BACKGROUND: Changes in out-stent plaque volume can be related to in-stent intimal hyperplasia. However, few data exist regarding the impact of out-stent plaque volume on in-stent intimal hyperplasia. METHODS: We prospectively performed volumetric intravascular ultrasound in 46 stable coronary patients (34 males, mean age of 66 years) immediately as well as 18 months after stenting. From the high-gain ultrasound images, out-stent plaque volume was calculated by extracting the stent volume from the external elastic membrane volume. Volumes of in-stent intimal hyperplasia and reference plaque were also evaluated. RESULTS: Out-stent plaque volume increased from 177.3 ± 100.8mm(3) to 190.7 ± 111.1mm(3) (p<0.05) in correlation with increases in-stent intimal hyperplasia (r=0.536, p<0.05). Under these conditions, changes in reference plaque volume correlated with those in LDL-C, which decreased from 121.2 ± 48.0mg/dl to 103.3 ± 48.9 mg/dl (r=0.43, p<0.05). Interestingly, increases in out-stent plaque volume in the silorimus-eluting stent (2.7 ± 1.2%) were lesser than those in the bare-metal stent (14.0 ± 11.0%, p<0.05). CONCLUSIONS: These results indicate that irrespective of LDL-C level, changes in out-stent plaque volume correlate with those in in-stent intimal hyperplasia. We suggest that silorimus-eluting stent can suppress in-stent intimal hyperplasia partially by affecting out-stent plaque, although further large-scale studies are required to define the role of out-stent plaque in the occurrence of in-stent intimal hyperplasia.
BACKGROUND: Changes in out-stent plaque volume can be related to in-stent intimal hyperplasia. However, few data exist regarding the impact of out-stent plaque volume on in-stent intimal hyperplasia. METHODS: We prospectively performed volumetric intravascular ultrasound in 46 stable coronary patients (34 males, mean age of 66 years) immediately as well as 18 months after stenting. From the high-gain ultrasound images, out-stent plaque volume was calculated by extracting the stent volume from the external elastic membrane volume. Volumes of in-stent intimal hyperplasia and reference plaque were also evaluated. RESULTS: Out-stent plaque volume increased from 177.3 ± 100.8mm(3) to 190.7 ± 111.1mm(3) (p<0.05) in correlation with increases in-stent intimal hyperplasia (r=0.536, p<0.05). Under these conditions, changes in reference plaque volume correlated with those in LDL-C, which decreased from 121.2 ± 48.0mg/dl to 103.3 ± 48.9 mg/dl (r=0.43, p<0.05). Interestingly, increases in out-stent plaque volume in the silorimus-eluting stent (2.7 ± 1.2%) were lesser than those in the bare-metal stent (14.0 ± 11.0%, p<0.05). CONCLUSIONS: These results indicate that irrespective of LDL-C level, changes in out-stent plaque volume correlate with those in in-stent intimal hyperplasia. We suggest that silorimus-eluting stent can suppress in-stent intimal hyperplasia partially by affecting out-stent plaque, although further large-scale studies are required to define the role of out-stent plaque in the occurrence of in-stent intimal hyperplasia.