Guidewire-Induced Coronary Artery Perforation and Tamponade During PCI: In-Hospital Outcomes and Impact on Long-Term Survival

Abstract: Background. Guidewire-induced coronary perforation (CP) rate is reported to have increased. Methods. We analyzed 23,399 PCIs and identified 73 patients complicated by CP, of which 31 were guidewire induced. Patients were divided into two groups: group A (guidewire-induced CP) and group B (non-guidewire induced CP). Characteristics and outcomes were compared and a multivariate model was developed to evaluate the independent contribution of guidewire-induced CP on mortality. Results. Group A patients had more PCIs on CTO lesions (P=.001). Group A showed a trend for higher tamponade (P=.08). Delayed tamponade occurred only in group A (P<.001). Polytetrafluoroethylene stents were used more often in group B (P<.01). In-hospital mortality was similar between groups (3.2% vs 7.1%; P=NS). Emergent cardiac surgery was needed in 5.5% of all CP patients and was similar between groups. Group A had a trend for better survival (hazard ratio [HR], 0.37; 95% CI, 0.12-1.10; P=.07). Tamponade conferred a 3-fold increase in the long-term probability of death (HR, 2.95; 95% CI, 1.07-8.13; P=.04). Guidewire-induced CP during elective PCI had the best survival (HR, 0.31; 95% CI, 0.11-0.87; P=.03). Conclusions. Guidewire-induced CP rate is low. In-hospital mortality was similar for patients with guidewire-induced and non-guidewire induced perforations. Presentation of tamponade was occasionally delayed and associated with increased early and late death. Percutaneous coronary intervention of lesions with an expected increased risk of CP should be undertaken with consideration of the short- and long-term risk, particularly during non-elective PCI since tamponade in this setting increased the risk of late death by nearly 3-fold.

J INVASIVE CARDIOL 2014;26(8):371-376

Key words: cardiac tamponade, guidewire, coronary perforation, coronary intervention

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Coronary perforation (CP) during PCI, although infrequent, represents one of the most dreadful complications.^1,2 Guidewire-induced CP has been reported to occur more frequently in the current era,^3-5 and is considered by many interventionalists more “benign,” easier to manage, and to have more favorable outcomes when compared to CP caused by balloon inflation, stent placement, or the use of debulking devices. We sought to define the incidence, management, clinical, procedural, and angiographic characteristics, and evaluate the in-hospital outcomes and long-term survival rate after guidewire-induced CP when compared with patients that experienced CP from other causes.

Methods

We analyzed a prospectively collected database of 23,399 PCIs performed at our institution, an urban tertiary-care teaching hospital, during an 8-year period (1999-2006). Patients were divided into two groups: group A (guidewire-induced CP) and group B (non-guidewire induced CP). The presumed cause of CP was identified after reviewing the medical record and the cineangiography. One patient who developed intraprocedural tamponade, and initially thought to have CP, was found to have ventricular rupture secondary to acute myocardial infarction and was excluded from the database. Tamponade was defined as the presence of fluid in the pericardial space requiring intervention during the procedure or before hospital discharge.⁶Delayed tamponade was defined as tamponade occurring after the patient had left the catheterization suite.

The cineangiograms of all 73 patients who experienced CP were reviewed retrospectively and angiographic data were obtained. All relevant clinical information was recorded from the medical records, including age, gender, history of diabetes mellitus, hypertension, hyperlipidemia, heart failure, ejection fraction, previous myocardial infarction, previous percutaneous coronary intervention (PCI), previous coronary artery bypas graft (CABG), history of stroke, carotid artery disease, peripheral arterial disease, abdominal aortic aneurysm, chronic kidney disease, hemodialysis status, chronic obstructive pulmonary disease (COPD), history of smoking, and number of affected vessels (coronary artery disease). Procedural data were recorded and included status of elective or emergent PCI, sheath size, use of glycoprotein (GP) IIb/IIIa inhibitors, use of bivalirudin, number of stents, intravascular ultrasound (IVUS) use prior to perforation, use of intraaortic balloon pump (IABP), measures to treat the CP (ie, protamine use, polytetrafluoroethylene [PTFE] use, coil use, perfusion balloon use, need for emergent cardiac surgery). Angiographic data that included the culprit perforated vessel, the class of coronary lesion according to American College of Cardiology/American Heart Association (ACC/AHA) lesion classification, angiographic evidence of coronary calcification (identified as readily apparent radioopacities within the vascular wall) and presence of proximal tortuosity were recorded. Proximal coronary tortuosity was defined as ≥2 bends of at least 45°. In-hospital short-term outcomes were recorded and included PCI success, length of hospital stay, ventricular tachycardia (VT) arrest, and in-hospital mortality. 

In-hospital death was defined as death occurring during the index admission. Successful PCI was defined as PCI that achieved angiographic success without the major clinical complications of death, procedural related myocardial infarction (MI), or need for emergent cardiac surgery. Emergent cardiac surgery was defined as unplanned surgery that was required emergently within 24 hours of PCI to treat a complication. Long-term patient survival data were secured from the United States Social Security Death Index database.

Statistical analysis. Continuous normally distributed data are presented as mean ± standard deviation and were analyzed with the unpaired t-test. Categorical data are presented as counts or proportions (percentage). Baseline clinical, procedural, and angiographic characteristics, as well as procedural outcomes, were compared between the two groups using either the Fisher’s exact test or the Mann-Whitney U-test. A multivariate model was developed to evaluate the independent contribution of guidewire-induced CP, development of tamponade, and elective PCI on mortality. Kaplan-Meier survival estimates were calculated for the guidewire-induced versus the non-guidewire induced CP groups, adjusted for status of PCI (elective PCI versus non-elective) and presence of tamponade. Kruskal-Wallis test was used to compare length of stay. A P-value <.05 was considered a priori to indicate statistical significance. SPSS software, version 16 (SPSS, Inc) was utilized for the statistical analyses. 

Results

Coronary perforations occurred in 73 of the 23,399 PCI patients (0.31%), of which 31 were guidewire induced. Patients were followed for an average of 1865.74 ± 1037.77 days (range, 0-3401 days). Male patients represented 60% of the cohort and median age was 72 years (range, 38 to 88 years). Presumed CP causes were guidewire (42.46%), balloon/stent (46.57%), cutting balloon (5.47%), or use of rotational atherectomy device (4.10%). One CP occurred after use of the Frontrunner device (1.37%). In group A (guidewire-induced CP), the presumed culprit guidewire was a “workhorse” guidewire in 38.7%, a hydrophilic guidewire in 22.6%, and a stiff guidewire in 38.7% of the cases.

The baseline clinical, procedural, and angiographic characteristics of the patients in the two groups are shown in Table 1. No CP occurred after PCI in ACC/AHA class A lesions. The majority of the CPs occurred in ACC/AHA class C lesions (72.6%). Both groups had similar angiographic evidence of coronary calcification and vessel tortuosity. The left anterior descending (LAD) coronary artery was the most common target vessel in both groups (P=NS) and there were no guidewire-induced CPs in grafts. Femoral artery vascular access was obtained in all but 2 patients in whom brachial artery access was used. More patients who experienced guidewire-induced CP (group A) had PCI procedures on chronic total occlusions (CTOs) (P=.001). The use of GP IIbIIIa inhibitors (9.7% and 14.3%, respectively; P=NS) and bivalirudin (12.9% and 9.5%, respectively; P=NS) was similar between the two groups. 

There was a trend for higher tamponade development in group A (P=.08) that appeared to be attributable to an increased risk of delayed tamponade (10 cases vs 0 cases; P<.001). All patients with tamponade were treated with pericardiocentesis in both groups. Delayed tamponade occurred in 10 patients and all occurred after presumed guidewire-induced CP (P<.001). In 9 of these delayed tamponade cases, the perforations appeared to have been located at the distal limit of the guidewire and not at the area of catheter intervention. In 1 additional patient, the cause of perforation could not be determined with certainty because tamponade developed 4 days after PCI for acute myocardial infarction and the distal wire tip location was uncertain due to poor distal perfusion. Causes other than guidewire perforation, such as ventricular rupture, are unlikely in this patient since he stabilized with pericardiocentesis alone.

Management of CP was undertaken by prolonged balloon inflation, reversal of anticoagulation, pericardiocentesis, use of PTFE-covered stents, and embolization coils, and urgent cardiac surgery according to the operator’s preference and perceived patient needs (Table 2). Protamine use was common but not universal for heparin recipients, and did not differ between groups. PTFE-covered stents were used more often in group B (P=.01). There was a trend for higher use of coil embolization in group A (P=.09) and a trend for higher use of perfusion balloons in group B (P=.07). Patients in group B had more stents placed (P=.02). 

In-hospital mortality was similar for the two groups (3.2% vs 7.1%, respectively; P=NS). Death during follow-up occurred in 5 patients of group A and 13 patients of group B (P=NS; Table 3). Death occurred in 1/15 patients who experienced tamponade in group A and 1/11 patients who experienced tamponade in group B. VT with arrest occurred more often in group B (P=.04). There was a trend for higher procedural success in group B (P=.08). Need for emergent cardiac surgery was similar in both groups (2 patients in each group) and there were no in-hospital deaths after emergent cardiac surgery.

The length of hospital stay was similar in both groups, but patients who experienced tamponade after guidewire-induced CP had longer hospital stays than patients in group A that did not have tamponade (P=.03). The length of hospital stay was similar between patients with and without tamponade within group B.

Patients in group A had a trend toward lower long-term probability of death (hazard ratio [HR], 0.37; 95% confidence interval [CI], 0.12-1.10; P=.07) compared with patients in group B (Figure 1); however, the circumstances of PCI greatly influenced survival (Table 4). The development of tamponade as a complication of CP conferred a 2.95-fold increase in the long-term probability of death (HR, 2.95; 95% CI, 1.07-8.13; P=.04) compared with those who sustained CP without tamponade (Table 4). Additionally, the patients who experienced CP as a complication of elective PCI had significantly higher survival compared to the non-elective PCI patients (HR, 0.31; 95% CI, 0.11-0.87; P=.03) (Table 4). 

Discussion

Coronary interventions are performed routinely in populations of high technical difficulty. Aggressive equipment manipulations, especially in the treatment of chronic total occlusions,⁷ use of hydrophilic-coated and high durometer guidewires⁴ and limited use of atheroablative devices^8,9 may explain recent reports of increased rates of coronary perforations (Table 5). Guidewire-induced CP may be due to distal branch puncture, perforation near the target lesion (a particular risk with CTO), or guidewire fracture, which may allow slow blood loss resulting in tamponade with a delayed presentation. In contrast, perforations not related to a guidewire typically have dramatic presentations: balloon rupture or similar device-related injury may cause sudden, large blood extravasation. These events are managed acutely, with less likelihood of a delayed complication. Most early reports on CP during PCI have not isolated guidewire-induced from non-guidewire causes, and the number of cases was limited. 

Clinical outcomes following guidewire-induced CP are generally thought to be less hazardous than CP from other causes, but our data suggest this may be incorrect. The rate of guidewire-induced CP in our study was similar to previous reports (Table 5). In-hospital mortality was numerically higher but not statistically greater for patients with non-guidewire induced CP (3.2% vs 7.1%), suggesting early risk may not be greatly less for patients with guidewire-related perforations. Overall CP incident rates are in line with previously reported rates.

Emergent cardiac surgery was needed infrequently, and was required overall in just 5.5% of patients with CP. This finding is consistent with reports from more recent studies (Table 5) and may represent improvements in identification of complications, equipment, and interventional techniques over time. In our study, the need of emergent cardiac surgery was similar over time (data not shown). There were no in-hospital deaths after emergent cardiac surgery. Other investigators¹⁰ have reported successful CP management with a PTFE-covered stent graft (which is currently more deliverable with lower risk for dislodgment), resulting in low in-hospital mortality without use of urgent cardiac surgery. 

The overall rate of tamponade development (0.11% of all PCIs and 36% of all CP patients) was similar to previously reported studies (Table 5). Interestingly, there was a trend toward higher tamponade occurrence in group A (48.4% vs 26.2%; P=.08), which is different than earlier reports.^11,12 This observation is important since it is widely thought that the adverse clinical outcomes resulting from CP correlate directly with the perforation grade and development of tamponade. Furthermore, delayed tamponade, recognized after the patient had left the catheterization suite, was observed in 10 patients (32.2% of cases in group A). All of these were presumed to be guidewire-induced CP (P<.001), in agreement with other reports demonstrating that guidewire-induced CP may manifest as delayed tamponade^5,13-15 Other studies¹⁶ have reported delayed tamponade without identifying a cause, but based on the observations made in our study and others, these cases may have been attributable to guidewire-induced CP. These findings highlight the need to remain vigilant for occult or unrecognized guidewire-induced CP. 

Ventricular tachycardia with arrest occurred more often in group B (0 vs 14.3%; P=.04), probably due to the faster accumulation of fluid in the pericardial space and/or the need for balloon occlusion of a large epicardial vessel as part of the CP management, subtending larger myocardial territory. 

There was a trend for higher rate of successful PCI in group B (54.8% vs 76.2%; P=.08). This may be due to several reasons, like usage of more PTFE stent-grafts (P=.01) and stents (P=.02), less use of coils (P=.09), lower incidence of tamponade (P=.08), or lower rate of CTO lesions (P=.01).

As reported in previous studies,^3,5,8,16-21 we noted that patients who experienced CP have complex anatomy: no CP occurred after PCI in ACC/AHA class A lesions. Evidence of coronary calcification was noted in 83.6% of CP cases. Although the distribution of CPs between the coronary arteries was similar, the LAD was the most frequent site of intervention in both groups, which is in accordance with most other investigators,^{4,5,13,16-18,20-25} although some studies suggest the right coronary artery is the most likely culprit vessel in CP.^8,26

Significantly more patients in group A had PCI procedures on CTOs (P=.01). The observed CTO rate (32.9%) in the overall CP population was similar to previously reported studies (reported range, 13%-63%).^{4,8,14,17-20,23} Also, the observed CTO rate (54.8%) in group A is similar to publications from more recent studies (reported range, 33.3%-75%).^3,5,25 In a recent study,⁸ the strongest independent predictor of CP was PCI on CTO lesion. 

The presumed culprit guidewire was a workhorse guidewire in 38.7%, a hydrophilic guidewire in 22.6%, and a stiff guidewire in 38.7% of the cases. Other researchers have reported that a hydrophilic wire was considered the culprit in the majority of the guidewire-induced CP (range, 50%-100%),^{3,18,19,23,27,28} while others found that non-hydrophilic guidewires were mostly the culprits.²⁰ Teis et al⁵ concluded that the use of hydrophilic wire was independently related to guidewire-induced CP, and other reports^14,15 have also attributed the development of delayed tamponade to the use of hydrophilic wires. The super-soft Stabilizer (Cordis Corporation) was identified by Dippel et al²⁹ to be the culprit in 10 out of 13 cases of guidewire-induced CP; this device was redesigned, and no further perforations were observed with the newer modified version. In our study, as stated, a workhorse wire was responsible for the CP in a substantial proportion of the cases, underscoring the need for meticulous monitoring of the wire tip position with frequent change in magnification (in order to monitor guidewire position in the distal coronary artery), especially in lengthy cases and procedures on complex lesions. While aggressive wires may present an increased risk of perforation, observational studies (including ours) will be biased by operator preferences. The relatively high rate of workhorse wire use we observed in cases complicated by perforation may have been driven by a strong preference for these wires in our practice. In any case, this observation makes clear that even non-aggressive wires pose risk.

GP IIb/IIIa inhibitor and bivalirudin use was similar between the  groups. Due to the small number of cases in each group, definite conclusions are difficult to make regarding one anticoagulant versus the other, although in-hospital outcomes were similar between the two anticoagulation groups in our cohort (results not shown). Recent reports suggest favorable outcomes may be expected with bivalirudin use, even when procedures are complicated by CP.^3,21

Patients in group A had a trend toward lower long-term probability of death (P=.07) compared with patients in group B (Figure 1). However, the circumstances of PCI greatly influenced survival (Table 4). The development of tamponade as a complication of CP conferred a 2.95-fold increase in the long-term probability of death (P=.04) compared with those who sustained CP without tamponade. This observation underscores the importance for prevention of this complication. In addition, the patients who experienced CP as a complication of elective PCI had significantly better survival compared to the non-elective PCI patients (P=.03) (Table 4), a finding that is consistent with data showing a higher risk of adverse events in patients presenting with acute coronary syndromes. Our data is supported by a recent study,¹⁶ which reported that most of the fatal CP cases (85.7%) were in patients with acute coronary syndromes; in 5 of these cases, the vessel thrombotically occluded and the patient died of cardiogenic shock, despite successful sealing of the perforation. 

Conclusion

Guidewire-induced CP is a rare complication of PCI, but the incidence may be rising relative to CP from other causes. A trend toward higher tamponade occurrence in group A was observed and appeared driven by an increased risk of tamponade with delayed presentation. Current data suggest that guidewire-induced CP is not a benign complication: tamponade occurred in nearly half of these patients, and tamponade was associated with a nearly 3-fold increase in risk of death. As in the past, prevention, early diagnosis, use of bedside echocardiography, and immediate implementation of therapy are keys to successful outcome, keeping in mind that guidewire-induced CP may have a more insidious subacute presentation.

Study limitations. This study was retrospective and descriptive and has the inherent limitations therein. We cannot exclude the possibility that guidewire-induced CP may have been underreported, especially among cases not complicated by tamponade. Due to the small sample size and the rarity of this complication and accompanied events, the probability of type 1 error is increased and the results should be interpreted cautiously. Finally, the presented data may not reflect practice at other institutions. 

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From the Lenox Hill Hospital, Heart and Vascular Institute of New York, Department of Cardiac and Vascular Interventional Services, New York, New York.

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

Manuscript submitted December 3, 2013, final version accepted December 27, 2013.

Address for correspondence: Ioannis Stathopoulos, MD, PhD, 30-10 38th Street, 2nd Floor, Astoria, NY 11103. Email: jastathopoulos@hotmail.com