Coronary Perforation 2006 — Watch for the Wire

The number of percutaneous coronary interventions (PCI) performed worldwide is increasing. With the improvement of technology and interventional tools, the number of procedures is expected to further increase. As the range of equipment available to the interventional cardiologist evolves, together with necessary operator expertise, not only will the number of procedures increase, but interventionists will be treating patients with complex disease and more challenging coronary anatomy. Among the most dreadful complications seen during PCI are abrupt vessel closure and perforations. Improvements in stent technology and antithrombotic therapy have almost completely resolved the need for emergent surgical intervention for cases of abrupt vessel closure.¹ In contrast, as calcified, tortuous and occluded vessels are increasingly treated by percutaneous means, vessel perforation is likely to persist as a rare but dreadful complication of PCI. Apparently, the widespread use of glycoprotein IIb/IIIa inhibitors, stiffer wires and high-pressure post-stenting balloon dilatation may further negatively influence the clinical consequences of vessel perforation. Perforations are divided into three classes (Table 1).² During PCI, coronary artery perforations can be caused by coronary wires and balloon angioplasty, but based on reports from the 1990s, they occur more frequently when atheroablative devices, stenting and excimer laser coronary angioplasty (ELCA) were used. Fortunately, the rate of this grave complication of percutaneous revascularization is low. Angiographic evidence of perforation has been reported in 0.1% of lesions treated with balloon angioplasty, 0.5–3.0% of lesions treated with rotational atherectomy, directional coronary atherectomy, TEC, or ELCA, and 0.2% when a stent is used (Table 2).^2–13 Perforations account for 20% of referrals for emergency bypass surgery.¹⁴ Patients who are especially at risk are elderly, women, those with complex lesion morphology (chronic total occlusion, vessel bifurcation, angulated calcified and tortuous arteries),^2,7,8 and those in whom atheroablative devices are used.^3,5,6 During PTCA, perforation may occur as a consequence of guidewire advancement, balloon advancement, balloon inflation or balloon rupture. Since PTCA results in dissection and stretching of the vessel wall, oversized balloons (balloon/artery ratio > 1.2) may extend these dissections through the adventitia, resulting in vessel perforation. Devices that alter the integrity of the vascular wall may also lead to perforation by tissue removal (TEC, DCA), pulverization (rotational atherectomy), or ablation (ELCA). With rotational atherectomy, morphologic features associated with perforation include lesion eccentricity, lesion length > 10 mm and vessel tortuosity.⁶ Oversized devices, especially when used to treat bifurcation lesions and lesions located in severely angulated vessel segments, substantially increase the risk of perforation. Intracoronary stenting can also lead to perforation from the use of stiff guidewires, oversized compliant balloons (for stent delivery), high-pressure balloons (for optimal stent expansion), or from subintimal passage of the stent into a vessel with severe dissection. In this issue of the Journal, Ramana et al.¹³ report a coronary perforation incidence of 0.5% (25 cases out of 4,886 PCI procedures). A similar incidence was reported by several groups (Table 2). Interestingly, in the present group of patients treated between 2001–2004, most perforations occurred due to guidewires, usually hydrophilic or extra-stiff. Witzke et al.¹² also reported that 51% of all perforations were guidewire-induced. Perforations can occur while trying to cross the lesion with the guidewire, with the distal wire or as a result of wire fracture. Stankivic et al.¹¹ divided the Milan experience into two phases. The early phase (before 1998) was characterized by a higher incidence of Class III perforations associated with IVUS-guided lumen optimization or the use of rotational atherectomy. Perforations were predominantly caused by compliant balloon catheters and frequently occurred in angulated lesions. The incidence of in-hospital MACE was higher in the early phase (51.4% versus 22.4%; p = 0.006), with an almost eightfold higher incidence of CABG and/or death (31.4% versus 4.1%; p = 0.001). Compared with the early phase, the late phase (1998 and beyond) was characterized as mainly Class II perforations that were frequently caused by a guidewire (RR 1.59; 95% CI 1.25–2.04; p = 0.001) in an attempt to re-open totally occluded vessels (RR 1.35; 95% CI 1.03–1.77; p = 0.033). These perforations responded well to protamine administration and/or prolonged balloon inflation. This may coincide with the introduction of hydrophilic coronary wires and special stiff wires designed to recanalize chronic total occlusions. Coronary perforation occurred more frequently with debulking techniques than with nondebulking (PTCA and stent) techniques. However, the use of debulking devices is decreasing in most catheterization laboratories worldwide. As a result, most cases of coronary perforation in the future are expected to occur from guidewires during PCI of complex total occlusion and tortuous lesions. These findings stress the importance in current practice of careful fluoroscopic observation of the progression of the guidewire through the arterial tree, as well as the need for frequent monitoring of guidewire position in the distal coronary artery, especially when hydrophilic or stiff wires are used. In addition, noting a guidewire perforation and monitoring its benign course in the catheterization laboratory it is not always a guarantee of the absence of late complications. Cardiac tamponade may present several hours after PCI, even without additional heparin administration after the procedure and without having used glycoprotein IIb/IIIa inhibitors during the procedure, and in rare cases, may not be recognized for up to 24 hours.¹⁵ Treatment. As in many fields in medicine, prevention is the best therapy. The interventional cardiologist should weigh carefully the risk-to-benefit ratio, especially when treating complex coronary anatomy. The poor prognosis associated with cardiac tamponade emphasizes the importance of taking steps to prevent this complication, such as careful guidewire advancement and positioning, avoidance of balloon or device oversizing, and meticulous attention to device selection and technique. During all percutaneous interventions, the tip of the guidewire should advance smoothly beyond the stenosis and retain torque response. If there is buckling of the guidewire, restricted tip movement or resistance to guidewire advancement, the wire may be subintimal and should be withdrawn and repositioned. If there is any concern that the balloon catheter may have entered a false lumen when an over-the-wire balloon is used, a gentle contrast injection may be indicative of the location of the tip of the balloon; however, such a maneuver can spark a distal dissection propagation. Persistent contrast staining indicates that a false channel has been entered and requires withdrawal and repositioning of both the guidewire and balloon, since balloon inflation within a false lumen may result in coronary artery rupture and rapid clinical deterioration. If coronary artery perforation does occur during PCI, sedation and pain relief measures should be considered. Meticulous monitoring and early echocardiography are recommended. Cardiovascular surgeons should be notified. Adverse clinical events following coronary perforations are related to their angiographic severity, occurring more frequently in patients who experienced Class 3 perforation. Initial management should focus on sealing the perforation as quickly as possible to prevent accumulation of blood within the pericardial space. In most cases this can be achieved using a prolonged balloon inflation, and if necessary, a perfusion balloon catheter to reduce myocardial ischemia. In cases of severe perforation, reversal of heparin anticoagulation with protamine to reach an activated clotting time (Jomed International AB, Helsingborg, Sweden) is a currently used covered stent. It is comprised of a layer of ultra-thin (75 µm) polytetrafluoroethylene (PTFE) graft material sandwiched between two stents of reduced wall thickness. Unfortunately, the current PTFE-covered stent has limited flexibility and a large profile, and is not available in diameters smaller than 3.0 mm. This stent also has high restenosis rates, however the PTFE-covered stents can successfully seal the site of coronary perforation and therefore decrease mortality and the need for emergency surgery in these patients. Monitoring after Successful Nonsurgical Management. Hemodynamic monitoring is done in the intensive care unit. Serial echocardiographic studies should be performed to monitor or detect pericardial effusion. Antiplatelet therapy consists of 325 mg/day of aspirin indefinitely, and 75 mg of clopidogrel for 3 months. Close clinical follow-up and stress tests are recommended. Coronary CT may provide valuable information regarding restenosis and vessel appearance at 2 to 4 months post-perforation, and repeated angiography should be considered if clinical restenosis is suspected. In summary, the incidence of coronary perforation also remains low in the current device era; it occurs more frequently with debulking devices and often as a consequence of guidewire migration and injury. However, since the use of debulking devices decreases, most future perforations will likely be guidewire-induced, followed by stent-induced perforations. Treatment of coronary perforation requires early detection, angiographic classification, immediate sealing of coronary extravasation and relief of hemodynamic compromise. Reversal of heparin anticoagulation, platelet transfusion in those patients treated with abciximab, and the use of covered stents need immediate attention. Pericardiocentesis should be performed for symptoms of cardiac tamponade, and perforations leading to severe hemodynamic compromise which cannot be treated and sealed appropriately, will occasionally require emergency surgery.

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