- 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 I||Extraluminal Crater without extravasation|
|Type II||Pericardial or myocardial blush without a ≥1mm exit hole and without contrast jet extravasation|
|Type III||Frank 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 perforationType 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
- 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 into coronary sinus or right ventricle is usually benign and can be managed conservatively
- Reverse anticoagulation.
- 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.
- 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.
- Deflate balloon and perform contrast injection- if persistent extravasation, reinflate balloon and start preparing for coil delivery microcatheter placement.
- 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.
- 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.
- Consider delivery of second coil if there is persistent leak.
- 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.
- Perform transthoracic echocardiogram on procedure table to rule out large pericardial effusion and perform emergent pericardiocentesis if evidence of tamponade.
- Monitor in the coronary care unit and obtain an echocardiogram the following day.
- Withhold antiplatelet agents for 12–24 hours and resume usual dose once uneventful.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.