Using serial volumetric intravascular ultrasonography, we evaluated the predictors of late intimal hyperplasia (IH) increases after drug-eluting stent implantation. All eligible patients who underwent 6-month angiography without visual restenosis were requested to undergo a 2-year follow-up examination. Complete serial (after stenting and early [6-month], and late [2-year] follow-up) angiographic and intravascular ultrasound data were available for 135 patients with 143 lesions: 99 sirolimus-eluting stents and 44 paclitaxel-eluting stents. The external elastic membrane, stent, lumen, and peri-stent plaque volumes (external elastic membrane minus stent) were normalized by stent length. The percentage of IH volume was calculated as IH volume/stent volume × 100. The early reduction in the minimum lumen area was greater than the late reduction in the minimum lumen area (−0.8 ± 0.8 vs −0.2 ± 0.5 mm 2 , p <0.001). A progressive increase occurred in the percentage of IH volume: 8.1 ± 7.1% from baseline to 6 months and 2.4 ± 3.9% from 6 months to 2 years (p <0.001, between the early and late increases in the percentage of IH). The use of paclitaxel-eluting stents was the only independent predictor for the percentage of IH volume at 6 months (β = 0.419, p <0.001). The use of paclitaxel-eluting stents (β = 0.365, p <0.001, 95% confidence interval 3.7 to 9.7) and the post-stenting normalized plaque and media volume (β = 0.195, p = 0.020, 95% confidence interval 0.1 to 1.6) were the only independent predictors for the percentage of IH volume at 2 years. However, when the percentage of IH at 6 months was forced into the model, the percentage of IH at 6 months and the post-stenting normalized plaque and media volume, not paclitaxel-eluting stent use, predicted the 2-year percentage of IH. In conclusion, although IH continued to increase beyond 6 months, the growth rate of intima and luminal loss attenuated with time.
Drug-eluting stents (DESs) reduce the rate of restenosis and the need for repeat revascularization compared to bare metal stents. Although delayed arterial healing, characterized by impaired endothelization and persistent fibrin deposition, has been suggested as a potential mechanism for late “catch-up” of neointimal growth after DES implantation, few long-term follow-up data have demonstrated late (after 1 year) DES-related vascular changes, including intimal hyperplasia (IH), stent–vessel wall apposition, and remodeling and their effect on late clinical prognosis. Although quantitative coronary angiography has been used to assess late loss of minimal lumen diameter, 3-dimensional intravascular ultrasound volumetric analysis can provide more detail and reliable information on the extent and distribution of intimal tissue and the nature and extent of vascular remodeling. We report the long-term, serial (baseline and early [6-month], and late [2-year] follow-up) intravascular ultrasound findings in patients treated with DES who did not experience clinical events between implantation and late follow-up.
Methods
The data were derived from the Serial Angiographic Analysis after Drug-Eluting Stent Placement by Six-month and Two-year Angiographic Follow-Up (DES-FU) study that included patients who had undergone DES implantation with sirolimus-eluting stents (SES Cypher stent, Cordis, Johnson & Johnson, Miami Lakes, Florida) and paclitaxel-eluting stents (PES Taxus stent, Boston Scientific, Natick, Massachusetts) at the Asan Medical Center (Seoul, Korea). The patients in this cohort had undergone stent implantation from March 2003 to August 2004. From the present analysis, we excluded patients with serious co-morbid diseases, graft lesions, restenosis on the 6-month angiogram, and those who had experienced adverse cardiac events, including death, myocardial infarction, stent thrombosis, or target vessel revascularization, before the late angiographic follow-up examination. In this registry, 531 patients with 766 lesions had undergone ≥2 scheduled follow-up angiograms, one at 4 to 12 months (6-month or early follow-up) and another at 13 to 46 months (2-year or late follow-up). As an intravascular ultrasound substudy, complete serial (after stenting and 6-month and 2-year follow-up) qualitative angiographic and volumetric intravascular ultrasound data were available for 135 patients (25.4%) with 143 lesions. All patients provided written informed consent.
All procedures were performed using standard techniques. The choice of DES (i.e., SES or PES) and the use of predilation, intra-aortic balloon pump, debulking atherectomy, or postdilation strategies were at the operator’s discretion. Heparin was administered during the procedure according to standard practice. The patients who had not previously been taking antiplatelet agents were pretreated with a 300- to 600-mg loading dose of clopidogrel or 500 mg of ticlopidine, followed by clopidogrel (75 mg/day) or ticlopidine (250 mg/day) for ≥6 months after PCI and aspirin (100 to 200 mg/day) indefinitely. The duration of clopidogrel was also dependent on the operator’s discretion. Similarly, cilostazol 200 mg/day was prescribed for ≥1 month in patients with high-risk clinical profiles or who had undergone complicated procedures.
All eligible patients who had undergone early 6-month angiography without restenosis were requested to return for a late 2-year angiographic follow-up examination. Qualitative angiographic measurements were done using standard techniques with automated edge-detection algorithms (CASS-5, Pie-Medical, Maastricht, The Netherlands) in the angiographic analysis center of the CardioVascular Research Foundation (Seoul, Korea). Angiographic image acquisition was performed at target sites using ≥2 angiographic projections of the stenosis at baseline, after stenting, and at 6 months and 2 years after stenting. Angiographic restenosis was defined as diameter stenosis of >50% at follow-up angiography.
Intravascular ultrasonography was performed after intracoronary administration of 0.2 mg nitroglycerin using a motorized transducer pull back (0.5 mm/s) and a commercial scanner (Boston Scientific/SCIMED, Minneapolis, Minnesota) consisting of a rotating 30- or 40-MHz transducer within a 3.2Fr imaging sheath. Quantitative volumetric intravascular ultrasound analysis was performed as previously described. Using computerized planimetry (EchoPlaque, version 2.7, Indec Systems, MountainView, California). The stent and reference segments were assessed every 1 mm. The reference segment external elastic membrane, lumen, and plaque and media (external elastic membrane minus lumen) areas were measured over a 5-mm length adjacent to each stent edge and averaged. In-stent measurements were also obtained every 1 mm and included the external elastic membrane, stent, lumen (intrastent lumen bounded by the borders of the stent and IH), peri-stent plaque and media (external elastic membrane minus stent), and IH (stent minus intrastent lumen) areas and volumes. The percentage of IH was defined as the IH volume divided by the stent. All volumes were calculated using Simpson’s rule and then normalized for analysis length (normalized volume).
Late stent malposition (LSM) was defined as the separation of at least one stent strut not in contact with the intimal surface of the arterial wall that was not overlapping a side branch, was not present immediately after stent implantation, and had evidence of blood speckling behind the strut. Within the LSM sections, the LSM and plaque and media (external elastic membrane minus stent minus LSM) volumes (and normalized volumes) were calculated using Simpson’s rule.
All statistical analyses were conducted using Statistical Package for Social Sciences software (SPSS, Chicago, Illinois). Categorical data are presented as numbers and percentages and compared using chi-square statistics or Fisher’s exact test. Continuous variables are presented as the mean ± SD and compared using the unpaired or paired Student t test. All p values were 2-sided, and p <0.05 indicated statistical significance.
Results
Complete serial (after stenting and 6-month and 2-year follow-up) qualitative angiographic and volumetric intravascular ultrasound data were available for 135 patients with 143 lesions (99 SES-treated lesions and 44 PES-treated lesions). The point of early and late follow-up was 7.0 ± 2.1 months (range 4.6 to 11.7) and 25.1 ± 3.6 months (range 21.7 to 30), respectively. The baseline clinical and procedural characteristics are summarized in Tables 1 and 2 .
| Variable | Total |
|---|---|
| Age (years) | 57 ± 10 |
| Men | 98 (73%) |
| Smoking | 41 (30%) |
| Hypertension ⁎ | 72 (53%) |
| Hypercholesterolemia † | 32 (24%) |
| Diabetes mellitus | 24 (18%) |
| Left ventricular ejection fraction (%) | 59 ± 8 |
| Previous percutaneous coronary intervention | 15 (11%) |
| Previous coronary bypass surgery | 2 (2%) |
| Clinical presentation | |
| Stable angina pectoris | 63 (47%) |
| Unstable angina pectoris | 57 (42%) |
| Acute myocardial infarction | 15 (11%) |
| No. of narrowed coronary arteries | |
| 1 | 54 (40%) |
| 2 | 39 (29%) |
| 3 | 41 (30%) |
| Isolated left main disease | 1 (1%) |
⁎ Defined as receiving antihypertensive treatment or having systolic blood pressure ≥140 mm Hg or diastolic blood pressure of ≥90 mm Hg.
† Defined as total cholesterol >200 mg/dl or receiving antilipidemic treatment.
| Variable | Total | Cypher | Taxus |
|---|---|---|---|
| Lesions (n) | 143 | 99 | 44 |
| 6-Month follow-up duration (mo) | 7.0 ± 2.1 | 7.2 ± 2.3 | 6.7 ± 1.7 |
| 2-Year follow-up duration (mo) | 25.1 ± 3.6 | 25.0 ± 3.3 | 25.2 ± 4.1 |
| Procedural findings | |||
| Direct stenting | 26 (18%) | 17 (17%) | 9 (21%) |
| Stent in side branch | 8 (6%) | 4 (4%) | 4 (9%) |
| Maximal balloon size used (mm) | 3.5 ± 0.4 | 3.5 ± 0.4 | 3.5 ± 0.5 |
| No. of drug-eluting stents/lesion | 1.2 ± 0.5 | 1.3 ± 0.5 | 1.2 ± 0.5 |
| Stent length (mm) | 29 ± 15 | 29 ± 15 | 29 ± 15 |
| Angiographic findings | |||
| Chronic total occlusion | 7 (5%) | 6 (6%) | 1 (2%) |
| In-stent restenosis | 6 (4%) | 5 (5%) | 1 (2%) |
| Severe calcification | 11 (8%) | 8 (8%) | 3 (7%) |
| Thrombolysis In Myocardial Infarction grade 0 | 9 (6%) | 7 (7%) | 2 (5%) |
| Thrombus | 9 (6%) | 4 (4%) | 5 (11%) |
| Coronary lesion site | |||
| Left anterior descending | 51 (36%) | 35 (35%) | 16 (36%) |
| Left circumflex | 38 (27%) | 30 (30%) | 8 (18%) |
| Right | 44 (31%) | 29 (29%) | 15 (34%) |
| Left main | 10 (7%) | 5 (5%) | 5 (11%) |
| Proximal reference diameter (mm) | 3.2 ± 0.4 | 3.2 ± 0.4 | 3.2 ± 0.5 |
| Distal reference diameter (mm) | 2.6 ± 0.4 | 2.6 ± 0.4 | 2.5 ± 0.5 |
| Minimal lumen diameter (mm) | |||
| Before intervention | 0.9 ± 0.5 | 0.9 ± 0.5 | 1.0 ± 0.5 |
| After intervention | 2.6 ± 0.4 | 2.6 ± 0.4 | 2.5 ± 0.5 |
| 6-Month follow-up | 2.5 ± 0.5 | 2.5 ± 0.4 | 2.3 ± 0.5 |
| 2-Year follow-up | 2.3 ± 0.6 | 2.4 ± 0.5 | 2.1 ± 0.6 |
| Coronary restenosis at 2 years | 5 (3%) | 2 (2%) | 3 (7%) |
Overall, 143 lesions were assessed with serial (baseline, early follow-up, and late follow-up) intravascular ultrasound examinations. The percentage of IH volume at 6 months was 8.1 ± 7.1%; this was followed by an increase of 2.4 ± 3.9% from 6 months to 2 years (p <0.001 vs 6-month percentage of IH), with no correlation between the early and late increases in the percentage of IH. Also, no relation was found between the late percentage of IH and the overall duration of follow-up. However, 122 lesions (86%) had an increase in the percentage of IH from 6 months to 2 years, and 21 lesions (15%) had a decrease in the percentage of IH from 6 months to 2 years. Although the overall percentage of IH volume at 2 years was 10.5 ± 8.5%, it was much greater in the PES-treated lesions than in the SES-treated lesions (16.3 ± 9.1% vs 7.9 ± 6.9%, respectively, p <0.001; Figure 1 ).
The IH volume in the 25 patients with diabetes mellitus was not different from that of the 110 patients without diabetes at 6 months (17.2 ± 15.9 vs 18.0 ± 20.8 mm 3 , p = 0.9) or 2 years (20.6 ± 18.5 vs 23.8 ± 26.2 mm 3 , respectively, p = 0.6). Similarly, the percentage of IH volumes in those with diabetes versus those without were virtually identical at 6 months (8.8 ± 6.9% vs 8.0 ± 7.2%, respectively, p = 0.6) and 2 years (10.5 ± 7.9% vs 10.5 ± 8.7%, p = 1.0). Finally, no significant difference was found in the late increase in the percentage of IH volume between those with (1.7 ± 3.1%) and without (2.5 ± 4.1%) diabetes (p = 0.4).
Univariate analysis demonstrated that PES use, acute coronary syndrome, and normalized post-stenting peri-stent plaque and media volume correlated with the percentage of IH volume at 6 months and at 2 years. These variables were entered into a multivariate model predicting the percentage of IH at 6 months and 2 years. Stepwise linear regression analysis identified PES use as the only independent predictor for the percentage of IH volume at 6 months (β = 0.419, p <0.001, 95% confidence interval [CI] 4.1 to 8.8). Additionally, the percentage of IH volume at 2 years was independently determined by PES use (β = 0.365, p <0.001, 95% CI 3.7 to 9.7) and the post-stenting normalized plaque and media volume (β = 0.195, p = 0.020, 95% CI 0.1 to 1.6). However, when the percentage of IH at 6 months was forced into the model, the independent predictors of neointimal hyperplasia at 2 years were the percentage of IH at 6 months and the post-stenting normalized plaque and media volume, not PES use. Finally, among the variables of normalized plaque and media volume, PES use, and acute coronary syndrome, the only independent determinant for the late increase in the percentage of IH volume (between 6 months and 2 years) was the immediate post-stenting normalized plaque and media volume (β = 0.262, p = 0.002, 95% CI 0.2 to 0.8).
Overall, the in-stent minimum lumen area decreased from 6.5 ± 1.8 mm 2 after stenting to 5.8 ± 1.7 mm 2 at 6 months (p = 0.001), with no subsequent reduction in minimum lumen area at 2 years of follow-up (5.5 ± 1.7 mm 2 , p = 0.3 vs at 6 months). The minimum lumen area changes in SES-treated and PES-treated lesions were similar in that a significant decrease in the minimum lumen area was noted only in the early follow-up phase ( Table 3 ).
| Variable | After Stenting | 6 Months of Follow-up | 2 Years of Follow-up | ||||||
|---|---|---|---|---|---|---|---|---|---|
| Total | Cypher | Taxus | Total | Cypher | Taxus | Total | Cypher | Taxus | |
| Lesions (n) | 143 | 99 | 44 | 143 | 99 | 44 | 143 | 99 | 44 |
| Proximal reference | |||||||||
| Mean external elastic membrane area (mm 2 ) | 15.6 ± 4.0 | 14.8 ± 3.8 | 17.3 ± 3.9 | 15.8 ± 3.9 | 15.1 ± 3.8 | 17.2 ± 3.7 | 15.6 ± 3.9 | 14.9 ± 3.7 | 17.1 ± 3.9 |
| Mean lumen area (mm 2 ) | 9.2 ± 2.6 | 9.2 ± 2.3 | 9.1 ± 3.0 | 9.0 ± 2.6 | 9.2 ± 2.5 | 8.6 ± 2.8 | 8.7 ± 2.8 | 9.0 ± 2.7 | 8.2 ± 2.9 |
| Mean plaque and media area (mm 2 ) | 6.4 ± 2.7 | 5.6 ± 2.4 | 8.2 ± 2.4 | 7.0 ± 3.1 | 6.1 ± 2.7 | 9.0 ± 3.0 | 6.9 ± 3.0 | 6.0 ± 2.7 | 8.9 ± 2.7 |
| Stented segment | |||||||||
| Minimum lumen area (mm 2 ) | 6.5 ± 1.8 | 6.6 ± 1.7 | 6.3 ± 1.8 | 5.8 ± 1.7 ⁎ | 6.0 ± 1.8 ⁎ | 5.1 ± 1.4 ⁎ | 5.5 ± 1.7 ⁎ | 5.8 ± 1.8 ⁎ | 4.9 ± 1.4 ⁎ |
| Stent volume (mm 3 ) | 215 ± 105 | 209 ± 110 | 227 ± 91 | 217 ± 14 | 212 ± 111 | 227 ± 88 | 217 ± 104 | 213 ± 111 | 228 ± 88 |
| Lumen volume (mm 3 ) | 215 ± 105 | 209 ± 110 | 227 ± 91 | 199 ± 97 | 200 ± 105 | 197 ± 76 | 194 ± 95 | 197 ± 105 | 187 ± 69 |
| Intimal hyperplasia volume (mm 3 ) | 0 ± 0 | 0 ± 0 | 0 ± 0 | 17.9 ± 20.0 | 12.4 ± 15.3 | 30.2 ± 23.5 | 23.2 ± 25.0 † | 15.7 ± 17.1 | 40.0 ± 31.2 |
| Intimal hyperplasia volume (%) | 0 ± 0 | 0 ± 0 | 0 ± 0 | 8.1 ± 7.1 | 6.1 ± 5.8 | 12.6 ± 7.8 | 10.5 ± 8.5 † | 7.9 ± 6.9 † | 16.3 ± 9.1 † |
| External elastic membrane volume (mm 3 ) | 391 ± 186 | 364 ± 190 | 451 ± 165 | 430 ± 204 | 412 ± 214 | 470 ± 175 | 446 ± 208 ⁎ | 436 ± 223 ⁎ | 467 ± 171 |
| Plaque and media volume (mm 3 ) | 176 ± 91 | 155 ± 88 | 223 ± 80 | 213 ± 107 ⁎ | 199 ± 110 ⁎ | 243 ± 95 | 225 ± 113 ⁎ | 219 ± 121 ⁎ | 238 ± 90 |
| Normalized stent volume (mm 2 ) | 7.9 ± 1.9 | 8.0 ± 1.9 | 7.8 ± 1.9 | 8.0 ± 1.9 | 8.1 ± 1.8 | 7.8 ± 1.9 | 8.0 ± 1.9 | 8.1 ± 1.9 | 7.9 ± 1.9 |
| Normalized lumen volume (mm 2 ) | 7.9 ± 1.9 | 8.0 ± 1.9 | 7.8 ± 1.9 | 7.4 ± 1.9 ⁎ | 7.6 ± 2.0 | 6.8 ± 1.6 ⁎ | 7.2 ± 1.9 ⁎ | 7.5 ± 2.0 | 6.5 ± 1.5 ⁎ |
| Normalized Intimal hyperplasia volume (mm 2 ) | 0 ± 0 | 0 ± 0 | 0 ± 0 | 0.6 ± 0.6 | 0.5 ± 0.4 | 1.0 ± 0.8 | 0.8 ± 0.7 | 0.6 ± 0.5 | 1.3 ± 0.8 |
| Normalized external elastic membrane volume (mm 2 ) | 14.3 ± 3.1 | 13.8 ± 3.0 | 15.6 ± 3.0 | 15.8 ± 3.2 ⁎ | 15.6 ± 3.4 ⁎ | 16.2 ± 2.9 | 16.4 ± 3.5 ⁎ | 16.6 ± 3.7 ⁎ | 16.1 ± 2.9 |
| Normalized plaque and media volume (mm 2 ) | 6.4 ± 1.9 | 5.8 ± 1.7 | 7.7 ± 1.5 | 7.8 ± 1.9 ⁎ | 7.5 ± 1.9 ⁎ | 8.4 ± 1.6 ⁎ | 8.3 ± 2.2 ⁎ , † | 8.3 ± 2.4 ⁎ , † | 8.2 ± 1.6 |
| Distal reference | |||||||||
| Mean external elastic membrane area (mm 2 ) | 10.5 ± 3.6 | 10.4 ± 3.6 | 10.7 ± 3.7 | 10.8 ± 3.5 | 10.7 ± 3.6 | 10.9 ± 3.2 | 10.9 ± 3.6 | 10.9 ± 3.6 | 11.0 ± 3.6 |
| Mean lumen area (mm 2 ) | 6.8 ± 2.3 | 6.9 ± 2.2 | 6.6 ± 2.7 | 6.9 ± 2.2 | 7.1 ± 2.2 | 6.4 ± 2.1 | 6.7 ± 2.2 | 7.0 ± 2.3 | 6.1 ± 1.8 |
| Mean plaque and media area (mm 2 ) | 3.7 ± 1.9 | 3.5 ± 1.8 | 4.2 ± 2.0 | 3.9 ± 1.9 | 3.6 ± 1.9 | 4.5 ± 1.8 | 4.1 ± 2.2 | 3.8 ± 2.0 | 4.9 ± 2.3 |
⁎ p <0.05 versus after stenting.
The in-stent minimum lumen area at 2 years of follow-up correlated negatively with the early increase in the percentage of IH volume at 6 months (r = −0.422, p <0.001) and also with the late percentage of IH volume increase (r = −0.293, p <0.001) and showed a positive relation with the baseline minimum stent area (r = 0.848, p <0.001).
No significant change was found in the normalized stent volume from baseline to 6 months or 2 years, but the normalized lumen volume decreased from 7.9 ± 1.9 mm 2 after intervention to 7.4 ± 1.9 mm 2 at 6 months (p = 0.017). The normalized external elastic membrane volume increased from 14.3 ± 3.1 mm 2 after stenting to 15.8 ± 3.2 mm 2 at 6 months (p <0.001). Late changes in the normalized lumen and external elastic membrane volumes were insignificant. The normalized plaque and media volume increased significantly during both the early follow-up period (from 6.4 ± 1.9 mm 2 after stenting to 7.8 ± 1.9 mm 2 at 6 months, p <0.001) and the late follow-up period (from 7.8 ± 1.9 mm 2 at 6 months to 8.3 ± 2.2 mm 2 at 2 years, p = 0.041), although the late increases in the normalized plaque and media volume were less than the early increases ( Table 4 ).
| Variable | Total | Cypher | Taxus |
|---|---|---|---|
| Lesions (n) | 143 | 99 | 44 |
| Between post-stenting and 6 months | |||
| Proximal reference | |||
| ΔMean external elastic membrane area (mm 2 ) | 0.2 ± 2.0 | 0.3 ± 0.5 | −0.1 ± 3.3 |
| ΔMean lumen area (mm 2 ) | −0.2 ± 1.5 | 0.0 ± 0.9 | −0.5 ± 2.2 |
| ΔMean plaque area (mm 2 ) | 0.6 ± 1.9 | 0.5 ± 1.2 | 0.9 ± 2.8 |
| Stented segment | |||
| ΔMinimum lumen area (mm 2 ) | −0.8 ± 0.8 | −0.6 ± 0.8 | −1.2 ± 0.8 |
| ΔStent volume (mm 3 ) | 1.9 ± 5.8 | 2.9 ± 3.7 | −0.3 ± 8.5 |
| ΔLumen volume (mm 3 ) | −15.8 ± 21.5 | −9.2 ± 15.8 | −30.6 ± 25.0 |
| ΔIntimal hyperplasia volume (mm 3 ) | 17.8 ± 20.0 | 12.4 ± 15.3 | 30.2 ± 23.6 |
| ΔIntimal hyperplasia volume (%) | 8.1 ± 7.1 | 6.1 ± 5.8 | 12.5 ± 7.8 |
| ΔExternal elastic membrane volume (mm 3 ) | 39.1 ± 32.2 | 47.8 ± 30.8 | 19.4 ± 26.4 |
| ΔPlaque and media volume (mm 3 ) | 36.5 ± 30.8 | 44.1 ± 29.7 | 19.7 ± 26.7 |
| ΔNormalized stent volume (mm 2 ) | 0.1 ± 0.2 | 0.1 ± 0.1 | 0.0 ± 0.3 |
| ΔNormalized lumen volume (mm 2 ) | −0.5 ± 0.6 | −0.3 ± 0.4 | −1.0 ± 0.8 |
| ΔNormalized external elastic membrane volume (mm 2 ) | 1.5 ± 1.0 | 1.8 ± 0.8 | 0.6 ± 0.9 |
| ΔNormalized plaque and media volume (mm 2 ) | 1.4 ± 0.9 | 1.7 ± 0.8 | 0.7 ± 1.0 |
| Distal reference | |||
| ΔMean external elastic membrane area (mm 2 ) | 0.2 ± 1.4 | 0.2 ± 0.4 | 0.2 ± 2.4 |
| ΔMean lumen area (mm 2 ) | 0.0 ± 1.0 | 0.1 ± 0.3 | −0.2 ± 1.8 |
| ΔMean plaque and media area (mm 2 ) | 0.2 ± 0.9 | 0.1 ± 0.2 | 0.3 ± 1.5 |
| Between 6 months and 2 years | |||
| Proximal reference | |||
| ΔMean external elastic membrane area (mm 2 ) | −0.1 ± 1.3 | 0.0 ± 0.5 ⁎ | −0.1 ± 2.1 |
| ΔMean lumen area (mm 2 ) | −0.2 ± 1.0 | −0.1 ± 0.3 | −0.3 ± 1.6 |
| ΔMean plaque area (mm 2 ) | −0.1 ± 1.8 ⁎ | −0.1 ± 0.9 ⁎ | −0.1 ± 2.7 |
| Stented segment | |||
| ΔMinimum lumen area (mm 2 ) | −0.2 ± 0.5 ⁎ | −0.2 ± 0.4 ⁎ | −0.3 ± 0.7 ⁎ |
| ΔStent volume (mm 3 ) | 0.5 ± 4.6 ⁎ | 0.4 ± 3.1 ⁎ | 0.8 ± 7.0 |
| ΔLumen volume (mm 3 ) | −5.0 ± 11.0 ⁎ | −3.2 ± 6.7 ⁎ | −9.0 ± 16.6 ⁎ |
| ΔIntimal hyperplasia volume (mm 3 ) | 5.3 ± 10.1 ⁎ | 3.3 ± 4.8 ⁎ | 9.8 ± 16.0 ⁎ |
| ΔIntimal hyperplasia volume (%) | 2.4 ± 3.9 ⁎ | 1.8 ± 2.7 ⁎ | 3.7 ± 5.7 ⁎ |
| ΔExternal elastic membrane volume (mm 3 ) | 16.7 ± 39.2 ⁎ | 24.2 ± 43.2 ⁎ | −3.5 ± 16.9 ⁎ |
| ΔPlaque and media volume (mm 3 ) | 12.7 ± 31.8 ⁎ | 20.3 ± 33.8 ⁎ | −4.4 ± 17.6 ⁎ |
| ΔNormalized stent volume (mm 2 ) | 0.0 ± 0.1 ⁎ | 0.0 ± 0.1 ⁎ | 0.0 ± 0.2 |
| ΔNormalized lumen volume (mm 2 ) | −0.2 ± 0.4 ⁎ | −0.1 ± 0.3 ⁎ | −0.3 ± 0.5 ⁎ |
| ΔNormalized external elastic membrane volume (mm 2 ) | 0.6 ± 1.5 ⁎ | 0.9 ± 1.7 ⁎ | −0.1 ± 0.6 ⁎ |
| ΔNormalized plaque and media volume (mm 2 ) | 0.5 ± 1.1 ⁎ | 0.8 ± 1.2 ⁎ | −0.1 ± 0.6 ⁎ |
| Distal reference | |||
| ΔMean external elastic membrane area (mm 2 ) | 0.1 ± 1.6 | 0.1 ± 0.7 | 0.1 ± 2.7 |
| ΔMean lumen area (mm 2 ) | −0.1 ± 1.0 | −0.1 ± 0.3 ⁎ | −0.3 ± 1.7 |
| ΔMean plaque and media area (mm 2 ) | 0.2 ± 1.0 | 0.1 ± 0.5 | 0.4 ± 1.6 |
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