CONTENT

A 62-year-old male patient presented with dyspnea. The cardiac troponin I (cTn-I) level was found to be 26 pg/mL (0.0-47.34 pg/mL) in the patient, with no significant ischemic change in his electrocardiography. It was learned that the patient had a history of hypertension, diabetes mellitus, and Behçet’s disease without follow-up and treatment. Echocardiography showed ejection fraction EF 30% and left ventricular global hypokinesia with dilatation. Diagnostic coronary angiography revealed a 70% stenosis in the mid part of the left anterior descending artery (LAD) with normal other coronary arteries. After a 2.5 × 20 mm balloon pre-dilatation, a 3.0 × 28 mm Everolimus-Eluting Platinum Chromium Coronary Stent System (Promus PREMIER, Boston Scientific) was implanted in the LAD. Post-dilatation was performed with a 3.5 × 15 mm non-compliant balloon at 14 atm and there was no significant residual stenosis (Figures 1a-d) (Video 1).

Twenty-eight days later, he admitted the typical chest pain, and cTn-I level was found to be 1250 pg/mL (0.0-47.34 pg/mL). In control coronary angiography, giant aneurysms were seen in the proximal and distal parts of the previously placed LAD stent and in the ostial part of the diagonal artery branch emerging from the stent (Figures 1d-f) (Video 2). The patient was referred for emergency coronary bypass graft surgery. Written informed consent was obtained from the patient for the publication of this case report.

Coronary artery aneurysm (CAA) is described as more than 50% dilatation of the reference coronary artery segment diameter.¹ If the CAA diameter is more than 4 times the normal coronary segment or the diameter is more than 20 mm, it may be described as a giant CAA.^2-4 Acquired CAA may happen due to atherosclerosis, Kawasaki disease, Takayasu arteritis, other connective tissue diseases, infections, trauma, percutaneous coronary intervention (PCI), and drug-eluting stent (DES) implantation.^1,5 Improvement of CAA after DES implantation is an infrequent complication. The possible mechanism of aneurysm formation is hypersensitivity and inflammatory reactions induced by the stent polymer. Although the stent polymers are highly tissue compatible, they can rarely stimulate a local severe inflammatory response with eosinophils and lymphocytes, including all three arterial layers, leading to aneurysm formation.^6-8 Also, four autopsies exposed intrastent eosinophilic infiltrate, thrombosis, and lack of intimal improvement. However, studies have shown that allergies to stents (such as nickel, stainless steel, and cobalt-chromium metals) increased in-stent restenosis, not predisposed to CAA formation. The optimal treatment method for DES-related coronary aneurysms is unknown. Covered stents or bypass operations may be indicated large or enlarging CAAs, due to the risk of coronary artery rupture risk.^5-9 Our case is unusual due to Everolimus-eluting stent-related early-time, multiple giant CAA development.

Footnotes

Informed Consent: Written informed consent was obtained from the patient for the publication of this case.

Declaration of Interests: The authors have no conflicts of interest to declare.

Video 1: Imaging of diagnostic coronary angiography and left anterior descending artery (LAD) stenting procedure

Video 2: Imaging of control coronary angiography, twenty-eight days after the first angiography

References

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