Coronary Artery Perforation Following Percutaneous Coronary Intervention

Abstract: Coronary artery perforation (CAP) is a rare but serious complication of percutaneous coronary intervention. Risk factors for CAP include female gender, older age, and lesion complexity. The most common causes of CAP include wire perforation, atherectomy, and aggressive sizing of balloons and stents. Complications of CAP vary greatly from clinical insignificance to hemodynamic collapse and death, depending on the severity of the CAP. Early recognition is of utmost importance to surviving CAP. Generally accepted treatment options depend on lesion severity, and include balloon inflation to tamponade the vessel, reversal of anticoagulation, covered stents, and embolization. Emergent pericardiocentesis or surgical evacuation may be required for the most severe cases.  

J INVASIVE CARDIOL 2016;28(3):122-131

Key words: coronary artery disease, coronary perforation, percutaneous coronary intervention

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Coronary artery perforation (CAP) is a rare but serious complication of percutaneous coronary intervention (PCI). The incidence of CAP during PCI ranges from 0.10%-3.00%.^1-4 Clinical sequelae range from spontaneous closure to cardiac tamponade leading to death. Mortality rates can be as high as 21.2%, depending on severity of vessel injury.³ Early recognition and treatment are paramount to survival. We review classification, risk factors, etiologies, consequences, and management options for CAP.

Diagnosis and Classification

Coronary angiography is the gold standard for the diagnosis of CAP. The Ellis classification for CAP includes three types (I, II, and III).⁵ Type I CAP is characterized by an extraluminal crater lesion without extravasations. It may be angiographically challenging to differentiate type I CAP from localized dissections. Type II CAP is characterized by formation of pericardial or myocardial blushing without contrast jet extravasation. Type III CAP is characterized by extravasation of blood through frank (≥1 mm) perforation. Type III also includes CAPs into an anatomical cavity chamber, such as the ventricle or coronary sinus. Other classifications for CAP are less recognized. Fukutomi et al proposed differentiating type I and type II forms through epicardial staining without or with extravasation,⁶ a classification that others have adopted.⁷ 

Angiographic and Demographic Risk Factors

CAP is more commonly observed in the presence of American College of Cardiology (ACC)/American Heart Association (AHA) type B2 or C lesions,^3,8-10 chronic total occlusions,^10,11 bifurcation lesions, angulated or tortuous lesions,¹⁰ heavily calcified vessels, lesions of right coronary and circumflex arteries,^3,9 and narrow-diameter vessels (Table 1).^3,10,12 

Women (46% vs 26%; P<.001) and older patients were at increased risk for CAP, which may be explained by smaller coronary arteries being more prone to damage during PCI.^{1,2,5,8,9,11-13} Additional risk factors include the use of clopidogrel,² lower baseline creatinine clearance,² hypertension,¹¹ previous coronary artery bypass grafting (CABG),^11,13 history of congestive heart failure,¹⁴ and multivessel coronary artery disease.^10\

Etiology of Coronary Artery Perforation

Many procedural factors have been implicated in CAP, including use of larger balloons in angioplasty, guidewire injury, atheroablative device use, and stent placement (Table 2).

Balloon oversizing. Larger balloon-to-artery ratio was associated with CAP (1.3 ± 0.3 vs 1.0 ± 0.3; P<.001) (Figure 1).¹⁵ In 62 patients with CAP, of those who underwent balloon angioplasty, the device-to-artery ratio was higher in patients who had CAP compared with those who did not have CAP (1.19 ± 0.17 vs 0.92 ± 0.16; P=.03).⁵ Another study reported that higher balloon-to-artery ratio was associated with CAP (odds ratio [OR], 7.62; 95% confidence interval [CI], 2.78-20.77; P=.01).¹⁰ The use of compliant balloons was a predictor of emergency CABG and/or in-hospital death (OR, 4.32; 95% CI, 1.60-11.65; P=.01).¹⁰ In addition, high-pressure inflation of resistant lesions may also increase the risk of CAP.

Guidewire perforation. Several studies reported guidewire-related CAP, with one study of 68 cases of CAP reporting as many as 88.9% of cases attributed to guidewires.^7,12,16-19 Understandably, the higher incidence has been found in patients with complex (type C) lesions and chronic total occlusion.^6,20 Injury can occur as a result of distal branch puncture or perforation at the target lesion site, especially with hydrophilic guidewires and stiff guidewires used for chronic total occlusions(Figure 2).²⁰ One study found a significantly increased risk of delayed tamponade in guidewire-associated CAP vs CAP from other causes.²⁰ The need for cardiac surgery is low in these patients (5.5%). 

Atheroablative devices. Atheroablative devices like rotational atherectomy are used in heavily calcified vessels for plaque modification.³⁵ In the period after rotational atherectomy devices gained popularity, the rate of CAP ranged from 0.8%-11.8%, with most studies reporting an incidence below 3%.^{5,9,12,15,21-29} The incidence of CAP was higher when atherectomy devices were used (2.8% vs 0.17%; P<.001; OR, 16.3; 95% CI, 7.1-37.4).¹⁴ One possible explanation for the higher risk of CAP with atheroablative devices is the effect on vascular wall integrity from debulking complex calcified lesions(Figure 3).⁸ Newer atheroablative devices, such as orbital atherectomy, show lower rates of CAP. In the prospective, multicenter, non-blinded ORBIT-II study involving 443 patients, 1.8% of patients suffered CAP,³⁰ which is on the lower end of the range of CAP incidence in rotational atherectomy studies.

Stent placement. Data on stent-induced CAP are mixed, but the majority of studies do not implicate stenting as a major cause, and injury is usually relegated to Ellis type II CAP.^3,13 One study even reported that patients with CAP were less likely to have undergone PCI with stents when compared to controls without CAP (73.5% vs 90.7%; P=.01).² Conversely, one study showed stent-associated CAP resulting in Ellis type III CAP, often necessitating urgent pericardiocentesis, covered-stent, or cardiac surgery.³¹

Clinical Consequences

Perforation classification and complications. Given that the majority of studies utilize the Ellis classification of CAP, the following discussion also uses that scheme. Ellis type I CAP is generally considered a benign condition that does not often lead to tamponade or death.^5,16 Ellis type II CAP is also usually benign, but there are higher rates of tamponade, emergency CABG, and death (Table 3).¹⁶ Ellis type III CAP is usually clinically more severe, with respect to need for urgent pericardiocentesis, intraaortic balloon pump insertion, emergent cardiac surgery, and mortality as compared with type I and II CAP.^11,12,16,31 When compared with type I CAP, types II and III CAP had higher rates of in-hospital death (21.9% vs 2.7%; P=.02), tamponade (37.5% vs 2.7%; P<.001), and composite endpoint of in-hospital death, cardiac tamponade, or emergent cardiac surgery (46.9% vs 5.6%; P<.001).³² Fortunately, type III CAP is rare, with an incidence of 0.23%.³³ Consequences of type III CAP are severe, however, with mortality of 7%-44%, tamponade up to 40%, and 20%-40% need for emergent CABG.^11,16,33,34 Lesion complexity is a critical risk factor for developing type III CAP. Of 56 patients with type III CAP, 96% of lesions were ACC/AHA type B2 or type C and 28.6% were chronic total occlusions.³³ 

Saphenous vein grafts (SVGs) can also perforate during PCI. In a case series of 12 SVG-CAPs,³ spontaneously sealed, 9 patients were treated with prolonged balloon inflation and 5 patients were treated with covered stent implantation.³⁵ Of the 7 patients who had follow-up angiography at 5 months to 2 years after the CAP, the SVG was occluded in 5 patients and had developed severe stenosis in the remaining 2 patients. 

Cardiac tamponade. CAP can lead to bleeding into the pericardium, resulting in cardiac tamponade and possibly hemodynamic collapse. The incidence of CAP that progress to tamponade ranges from 10%-60%.⁴ Important factors that influence that range include type of CAP, type of anticoagulation, and rate of blood accumulation. Cardiac tamponade is associated with complex lesions, mainly type B2 and C lesions,^36,37 and type III CAP^1,3,5,13 as well as atheroablative devices.^36,38

As little as 100 mL of fluid accumulation in the pericardial space, in an acute setting, can cause hemodynamic instability.³⁹ Tamponade should be suspected when patients develop hypotension, chest pain, shortness of breath, dizziness, bradycardia, or engorged neck veins. The key to diagnosis and evaluation is emergent bedside echocardiography. Right heart catheterization can facilitate the diagnosis of tamponade, looking specifically for equalization of diastolic pressures. 

In a study of 73 patients who suffered CAP after PCI, 26 were complicated by tamponade.⁴⁰ Although in-hospital mortality was not significantly different (7.7% in those with tamponade vs 4.3% in those without), there was a three-fold increase in overall risk of death in the tamponade group at long-term follow-up (OR, 3.3; 95% CI, 1.01-10.65; P=.047; average follow-up period, 1865.74 days). Compared with earlier studies where the percentage of patients who required emergent surgery approached 50%, only 11.5% needed surgical intervention, which the authors attributed to advances in complication identification and management over time.

Patients suffering from CAP may also be at risk for delayed tamponade, defined as the presence of fluid in the pericardial sac requiring intervention after the patient has left the cardiac catheterization laboratory but prior to discharge.^5,8,37 Delayed tamponade has been observed anywhere between 30 minutes and 9 days after PCI.³⁷ Similar to immediate tamponade from CAP, delayed tamponade is mainly associated with complex lesions. Fukutomi et al reported that all 13 patients with delayed tamponade had PCI for chronic total occlusions.⁶ Another study examining 10 cases of delayed tamponade reported an association with chronic total occlusions, lesions in 2-3 vessels or branches, and history of previous PCI in 50%.³⁷ Mortality was found to be significantly higher in acute tamponade compared with delayed tamponade (59% vs 21%, respectively; P=.04).³⁶ Delayed tamponade poses a diagnostic challenge since it occurs outside the catheterization lab, lacking typical angiographic and hemodynamic signs. This suggests that even in cases of relatively mild CAP, hemodynamic monitoring for at least 48 hours after PCI would be warranted, especially in cases involving more complex lesions.

Pseudoaneurysms. Coronary pseudoaneurysms are defined as areas of local vessel dilation 1.5 times larger than adjacent normal segments. These are rare events, and most studies are relegated to case reports and case series.^6,41-44 While there are no controlled studies examining the rate of pseudoaneurysm rupture, the theoretical risk remains concerning.⁴⁴ Although pseudoaneurysms have been reported to develop as early as 10 minutes following PCI, most have been noticed from 2 weeks to 3 months after CAP.⁴¹ In one of the larger studies, 28.6% of 67 CAP patients were found to have pseudoaneurysm after a mean angiographic follow-up of 13.4 ± 11.3 months following PCI.⁶ Pseudoaneurysms were associated with more severe CAP that demonstrated epicardial staining with contrast extravasation on angiography compared to staining without contrast extravasation (72.2% vs 11.1%, respectively; P<.001). They were also more commonly found after directional atherectomy and cutting balloon angioplasty.⁶ After 6-month angiography following the diagnosis of pseudoaneurysm, there was variation in clinical course (6 stayed the same, 8 contracted and/or became occluded, and 4 enlarged). None ruptured during the 3-year follow-up period. Considering how the majority of pseudoaneurysms have been found incidentally, it is possible that pseudoaneurysms occur at a higher rate than conventionally thought. Given the scarcity of data, optimal evaluation and management remain unclear. 

Impact of antithrombotic therapy on CAP. While protamine can reverse the effects of heparin, adjunctive antithrombotic agents such as glycoprotein (GP) IIb/IIIa inhibitors and bivalirudin lack a specific agent to counteract their effects. However, immediate reversal of antithrombotic agents theoretically may increase the risk of stent thrombosis, which may further complicate the management of CAP.¹³ 

Bivalirudin is thought to be safe because of its ability to reversibly bind to thrombin, as well as its short half-life.⁷ In patients with CAP due to wire perforation, major adverse cardiac events and cardiac tamponade were more common with use of heparin compared with bivalirudin (50% vs 0%, respectively; P<.01).⁷ In a study of 69 patients, Romaguera et al found a lower rate of cardiac surgery for CAP when bivalirudin was used compared with heparin (2.4% vs 17.9%, respectively; P=.04), but no difference between groups in the composite endpoint of in-hospital death, tamponade, and emergent surgery (OR, 1.42; 95% CI, 0.47-4.29; P=.53).³² The authors suggested that the time needed for full reversal of heparin may not be as different as the half-life of bivalirudin, which may explain the similar outcomes. Some studies have examined CAP outcomes in cases involving bivalirudin alone vs use of a combination of unfractionated heparin and GP IIb/IIIa inhibitors. A pooled analysis of 35 CAP patients from the REPLACE-2, ACUITY, and HORIZONS-AMI trials showed that bivalirudin alone was not associated with worse outcomes.²

The data on the impact of GP IIb/IIIa inhibitors are mixed. Gunning et al found that 9 of 10 patients with CAP on abciximab were associated with tamponade that needed pericardial drainage, and 4 of these 9 tamponade cases were found more than 2 hours after PCI.⁸ Stankovic et al reported a trend toward higher incidence of CAP in patients treated with GP IIb/IIIa inhibitors (OR, 1.86; 95% CI, 0.95-3.63).¹⁰ Fasseas et al reported a nearly 10-fold greater requirement for covered stent placement or cardiac surgery in patients with CAP while on GP IIb/IIIa inhibitors (33.3% vs 3.2%).¹³ Overall clinical outcomes with respect to tamponade, myocardial infarction, or death were similar between groups. However, others did not find a relationship between PCI-related CAP, adjunctive GP IIb/IIIa inhibitor use, and worsening of clinical course.^14,18,17,36

Management

Early recognition and treatment are crucial for survival after CAP. The goal of CAP management is to seal the site of extravasation and to treat hemodynamic instability from pericardial effusion or tamponade. Although there have been proposed algorithms for CAP management,^3,7,14,32,33 there is no consensus on optimal treatment of CAP and protocols may vary by institution (Figures 4 and 5). Several factors impact the management of CAP, including CAP grade, presence/duration of pericardial effusion or tamponade, and hemodynamic status. 

Prolonged balloon inflation. Low-pressure balloon inflation may help seal the CAP while allowing distal vessel perfusion to prevent ischemia. Ellis type I and II CAP have been successfully managed with prolonged balloon inflation.^10,31 In a retrospective study of 30 CAP cases, 29 were treated with balloon inflation.³¹ All patients with type I and II CAP were successfully treated with prolonged balloon inflation with or without pericardiocentesis, while only 64% of type III CAP were successfully treated. Of the patients with type I and II CAP, 84% were managed by balloon inflation alone. There was a numerically higher incidence of tamponade and pericardiocentesis with type III CAP compared with type I/II CAP that were treated with balloon inflation (11% vs 27%). Balloon inflation time was significantly longer in cases of stent-related CAP compared with cases of wire/balloon-related CAP (44 ± 37 minutes vs 21 ± 13 minutes, respectively; P<.05). Duration was also significantly longer in type III CAP compared with type I/II CAP (48 ± 37 minutes vs 20 ± 13 minutes; P<.05).³¹

Reversal of anticoagulation. The decision to reverse anticoagulation should be dependent on the size of the CAP and how it responds to balloon inflation. If the CAP is large or extravasation continues after a prolonged period (up to 30 minutes) of balloon inflation, protamine to reverse the effects of heparin can be administered. In a study of 90 patients who received protamine for procedural complications after stent placement, none had stent thrombosis or adverse hemodynamic consequences.⁴⁵ If the CAP is small and balloon inflation successfully seals it, reversal of anticoagulation may not be necessary, especially if a stent has been implanted. If CAP has occurred but no stent has been implanted, the threshold for reversing anticoagulation may be lower given that stent thrombosis will not occur. In the case of abciximab use, platelet transfusion may be warranted.¹⁴ As described above, the benefit of bivalirudin is its short half-life, which does not predispose to bleeding complications.

Covered stents. Polytetrafluoroethylene (PTFE)-covered stents consist of a balloon-expandable layer of PTFE between two stainless-steel stents that prevent blood leakage between stent struts.³ PTFE-covered stents decrease the incidence of in-hospital major adverse cardiac events in type III CAP.¹⁰ In a multicenter study of patients in whom reversal of anticoagulation and prolonged balloon inflation were unsuccessful, use of PTFE-covered stents vs non-covered stents led to less need for CABG (18% vs 88%, respectively; P<.001), tamponade (8% vs 82%, respectively; P<.001), and major adverse cardiac events (18% vs 88%, respectively; P<.001).⁴⁶ An international retrospective registry of CAP treated with PTFE-covered stents reported a success rate of 92.9% for completely sealing CAP.⁴⁷ No in-hospital Q-wave myocardial infarction, emergent CABG, or deaths were reported. The disadvantage of covered stents is that they are bulky and rigid, making them difficult to deliver in calcified and tortuous vessels, particularly in emergency situations and in arteries <2.75 mm in diameter.³² However, one study has shown no difference in rates of tamponade, emergency CABG, and in-hospital death with the use of PTFE-covered stents compared with perfusion balloons and non-covered stents.¹⁶ Dual-antiplatelet therapy with aspirin and clopidogrel should be continued for at least 6 months to minimize the risk of stent thrombosis.³² 

The time between the sealing balloon deflation and covered stent delivery is disadvantageous. Dual-catheter strategies that avoid this problem have been offered.⁴⁸ In a study with 26 patients, there was a trend toward less tamponade (27.3% vs 53.3%; P=NS), shock (18.2% vs 40%; P=NS), postprocedural myocardial infarction (63.6% vs 80%; P=NS), and death (9.1% vs 20%; P=NS) with the dual-catheter vs single-catheter approach, respectively.

Newer stents that have been successfully used in CAP claim increased flexibility due to unique materials. Initially developed for SVG intervention as a way to decrease rates of embolization, equine pericardium-covered stents have shown effectiveness in case reports of CAP, with some reporting smaller profiles and improved flexibility.⁴⁹ Papyrus stents have also been recently developed for the use of CAP, and report increased flexibility due to use of an electrospun polyurethane membrane. These stents can also be used with a wider variety of guide catheters, which may decrease time of deployment. Mesh stents using thin layers of polyethylene terephthalate have also been shown in case studies to be effective in CAP.⁵⁰ Given that these are novel devices and CAP incidence is rare, more robust studies of these devices are warranted. 

Embolization. The deployment of covered stents is limited to more proximal vessels due to their bulky, rigid properties. Although mainly limited to case studies, microcoil embolization was used to successfully treat distal CAP^51-54 as well as pseudoaneurysm secondary to CAP.⁴⁴ Microcoils of small diameter (2-3 mm) have been used successfully in distal coronary arteries, and multiple microcoils can be used simultaneously as required.^44,51 Microcoils can stop bleeding without the need for reversing anticoagulation, which can decrease the risk of thrombosis, a complication that is low risk yet still possible. Most microcoils are made of platinum to enhance radioopacity, and can be coated with thrombogenic fibers or gel to promote success.⁵¹ One report involving a guidewire-induced Ellis type III CAP that was treated with microcoil embolization initially showed favorable results.⁵⁵ However, at 1-year angiographic follow-up, blood flow continued through the embolized vessel. The authors hypothesize that this was due to poor adherence of the coil to the vessel wall in the setting of dual-antiplatelet therapy. Although formal studies of microcoils in CAP are lacking, coil embolization remains a viable technique in the appropriate setting and in expert hands. 

Other materials that have been used for embolization include synthetic glues, two component adhesives made of fibrinogen and thrombin, collagen, polyvinyl alcohol particles, autologous blood clot, protamine, and thrombin.^56-61

Pericardiocentesis. The primary management of CAP complicated by tamponade is pericardiocentesis. In a study of 31 patients who suffered from tamponade after PCI, those with early onset were more likely than those with late onset to require intraaortic balloon pump, cardiopulmonary resuscitation, ventilator support, and blood transfusions.³⁶ In 97% of all patients in the study, emergent pericardiocentesis was performed; of those, 60% were treated by drainage alone and 40% required emergency surgery. A pericardiocentesis tray should be requested as soon as CAP is suspected in the catheterization lab in order to prevent delay should urgent drainage be indicated. Right atrial catheterization placement soon after suspected tamponade can also aid in monitoring central venous pressure. Serial echocardiograms are useful in monitoring patients for complications after drainage, including possible myocardial puncture and fluid reaccumulation.

Emergent surgery. If tamponade develops and pericardiocentesis is not feasible or is ineffective, a cardiac surgeon should be consulted. Data are limited on outcomes after emergent surgery following CAP. In one study of 56 patients with Ellis type III CAP, 16% needed emergent CABG, and 44.4% of these had successful repair of the rupture.³³ In a study of 31 patients who developed tamponade following CAP, 12 patients needed emergent surgery, of which there was a 50% mortality rate.³⁶

Conclusion

Despite numerous advances in PCI, CAP is still a feared complication. Data on predisposing risk factors are largely mixed, but the one largely agreed upon risk factor is lesion complexity. PCI of complex lesions (type C lesions, calcifications, and chronic total occlusions) plays a role in the incidence of CAP. Many devices and techniques have been associated with perforation. The ultimate concern continues to be the risk of tamponade and hemodynamic compromise. While standard measures of managing tamponade should always be kept in mind, it is important to maintain a high index of suspicion for delayed tamponade even after seemingly successful procedures, especially in cases of complex lesions. Generally accepted forms of treatment include reversal of antithrombotic agents, prolonged balloon inflation, covered stents, and embolization. There remains a need for development of thinner and more flexible covered stents, capable of delivery in shorter time intervals. Data on optimal treatment are limited by lack of randomized trials. As a result, management protocols may vary by institution.

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From the Division of Cardiology, UCLA Medical Center, Los Angeles, California.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. They report no conflicts of interest regarding the content herein.

Manuscript submitted January 20, 2015, provisional acceptance given February 12, 2015, final version accepted April 22, 2015.

Address for correspondence: Michael S. Lee, MD, UCLA Medical Center, 100 Medical Center, Suite 630, Los Angeles, CA 90095. Email: mslee@mednet.ucla.edu