Several studies found that older age and female gender are associated with an increased incidence of coronary perforation (2, 3, 4,6,8). In a multicenter study by Ellis et al. (2), patients who developed perforation were almost 10 years older than those who had no perforation; in the same study, women represented 46% of the patients with perforation, compared with 16% of women among patients without this complication (2). However, women and the elderly are at increased risk to experience coronary perforation probably because of smaller vessel diameter and/or specific vessel characteristics. Intervening in vessels with severe calcification or fibrosis and/or extreme tortuosity or angulation is known to increase the risk of perforation; the
same is true regarding chronic total occlusion and bifurcation lesion sites (6,12,15).

Whether the use of platelet glycoprotein IIb/IIIa inhibitors is related to the increased incidence of coronary perforations is contradictory. In two studies, the incidence of coronary perforation was not related to adjunctive peri-PCI therapy (3,9); in another study, a trend was observed toward a higher incidence of coronary perforation in the setting of platelet glycoprotein IIb/IIIa inhibitors (6). The rates of coronary perforation in the randomized EPIC, EPILOG, CAPTURE, and EPISTENT trials did not differ significantly between patients treated with platelet GP IIb/IIIa receptor inhibitors and the placebo arm (0.4% versus 0.2%, p = 0.24) (16, 17, 18, 19).

The use of oversized balloons, coupled with relatively high inflation pressure intended for full stent expansion to minimize residual stenosis after stent implantation, may cause vessel wall perforation by several mechanisms, including overstretching of the most compliant coronary artery segment, a high-pressure jet due to balloon rupture, and outward pushing of a stent strut through the vessel wall. Procedural success and complication rates as a function of balloon-to-vessel ratio and high inflation pressure have been shown in several studies. In phase I of a study by Tobis (20), the use of high balloon-to-vessel ratio (1.2:1) with a mean pressure of 12 atm for the treatment of coronary stenosis in 60 patients was associated with the mean final percentage stenosis of −8%, with one case of coronary rupture. In phase II, applying the same balloon-to-vessel ratio but higher inflation pressure (a mean of 15 atm) in the next 300 patients yielded a slight improvement in the final percentage stenosis (mean −10%), but at the expense of an increase in vessel rupture and major dissection (3.4%). Finally, in phase III, using a smaller balloon-to-vessel ratio
of only 1.0 but with a higher mean pressure (16 atm) in 162 patients, the percentage of stenosis was only 1%; the rate of coronary rupture also was diminished significantly (0.7%). Likewise, in a series by Ellis et al. (2), the mean balloon-to-artery ratio in patients treated with plain balloon angioplasty was significantly higher in those who developed coronary perforation compared with those who did not (1.19 ± 0.17 versus 0.92 ± 0.16, p = 0.03); the same observation was made by Stankovic et al. (6), where high balloon-to-artery ratio was associated with a 7.6-fold increase in the odds of coronary perforation (p = 0.001).

Any device introduced into the coronary artery or saphenous vein graft (SVG) may potentially cause perforation of the vessel. Reports have described coronary perforation caused by guidewire, plain balloon (especially if the latter ruptures), stent, intravascular ultrasound (IVUS) catheter, and embolic protection device (6,21,22). Coronary perforation as a result of the forceful injection of contrast media has also been reported (23).

However, certain devices are known to substantially raise the incidence of coronary perforation. In the series by Stankovic et al. (6), atheroablative techniques were associated with an increased risk of coronary perforation by both univariate and multivariate analysis (OR = 3.54; 95% CI, 1.93-6.55, p = 0.001). Of importance, atheroablative devices also are known to increase the severity of coronary perforation. As shown in a study by Ellis et al. (2), type II or III perforation developed in 65% of the cases caused by plain balloon versus almost 80% of the cases caused by atheroablative techniques. Likewise, in a study by Dippel et al., all perforations caused by atheroablative devices were either type II (46%) or type III (54%), and the use of atheroablative devices was associated with a 28-fold increase in the odds of perforation (3).

The true incidence of guidewire-related coronary perforation is most likely higher than reported because some of the complications remain unrecognized and are self-limited. According to the published literature, the rates of coronary perforations secondary to guidewire were 0.21% in the series by Dippel et al. (3) and 0.36% in the series by Fukutomi et al. (5). In the latter series, perforation occurred at the treatment site in 12 cases, in distal vessel in 10 cases, and could not be localized in 5 cases (5). In the series by Witzke et al. (9), coronary perforation due to guidewire was observed in 20 of 39 cases of perforations (51%). Of these cases, perforations emerged while trying to cross the lesion with the guidewire in 11 patients (55%), with the distal wire in 7 patients (35%), and as a result of wire fracture in 2 patients (10%). Based on these data, the authors emphasize that the distal migration of the guidewire is an important factor for coronary perforation, and that meticulous care of the guidewire should be taken, especially in patients treated with platelet GP IIb/IIIa receptor inhibitors (9). A careful fluoroscopic observation during passage of the guidewire through the vessel, coupled with sufficient magnification to monitor guidewire position in the distal vessel, are strongly recommended. Several wires are known to increase the risk of perforation. In a study by Dippel et al. (3), 10 of 13 cases of guidewire-induced coronary perforations occurred with the same coronary guidewire (Super Soft Stabilizer, Cordis, Miami, Florida); the wire was subsequently redesigned to enhance flexibility of the distal segment. Stiff guidewires (Athlete, Asahi Intec, Nagoya, Japan; Hi Torque ACS, Guidant, Indianapolis, Indiana) provide the ability to steer, shape, and push, thus allowing accurate advancement through hard fibrous tissue. Because of the high risk of vessel perforation using stiff wires, visualization of the distal vessel is of paramount importance. Hydrophilic guidewires (Choice PT, Boston Scientific Scimed, Natick, Massachusetts; Crosswire, Terumo Medical Corporation, Somerset, New Jersey; Shinobi, Cordis, Miami, Florida) represent floppy wires with hydrophilic coating; they possess excellent gliding characteristics and reduced friction. However, these wires are known for their limited ability to steer and push. This increases the risk of creating a dissection and/or perforation (9). These wires, therefore, should always be used carefully and never pushed against resistance.