Early neoatherosclerosis as a cause of second-generation drug-eluting stent restenosis

Chamié, Daniel; Costa Jr., J. Ribamar; Abizaid, Alexandre

doi:10.1590/S2179-83972012000300019

Abstracts

We report a case of everolimus-eluting stent restenosis caused by neoatherogenesis. Optical coherence tomography indicated the presence of a superficial arch with high optical intensity in the in-stent mid-segment, followed by significant signal attenuation, with poorly defined borders, indicating the presence of lipid infiltration and/or necrotic core, similar to that observed in de novo coronary lesions. Signs suggesting macrophage/foam cell infiltration were observed inside the fibrous cap, indicating the presence of local inflammatory activity. The development of new in-stent atherosclerosis at the site of a pre-existing neointimal tissue (neoatherosclerosis) was recently identified as an additional cause of coronary stent failure. The present report is one of the first to demonstrate the finding of neoatherosclerosis as a second generation drug-eluting stent failure.

Coronary artery disease; Coronary restenosis; Angioplasty; Drug-eluting stents

Relatamos um caso de reestenose de stent eluidor de everolimus causada por neoaterogênese. A tomografia de coerência óptica revelou, no segmento médio intrastent, presença de arco superficial com alta intensidade óptica, seguido por significativa atenuação do sinal luminoso, com limites mal definidos, indicando presença de infiltração lipídica e/ou núcleo necrótico, semelhante ao observado em lesões coronárias de novo. Sinais sugerindo infiltração de macrófagos/foam cells puderam ser observados no interior da capa fibrosa, denotando presença de atividade inflamatória local. O surgimento de nova aterosclerose intrastent, no local de um tecido neointimal já formado (neoaterosclerose), tem sido recentemente identificado como causa adicional de falência de stents coronários. O presente relato é um dos primeiros a demonstrar o achado de neoaterosclerose como falha de um stent farmacológico de segunda geração.

Doença da artéria coronariana; Reestenose coronária; Angioplastia; Stents farmacológicos

CASE REPORT

^IPhysician, interventional cardiologist of the Invasive Cardiology Service of the Instituto Dante Pazzanese de Cardiologia. São Paulo, SP, Brazil

^IIPhysician, interventional cardiologist of the Invasive Cardiology Service of the Instituto Dante Pazzanese de Cardiologia. São Paulo, SP, Brazil

^IIIAssociate Professor. Director of the Invasive Cardiology Service of the Instituto Dante Pazzanese de Cardiologia. São Paulo, SP, Brazil

Correspondence to

ABSTRACT

A case of everolimus-eluting stent restenosis caused by neoatherogenesis is reported. Optical coherence tomography indicated the presence of a superficial arch with high optical intensity in the in-stent mid-segment, followed by significant signal attenuation with poorly defined borders, indicating the presence of lipid infiltration and/or a necrotic core, similar to that observed in de novo coronary lesions. Signs suggesting macrophage/foam cell infiltration were observed inside the fibrous cap, indicating the presence of local inflammatory activity. The development of new in-stent atherosclerosis at the site of pre-existing neointimal tissue (neoatherosclerosis) was recently identified as an additional cause of coronary stent failure. The present report is one of the first to demonstrate the finding of neoatherosclerosis as a second-generation drugeluting stent failure.

Descriptors: Coronary artery disease. Coronary restenosis. Angioplasty. Drug-eluting stents.

The case of a 58-year-old male patient is reported, an ex-smoker, with hypertension and prior coronary artery bypass grafting surgery, who presented with acute myocardial infarction without ST-segment elevation on January 1, 2012, and was submitted to percutaneous coronary intervention on January 18, 2012, with implantation of an everolimus-eluting stent in the middle third of the left circumflex artery.

Six months after the procedure, the patient returned complaining of stable angina class II according to the classification of the Canadian Cardiovascular Society (CCS).

A new angiography showed focal in-stent restenosis (Figure 1). An optical coherence tomography was performed (Figures 2 and 3) and demonstrated a heterogeneous vascular response pattern throughout the previously treated segment. The distal segment of the stent had a satisfactory vascular healing pattern, with a thin layer of neointimal hyperplasia with circumferential distribution and regular borders, in which the tissue had a homogeneous pattern of high optical intensity¹(Figure 2, panel 1). In contrast, the proximal intrastent segment showed more pronounced neointimal suppression, with the heterogeneous distribution of a fine layer of neointimal tissue and presence of several struts with no tissue covering them (Figure 2, panel 3).

In the medium intrastent segment (Figure 2, panel 2), significant neointimal proliferation with expressive involvement of the luminal area was observed. A high optical intensity shallow arch, followed by significant attenuation of the light signal in which boundaries were poorly defined was observed, suggesting the existence of fatty infiltration and/or a necrotic core similar to de novo coronary lesions,² showing new intrastent atherosclerosis.³The optical signal attenuation was so expressive that it prevented the identification of the structure of the metallic stent struts. Signs of local inflammatory activity could be inferred by visualising a 'flecked' glow within the fibrous cap, with an optical intensity greater than the surrounding fibrous tissue, suggesting the infiltration of clusters of macrophages/ foam cells.

In the three-dimensional reconstruction of the optical coherence tomography images, there was a discontinuity image in the central region of the stent structure (restenosis site) resulting from the hyperattenuation of the optical signal by the neoatherogenic tissue (Figure 3A).

The development of new intrastent atherosclerosis at the site of already formed neointimal tissue ('neoatherosclerosis') has recently been identified as an additional cause of failure (restenosis or thrombosis) of coronary stents.^4-6A series of 299 autopsy cases demonstrated that the incidence of neoatherosclerosis is greater in lesions treated with first-generation drug-eluting stents (DES; 31%) compared with bare-metal stents (BMS; 16%), and the time to its onset is shorter after implantation of a DES (420 days - 361 days to 683 days) when compared to BMS (2,160 days - 1,800 days to 2,880 days).⁷To date, descriptions of encountering neoatherosclerosis in second-generation DES are scarce. The present report is one of the first to report the finding of neoatherosclerosis as a second-generation stent failure. The prematurity of this phenomenon is noteworthy and deserves further investigation.

CONFLICTS OF INTEREST

The authors declare no conflicts of interest.

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