Coronary Artery Perforation During Percutaneous Coronary Intervention: Incidence and Outcomes in the New Interventional Era

Coronary artery perforation (CP) is a rare and potentially life-threatening complication of percutaneous coronary intervention (PCI). CP has historically been reported to occur in 0.1–3.0% of PCI procedures.^1–5 Although CP can be caused by coronary wires and balloon angioplasty,⁶ they are more frequently reported in PCI using atheroablative devices, stenting and excimer laser coronary angioplasty.² In coronary artery perforations, the vessel damage may range from vessel puncture by the coronary wire, resulting in minimal dye staining to vessel rupture, followed by brisk extravasation of blood and dye into the pericardial space leading to hemodynamic collapse.¹² Nonsurgical treatment of CP includes prolonged balloon inflation with perfusion balloons, pericardial drainage and coil embolization.^{1–5,17–21} Covered stents have emerged as a new treatment modality in a select group of patients.^4,5 Briguori et al. reported a 91% successful closure rate of Type 1 and 2 perforations with polytetrafluoroetylene-covered stents and a significantly lower incidence of cardiac tamponade, mediastinal hemorrhage, myocardial infarction or need for emergency surgery.¹ Previous studies have determined risk factors that place patients at higher risk for CP. These risks include increasing age, female gender, heavy calcification, target lesions in the left circumflex and right coronary arteries, long target lesions (> 10 mm) and eccentric lesions.^6–11 Interventional cardiology techniques have evolved over the last decade with the advent of new stents, atheroablative devices and the use of glycoprotein (GP) IIb/IIIa agents. Therefore, we hypothesized that the incidence, cause and outcomes of CP should differ from that previously described. Methods All patients who underwent PCI at our medical institution from January 2001 to December 2004 were identified. Data were extracted by chart review and a prospectively filled computer database. Patient age ranged from 35 to 95 years old (mean age: 67 years) and 64% percent were men. The majority of lesions treated in these patients were classified as AHA/ACC Class B (48%) and Class C (41%) lesions. The choice of access and equipment were determined by the treating interventional cardiologist. All patients received heparin during the procedure for an ACT above 300 seconds or above 200 seconds when GP IIb/IIIa agents were used. Dual antiplatelet therapy with aspirin and clopidogrel (or ticlopidine) was administered periprocedurally. GP IIb/IIIa use was at the discretion of the interventional cardiologist. CPs were classified according to the previously stated angiographic criteria of Ellis et al.²: Type 1 CP, described as a crater extending outside the lumen only; Type 2 CP, resulting in pericardial or myocardial blush without a > 1 mm exit hole; Type 3, described as frank streaming of contrast through a > 1 mm exit hole; and Type 3, with cavity spilling as a perforation into an anatomic chamber. Results A total of 4,886 PCI procedures were performed from January 2001 to December 2004. Atherectomy devices were used in 329 patients (6.7%) and GP IIb/IIIa agents in 2,200 (45%): integrilin (51.2%), tirofiban (44.6%) and abciximab (4.2%). Twenty-five CPs were identified for an incidence of 0.5%. There were 6 Type 1 CPs (24%), 10 Type 2 CPs (40%) and 9 Type 3 CPs (36%). All 6 Type 1 CPs were caused by coronary wires and nearly all (4/6) occurred with the use of hydrophilic and extra stiff wires. Three of the five Type 1 perforations occurred while attempting to cross chronic total vessel occlusions. GP IIb/IIIa agents were used in 2 of the patients (Figure 1). Type 2 perforations were caused by coronary wires in 8/10 CPs and by stent placement in 2/10 CPs. Five patients (50%) had received GP IIb/IIIa agents and 5 perforations occurred while attempting to cross chronic total vessel occlusions. Although 2 myocardial infarctions resulted, no pericardial drainage or surgical intervention was required (Figure 2). Type 3 perforations were caused by stent placement in 4/9 CPs, by rotational atherectomy devices in 2/9 CPs and by coronary wires in 3/9 CPs. Type 3 perforations most often occurred in ACC Type B lesions (44%) and Type C lesions (56%). Seven of the Type 3 perforations (78%) were associated with significant calcification. Seven patients (78%) had received GP IIb/IIIa. agents. None were chronic total vessel occlusions. Six Type 3 perforations were treated by percutaneous methods alone, 2 needed surgical intervention and one required surgical intervention after failing percutaneous method therapy (covered stent). Of the perforations solely treated by percutaneous methods,6 3 patients were treated by covered stent, 1 required pericardial drainage, 1 was treated by perfusion balloon and 1 was treated by heparin reversal alone. Five patients (56%) sustained a myocardial infarction and 2 patients (22%) died. One patient underwent surgical intervention after failing percutaneous therapy (covered stent) and died (Figure 3). Discussion Coronary perforation continues to be an infrequent, but serious, complication of percutaneous coronary intervention. The incidence of CP has previously been shown to increase with the use of atherectomy devices.² However, it remains unclear if the current liberal use of GP IIb/IIIa agents is associated with worse outcomes in CPs. Some have reported that a significant amount of hemodynamically significant perforations were associated with the use of abciximab,¹² while others report that the occurrence and severity of CP was not increased with the use of abciximab.²² We demonstrate that the majority of CPs occurring during PCI are Type 1 and Type 2 perforations, and are most often caused by coronary wires. The use of GP IIb/IIIa agents did not worsen the hemodynamic effect of this type of perforation. Our data suggest that these patients can be managed conservatively: by reversal of anticoagulation, discontinuing ongoing GP IIb/IIIa use and careful observation of the patient. Type 3 perforations continue to be associated with significant morbidity and mortality. Contrary to earlier studies, we did not observe an increased risk of perforation with atheroablative devices when compared to coronary stenting. While the exact explanation remains unknown, we postulate that this may be due to the change in interventional practice which aims for optimal stent deployment using high-pressure inflation. The decreased perforation rates occurring with atheroablative devices may be due to the increased awareness of the risk of perforation with these devices and the avoidance of their use when multiple risk factors for coronary perforation exist. With regard to the treatment of Type 3 perforations, our data continue to reinforce percutaneous management. The majority of cases were treated by percutaneous methods, including pericardial drainage, perfusion balloon and placement of polytetrafluoroethylene (PTFE)-covered stents. All patients had heparin reversed and GP IIb/IIIa use immediately discontinued. However, Type 3 perforations continue to be associated with increased mortality and morbidity. In conclusion, Type 1 and 2 perforations are predominately caused by hydrophilic and stiff wires, and do not require pericardial drainage or surgical intervention. Type 3 perforations are more often associated with stent placement, and most can be managed with percutaneous methods.

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