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  3. Dissection Type F – Case 1

Dissection Type F – Case 1

Clinical Presentation

  • 86-year-old female who presented with chest pain to an outside hospital and underwent cardiac catheterization showing severe 3-Vessel CAD with LM involvement. She was referred for complex PCI.

Past Medical History

  • HTN, HLD, CAD, AAA s/p Repair, Carotid Stenosis (Right Total Occlusion, 60% Stenosis on Left), Moderate AS, COPD on 2L O2 NC at Home

Clinical Variables

  • Prior Cardiac Catheterization: LM 70-80% stenosis, and RCA 80-90% stenosis.


  • Home Medications: Clopidogrel, Metoprolol Tartrate, Amlodipine, Furosemide, Albuterol, Tiotropium
  • Adjunct Pharmacotherapy: Clopidogrel, Bivalirudin


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Left coronary artery angiography
  • 70-80% calcified left main (LM) lesion
  • 60-70% left anterior descending (LAD) stenosis
  • mild diffuse disease in left circumflex (LCx) coronary artery.
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Left coronary artery angiography

  • 70-80% calcified left main (LM) lesion
  • 60-70% left anterior descending (LAD) stenosis
  • mild diffuse disease in left circumflex (LCx) coronary artery.
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Right coronary artery (RCA) angiography

  • 60-70% lesion in the proximal RCA.
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Wiring of the LAD with a Fielder wire with use of a Finecross microcatheter for support.

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Rotational atherectomy of the LM using a 1.5 mm Burr at 150K rpm.

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Angiography of the LAD after rotational atherectomy with presence of a minor LM dissection.

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Pre-dilatation of the LM with a Quantum Apex 3.5/15 mm balloon.

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Angiography of the LM concerning for an imminent flow-limiting, Type F dissection of the LM extending into the LAD.

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Balloon inflation of the LM using a Quantum Apex 3.5/15 mm balloon.

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Angiography of the LM after balloon inflation showing abrupt vessel closure. Patient become hemodynamically unstable with VF which was successfully defibrillated with one shock.

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Deployment of a Xience V 3.5/15 mm stent in the distal LM extending into the LAD.

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Angiography of the LAD after stent placement showing successful treatment of the dissection with restoration of TIMI 3 flow.

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Deployment of a Xience 4.0/12 mm stent in the ostial LM.

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Post dilatation of stent placed in the LM with a Quantum Apex 3.5/15 mm balloon.

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Angiography after post dilatation of the stent placed in the LM showing successful treatment and restoration of TIMI 3 flow.

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Final angiography showing successful treatment of the LM-LAD dissection with restoration of TIMI 3 flow.

Post-procedure EKG

Case Overview

  • Underwent complex intervention of the LM.
  • Rotational atherectomy was done leading to a minor dissection which evolved into a Type F dissection with AVC after pre-dilatation.
  • Patient became hemodynamically unstable with VF arrest that was successfully treated with a single defibrillation.
  • Two stents were placed in the LM extending into the LAD with restoration of flow.
  • An additional stent was placed, effectively treating the dissection.
  • Troponin-I peaked at 43.8 ng/mL and CK-MB peaked at 108.8 ng/mL.
  • Patient was discharged home 7 days after without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • Wire bias altering the trajectory of the rotational atherectomy device.
  • How could the complication have been prevented?
    • We should have performed rotational atherectomy starting with a smaller 1.25mm rota burr and upsized to a larger 1.5mm or 1.75mm rotational burr. This approach would have better modified the plaque in the tortuous distal LM and in turn reduce wire bias which was responsible for altering the trajectory of the rotational burr while performing rotational atherectomy.
    • Could have considered using an alternative atherotomy device such as a cutting balloon.
    • Use of a guide catheter which provides coaxial engagement will help reduce unfavorable guidewire bias.
  • Is there an alternate strategy that could have been used to manage the complication?
    • Sometimes wire bias can possibly be prevented by use of a Rota Extra Support wire instead of a Rota Floppy wire. A stiffer wire can be used to straighten the vessel or lesion to lessen the resistance and possibly reduce wire bias.
  • What are the important learning points?
    • “Failure to plan is planning to fail” – Benjamin Franklin
    • Need to be extremely cautious when using atherectomy devices in extremely tortuous vessels. Wire bias can occur in tortuous vessels, increasing the risk of dissection or perforation.
    • Minor dissections are expected after atherectomy or balloon dilatation of a calcified vessel. Rarely, do they result in Type D to F dissections. Therefore, it is advised to keep appropriate balloons and stents ready when performing complex interventions to manage unexpected complications.
    • Once a dissection is identified, rotational atherectomy should be stopped, and primary focus should be on maintaining wire position. Once assures the wire is in the true lumen, the dissection should be treated accordingly with balloon inflation and placement of a stent.
    • Guidewire bias is when you have divergence from the central axis of the vessel and can result in ablation of normal tissue if the tension on the wall exceeds the elasticity of the vessel. To reduce sidewall tension:
      • Keep the tip of the guidewire just beyond the lesion.
      • Use a stepped-burr approach starting with an undersized burr is preferred.
      • When advancing the burr, do so at low speed to reduce there is less tension in the wire.
    • There are two kinds wires that can be used when performing rotational atherectomy:
      • Rota Floppy Wire: Used in most cases, and is more flexible with a longer taper and shorter spring tip compared with the Rota Extra Support wire. This wire causes less vessel straightening, less wire bias, and allows for atherectomy along the greater curvature of an angulated lesion.
      • Rota Extra Support Wire: Used in tortuous vessels or in situations when one suspects wire bias as a reason for the burr not crossing the lesion. Wire is stiffer, and with a shorter taper and longer spring tip compared with the Rota floppy wire. This wire causes the vessel to straighten out the tortuosity to allow the burr to advance to a lesion, and is useful in ablation of plaque at the lesser curvature of angulated lesions, aorto-ostial lesions and distal lesions. However, this wire can result in proximal vessel spasm and ‘pseudo-stenosis’.
    • A stiffer guidewire does not always result in unfavorable bias, and may result in a favorable bias, especially when performing rotabalation of an angulated and heavily calcified lesion.
Educational Content


  • AVC is the commonest major complication of PCI1
  • Incidence: 0.3% [used to be 3% in pre-stent era]2
  • Risk factors:3
    • 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:3
    • 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.2

  • 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:4
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.5 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.6 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic serotonin and thromboxane, oxidative stress,and reperfusion injury.6 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.
    • 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.
    • 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


        • 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
        • 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.
        • 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


      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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