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Dissection Type C – Case 2

Clinical Presentation

  • 82-year-old female who presented with chest pain (CCS Class III). Referred for staged PCI of LAD/D1 bifurcation.

Past Medical History

  • HTN, HLD, CAD s/p PCI, Hypothyroidism
  • LVEF 60%

Clinical Variables

  • Prior Cardiac Catheterization: Proximal LAD 30-40% stenosis, mid LAD 80-90%, D1 70-80% stenosis with severe calcification of the LAD.

Medications

  • Home Medications: Aspirin, Clopidogrel, Rosuvastatin, Metoprolol Succinate, Amlodipine, Enalapril, Levothyroxine
  • Adjunct Pharmacotherapy: Clopidogrel, Bivalirudin

Pre-procedure EKG

Angiograms

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Right coronary artery (RCA) angiography
  • 50-60% proximal RCA lesion.
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Right coronary artery (RCA) angiography

  • 50-60% proximal RCA lesion.
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Left coronary artery angiography

  • 30-40% proximal and 90% mid left anterior descending (LAD) lesion
  • 70-80% stenosis in the first diagonal branch (D1)
  • no significant lesion in the left circumflex (LCx) coronary artery.
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Rotational atherectomy of the LAD using a 1.5 mm Burr at 150K rpm.

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Angiography of the LAD after rotational atherectomy showing slow flow.

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Pre-dilatation of mid LAD lesion with a Trek 2.5/15 mm balloon with use of a Guidezilla support catheter.

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Positioning of a Trek 2.5/15 mm balloon in the distal LAD.

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Angiography of the LAD after lesion pre-dilatation showing a Guidezilla support catheter, non-flow limiting Type C dissection of the LM. When contrast is injected, the catheter thrusts forward and causes direct injury of the LM, leading to a dissection.

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Guidezilla support catheter induced, non-flow limiting Type C dissection of the LM.

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Angiography of LAD after Xience Alpine 2.5/33 mm stent placement in the distal LAD.

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Deployment of a Xience Alpine 3.0/33 mm stent in the mid LAD.

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Angiography of the LAD after stent placement.

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Wiring of the side branch (LCx).

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Positioning of a Resolute Onyx 5.0/12 mm stent in the LM.

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Angiography of the LM after stent placement.

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Final angiography showing successful treatment of the LM dissection flap with TIMI 3 flow in the LCA. However, retrograde extension of the dissection into the left coronary sinus/aortic is also seen angiographically.

Post-procedure EKG

Case Overview

  • Underwent staged intervention of the LAD.
  • Procedure complicated by slow flow following rotational atherectomy due to micro-particulate distal embolization.
  • This was followed by a Guidezilla support catheter induced, non-flow limiting Type C dissection of the LM.
  • In addition, there was significant residual contrast staining with mild retrograde extension of the dissection into the left coronary sinus/aortic wall.
  • Procedure was continued and a two stent were placed in the mid to distal LAD.
  • Subsequently, side branch (LCx) was wired and direct stenting of the LM dissection was performed with direct placement of a stent, effectively treating the dissection.
  • Post procedure, minor EKG changes were noted. However, patient remained hemodynamically stable and without chest pain. Taking this into account along with retrograde extension of the dissection into the left coronary sinus/aortic wall, administration of adjunct pharmacotherapy (Gp2B/3A inhibitor, Cangrelor, etc.) and/or placement of an IABP was deferred.
  • Troponin-I peaked at 4.25 ng/mL and CK-MB peaked at 21.0 ng/mL.
  • Patient was discharged home two days later without any sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • Type C dissection of an angiographically normal LM due to Guidezilla support catheter injury.
      • As contrast was injected through the Guidezilla support catheter, it lunged forward with excessive force injuring the LM and caused a dissection.
    • Slow flow due to distal micro-particle embolization during rotational atherectomy.
  • How could the complication have been prevented?
    • When the Guidezilla support catheter is placed within the coronary it is best to minimize contrast use and administer IC agents with a lower pressure. The outlining of the Guidezilla catheter is coated and more lubricious compared with outer extension guide catheters, therefore making the Guidezilla catheter more susceptible to movement during a procedure.
  • What are the important learning points?
    • This is a Type C dissection because of the persistence of extraluminal contrast seen well after contrast injection.
    • When injecting IC agents/contrast through a support catheter, remember to inject slowly with low pressure. This helps reduce catheter movement which can result in vessel trauma, and if a dissection is present, further propagation of the dissection.
    • Dissection of the LM and RCA can propagate both antegrade or retrograde. In this case the dissection extended in both directions. Fortunately, the retrograde extension of the dissection was only minimal involving the left coronary sinus alone. In majority of cases, stenting of the ostium of the vessel involved typically treats the dissection flap preventing further progression.
    • If a dissection extends into the coronary sinus/aorta follow up imaging with TEE and/or Cardiac CTA should be performed on a case by case basis. In this case, Cardiac CTA was deferred because of minimal retrograde extension with only the coronary sinus being involved.
    • This case was performed during the CCC Live Case Symposium and can be viewed in full with case discussion by clicking on the following link: https://ccclivecases.org/new/complex-coronary/september-2017-ccc-live-case.
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 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
    • 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
  • 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

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.
  1. 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.
  2. Rezkalla S.H., Kloner R.A. (2002) No-reflow phenomenon. Circulation 105:656–662.
  3. 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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