A 47-year-old non-diabetic, non-smoker, normotensive male presented with chronic stable angina and positive treadmill test in June 2013. His clinical examination was unremarkable. Two-dimensional echocardiography revealed no regional wall motion abnormality and left ventricular ejection fraction of 60%. His coronary angiography revealed mid-left anterior descending artery (LAD) 90% tubular stenosis, which was successfully stented with a 3.5 × 28 mm bioresorbable vascular scaffold (BVS) (Absorb stent, Abbott Vascular, Santa Clara, CA, USA) (Video 1). He remained asymptomatic on aspirin 150 mg, clopidogrel 75 mg, and atorvastatin 20 mg daily doses of medicines, for the next 6 years. Recently, he presented with Class II angina with an inconclusive treadmill test. A check angiogram revealed a patent LAD lumen with no in-stent restenosis. An optical coherence tomography (OCT) imaging (Illumien Optis, Abbott/St Jude Medical, Westford, MA, USA) across the LAD revealed no significant luminal stenosis and completely resorbed struts (Video 2). A signal rich fibrotic neoplaque (intima) with areas of neoatherosclerosis (Figure 1) and multiple neovascular channels (Figure 2) could be seen. The distal and proximal platinum markers of BVS (Supplementary material online, Figure S1) could be seen as high intensity thin linear signal with backscattering, separated by a distance of 28 mm.
Figure 1.
Optical coherence tomography imaging of mid-left anterior descending artery showed a neovascular channel (white arrow) and lipid-rich plaque (white asterisk).
Figure 2.
Optical coherence tomography imaging of mid-left anterior descending artery showed multiple neovascular channels (white arrows).
The intimal proliferation following metallic drug-eluting stent and BVS implantation is named as ‘neointima’ and ‘neoplaque’, respectively.1 Our case illustrates OCT findings consistent with the formation of neovascular channels within the neoplaque after BVS implantation. Neointimal neovascularization is known to trigger in-stent restenosis, neoatherosclerosis, and subsequent plaque rupture in metallic stents.2 The BVS is expected to reduce such complications by the formation of a homogenous fibrotic neointimal layer that may shield necrotic plaque components towards the lumen preventing plaque rupture.3
However, neointimal neovascularization in our patient points towards a need for a better understanding of such a phenomenon. Is it a normal physiological healing response as observed in the index case or a pathological response potentially associated with pronounced inflammation, neoatherogenesis, and adverse clinical outcomes as observed with metallic stents has to be determined.3
Few authors have reported asymptomatic follow-up of 2–5 years, despite neovascularization in BVS implanted patients.3 We hereby reported a 6-year of asymptomatic follow-up in a patient despite neovascularization following BVS implantation. As such, our observation might contribute to the understanding of causes for late scaffold failures, although its direct clinical implications have yet to be seen.
Supplementary material
Supplementary material is available at European Heart Journal - Case Reports online.
Supplementary Material
Acknowledgements
Mr Puneet Sharma, BSc, regional manager, Abbott Vascular India Ltd, helped in analysing the OCT images.
Consent: The author/s confirm that written consent for submission and publication of this case report including image(s) and associated text has been obtained from the patient in line with COPE guidance.
Conflict of interest: none declared.
References
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