Coronary artery perforation is an infrequent but serious complication of percutaneous coronary intervention (PCI), occurring in some 0.3–0.6%.1–4 The classification by Ellis et al1 describes perforation as type I, an extraluminal crater without extravasation; type II, epicardial fat or myocardial blush without contrast jet extravasation; type III, extravasation through frank (> 1 mm) perforation; and type IV, extravasation of dye into a cardiac chamber or cavity (but not the pericardial space). Type III perforations are associated with cardiac tamponade, a need for urgent bypass surgery and a high mortality rate.1–4 Algorithms for the nonsurgical management of type II and type III perforations involve prolonged balloon or perfusion balloon inflation, reversal of anticoagulation with protamine, or with or without platelet transfusion, placement of covered stents and pericardial drainage for hemodynamic compromise.
In PCI of complex lesions, including chronic total occlusions (CTOs) and bifurcation lesions, hydrophilic guidewires more prone to distal migration may be required for access to a significant side-branch vessel. This increases the risk of distal perforation where there may be no use for a covered stent, and reversal of anticoagulation may not be optimal if a stent has already been deployed in the parent vessel. Strategies to seal the perforation such as polyvinyl alcohol foam embolization,5,6 microcoil embolization,7–10 gelfoam embolization,11 clotted autologous blood,12 intracoronary thrombin,13 microfibrillar collagen14 and use of subcutaneous tissue15 have been employed with various success.
We describe two cases of type III distal artery perforation of a significant branch vessel treated with microcoil embolization without altering the primary treatment strategy or reversing anticoagulation or antiplatelet therapy.
Case 1. PCI was planned to the left anterior descending (LAD)/left anterior descending diagonal (LADD1) bifurcation using a provisional T-stent strategy in a 77-year-old male with troponin-positive acute coronary syndrome (Figure 1A). A 6 Fr JL5 guide catheter (Medtronic, Minneapolis, Minnesota) engaged the left main coronary artery after 90 u/kg of intraarterial (IA), unfractionated heparin, clopidogrel loading (300 mg) more than 24 hours previously and chronic aspirin (75 mg). Both lesions were crossed with hydrophilic Whisper wires (Guidant Corp., Indianapolis, Indiana). The LAD lesion was predilated with a 2.5 x 12 mm Maverick balloon (Boston Scientific, Natick, Massachusetts) after a 20.6 mg bolus of IV abciximab. A 3.0 x 20 mm Taxus® drug-eluting stent (Boston Scientific) was then deployed at 8 atm. The LADD1 was rewired with a Whisper wire and dilated with a 2.5 x 12 mm Maverick balloon to 12 atm before a kissing inflation, using a 3.0 x 15 mm Maverick balloon to the LAD (12 atm) and a 2.0 x 12 mm Maverick balloon to the LADD1 (12 atm). Angiography then revealed TIMI 3 flow in the LAD and TIMI 3 flow with extravasation of blood through the distal LADD1 vessel (Figure 1B).
Initial management included prolonged balloon inflation in the LADD1, just proximal to the perforation, but after two 20-minute intervals, angiography showed continued extravasation of dye into the pericardium. Urgent transthoracic electrocardiography showed a small pericardial effusion and no evidence of tamponade. Given the deployment of the stent in the LAD, reversal of heparin anticoagulation with protamine was deferred and platelet transfusion was not performed.
The LADD1 perforation was occluded with three 0.018 inch 3 x 2 mm Tornado microcoils (Cook, Bjaeverskov, Denmark) delivered through a 3 Fr, 0.018 inch MicroFerret infusion catheter (Cook) initially advanced over the LADD1 Whisper wire and positioned in the mid-distal LADD1. Each microcoil was positioned with a 2 ml saline flush through the delivery catheter. Extravasation ceased after the third coil and was confirmed on angiography 15 minutes later (Figure 1C).
The next day, transthoracic electrocardiography demonstrated a trivial residual pericardial effusion. Aspirin and clopidogrel were continued. The patient suffered pleuropericardial chest pain for 24 hours. Troponin I at 24 hours was 0.7 ug/L, and there were no significant electrocardiographic changes.
Repeat angiography 4 days post-PCI demonstrated a patent LAD stent, occlusion of the LADD1, with microcoils in situ and no extravasation. The patient was discharged 48 hours later.
Case 2. PCI was planned for tandem LAD lesions, including LAD/LADD1 bifurcational disease in an 83-year-old female with prior myocardial infarctions (1991 and 2004) (Figure 2A). A 6 Fr JL4 guide catheter (Medtronic) engaged the left main coronary artery after 90 u/kg IA unfractionated heparin, clopidogrel loading (300 mg) more than 24 hours previously and chronic aspirin (75 mg). The LAD l and LADD1 lesions were crossed with Whisper wires. The proximal LAD lesion was predilated with a 2.5 x 12 mm Maverick balloon before a 3 x 12 mm Driver stent (Medtronic) wasdeployed at 16 atm. Angiography then revealed TIMI 3 flow in the LAD and TIMI 3 flow with extravasation of blood through the LADD1 related to distal migration of the Whisper wire (Figure 2B). The jailed Whisper wire was withdrawn and used to rewire the LADD1.
Initial management included prolonged balloon inflation in the LADD1, just proximal to the perforation, but after two 20-minute intervals, angiography showed continued extravasation of dye to the pericardium. Urgent transthoracic electrocardiography showed only a small pericardial effusion without evidence of tamponade. The maximum activated clotting time (ACT) during the procedure was 347 seconds. Given the deployment of the stent in the LAD, reversal of heparin anticoagulation with protamine was deferred.
The LADD1 perforation was occluded with three 0.018 inch, 3 x 2 mm Tornado microcoils, as in Case 1, and delivered through a 3 Fr, 0.018 inch MicroFerret infusion catheter positioned in the mid-distal LADD1. After delivery of the third coil, extravasation significantly slowed and ceased over 15 minutes (Figure 2C).
During microcoil insertion, the patient’s blood pressure was 90 mmHg, with a 40 mmHg paradox associated with echocardiographic evidence of right atrial collapse. Using pericardiocentesis, 350 ml of blood was aspirated and a drain was left in situ. Repeat transthoracic electrocardiography showed no residual collection and the intrapericardial drain was removed after 24 hours. The patient’s course was complicated by transient atrial fibrillation, but she was discharged without further complication 3 days later.
The perforation grade and the presence of chronic renal insufficiency are predictors of mortality in coronary artery perforation. 16 The consequences of type III coronary artery perforations are significant, including emergency bypass surgery (50%) and death (21%).17 The management depends on the type, site and mechanism of the perforation.1 Distal coronary perforations often involve significant side branches that may not respond toprolonged balloon inflation, and this may trigger reversal of both the anticoagulation and platelet inhibition, as well as attempts to seal the hole. If a stent has already been deployed in the parent vessel, this potentially increases the risk of acute stent thrombosis.18 A further hazard is the formation of semi-clotted intrapericardial hematoma secondary to reversal of heparin and/or platelet inhibition, which may make emergency pericardiocentesis difficult and less effective.
The two cases represent typical type III perforations caused by hydrophilic guidewires. Routine use of these wires should be avoided unless necessary, and the distal tip should always be visualized to prevent distal migration. Both cases involved significant side branch vessels (> 1 mm), and one was in the setting of glycoprotein (GP) IIb/IIIa inhibition with abciximab. Both occurred after stent deployment in the parent vessel. One case required pericardiocentesis for cardiac tamponade. In each case, rapid and effective coil embolization was achieved without reversal of standard antiplatelet and anticoagulant strategies.
Successful strategies for sealing have included polyvinyl alcohol and gelatin foam, but these methods are more suited to small (< 1 mm) diameter arteries, and caution is required to prevent reflux of embolizing materials to the more proximal vessel. Other successful strategies include delivery of subcutaneous tissues, thrombin, and autologous clot formation, which may have proven difficult in the setting of glycoprotein IIb/IIIa inhibition, as in Case 1.
The microcoils (Cook) have a soft platinum structure with synthetic fibers that maximize thrombogenicity. The Tornado configuration (3 mm proximally and 2 mm distally) maximizes coil exposure to the cross-section of lumen for disruption of flow and is designed for vessel taper (Figure 3). Microcoils are also compatible with magnetic resonance imaging.
There are several advantages of using microcoils in the cases described. Firstly, they are readily accessible and relatively inexpensive. Secondly, they can be prepared easily and deployed rapidly. The culprit wire causing the distal perforation is pulled back into the arterial lumen and a 3 Fr microcatheter with a distal radiopaque tip is inserted over the wire, just proximal to the perforation site and the wire is then removed. A single Tornado microcoil is supplied preloaded within a loading cannula that is attached to the microcatheter hub with a Luer lock. The microcoil is then positioned through the distal microcatheter tip using a brisk 2 ml saline flush connected to the loading cannula. Further microcoils can be used in the same way until extravasation has ceased. Thirdly, by using a microcatheter as a delivery device, microcoils can be inserted distally and accurately without danger to the parent vessel. Fourthly, they come in various sizes, and the number used (usually one to three) is determined by cessation of extravasation on angiography. Finally, once extravasation has ceased, there is little or no potential to rebleed and therefore, reversal of heparin may be avoided.
The clinical sequelae of type III coronary artery perforations are related to the degree of extravasation. In distal perforations of significant side branches (> 1 mm), which are not controlled with prolonged balloon inflation, we believe the deployment of microcoils provides a simple, rapid and safe solution to ongoing extravasation. While heparin reversal is currently the accepted practice in these cases, reversal of antiplatelet and anticoagulant therapy may not be mandatory, allowing high procedural success, particularly when stenting has already been undertaken. We recommend that microcoils be readily available for this purpose.
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