CASE REPORTS

Coronary Artery Aneurysm following Drug-Eluting Stent Implantation

S. Anandaraja, MD, DM, Nitish Naik, MD, Kewal Talwar, MD
S. Anandaraja, MD, DM, Nitish Naik, MD, Kewal Talwar, MD
Percutaneous coronary interventions (PCI) are uncommon causes of coronary artery aneurysms (CAA). The incidence of CAA after percutaneous transluminal coronary angioplasty (PTCA) ranges from 3.9–5%,1,2,5–7 and after directional coronary atherectomy from 2–10%.3,4 Though CAA after implantation of a stent is rare, it has been recently reported after implantation of a drug-eluting stent.8 We report a similar case of CAA following stenting with a drug-eluting stent. Case Report. A 45-year-old woman with a known case of hypertension presented to our center with recent-onset NYHA class III angina despite being on optimal medical therapy. She was thus taken for coronary angiography and possible revascularization. Coronary angiography showed total occlusion of the mid-left anterior descending (LAD) artery, with no significant lesions in the left circumflex or right coronary arteries and normal left ventricular function (Figure 1). The patient was taken the catheterization laboratory for PCI. The totally occluded LAD was easily crossed with a 0.014 inch BMW Guide Wire (Guidant Corp., Indianapolis, Indiana) and dilated with a 2.5 x 15 mm Crosssail® balloon catheter (Guidant) at 8 atm. There was no dissection after balloon angioplasty. Following this, a 2.75 x 20 mm Taxus® drug-eluting stent (Boston Scientific Corp., Natick, Massachusetts) was deployed in the LAD at a pressure of 12 atm, resulting in TIMI 3 flow (Figure 2). The patient who was on regular follow-up was readmitted 6 months later with unstable angina. The electrocardiogram did not reveal any significant ST-T changes. She was sent for a coronary angiogram which revealed focal in-stent restenosis and a saccular aneurysm of 3.5 x 8 mm within the mid-portion of the stent (Figure 3). Discussion. CAA following PTCA is usually a delayed finding. It is caused by the use of oversized balloons or high-pressure inflation of the balloon, resulting in intimal and medial tearing with continuous weakening and stretching of the artery,5–7 perforation of the media without penetration of blood through the adventitia, or deep resection by directional coronary atherectomy. Conversely, there have also been reports of rupture or rapid enlargement of an aneurysm in the early stages following PCI. These were likely perforations that progressed to pseudoaneurysms.9 Development of CAA after stenting in the present day is rare. Rab et al.10 reported CAA in 32% of patients who received glucocorticoid following bailout stenting. They suggested that steroid-mediated impairment of vascular healing might have led to weakening of the arterial wall and aneurysm formation, despite the presence of a reinforcing stent. Most reports have been associated with bailout stenting for coronary artery dissection following balloon angioplasty. Also, high-pressure balloon inflations commonly used to optimize the expansion of coronary stents may lead to small uncovered dissections and CAA formation.11 Incomplete coverage of edge dissection may lead to long-term coronary artery aneurysm formation. In the study by Slota et al.,12 CAA was higher in patients with dissection (8.9 versus 4.7%). In their study of 410 patients (PTCA = 203 patients and stent = 207 patients), the incidence of CAA was 5.4% at 6-month angiographic follow-up (3.9% in the stent group and 7% in the PTCA group). This study was performed before the routine use of high-pressure balloon inflation during stent implantation. They could not find a predictive factor for the development of CAA. The restenosis rate and major cardiac events at 1-year follow-up were not different when patients with and without CAA were compared. The incidence of aneurysm formation is lower after stent implantation with currently used techniques. In the recently reported instances of CAA following implantation of sirolimus-eluting stents,8,13 the authors postulated that patient-specific sensitivity to the drug and incomplete stent apposition could have played a role. Since intravascular ultrasound assessment was not done in our patients, we cannot comment on whether incomplete stent apposition was responsible. Minor dissections, a universal phenomenon following balloon angioplasty, usually seal off and heal after stenting. However, drug-eluting stents having an antiproliferative action may be responsible not only for delay in intimal healing, but also for the tunica media. This delayed and inappropriate healing may be responsible for weakening of the arterial wall and delayed aneurysm formation.
References
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