss or entrapment is treated with retrieval of the lost coverage or by covering it with stents.
CONCLUSIONS Coronary thrombus can be both the cause and the result of coronary complications. An intensive antithrombotic regimen that combines antithrombin and antiplatelet treatments is critical to preventing and managing thrombus. A stepwise systematic approach to the management of thrombotic lesions could improve the likelihood of restoring antegrade flow, while minimizing the risk of distal embolization or other complications. Treating the underlying coronary pathology that led to thrombus formation during PCI is important for minimizing its consequences and reducing the risk for recurrence.
DISCLOSURES Dr. Karacsonyi: none. Dr. Ungi: none. Dr. Banerjee: research grants from Gilead and the Medicines Company; consultant/speaker honoraria from Covidien and Medtronic; ownership in MDCARE Global (spouse); intellectual property in HygeiaTel. Dr. Henry: none. Dr. Brilakis: consulting/speaker honoraria from Abbott Vascular, Asahi, Cardinal Health, Elsevier, GE Healthcare, and St. Jude Medical; research support from Boston Scientific and InfraRedx; spouse is employee of Medtronic.
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Rheolytic thrombectomy with percutaneous coronary intervention for infarct size reduction in acute myocardial infarction: 30-day results from a multicenter randomized study. J Am Coll Cardiol July 18, 2006;48(2):244e52. 16843170. [25] Parodi G, Valenti R, Migliorini A, Maehara A, Vergara R, Carrabba N, et al. Comparison of manual thrombus aspiration with rheolytic thrombectomy in acute myocardial infarction. Circulation Cardiovascular interventions June 2013;6(3):224e30. 23735474. [26] Vergara R, Valenti R, Migliorini A, Parodi G, Giurlani L, Marrani M, et al. Rheolytic thrombectomy for acute myocardial infarction complicated by cardiogenic shock. J Invasive Cardiol December 2016;28(12):E193e7. 27187985. [27] Svilaas T, Vlaar PJ, van der Horst IC, Diercks GF, de Smet BJ, van den Heuvel AF, et al. Thrombus aspiration during primary percutaneous coronary intervention. N Engl J Med February 07, 2008;358(6):557e67. Epub 2008/02/08. eng, 18256391. 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[37] Stone GW, Maehara A, Witzenbichler B, Godlewski J, Parise H, Dambrink JH, et al. Intracoronary abciximab and aspiration thrombectomy in patients with large anterior myocardial infarction: the INFUSE-AMI randomized trial. J Am Med Assoc May 02, 2012;307(17):1817e26. 22447888. [38] Sardella G, Mancone M, Bucciarelli-Ducci C, Agati L, Scardala R, Carbone I, et al. Thrombus aspiration during primary percutaneous coronary intervention improves myocardial reperfusion and reduces infarct size: the EXPIRA (thrombectomy with export catheter in infarct-related artery during primary percutaneous coronary intervention) prospective, randomized trial. J Am Coll Cardiol January 27, 2009;53(4):309e15. Epub 2009/ 01/24. eng, 19161878.
The Impact of Thrombus as a Cause and as a Result of Complicated Percutaneous Coronary Intervention Judit Karacsonyi1, 2, Timothy Henry3, 4, Imre Ungi2, Subhash Banerjee1 and Emmanouil S. Brilakis1, 3 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
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 devices. 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 restore 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 for 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 with 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 antagonists are being used, a 70e100 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 (Vascular 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 negative 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 thrombectomy 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 Aspiration Thrombectomy Event Rate
PCI-Only Event Rate (%)
Trial
Author
Year
n
Primary End Point
TOTAL [31]
Jolly et al.
2015
10,732
Composite of cardiovascular death, recurrent MI, cardiogenic shock, or NYHA class IV heart failure within 180 days
6.9%
7.0
.86
TASTE [36]
Lagerqvist et al.
2014
7,244
All-cause mortality at 30 days; secondary end point, all-cause mortality at 1 year
5.3%
5.6
.57
TASTE [29]
Frobert et al.
2013
7,244
All-cause mortality at 30 days
2.8%
3.0
.63
INFUSE-AMI [37]
Stone et al.
2012
452
Infarct size (percentage of total left-ventricular mass) at 30 days assessed by cardiac MRI
Infarct size: 17%
17.3
.51
EXPIRA [38]
Sardella et al.
2009
175
Occurrence of myocardial blush grade 2 and the rate of 90-min ST-segment resolution >70%.
Myocardial blush grade 2: 88%
60
.001
ST-segment resolution >70%: 64%
39
.001
.020
TAPAS [28]
Vlaar et al.
2008
1,060
Cardiac death or nonfatal reinfarction after 1 year
3.6%
6.7
TAPAS [27]
Svilaas et al.
2008
1,071
Myocardial blush grade of 0 or 1 (defined as absent or minimal myocardial reperfusion)
Myocardial blush grade of 0 or 1 occurred in 17.1%
26.30
P
<.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 associated with an increased risk of stroke at 30 days (0.7% vs. 0.3%, P ¼ .02) [31]. The 1-year follow-up results were 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 ischemic 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 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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FIGURE 14.7 Thrombus embolization during percutaneous coronary intervention of a right coronary artery chronic total occlusion (RCA CTO). A 64-year-old man presented with stable angina and newly diagnosed decreased left-ventricular systolic function. (A) Angiography revealed an RCA CTO (yellow arrow) with a clear proximal cap, length 50 mm, septal and epicardial collaterals. (B and C) The RCA ostium was engaged with an 8-Fr Amplatz Left 1 and the left coronary ostium was engaged with an 8-Fr EBU 3.75 guide catheter. The CTO was successfully crossed using the CrossBoss catheter (yellow arrow) and the “fast spin” technique (“true to true” crossing), as confirmed on orthogonal projections (yellow arrow). (D) The lesion was predilated with a 2.5 30-mm balloon and intravascular ultrasound revealed underexpanded stents and neointimal hyperplasia. (E) The lesion was predilated multiple times with a 3.5 15-mm Angiosculpt balloon followed by implantation of a 3.5 38-mm drug-eluting stent (DES) in the mid-RCA and a 4.0 28-mm DES in the proximal RCA, covering the ostium. Postdilation was performed with a 3.5 25-mm noncompliant balloon and a 4.0 8-mm Ostial flash balloon (yellow arrow). (F and H) Final angiography revealed a lesion at the distal RCA bifurcation (yellow arrow), followed by occlusion of the right posterolateral branch (yellow arrow). Activated clotting time was 259 s. Aspiration thrombectomy with an Export catheter (Medtronic) retrieved a large thrombus (as confirmed by histologic examination [G]), (I) followed by restoration of antegrade TIMI 3 flow in all distal branches.
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Treatment of coronary complications leading to coronary thrombus formation should consist of (1) general treatment measures for coronary thrombus (Fig. 14.2) and (2) specific treatment of the underlying coronary complication (Fig. 14.4). For example, coronary dissection is treated with stent implantation (ensuring that guidewire position is not lost), stent underexpansion is treated with high-pressure balloon inflations, and equipment loss or entrapment is treated with retrieval of the lost coverage or by covering it with stents.
CONCLUSIONS Coronary thrombus can be both the cause and the result of coronary complications. An intensive antithrombotic regimen that combines antithrombin and antiplatelet treatments is critical to preventing and managing thrombus. A stepwise systematic approach to the management of thrombotic lesions could improve the likelihood of restoring antegrade flow, while minimizing the risk of distal embolization or other complications. Treating the underlying coronary pathology that led to thrombus formation during PCI is important for minimizing its consequences and reducing the risk for recurrence.
DISCLOSURES Dr. Karacsonyi: none. Dr. Ungi: none. Dr. Banerjee: research grants from Gilead and the Medicines Company; consultant/speaker honoraria from Covidien and Medtronic; ownership in MDCARE Global (spouse); intellectual property in HygeiaTel. Dr. Henry: none. Dr. Brilakis: consulting/speaker honoraria from Abbott Vascular, Asahi, Cardinal Health, Elsevier, GE Healthcare, and St. Jude Medical; research support from Boston Scientific and InfraRedx; spouse is employee of Medtronic.
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