TY - JOUR
T1 - Increased thin-cap neoatheroma and periprocedural myocardial infarction in drug-eluting stent restenosis multimodality intravascular imaging of drug-eluting and bare-metal stents
AU - Ali, Ziad A.
AU - Roleder, Tomasz
AU - Narula, Jagat
AU - Mohanty, Bibhu D.
AU - Baber, Usman
AU - Kovacic, Jason C.
AU - Mintz, Gary S.
AU - Otsuka, Fumiyuki
AU - Pan, Stephen
AU - Virmani, Renu
AU - Sharma, Samin K.
AU - Moreno, Pedro
AU - Kini, Annapoorna S.
PY - 2013/10
Y1 - 2013/10
N2 - Background-Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. Methods and Results-Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. Median duration poststent implantation was 33 months. Optical coherence tomography-verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P=0.02), anddemonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P=0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12-92] versus 9 [interquartile range, 0-32]; P<0.001) and the density of lipid core burden index (lipid core burden index/4 mm, 144 [interquartile range, 60-285] versus 26 [interquartile range, 0-86]; P<0.001) were higher in DES compared with baremetal stents. Topographically, NA was classified as I (thin-cap NA), II (thick-cap NA), and III (peri-strut NA). Type I thin-cap neoatheroma was more common in DES (20% versus 3%; P=0.01) and in areas of the stented segment without significant in-stent restenosis (71%). Periprocedural myocardial infarction occurred only in DES (11 versus 0; P=0.05), of which 6 (55%) could be attributed to segments with >70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7-27; P=0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1-2.4; P=0.05). Conclusions-In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure.
AB - Background-Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. Methods and Results-Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. Median duration poststent implantation was 33 months. Optical coherence tomography-verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P=0.02), anddemonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P=0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12-92] versus 9 [interquartile range, 0-32]; P<0.001) and the density of lipid core burden index (lipid core burden index/4 mm, 144 [interquartile range, 60-285] versus 26 [interquartile range, 0-86]; P<0.001) were higher in DES compared with baremetal stents. Topographically, NA was classified as I (thin-cap NA), II (thick-cap NA), and III (peri-strut NA). Type I thin-cap neoatheroma was more common in DES (20% versus 3%; P=0.01) and in areas of the stented segment without significant in-stent restenosis (71%). Periprocedural myocardial infarction occurred only in DES (11 versus 0; P=0.05), of which 6 (55%) could be attributed to segments with >70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7-27; P=0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1-2.4; P=0.05). Conclusions-In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure.
KW - Atherosclerosis
KW - Coronary restenosis
KW - Percutaneous coronary intervention
UR - http://www.scopus.com/inward/record.url?scp=84892145707&partnerID=8YFLogxK
U2 - 10.1161/CIRCINTERVENTIONS.112.000248
DO - 10.1161/CIRCINTERVENTIONS.112.000248
M3 - Article
C2 - 24065447
AN - SCOPUS:84892145707
SN - 1941-7640
VL - 6
SP - 507
EP - 517
JO - Circulation: Cardiovascular Interventions
JF - Circulation: Cardiovascular Interventions
IS - 5
ER -