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Acute Stent Thrombosis – Case 1

Clinical Presentation

  • 63-year-old male who presented with chest pain (CCS Class 3), and was referred for PCI of the LM trifurcation.

Past Medical History

  • HTN, HLD, DM, Former Tobacco Use, CAD s/p 3-Vessel CABG and Multiple PCI’s, ESRD on iHD, PVD s/p Fem-Pop Bypass and Bilateral Toe Amputations, BPH
  • LVEF 53%

Clinical Variables

  • Stress MPI: Mild anterolateral ischemia and moderate posterior scarring.
  • Prior Cardiac Catheterization: Ostial LM 70-80%, distal LM 60-70% stenosis, proximal LAD 70-80% stenosis, D1 90% stenosis, OM1 total occlusion and fills via SVG, LPL 60-70% stenosis, proximal RI 70-80% stenosis, proximal RCA 80-90% stenosis and fills retrograde via SVG; SVG-Y graft to RPDA and OM1 (patent), LIMA to LAD known to be occluded.

Medications

  • Home Medications: Aspirin, Clopidogrel, Rosuvastatin, Carvedilol, Valsartan-Hydrochlorothiazide, Isosorbide Monnitrate, Clonidine, Doxazosin, Insulin, Calcium Acetate, Calcitriol, Epoetin-Alpha
  • Adjunct Pharmacotherapy: Clopidogrel, Bivalirudin

Pre-procedure EKG

Angiograms

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Patent radial artery Y graft to the right posterior descending artery (RPDA) and to the first obtuse marginal branch (OM1).
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Patent radial artery Y graft to the right posterior descending artery (RPDA) and to the first obtuse marginal branch (OM1).

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Right coronary artery (RCA) angiography

  • no obstruction in the right coronary artery (RCA).
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Left coronary artery angiography

  • distal left main (LM) (60-70%) trifurcation lesion with 70-80% stenoses in the ostial segments of the left anterior descending (LAD), left circumflex (LCx) and ramus intermedius (RI).
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Wiring of LM trifurcation followed by cutting balloon angioplasty of the LAD with a Flextome 3.0/6mm balloon.

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Pre-dilatation of the LCx lesion with a Trek 2.5/15mm balloon.

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Pre-dilatation of the proximal LAD lesion with a Quantum Apex 3.0/12mm balloon.

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After lesion pre-dilatation, patient has circulatory collapse, and IABP was emergently placed. Angiography of the LCA showing that abrupt vessel closure (AVC) was most likely due to thrombus. Patient developed ventricular tachycardia followed by ventricular fibrillation, which was successfully treated with a single debrillator shock of 200 J.

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IC vasodilators were administered through the guide catheter without improvement in flow. This was followed by serial balloon inflations of the LM trifurcation performed with a Quantum Apex 3.0/12mm balloon.

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Deployment of a Xience Xpedition 3.25/23mm stent in the LM extending into the proximal LAD.

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Angiography of the LCA after stent placement showing restoration of TIMI 3 flow in the LAD. However, the procedure was further complicated by stent jailing of the RI and LCx.

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Balloon dilatation of the ostium of the LCx with a Trek 2.5/15mm balloon.

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Angiography of the LCA after balloon dilatation of the LCx ostium showing restoration of flow.

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Deployment of a Xience Xpedition 3.0/12mm stent in the proximal LCx.

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Kissing balloon inflation (KBI) of the LAD and LCx with Trek NC 3.5/12mm and Trek NC 3.0/12mm balloons respectively.

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Angiography of the LCA after KBI concerning for embolization of thrombus in the distal LAD.

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Angiography of the LAD after wiring across the thrombus showing restoration of flow (TIMI 3).

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Repeat KBI of the LM-LAD and LCx performed using the same balloons.

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Final angiography of the LCA showing successful intervention of the LM-LAD and LCx.

Post-procedure EKG

Case Overview

  • Underwent complex intervention of LM trifurcation.
  • Procedure was complicated by abrupt vessel closure (AVC) of the LM likely due to acute thrombus/Type F dissection following lesion pre-dilatation.
  • Patient acutely decompensated and an IABP was emergently placed.
  • Subsequently, patient developed ventricular tachycardia followed by ventricular fibrillation which was successful treated with a single debrillator shock of 200 J.
  • Serial balloon inflations of the LM performed without improvement in flow.
  • Procedure was continued and a stent was placed in the LM extending into the proximal LAD.
  • Follow up angiography showed successful restoration of flow in the LM-LAD; however, the procedure was further complicated by stent jailing of the RI and LCx.
  • PTCA of the ostial LCx was performed, restoring flow in the LCx.
  • Next, a stent was successfully placed in the LCx. This was followed by KBI of the LM-LAD and LCx.
  • However, procedure was now complicated by embolization of thrombus to the distal LAD.
  • A wire was used to traverse the distal LAD thrombus, successfully restoring flow in the distal LAD.
  • PTCA of the stent jailed RI was performed, but unsuccessful.
  • Troponin-I peaked at 38.2 ng/mL and CK-MB peaked at 16.9 ng/mL.
  • Patient was discharged home two days later without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • Abrupt vessel closure (AVC) due to acute thrombosis/Type F dissection following lesion pre-dilatation.
  • How could the complication have been prevented?
    • Assure patient is given adequate periprocedure antithrombotic therapy (antiplatelets and anticoagulants).
      • Pay close attention to the ACT during the procedure and dose anticoagulation accordingly to maintain ACT >300 prior to performing an intervention (Hemochron machine).
    • Avoid aggressive, high pressure, over sized balloon dilatation of a calcified lesion as this can result in complications.
    • Avoid placement of multiple wires (≥3 wires) within the coronary system simultaneously because this increases the risk for thrombosis within the guide catheter and coronary arteries.
    • Lesions preparation with atherectomy (rota, orbital or laser) prior to performing lesion pre-dilatation could have helped reduce calcified plaque burden, and made it safer to prepare and reduce the chance of dissection.
  • Is there an alternate strategy that could have been used to manage the complication?
    • Intravascular imaging of the coronaries with IVUS would have helped with determining the etiology of AVC, and guide further management but given the certainty of AVC being due to acute thrombosis/Type F dissection the complication was immediately treated with PTCA followed by placement of a stent.
  • What are the important learning points?
    • When AVC occurs after PTCA or stent placement you have to consider a broad differential which includes the possibility of a coronary spasm, thrombus or debris with distal embolization, and dissection.
    • A stent should not be placed prior to restoration of flow in the vessel with AVC unless you are confident the complication is due to a dissection. Generally, a stent should only be placed after flow has been restored in a vessel which has AVC.
    • In this case, following pre-dilatation of a calcified lesion there was AVC of the LM due to acute thrombosis/Type F dissection. Intracoronary vasodilators were given with no improvement in flow. We were confident the cause for AVC was due to acute thrombosis/Type F dissection, and PTCA was performed as a bridge with no improvement in flow. A stent was subsequently placed with immediate improvement in flow noted, confirming our suspicion for acute thrombosis/Type F dissection. However, the procedure was further complicated by stent jailing of the LCx and RI. Alternatively, if our concern for AVC was due to thrombus without dissection, we could have performed aspiration thrombectomy prior to placement of a stent.
    • If you are performing stenting with side branch wiring, and the side branch is stent jailed with the wire still in position, it is imperative you do not remove that wire. Instead, place a second wire across the vessel which is stent jailed, and then remove the wire. If this is not feasible, use a 1.0 compliant balloon and advance it over the wire which is stent jailed and wedge it at the ostium of the stent and remove the wire. Next, introduce another wire across this vessel and continue with the procedure.
Educational Content

ABRUPT VESSEL CLOSURE (AVC)

  • AVC is the commonest major complication of PCI8
  • Incidence: 0.3% [used to be 3% in pre-stent era]9
  • Risk factors:10
    • Proximal vessel tortuosity
    • Diffuse lesion
    • Pre-existing thrombus
    • Degenerated vein graft
    • Extremely angulated lesion
    • Unstable angina
    • Multivessel disease
    • Female gender
    • Chronic renal failure
  • Common causes:10
    • Coronary dissection
    • Intracoronary thrombus formation
    • Native thrombus (or atheroma) embolization
    • Air injection
    • Coronary no-reflow
    • Coronary vasospasm

In the current DES era, commonest causes of AVC are stent edge dissection and acute stent thrombosis. However, the cause is indeterminate in almost 50% of patients.9
  • Classification of coronary perforation: As per the National Heart, Lung and Blood Institute scheme, types A–F classification remains useful to describe the severity of luminal injury:11
Type AMinor radiolucency within the coronary lumen without dye persistence
Type BParallel tracks or double lumen separated by a radiolucent area during angiography without dye persistence
Type CExtraluminal, persisting extravasation of contrast
Type DSpiral luminal filling defects
Type EPersistent lumen defect with delayed antegrade flow
Type FFilling defect accompanied by total coronary occlusion
  • Prevention:
    • Maintain ACT > 300 throughout procedure
    • Make sure interface is free of air
    • Avoid high-pressure balloon dilatation or stenting
    • Avoid unnecessary post-dilatation and very long stents
    • Use distal protection devices in vein graft PCI
    • Be careful when retrieving delivery after stent implantation
    • Avoid geographical miss during stenting
    • Avoid aggressive post-dilatation at the stent edges
    • Be careful while positioning wire distal tip in tortuous vessel
  • Management: Abrupt closure results in acute ischemia manifesting as ECG changes, hypotension, bradycardia, chest pain and ventricular arrhythmias. The first step is to identify the underlying cause of AVC and then treat it accordingly.
    • Immediate priority should be to ensure intraluminal position of coronary guidewire and, if in doubt, an over-the-wire balloon catheter or Twin-Pass or other microcatheter should be advanced distal into the target vessel to allow minimal contrast media injection and confirm wire position.
    • If intraluminal guidewire position is confirmed, the most likely mechanism underlying AVC is dissection or intraluminal thrombus. Prompt balloon inflation should be attempted to establish antegrade flow. If flow returns immediately after balloon inflation the likely cause of AVC is dissection and urgent stenting is useful for stabilizing.
    • If the distal flow after balloon inflation is sluggish (TIMI 0 or 1), the likely cause of AVC is distal thromboembolism. Using a Twin-Pass or microcatheter to administer distal vasodilators can help reestablish flow.
    • If initial contrast agent injection reveals guidewire position within a false lumen, careful exploration of the occluded segment using a second guidewire must be performed.
    • Aspiration thrombectomy and Glycoprotein IIb/IIIa antagonists may be helpful if acute closure is due to thrombus. Control of anticoagulation is of paramount importance to avoid thrombotic occlusion of stented artery. ACT should be measured every ~30 minutes to keep ACT > 300 throughout the procedure and dose of anticoagulation is adjusted accordingly. If ACT is not reaching therapeutic levels consider resistance to anticoagulant and a possible reason for suspected thrombus formation causing AVC.
    • Intravenous fluids, vasopressors, inotropes and intra-aortic balloon pump (IABP) should be considered for unstable hemodynamics.
    • Emergency CABG should be considered if patient have persistent AVC depending on the location of the occlusion, patient’s clinical condition and assessment of risks and benefits.

Coronary slow flow/no-reflow phenomenon

Slow flow/No-reflow is an acute reduction in coronary flow (TIMI grade 0–1) in a patent vessel with absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion.12 The underlying mechanism is complex and not completely understood, but some proposed mechanisms include distal embolization of calcium, plaque or thrombus and microvascular spasm caused by release of vasoconstrictor substances like serotonin and thromboxane, oxidative stress, and reperfusion injury.13 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic dysfunction or hemodynamic instability, long calcified lesions, ostial lesions, chronic total occlusion of right coronary artery, thrombotic lesions, and vein graft lesions. Use of rotational atherectomy is also associated with a higher incidence of no-reflow.
Prevention
  • Direct stenting whenever feasible
  • Use of distal embolic protection devices for vein graft interventions.
  • Aspiration thrombectomy in STEMI cases if there is large thrombus burden
  • For cases involving rotational atherectomy, the use of rota flush, small initial burr sizes, shorter rotablation runs, avoiding drops in rotations per minute (RPMs), and prevention of hypotension/bradycardia

Management: Coronary no re-flow must be immediately differentiated from AVC due to dissection as placement of stent in a vessel with no reflow may worsen the situation. Exclusion of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion suggests no-reflow.
  • Stabilize hemodynamics with medications/intra-aortic balloon pump (IABP)
  • IC verapamil (100–200 μg)
  • IV adenosine (10–20 μg)
  • IC nitroprusside (50–200 μg)
  • Moderately forceful injection of blood or saline through the manifold
  • GPIIb/IIIa agents, IV cangrelor may also be helpful

Air Embolism

Intracoronary air embolism is a potentially lethal but rare complication. It could result in hypotension, hemodynamic collapse, cardiac arrest, and in rare cases death. Coronary air embolism is almost always iatrogenic. It occurs mostly when
  • Catheters are not adequately aspirated and flushed
  • During introduction or withdrawal of a guidewire, balloon catheter or other interventional devices
  • Rupture of a balloon during high inflation
  • During intracoronary medication injection

Diagnosis: Coronary air embolism is detected fluoroscopically as intracoronary filling defects during dye injection. It could also be seen as abrupt cutoff of a vessel secondary to occlusion of distal circulation with air column. Clinically small air embolism may be asymptomatic. Larger air embolism may present as chest pain, hypotension, ischemic EKG changes, or cardiac arrest.
Prevention
  • Do not engage the left main coronary when pulling out the guiding wire unless the patient has excessive aortic tortuosity or an enlarged aortic root.
  • Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if the catheter already has a column of air inside it.
  • Draw back at least 2 cc of blood into the injection syringe and make sure that the interface is free of air prior to injection.
  • Inject some dye into the ascending aorta prior to engaging left main.
  • Always ensure that all the catheters and tubings are aspirated, flushed and free of air.
  • Take adequate care when prepping stents or balloons and ensure that the syringe tip is facing downwards.
  • Always inject with the syringe tip facing downwards

Treatment
  • Put patient on 100% oxygen.
  • Flush air free saline vigorously into the coronary arteries. Aspirate blood and air column via guide catheter and reinject saline forcefully back into coronary arteries.
  • Administer IV phenylephrine 200 μg for hypotension. Repeat, as needed every minute. If significant hypotension or hemodynamic collapse is present, push IV 1 cc epinephrine (1:10,000 dilution).
  • Intracoronary injection of vasodilators (adenosine, nitroprusside, verapamil) may be attempted.
  • Supportive measures should be instituted (IABP for persistent hypotention) and patient admitted to intensive coronary care unit for further monitoring

Coronary Vasospasm

Coronary vasospasm can be induced by PCI secondary to endothelial denudation and nitric oxide loss.
  • Some cases are catheter-induced which is caused by a contact of a catheter without balloon deployment. It is usually short-lived and is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm
  • Rotablator cases are more prone to vasospasm

Diagnosis
  • Coronary vasospasm is detected by presence of EKG changes of ST segment elevation in association with angina, and then EKG completely returns to baseline upon resolution of symptoms.
  • The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven reversible by the administration of intracoronary vasodilators.

Treatment
  • Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates [nitroglycerin 100-300 mcg, verapamil 100 mcg/min, up to 1.0-1.5 mg, nicardipine 100-300 mcg, nitroprusside 100-300 mcg]
  • IV atropine can be useful if there is associated hypotension of bradycardia
  • If vasospasm persists, remove all hardware and leave the guide wire in place to maintain position. This may minimize distal vessel spasm
  • Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres)
  • Stenting should be reserved in cases if all the above measures have failed, as it may lead to propagation of spasm to a new location
  • Refractory vasospasm may be indicative of dissection, which is also an indication for stenting



Abrupt Vessel Closure Summary

  • Dissection
    • Minor dissections - usually heal without clinical sequelae, no treatment required
    • Major dissections - repeated prolonged low-pressure balloon [distal vessel], stenting [Proximal/mid vessel segment or impaired flow due to dissection]
  • Thromboembolism
    • Twin-Pass or microcatheter to administer vasodilators distally
    • Check ACT to keep > 300. Consider starting IV Cangrelor or bailout GPIs
    • Balloon dilatation and/or thrombus aspiration in case of stent thrombosis
    • Stenting on case of thrombosis in in unstented vessel segment
  • No-reflow
    • Intracoronary Adenosine, Nitroprusside, Nicardipine, Verapamil, or GPI’s
    • A transit catheter or over-the-wire balloon should be used to deliver the vasodilators to the distal microvasculature
    • Insertion of IABP to improve flow
  • Air embolism
    • Start 100% oxygen
    • Flush air free saline vigorously into the coronary arteries. Aspirate blood via guide catheter and reinject forcefully back into coronaries
    • IV phenyl epinephrine or epinephrine as needed
    • Intracoronary injection of vasodilators
  • Vasospasm
    • Intracoronary Nitroglycerin, Adenosine, Nitroprusside, Nicardipine, or Verapamil
    • IV fluid bolus and/or atropine as needed
    • Remove all hardware and leave the guide wire in place to maintain position
    • Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres)
  • Unknown etiology
    • Maintain wire position distally and pass a microcatheter distally to inject contrast
    • If flow distally, problem at site of vessel closure and needs to be investigated
    • If no flow distally, consider no reflow and give IC vasodilators



References

  1. de Feyter P.J., de Jaegere P.P.T., Murphy E.S., Serruys P.W. (1992) Abrupt coronary artery occlusion during percutaneous transluminal coronary angioplasty. Am Heart J 123:1633–1642.
  2. Francesco Giannini, Luciano Candilio, Satoru Mitomo, Neil Ruparelia, Alaide Chieffo, Luca Baldetti, Francesco Ponticelli, Azeem Latib, Antonio Colombo. Practical Approach to the Management of Complications During Percutaneous Coronary Intervention. J Am Coll Cardiol Intv. 2018 Sep, 11 (18) 1797-1810.
  3. Klein L. (2005) Coronary complications of percutaneous coronary interventions: a practical approach to the management of abrupt closure. Catheter Cardiovasc Interv 64:395–401.
  4. Huber MS, Mooney LF, Madison J, et al. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am J Cardiol 1991;68:467–71.
  5. Rezkalla S.H., Kloner R.A. (2002) No-reflow phenomenon. Circulation 105:656–662.
  6. Piana R., Paik G., Moscucci M., et al. (1994) Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 89:2514–8.

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