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Perforation – Atherectomy – Case 1

Clinical Presentation

  • 54-year-old female who presented with chest pain (CCS Class III) and was referred for IVBT.

Past Medical History

  • HTN, HLD, Active Tobacco Use, CAD s/p Multiple PCI’s, Sarcoidosis, Neuropathy (receiving IVIG therapy), Pulmonary Fibrosis, COPD
  • LVEF 70%

Clinical Variables

  • Stress MPI: Moderate ischemia along the antero-lateral wall.


  • Home Medications: Aspirin, Ticagrelor, Atorvastatin, Metoprolol Succinate, Nifedipine ER, Hydrocholorothiazide, Mycophenolate Mofetil, Mirtazapine, Fluticasone-Salmeterol, Aclidinium Bromide, Colchicine, Cylcobenzaprine, Famotidine
  • Adjunct Pharmacotherapy: Ticagrelor, Bivalirudin

Pre-procedure EKG


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Right coronary artery angiography
  • mild diffuse disease, no significant obstruction.
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Right coronary artery angiography

  • mild diffuse disease, no significant obstruction.
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Left coronary artery angiography

  • 90-95% in-stent restenosis in the first diagonal branch (D1) of the left anterior descending (LAD) coronary artery.
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Branching D1 successfully wired.

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Pre-dilatation of the anterior branch of D1 with a Mini Trek 2.0/12mm balloon.

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Angiography of the branching D1 after lesion pre-dilatation.

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Cutting balloon angioplasty of the anterior branch of D1.

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Angiography after cutting balloon angioplasty of the anterior branch of D1.

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Rotational atherectomy (RA) with 1.25mm burr at 150k RPM led to a fracture of Rota Extra Support wire and a type 3 coronary perforation.

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Prolonged balloon inflation with a NC Emerge 2.5/15mm balloon sealed the D1 perforation. The procedure was further complicated by abrupt vessel closure (AVC) of the LAD due to thrombus embolization. Flow in the LAD was successfully restored with aspiration thrombectomy using a Pronto catheter.

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Follow up angiography showing persistent closure of D1.

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Final angiography showing closure of D1 and sealing of the perforation involving the D1 carina.

Post-procedure EKG

Post-procedure Echocardiography

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Case Overview

  • Underwent intervention of D1.
  • During rotational atherectomy in a tortuous lesion, the burr transected the rota wire and the burr advanced outside the lumen, causing a type 3 perforation.
  • Antiplatelet/Anticoagulation therapy was immediately stopped, and prolonged balloon inflation to tamponade the vessel was performed.
  • Thrombus formed leading to abrupt closure of D1, sealing the perforation.
  • Procedure was further complicated by AVC due to embolization of thrombus into the LAD.
  • Aspiration thrombectomy of the LAD was performed, successfully restoring flow in the LAD.
  • Echocardiography showed no pericardial effusion or tamponade physiology.
  • Troponin-I peaked at 5.71 ng/mL and CK-MB peaked at 28.7 ng/mL.
  • Patient was discharged home 2 days later without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • While performing stent ablation using rotational atherectomy of an angulated, long segment in-stent restenosis lesion with multiple stent layers, the stiffness of the rota wire created significant wire bias. Although, RA was performed cautiously, it resulted in wire fracture and subsequent burr advancement outside the vessel leading to a type 3 coronary perforation.
    • In this case, stopping anticoagulation and prolonged balloon inflation to tamponade the perforated vessel (D1) resulted in AVC from thrombus formation with thrombus then embolizating to the LAD.
  • How could the complication have been prevented?
    • Rotational atherectomy should be considered on a case by case bases, especially when the lesion is long, severely calcified and/or with severe angulation/tortuosity. In this case we should have been less aggressive with performing rotational atherectomy and considered performing cutting/scoring balloon angioplasty in the distal RCA/RPDA.
    • Technical modifications to prevent rotablation related perforation:
      • Use a small burr size (start with 1.25 burr)
      • Bending the wire technique
      • Use of Rota Extra Support wire
      • Pre-dilatation with small balloon
      • Avoid GP IIB/IIA prior to rotablation
  • Is there an alternate strategy that could have been used to manage the complication?
    • Ellis Type 1 and 2 perforations usually seal spontaneously and are conservatively managed. Such patients should be closely monitored in the catheterization lab, and serial echocardiography should be performed, particularly if there is an Ellis Type 2 coronary perforation because it may lead to cardiac tamponade. Ellis Type 3 perforations are associated with increased risk of cardiac tamponade and mortality, and require immediate intervention/treatment. Ellis Type 3 Cavity Spilling perforation management is unclear. Usually they are conservatively managed, unless there is significant extravasation or the patient is symptomatic.
    • Coronary perforation management algorithm:
      • 1st: Prolonged balloon inflation: Position the balloon (or stent-balloon post stent deployment) just proximal or at the level of the perforation to prevent ongoing extravasation and development of hemo-pericardium. Ideally, the balloon to artery ratio should be 1:1. Inflate for 5-10 minutes followed by test deflations with contrast given in between inflations to evaluate the status of the perforation. If there is ongoing extravasation, re-inflate the balloon to stop further extravasation of blood into the pericardial space. This strategy helps stabilize the patients and gain control of the situation, while the operator prepares for echocardiography, pericardiocentesis, and more definitive treatment to seal the perforation.
      • 2nd: Anticoagulation management: ‘STOP’ all anticoagulation immediately if you suspect or visualize a perforation. We consider ‘REVERSING’ heparin with protamine sulfate (to achieve ACT <225s) after coronary equipment is removed to prevent thrombosis within the vessel. If using bivalirudin, it can take up to 1-2 hours for its anticoagulation effect to a normalize after it is stopped. If patient was on glycoprotein IIB/IIIA inhibitors: For abciximab, consider giving platelet transfusion; tirofiban and eptifibatide have a short half life and their reversal can typically be achieved by stopping there infusion or in extreme cases with hemodialysis. Cangrelor has a short half life and its reversal can be achieved by stopping its infusion.
      • 3rd: Covered stent: Standard of care for a perforation located in the proximal to mid segment of a vessel of appropriate size (≥2.5 mm), with no major side branch across the region where the stent will be placed. If a covered stent can be delivered to a distal vessel perforation, and the vessel is of appropriate size, covered stent placement to seal the perforation is reasonable. If the clinical situation allows, proceed with direct stent placement whenever possible using a single catheter or two-catheter (Ping-Pong) strategy. The stent should be quickly positioned and immediately deployed to high pressure. This should be followed by high pressure post-dilatation (18-20 atm) to achieve appropriate stent apposition.
      • 4th: Embolization of distal vessel perforations: Non-surgical techniques for distal vessel embolization include: Coils, Gel Foams, Glues, Microspheres, Thrombin injection, Subcutaneous tissue, Autologous Blood Clots and multiple other agents (depending on what is available in an individual catheterization lab). Embolization leads to loss of vessel flow beyond point where embolized material is delivered and subsequent infarct in the vessel territory.
      • 5th: Surgery Intervention: Ligation or suturing of the vessel for hemostasis with bypass grafting to the distal vessel. Pericardial patch/Teflon with possible bypass grafting to the distal vessel (consider this approach if vessel has multiple stents and/or presence of a subepicardial hematoma).
  • What are the important learning points?
    • Need to be extremely cautious when using atherectomy devices, especially in tortuous vessels where there is increased guidewire bias, which increases the risk of dissection and perforation.
    • The harbinger of rotational atherectomy related complications is intermittent stalling of the burr. Feedback for from the rotablation system is important in preempting complications and can be perceived by the following:
      • Visual: smooth advancement under fluoroscopy and monitoring decelerations in the speed (RPM) on the monitor
      • Auditory: listen for changes in the frequency of sound as the burr encounters resistance
      • Tactile: advancer knob resistance or driveshaft vibration (consider the following: excessive load on burr, too rapid advancement, a kini in the drive shaft coil, too large of a burr)
    • 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, particularly when performing rotabalation of an angulated and heavily calcified lesion.
    • When a wire is fractured within a coronary vessel, an attempt should be made to percutaneously retrieve the remnant wire or exclude it with a stent, particularly if the remnant wire is located proximal in a large caliber vessel. If the remnant wire is located more distal, it is reasonable to defer intervention. In this case, the fractured wire was located more distal within the vessel, and attempts to retrieve the remnant wire were abandoned as the vessel had already thrombosed due to prolonged balloon inflation to tamponade the vessel.
Educational Content


  • Common complications associated with rotational atherectomy are:1
    • Slow flow / No-reflow
    • Coronary Dissection
    • Coronary Perforation
    • Burr entrapment

Slow flow / No-reflow

  • It is most feared and preventable operator-dependent complication of Rotational Atherectomy (RA)
  • Incidence- 2.6% in the drug-eluting stent era2
  • Omens of slow-flow / no-reflow include sudden decelerations and visual, tactile or auditory clues of high resistance to burr advancement
  • Be mindful of incident chest pain, ST-segment elevations, hemodynamic instability, and bradyarrhythmia while burring which could signal no-reflow phenomenon
  • Prevention
    • Optimal antiplatelet and anticoagulant therapy
    • Continuous flush cocktail
    • Smaller burr sizes (Max burr to artery ratio 0.4-0.6)
    • Lower speeds (140-150K rpm)
    • Short ablation runs of 15-20 seconds
    • Pause between runs
  • Treatment
    • Correction of hypotension with fluids, vasopressors, and pacing as required
    • Administration of intracoronary vasodilators, such as adenosine, nitrates, nitroprusside, nicardipine, and verapamil administered distally in the vessel
    • If hemodynamically unstable, insertion of an intraaortic balloon pump to augment coronary perfusion pressure

Coronary Dissection

  • Dissections during RA are described and graded in standard fashion using the NHLBI classification system (A-F)
  • Incidence: 1.7% - 5.9% in the drug-eluting stent era 3
  • Like slow-flow / no-reflow, dissection can present with signs and symptoms of acute myocardial ischemia including chest pain, ST-segment elevations, and hemodynamic or electrical instability
  • Prevention:
    • Avoid rotablation in excessively tortuous vessels
    • Avoid excessive angulation while burring
    • Smaller burr sizes
  • Treatment:
    • Stop further ablation
    • Maintain wire position
    • Expeditious completion of PCI via balloon angioplasty and stenting if feasible

Coronary Perforation

  • Perforation represents a more severe variant of dissection in which disruption extends through the full thickness of the arterial wall.
  • Incidence: 0-2% in the drug-eluting stent era3
  • Coronary perforations during RA are described and graded in standard fashion using the Elis classification scheme (I-III)
  • Although RA is considered a risk factor for perforation,4 the majority of type III perforations result from balloon angioplasty 5
  • Risk factors: lesion-specific predictors of perforation include eccentricity, tortuosity, length >10 mm, and location in the right coronary artery or left circumflex artery
  • Prevention:
    • Correct burr sizing
    • Avoid aggressive burring
    • Avoid excessive angulation
    • Lower speeds
  • Treatment:
    • Stop further ablation
    • Maintain wire position
    • Discontinuation of anticoagulation
    • Prolonged balloon inflation (10-15 min) proximal or at site of injury. If still bleeding, repeat prolonged balloon inflation
    • If extravasation persists, seal the site with either occlusive coils [perforation site distal main vessel] or by implantation of polytetrafluoroethylene (PFTE) covered stent [perforation siteproximal main vessel, distal side branch which can be excluded with covered stent]
    • If extravasation still persists or site of injury is proximal main vessel with bifurcation (covered stent not an option) consider emergent surgery
    • Aggressive treatment with intravenous fluids, atropine, vasopressors, mechanical circulatory support if hemodynamics deteriorate

Burr Entrapment

  • Entrapment consists of burr embedding in a severe stenosis, preventing both further burr advancement and retrieval
  • Presence of diamond chips on the front, but not the rear, of the burr abets an opportunity for the burr to lodge within a lesion and become entrapped.
  • Once stuck and stalled within a lesion, retrograde ablation is not possible and friction associated with retrograde motion cannot be orthogonally displaced.
  • During ablation, the operator should be attentive to potential warning signs, which may be visual (lack of smooth advancement under fluoroscopy), auditory (pitch changes with variation in resistance encountered by burr), or tactile (resistance in advancer knob or excessive driveshaft vibration)
  • Incidence: 0.5% to 1%3
  • Prevention:
    • Meticulous relief of system tension before RA
    • Gentle pecking motions
    • Short ablation runs
    • Avoid excessive tortuosity
    • Do not stop spinning within a lesion
  • Treatment:
    • Apply forceful pull on the Rota wire with guide disengaged taking advantage of the wire’s 0.014 inches spring tip
    • Administer high dose of vasodilators and aggressively pull the Rota burr
    • Manual traction with on-Dynaglide or off-Dynaglide rotation
    • If above measures fail, potential catheter-based solutions to facilitate burr retrieval include
      • Obtain second arterial access and advance Fielder wire and a small (1~1.25mm) balloon distally, inflate at the level of Rota burr, then aggressively pull the Rota burr
      • Advance Guide extension catheters on the Rota Burr

7Fr Guide extension
Cut the Rota burr shaft at the connection outside the body, then advance 7Fr guide extension on the shaft until the Rota burr and pull aggressively.

6Fr Guide extension catheter
  • Cut the Rota burr and aggressively pull the Teflon covering sheath.
  • once done, then advance 6Fr Guide extension on the shaft until the Rota burr and pull aggressively
    • Subintimal tracking and reentry with balloon dilatation adjacent to the entrapped burr6, 7


Differential sanding of Orbital atherectomy (OA) permits healthy tissue to flex away from the crown during orbit and can be used with speed selection options for low speed (80,000 rpm), high speed (120,000 rpm), or GlideAssist (5000 rpm).

Common complications associated with rotational atherectomy are:

  • Slow flow / No-reflow
  • Coronary Dissection
  • Coronary Perforation

Slow flow / No-reflow

Incidence: 0.9% in Orbit II trial and 0.7% in real work registry analysis.8, 9

The unique mechanism of action, differential sanding, combined with an average particle size of debris of 2.04 μm – smaller than a red blood cell – may contribute to lower rates of no-reflow and transient heart block with orbital atherectomy.10

  • Optimal anticoagulant and antiplatelet therapy
  • Continue ViperSlide infusion
  • Always keep the crown advancing or retracting with slow advancement (1mm/sec)
  • Short run timetime ( <20 seconds)
  • Rest time = or > run time
  • Ensure to keep the optimal blood pressure (SBP > 100Hg) and give fluids, vasopressors, and pacing as needed
  • Administer intracoronary vasodilators, such as adenosine, nitrates, nitroprusside, nicardipine, and verapamil administered distally in the vessel if necessary, via twin-pass dual access catheter
  • If hemodynamically unstable, place an intra-aortic balloon pump to augment coronary perfusion pressure

Coronary Dissection

  • Coronary artery dissection can be categorized by using NHLBI classification system (A-F)
  • Incidence: 3.4 % in Orbit II trial and 0.9% in Real world registry8, 9
  • Dissection can manifest with acute onset of chest pain, new EKG changes with ST elevations, and hemodynamic or conduction disturbances. Prevention
  • Avoid high speed run
  • Avoid in very tortuous coronary anatomy or > 2 bends exceeding 90° angulations
  • Use of ViperWire advance with flex tip in a setting of tortuous artery

  • Treatment
    • Stop ablation immediately
    • Reassess hemodynamic and patient status, then give vasopressor as needed
    • Completion of PCI with balloon angioplasty and stent placement if possible

    Coronary Artery Perforation

    • Coronary perforation is the most serious complication that can occur with OA.
    • With unique mechanism with pulsatile forces in OA, it can result in more significant tissue modification while having a higher risk of deep dissections and perforation.
    • Incidence: 0.7-2%8, 9, 11
    • Coronary perforations during OA can be graded in standard fashion using the Elis classification scheme (I-III).

    Risk factors: Very tortuosity, use of higher speed (120,000 rpm), presence of lipid rich plaque and smaller calcification arc (less than 2 quadrants in OCT/IVUS)12
    • Use of lower speed (80,000 rpm)
    • Avoid excessive angulation( >2 bends exceeding 90° angulations)
    • Careful advancement when evidence of wire wrinkling from tension buildup is present leading to vessel straightening
    • Avoid high speed if the vessel diameter is less than 3 mm
    • Advance the burr slowly with a speed of 1 mm per second

    • Stop further ablation immediately
    • Maintain wire position
    • Discontinuation of anticoagulation
    • Prolonged balloon inflation (10-15 min) proximal or at site of injury. If still bleeding, repeat prolonged balloon inflation
    • If extravasation persists, consider to use coils or covered stent
    • Reassess the perforation and patient status with angiogram
    • Be ready to do emergency pericardiocentesis if necessary
    • If extravasation remains present and/or site of injury is proximal main vessel with bifurcation (covered stent not an option), consider emergent surgery
    • Aggressive treatment with intravenous fluids, atropine, vasopressors, mechanical circulatory support if hemodynamics deteriorates


    1. Sharma SK, Tomey MI, Teirstein PS, et al. North American Expert Review of Rotational Atherectomy. Circ Cardiovasc Interv. 2019;12(5):e007448. doi:10.1161/CIRCINTERVENTIONS.118.007448
    2. Naito R, Sakakura K, Wada H, Funayama H, Sugawara Y, Kubo N, Ako J, Momomura S. Comparison of long-term clinical outcomes between sirolimus-eluting stents and paclitaxel-eluting stents following rotational atherectomy.Int Heart J.2012; 53:149–153
    3. Tomey MI, Kini AS, Sharma SK. Current status of rotational atherectomy.JACC Cardiovasc Interv.2014; 7:345–353. doi: 10.1016/j.jcin.2013.12.196
    4. Shimony A, Joseph L, Mottillo S, Eisenberg MJ. Coronary artery perforation during percutaneous coronary intervention: a systematic review and meta-analysis. Can J Cardiol 2011;27:843–50.
    5. Al-Lamee R., Ielasi A., Latib A., et al. (2011) Incidence, predictors, management, immediate and long-term outcomes following grade III coronary perforations. J Am Coll Cardiol 4:87–95
    6. Sulimov DS, Abdel-Wahab M, Toelg R, Kassner G, Geist V, Richardt G. Stuck rotablator: the nightmare of rotational atherectomy.EuroIntervention.2013; 9:251–258. doi: 10.4244/EIJV9I2A41
    7. Tanaka Y, Saito S. Successful retrieval of a firmly stuck rotablator burr by using a modified STAR technique. Catheter Cardiovasc Interv.2016; 87:749–756. doi: 10.1002/ccd.26342
    8. Chambers JW, Feldman RL, Himmelstein SI, et al. Pivotal trial to evaluate the safety and efficacy of the orbital atherectomy system in treating de novo, severely calcified coronary lesions (ORBIT II). JACC Cardiovasc Interv. 2014;7(5):510-518. doi:10.1016/j.jcin.2014.01.158
    9. Lee MS, Shlofmitz E, Kaplan B, Alexandru D, Meraj P, Shlofmitz R. Real-World Multicenter Registry of Patients with Severe Coronary Artery Calcification Undergoing Orbital Atherectomy. J Interv Cardiol. 2016;29(4):357-362. doi:10.1111/joic.12310
    10. Sotomi Y, Shlofmitz RA, Colombo A, et al. Patient selection and procedural considerations for coronary orbital atherectomy system. Interv Cardiol 2016;11:33
    11. Parikh K., Chandra P., Choksi N., et al: Safety and feasibility of orbital atherectomy for the treatment of calcified coronary lesions: the ORBIT I trial. Catheter Cardiovasc Interv 2013; 81: pp. 1134-1139
    12. Kini AS, Vengrenyuk Y, Pena J, et al. Optical coherence tomography assessment of the mechanistic effects of rotational and orbital atherectomy in severely calcified coronary lesions. Catheter Cardiovasc Interv. 2015;86(6):1024-1032. doi:10.1002/ccd.26000

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