Giant coronary pseudoaneurysm associated with stent fracture treated successfully with coil embolization and a vascular plug

A coronary artery aneurysm (CAA) caused by a stent fracture is a rare complication of percutaneous coronary intervention (PCI). It may lead to life-threatening events, such as coronary embolism or rupture of the aneurysm, which may lead to cardiac tamponade. Some therapeutic strategies, such as observation, antiplatelet or antithrombotic therapies, surgical treatment, stent or covered stent implantation, and coil embolization, have been used for the treatment of coronary pseudoaneurysm. However, the natural history, clinical outcome, and optimal management strategies are not clearly understood. We report a case of a giant coronary pseudoaneurysm successfully treated using coil embolization and a vascular plug after conventional management, such as observation, covered stent implantation, and surgical treatment, had failed.

A 59-year-old man hospitalized in another hospital for rehabilitation after cerebral hemorrhage was transferred to our hospital to treat acute cholangitis. He was referred to the department of cardiology because a coronary artery aneurysm (CAA) was incidentally detected on contrast-enhanced computed tomography (CECT). He had slight right upper abdominal point tenderness and fever and was hemodynamically stable without chest pain. The patient had undergone percutaneous coronary interventions (PCIs) previously. Twelve years prior, a sirolimus-eluting stent (Cypher 3.5 × 33 mm, Cordis, Johnson & Johnson, Warren, New Jersey) and a paclitaxel-eluting stent (TAXUS 3.5 × 20 mm, Boston Scientific Corporation, Marlborough, Massachusetts) had been implanted in the mid-left anterior descending artery (LAD) and distal left circumflex artery (LCX), respectively, and an everolimus-eluting stent (Synergy 3.5 × 32 mm, Boston Scientific Corporation, Marlborough, Massachusetts) was implanted in the proximal LAD four years earlier. Coronary computed tomography angiography and coronary angiography (CAG) revealed complete separation (20 mm) of the paclitaxel-eluting stent in LCX and a pulsating giant CAA (19 × 17 mm) with evidence of blood inflow (Fig. 1). The right coronary artery (RCA) had a chronic total occlusion (CTO), and there were good collateral vessels from LAD to the distal RCA. The onset and growth rate were unknown, with no evidence of ongoing ischemia, arrhythmia, or mechanical complications. We initially treated the acute cholangitis with antibiotics, followed by conservative management of the aneurysm. Blood cultures were negative; therefore, we ruled out an infectious aneurysm. On day 7 of admission, a follow-up CECT showed an expanded aneurysm (23 × 26 mm), and we considered this to be an indication for early invasive therapy. The patient and his family declined surgery for his decreased activity due to prior cerebral hemorrhage, and we decided to treat him with a covered stent. During the PCI procedure, the wire control and delivering devices were exceedingly difficult to use because of the fractured stent and disruption of the vessel wall. We performed an intravascular ultrasound (IVUS) (Fig. 2), which showed a loss of vascular layers at the site of the aneurysm, indicating a pseudoaneurysm. Severe stenosis with calcification in the vessel distal to the pseudoaneurysm impeded the delivery of a balloon as small as 1.2 × 12 mm, which made us stop the insertion of the covered stent. The patient and his family refused surgery for a second time, and we continued to manage the pseudoaneurysm conservatively. During this period, the cholangitis resolved due to antibiotic therapy. A CECT performed on day 29 of admission revealed that the original pseudoaneurysm had expanded into two pseudoaneurysms (31 × 30 mm, 25 × 20 mm) (Fig. 1). The patient and his family agreed to undergo surgical treatment, which was performed on day 35 of admission, however they refused coronary artery bypass grafting for RCA CTO lesion since they wanted to avoid highly invasive procedure. The surgeons identified the pseudoaneurysms during off-pump surgery because they considered that it was easier to identify the pseudoaneurysms when there was blood flow. However, the pseudoaneurysms were located on the posterior side of the heart, making the procedure difficult to perform. The pseudoaneurysms were incised and plicated with felts. However, on day 45, a postoperative CECT showed a persistent pseudoaneurysm (measuring 18 × 27 mm). Subsequently, we decided to perform embolization to treat this pseudoaneurysm. We engaged a 7Fr guiding catheter and carefully crossed a 0.014″ guidewire, over which a 4.2Fr child catheter was introduced into the pseudoaneurysm. Three microcoils (AZUR CX35 13 mm × 24 cm, Terumo, Tokyo, Japan) were sequentially introduced into the pseudoaneurysm, and we deployed an AMPLATZER Vascular Plug4® (St. Jude Medical, Inc., St. Paul, Minnesota) at the proximal vessel proximal to the pseudoaneurysm (Fig. 3) (Supplementary data).

The patient remained well after the procedure without arrhythmias or mechanical complications. Creatine kinase peaked on postoperative day 1 (485 IU/L). A follow-up CAG 10 days after surgery showed that the pseudoaneurysm was sealed, and collateral network from LAD to the distal LCX was identified (Fig. 3). The patient was discharged without any symptoms or complications.

The incidence of CAA after first-generation drug-eluting stent implantation is reported to range from 0.2 % to 2.3 %, similar to that for bare-metal stents (BMSs) (0.3 % to 3.9 %) []. CAAs may cause life-threatening events, such as distal thrombosis, acute coronary syndrome, or rupture, further leading to cardiac tamponade []. So far, some strategies, such as observation, antiplatelet or antithrombotic therapies, surgical treatment, stent or covered stent implantation, and coil embolization, are reported, but there are no established treatments and management for CAAs with stent fracture. Each strategy was found to have its own strengths and weaknesses. Antiplatelet or antithrombotic therapies can reduce thrombosis and distal embolization but cannot reduce the risk of rupture. BMSs block blood inflow into pseudoaneurysms by covering themselves with neointima. The procedure is comparatively easy, but unreliable, and there is a high restenosis rate. Drug-eluting stents (DESs) have a low restenosis rate, but it takes a long time to be covered by neointima. Covered stents have immediate effect and certainty, but some problems include restenosis, thrombosis, size of stent, and side branch obstruction. Moreover, if we implant a new stent over a fractured stent, the mechanical stress will continue, and the risk of recurrence of stent fracture remains. In cases of emergency, these complications were not the major concern to rescue patients, but in this case, since even a balloon as small as 1.2 × 12 mm was not able to be delivered to the vessel distal to the pseudoaneurysm due to its severe stenosis with calcification, we thought we could not secure sufficient landing zone and had to cease the insertion of the covered stent. DES and BMS implantation were thought to be inappropriate strategy for such a giant pseudoaneurysm.

We used both filling the aneurysm with coils and embolizing the proximal neck with a vascular plug. It was difficult to embolize the vessel distal to the pseudoaneurysm. However, if we performed only proximal embolization, collateral circulation would develop in the chronic period and prevent the pseudoaneurysm from thrombosing, which meant the pseudoaneurysm would not be cured. In contrast, if we perform coil embolization alone, it was unclear that coil embolization could completely embolize the giant pseudoaneurysm. We used AMPLATZER Vascular Plug4® (AVP4) for this lesion. AVP4® can be delivered via a 0.038-inch 4-F or 5-F diagnostic catheter without the need for exchange of a vascular sheath or a guiding catheter. It has a low profile and is packaged with a 155 cm long polytetrafluoroethylene-coated delivery wire, which makes it much easier to be delivered through tortuous and small vessels compared to other plugs.

Although embolization causes myocardial infarction, we expected that embolization would not cause a large infarction because this was a distal LCX lesion, which was confirmed by a slight elevation in the level of creatine kinase.

It is intriguing that a pseudoaneurysm, which usually progresses slowly, expanded rapidly without additional identifiable factors that could have affected its growth rate. Blood cultures were negative, and the surgical pathological examination of the tissue around the pseudoaneurysms showed no evidence of inflammation; therefore, an infectious aneurysm could be ruled out. We hypothesize that the stent fracture was caused by mechanical stress from cardiac contractions on the curve of the LCX artery. The timing of the appearance of a pseudoaneurysm at the implanted DES site is usually reported within 10 months []. In the present case, although the accurate timing of the onset of the pseudoaneurysm was unclear, DES implantation had been performed twelve years prior. The reason why CAAs developed at the probably old DES-fractured cite and expanded in such a short period are unknown.

We report a case of a giant CAA associated with complete stent separation that was successfully treated using coil and plug embolization. We suggest that if conventional management fails, treatment with coil embolization and a vascular plug should be considered.

The following is the supplementary data related to this article.

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  Supplementary data

  Coil insertion and embolization with a vascular plug.

We are grateful to members of Kansai Electric Power Hospital for helpful discussions and comments on treatment strategies.