Coronary Perforations: Old Screenplay, New Actors!

Coronary perforation remains one of the most serious complications in the catheterization laboratory, with multiple studies demonstrating very poor outcomes, particularly in relationship to myocardial infarction and death. Angiographic evidence of perforation has been reported in 0.1% to 3.0% of lesions treated with various intervention techniques^1–8 and even today accounts for 20% of referrals for emergency by-pass surgery.9 Patients who are especially at risk are elderly, female patients, those with calcified and tortuous arteries^1,5,6,8 and those in whom atheroablative devices are used.^{3,4,6,8,10,11} In our own series, we noted an 8% incidence of death, 18% incidence of MI, and a 13% need for emergency coronary bypass surgery.⁸ Recent advances in device technology, intense pharmacological management and improvement in operator experience and technique resulted in a shift of interventional cardiology towards the treatment of more complex patient and lesion subsets compared to historical controls. Whether that change in clinical practice has influenced the coronary perforation rate and severity is not well established. In this issue of the Journal, Witzke, et al. report the incidence, management, and clinical outcome of coronary perforations in a large database of 12.658 patients undergoing PCI in the current device era.¹² Coronary perforation occurred in 39 patients (0.3%) and 31 of them were class II or III according to the angiographic classification proposed by Ellis et al.¹ Similar to prior reports, incidence of perforations varied with different devices used, and was the lowest (0.15%) with stent procedures and the highest with debulking procedures (1%).^1,3–8,11 However, although use of debulking techniques was a predictive of perforation in their study, the likelihood of developing a type III perforation was not significantly greater in the debulking group in comparison to the non-debulking technique. See Witzke, et al. on pages 297–301 It is interesting to note that 51% of all perforations were induced by guidewire. In our own series we also observed the increase in the rate of guidewire perforations in recent years (1998 onwards) which may coincide with the introduction of hydrophilic coronary wires and special stiff wires designed to recanalize chronic total occlusions.⁸ The risk of this complication is in direct relation to the magnitude of the perforation. Although Witzke et al do not report angiographic severity of guidewire induced perforations in their series, we found that most of those perforations were angiographic class II and had good clinical outcomes (none of them required emergency CABG or resulted in death of the patient in our study). However, these findings stress the importance of careful fluoroscopic observation of the progression of the guidewire through the arterial tree, as well as the need for frequent change in magnification in order to monitor guidewire position in the distal coronary artery when hydrophilic, taper 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 about absence of late complications. In few cases we observed tamponade occurring 6 or 8 hours after the procedure even without additional heparin administration after the procedure and without having used IIb/IIIa inhibitors during the procedure. Another important observation of the present study is that although 48% of their 12.658 patients received glycoprotein IIb/IIIa inhibitors occurrence of coronary perforations was not affected by the use of those agents (perforations occurred in 0.26% of the patients treated with these agents and in 0.3% of those who were not). Although detailed outcome of the patients with coronary perforations treated with IIb/IIIa antagonists is not presented, occurrence of cardiac tamponade, as the most severe clinical manifestation, was also not affected by those agents. While in some recent reports use of GP IIb/IIIa agents was also not related to coronary perforation⁶, in our own series we found a non-significant trend for a higher incidence of perforation with the use of GP IIb/IIIa agents.⁸ Possible explanations for the association of perforation with the use of GP IIb/IIIa agents may be that they unmask a minimal vessel tear and convert it in to overt perforation, or case selection in our study could bias the results. As previously reported, adverse clinical events following coronary perforations in the present study were related to their angiographic severity, occurring more frequently in patients who experienced type III perforation.^{1,2,6,8,13,14} Ellis at al. first reported that class III perforations (extravasation through a frank >=1mm perforation) were associated with a very high incidence of major adverse events (death, 19%; emergency CABG, 63%; Q-wave myocardial infarction, 15%; cardiac tamponade, 63%).¹ Regarding the treatment options, present study confirms a value of recently proposed algorithms for percutaneous management of coronary perforations.^6,8 Prevention, early diagnosis, adjusted risk evaluation, and immediate implementation of therapeutics resources are the keys to coronary perforation control. Prevention is especially important in situations that potentially increase the risk of perforation (as the high risk patient or lesion subsets, or use of debulking techniques or hydrophilic, taper or stiff guidewires). Early diagnosis is based on the correct evaluation of symptoms and careful monitoring of clinical signs, such as a puncture-like chest pain during guidewire advancement or with resistance to wire and device progression. Risk of this complication significantly increases when we attempt to overcome a resistant lesion by overinflating a semi-compliant balloon or by using a balloon larger than the media-to-media diameter. It is important to take into consideration that some severely calcified lesions will not expand even at high pressure. In these cases, a conservative strategy may be more appropriate than an obstinate pursuit of an optimal result. An important caveat to prevent a perforation is to appropriately pre-treat a calcified lesion with rotational atherectomy rather than insisting with an aggressive postdilation sometimes utilizing an oversized balloon in an attempt to obtain complete stent expansion. Among the devices sometimes found to be associated with perforations we cannot dismiss the cutting balloon especially when used to dilate a calcified lesion when the calcium is asymmetrically distributed, in this regard the operator needs to maintain a high level of attention. The all field of coronary perforations is becoming more and more important due to the fact that stent implantation (with a drug-eluting stent) is becoming an essential step in the treatment of a coronary stenosis: stent implantation is not only performed to treat or prevent dissection but to effectively lower restenosis in any type of lesion. When a perforation occurs and it is large to require more than conservative treatment two major options are available: distal vessel embolization (as in some guidewire perforations) or sealing of the wall of the ruptured vessel with a covered stent. Distal embolization is performed with gel foam particles, polyvinyl alcohol particles or with coils. When none of the above are available I recently became aware of a successfully managed distal perforation utilizing a cloth created on the catheterization table with the patient own blood and injected distally utilizing a Transit catheter (Cordis, a Johnson and Johnson Company, Warren, New Jersey). When there is rupture of an epicardial vessel the implantation of PTFE (polytetrafluoroethylene) covered stents appears to be the best strategy for class III perforations, while a conservative approach, combining protamine administration and prolonged balloon inflation, is appropriate for class II perforation. Unfortunately we have only one type of PTFE covered stent with a limited flexibility, an unacceptable large profile and not available in diameters smaller than 3.0 mm. We hope we will see soon some new covered stent able to fully address this rare but unacceptable complication frequently associated with a poor clinical outcome.