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  3. Perforation Type 2 Wire – Case 1
 Coronary Perforations

Perforation Type 2 Wire – Case 1

Clinical Presentation

  • 70-year-old male who presented with chest pain (CCS Class III).

Past Medical History

  • HTN, HLD, CAD, DVT/PE (2009)
  • LVEF 60%

Clinical Variables

  • Cardiac CTA: Severe 3-Vessel CAD.
  • Prior Cardiac Catheterization: Distal LM 60-70% stenosis, proximal LAD 70-80% stenosis, and proximal LCx 80-90% stenosis with severe calcification of the vessels.

Medications Heading

  • Home Medications: Home medications: Aspirin, Clopidogrel, Simvastatin, Ezetimibe, Fenofibrate, Atenolol, Amlodipine, Ranolazine
  • Adjunct Pharmacotherapy: Clopidogrel, Ticagrelor, Bivalirudin

Pre-procedure EKG Heading

Angiograms

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Right coronary artery (RCA) angiography
  • 70-80% ostial stenosis in the RCA
  • ulcerated subtotal lesion in the proximal to mid RCA
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Right coronary artery (RCA) angiography

  • 70-80% ostial stenosis in the RCA
  • ulcerated subtotal lesion in the proximal to mid RCA
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Left coronary artery angiography

  • 30-50% in-stent restenosis in distal LIMA to LAD bypass graft.
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Left coronary artery angiography

  • 90-95% calcified distal left main (LM) bifurcation lesion
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Rotational atherectomy of the LM using a 1.25mm burr at 150k RPM.

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Angiography of the LM after rotational atherectomy with 1.25mm burr at 150k RPM.

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Rotational atherectomy of the LM using a 1.75mm burr at 150k RPM.

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Angiography of the LM after rotational atherectomy with 1.75mm burr at 150k RPM.

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Pre-dilatation of the LM lesion with a Quantum Apex 3.0/15mm balloon.

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Angiography of the LM after lesion pre-dilatation.

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Deployment of a Synergy 3.5/24mm stent in the LM.

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Angiography of the LM after stent placement.

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Post-dilatation of the stent placed in the LM with a Trek NC 4.0/12mm balloon (20 atm).

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Angiography of the LM after stent post-dilatation showing a type 2 distal wire perforation.

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Final angiography of the LCA showing a type 2 wire perforation which is self contained with staining of the myocardium.

Post-procedure EKG

Case Overview

  • Underwent OCT guided PCI of the distal LM bifurcation (distal LM MLA of 5.1 mm²).
  • SKS technique was used to place a stent in the LM bifurcation.
  • Procedure was complicated by a non-flow limiting, Type B dissection of the LM proximal to the newly placed stents.
  • Two stents were placed in a ‘parallel, double barrel’ manner overlapping into the previously placed stents in the LM.
  • Follow up angiography revealed, inadequate treatment of the dissection with incomplete coverage of the dissection flap.
  • Patient was observed on the catheterization table and repeat angiography showed no change in the residual dissection.
  • Post intervention OCT showed LM MLA 10.9 mm² with residual minor proximal edge dissection (residual dissection was < 2 mm in length). Therefore, further intervention was deferred.
  • Troponin-I peaked at 0.4 ng/mL and CK-MB peaked at 2.6 ng/mL.
  • Patient was discharged the next day without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • High pressure post-dilatation of the proximal stent edge.
  • How could the complication have been prevented?
    • Optimize balloon position and assure it is not outside the proximal or distal stent edge prior to balloon inflation.
    • Post-dilate the stent edges using a lower balloon inflation pressure.
      • When performing SKS, KBI maximal pressure dilatation of the stent balloons is 12 atm simultaneously.
      • When performing individual dilatation of the stents after SKS are placed, the maximal pressure to inflate the stent balloons is 16 atm.
    • Consider using separate shorter NC balloons instead of the stent balloons after SKS were deployed.
  • Is there an alternate strategy that could have been used to manage the complication?
    • Consider an alternative stenting technique to treat the dissected segment such as reverse crush.
    • Convert SKS into crush technique by crushing the LM-LCx stent with a balloon placed inside the LM-LAD stent, followed by recrossing of LCx and performing final KBI.
  • What are the important learning points?
    • This is a type B dissection because of the presence of a parallel tract linear defect seen during contrast injection.
    • Maintaining wire position is extremely important, especially when dealing with complex interventions. Be cautious to avoid loss of wire position and possible wire entrapment.
    • Guide catheter induced dissection should always be considered in the differential when there is a LM dissection.
    • The larger the size of the guide catheter the higher the risk for guide catheter induced dissection. We used a large sized guide catheter (8 Fr) to accommodate the large size rota burr (2.15 mm).
    • Optimize post dilatation technique.
      • Use a noncompliant, short balloon for post-dilatation of a stent.
      • Keep the balloon just inside the stent edge when performing post-dilatation of the proximal or distal stent edges.
      • Use Stent Boost (Philips) or Stent Viz (GE) to assess the positioning of the NC balloon prior to inflation.
    • Post intervention imaging with OCT was performed and the dissection length was < 2 mm. Conservative management is appropriate if the dissection length is < 2 mm and dissection is not propagating.
      • The patient remained in the cardiac catheterization lab for 30 minutes. Repeat angiography was performed and dissection was stable; therefore, we opted for conservative management instead of performing further intervention.
    • Note: SKS technique is now rarely being used.
Educational Content

CORONARY PERFORATION

  • Coronary perforation although rare is one of the most feared complication of percutaneous coronary intervention (PCI)1
  • Incidence: 0.4%2
  • Risk factors:3
    • Chronic total occlusions
    • Angulated calcified type B2 and type C lesions
    • Long lesions (>10 mm)
    • Eccentric lesions
    • Smaller vessel size
    • Older age
    • Female sex
    • Renal failure
    • Previous coronary artery bypass graft surgery
  • Common causes:3
    • Oversizing of the dilatation catheter and balloon/stent mismatch [Balloon - artery ratio >1.3/1]
    • Inflation of a non-compliant balloon to very high pressures
    • Use of atheroablatives devices or cutting balloons
    • IVUS directed optimal PCI with high pressure stenting
  • Classification of coronary perforation: There are two classification schemes for coronary perforation - Ellis4 and Kini classification.5 Ellis classification scheme, more commonly used describes wire and device perforations into following categories:
Type IExtraluminal Crater without extravasation
Type IIPericardial or myocardial blush without a ≥1mm exit hole and without contrast jet extravasation
Type IIIFrank extravasation of contrast and a ≥1mm exit hole
Type III- Cavitary Spilling (CS)Perforation into an anatomic cavity chamber, such as
the coronary sinus, or the right ventricle

Kini classification scheme is more simplistic, focused on wire perforations and describes two types of wire perforations:

  • Type I described as "myocardial stain" with no frank dye extravasation and
  • Type II as "myocardial fan" with dye extravasation into pericardium, coronary sinus, or cardiac chambers
  • A significant proportion of perforations occur with guidewires crossing the lesion, with distal wire perforation or wire fracture. Extra stiff wires and low friction hydrophilic-coated wires are associated with higher incidence of perforation.6,7 This may reflect either use of specialty wires to facilitate passage through more complex lesions or their ease of distal migration.
  • Prevention: meticulous attention to guidewire position, careful and appropriate sizing of the balloon or stent prior to inflation, and avoiding over dilation or high pressure inflation exceeding the balloon's burst pressure
  • Management: Clinical suspicion should rise if patient develops sudden onset of acute/sharp chest pain or have sudden explained severe hypotension, particularly when inflating balloon or deploying a stent. If clinical suspicion arises, pull balloon immediately into the guide and perform angiography to confirm diagnosis.
    • The first aim is to prevent cardiac tamponade by immediate balloon inflation [SDS or the balloon present in the guide] proximal or at site of perforation at the lowest pressure possible. Usually 2-4 atmospheres for about 5-10 minutes is sufficient. However, may need to go to higher pressure and or longer duration to achieve hemostasis. Assess for hemostasis throughout intervention by injecting contrast at regular intervals.
    • Consider anticoagulation reversal: Decision to reverse needs to be balanced against potential risk of acute thrombosis, especially if a stent was just deployed. Heparin reversal: protamine sulfate 1mg IV/100 units of UFH (to achieve activated clotting time of <150s). Bivalirudin reversal: fresh frozen plasma is preferred and it results in partial reversal.
    • Aggressive treatment with intravenous fluids, atropine, vasopressors, mechanical circulatory support may be required if hemodynamics deteriorate. Call CT surgery for backup.
    • Emergent bedside echocardiogram should be obtained. If patient has significant effusion with tamponade physiology, perform emergent pericardiocentesis.

Treatment of coronary perforation

Type 1 perforation
  • Often resolves without intervention and reversal of anticoagulation
  • If above measure fails, perform prolonged balloon inflation (10-15 min) proximal or at site of injury
  • If still persists, follow steps for type II/III/III CS perforations as explained below

Type II/III/III CS perforation
  • Prolonged balloon Inflation proximal or over perforation site and reversal of anticoagulation. 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 site proximal 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
  • Type III CS draining in to coronary sinus or right ventricle is usually benign and can be managed conservatively

Step by step guide for management of coronary wire perforation5
  1. Reverse anticoagulation.
  2. Inflate appropriately sized balloon to low atmospheric pressure proximal or at the site of perforation and confirm sealing of further extravasation with contrast injection from guiding catheter.
  3. Perform prolonged balloon inflation (10–20 min) proximal or at the site of perforation if the perforation is in distal territory or in tertiary branches.
  4. Deflate balloon and perform contrast injection- if persistent extravasation, reinflate balloon and start preparing for coil delivery microcatheter placement.
  5. Remove the balloon and track the coil delivery microcatheter over the guide wire and place it about 1 mm proximal to the site of perforation.
  6. Load the occlusive coil into the microcatheter and advance it by pushing with either a 0.018” guidewire or the stiffer backend of workhorse guidewire. Push the coil out distally and withdraw the catheter simultaneously.
  7. Consider delivery of second coil if there is persistent leak.
  8. In some cases with persistent coronary leak from a side branch, a covered stent can be placed in the main vessel, cutting off the blood supply to the side branch with resultant resolution or minimization of leakage.
  9. Perform transthoracic echocardiogram on procedure table to rule out large pericardial effusion and perform emergent pericardiocentesis if evidence of tamponade.
  10. Monitor in the coronary care unit and obtain an echocardiogram the following day.
  11. Withhold antiplatelet agents for 12–24 hours and resume usual dose once uneventful.


References

  1. 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.
  2. Kinnaird T, Kwok CS, Kontopantelis E, et al. Incidence, determinants and outcomes of coronary perforation during percutaneous coronary intervention in the United Kingdom between 2006 and 2013. An analysis of 527121 cases from the British Cardiovascular Intervention Society Database. Circ Cardiovasc Interv 2016;9:e003449.
  3. Ellis SG, Roubin GS, Kinh SB, et al. Angiographic and clinical predictors of acute closure after native vessel coronary angioplasty. Circulation 1988;77:372–9.
  4. Ellis S.G., Ajluni S., Arnold A.Z., et al. (1994) Increased coronary perforation in the new device era. Incidence, classification, management, and outcome. Circulation 90:2725–2730.
  5. Kini AS, Rafael OC, Sarkar K, et al. Changing outcomes and treatment strategies for wire induced coronary perforations in the era of bivalirudin use. Catheter Cardiovasc Interv. 2009;74(5):700‐707. doi:10.1002/ccd.22112.
  6. 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.
  7. De Marco F., Balcells J., Lefèvre T., Routledge H., Louvard Y., Morice M.C. (2008) Delayed and recurrent cardiac tamponade following distal coronary perforation of hydrophilic guidewires during coronary intervention. J Invasive Cardiol 20:E150–E153.

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