Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge: a volumetric intravascular ultrasound study

Lumen enlargement during coronary stenting results from vessel expansion and axial redistribution of atheromatous plaque along the stented segment and proximal and distal reference segments. Plaque burden predicts stenosis at the stent edge. The aim of this study was to investigate the fate of shifted plaque with special reference to whether or not plaque shift (PSh) correlates with late lumen reduction. This is a prospective study conducted on 54 consecutive patients who underwent bare metal stenting. In all stent edges (108 edges), PSh volume was measured as postintervention plaque-media volume (PMV) minus preintervention PMV. Changes in lumen volume (DeltaLV), vessel volume (DeltaVV), and PMV (DeltaPMV) were measured by serial intravascular ultrasound (IVUS) examination. After stenting, PSh was detected in 81.5% of proximal edges versus 72.2% of distal edges (P = 0.36). It correlated significantly with DeltaVV (r = 0.34, P = 0.002), and inversely with DeltaLV (r = 0.32, P = 0.003). However, at 6-month follow-up, it did not correlate with DeltaLV (r = -0.03, P = 0.8), DeltaVV (r = 0.1, P = 0.6), or DeltaPMV (r = 0.1, P = 0.4). Furthermore, DeltaLV correlated more strongly with DeltaVV (r = 0.62, P < 0.00001) than with DeltaPMV (r = -0.39, P = 0.001). By multivariate analysis, PSh area was an independent predictor of the postintervention change in lumen area (partial eta squared 0.21, P = 0.01), but not the follow-up change. Two patients (3.7%) developed proximal edge stenosis with no evident PSh after stenting. Thus, axial redistribution of atheromatous plaque into the reference segments was frequently encountered after stenting. Although PSh correlated with the immediate reduction in stent edge lumen volume, it did not correlate with the late lumen reduction.     

Preintervention arterial remodeling as a predictor of intimal hyperplasia after intracoronary stenting: a serial intravascular ultrasound study.

BACKGROUND: The impact of vascular remodeling pattern on intimal hyperplasia (IH) after coronary stenting is unknown. HYPOTHESIS: The preintervention remodeling pattern of the lesion might be associated with IH after the coronary stenting procedure. METHODS: Serial (pre-, post-stent implantation, and follow-up) intravascular ultrasound (IVUS) images were obtained in 58 patients with single-stent implantation (GFX stents in 41 and NIR in 17). The matching IVUS image slices at the preintervention lesion site were selected for serial comparisons. The remodeling index (RI) was defined as lesion/proximal reference external elastic membrane cross-sectional area (CSA) at preintervention lesion site. Adequate remodeling was defined as a RI > 0.95 and inadequate remodeling as a RI < or = 0.95. Vessel stretching, percent vessel stretching, and percent IH CSA, as well as pre- and postintervention IVUS variables were evaluated according to the remodeling pattern. RESULTS: The percent IH CSA was 31% in adequate remodeling (n = 29, mean RI = 1.05) and 41% in inadequate remodeling (n = 29, mean RI = 0.88) (p = 0.049). Percent vessel stretching was 15% in adequate remodeling and 22% in inadequate remodeling (p = 0.007). The RI inversely correlated with percent vessel stretching (r = -0.435, p = 0.001). CONCLUSIONS: Compared with preintervention adequate remodeling, inadequate remodeling was associated with increased percent IH CSA, which might be related with more vessel stretching.     

Effect of plaque volume on subsequent vessel remodeling at edges of sirolimus-eluting stents

Serial (baseline and 9-month follow-up) intravascular ultrasound analysis was performed at 5-mm reference segments immediately proximal and distal to the sirolimus-eluting stent (SES) in 33 lesions. Proximal and distal reference segments were divided into 1-mm subsegments. Between postintervention and follow-up intravascular ultrasound studies, there were significant decreases in the lumen and increases in plaque & media areas in the subsegment closest to the distal edge, with no change in external elastic membrane area. There was no significant change in external elastic membrane, lumen, and plaque & media areas within the other subsegments. At the nearest 1-mm subsegment from the proximal and distal edges, baseline plaque & media area was associated with subsequent vessel remodeling. In conclusion, a large amount of plaque at the SES edge may be a risk of negative remodeling at follow-up (stent edge restenosis). It supports the importance of "normal-to-normal" SES deployment.     

Peri-stent reference segment plaque burden is associated with disease progression in saphenous vein grafts (a serial intravascular ultrasound assessment)

We are aware of no studies of peri-stent disease progression or luminal compromise in saphenous vein graft (SVG) lesions. We used serial intravascular ultrasound (IVUS) to assess disease progression in peri-stent saphenous vein bypass graft reference segments. We studied 37 peri-stent SVG reference segments in 21 patients; 16 were proximal and 21 were distal to the stent. The same anatomic image slice was analyzed after the intervention and at follow-up; this site was 3.68 +/- 2.22 mm from the stent edge. Graft age was 10.1 +/- 5.4 years, and mean follow-up duration was 13 months (range 3 to 61). Overall, change in SVG area, change in lumen area, and change in plaque burden correlated with postintervention plaque burden (r = 0.448, p = 0.005; r = -0.584, p <0.001; and r = 0.507, p = 0.001, respectively). For the proximal edge, change in lumen area correlated with change in plaque area (r = -0.951, p <0.001), but not with change in SVG area (r = -0.337, p = 0.201). For the distal edge, change in lumen area correlated more strongly with change in plaque area (r = -0.982, p <0.001) than with change in SVG area (r = -0.624, p = 0.003). When peri-stent reference segments were divided into 2 groups according to postintervention plaque burden (>50% [n = 20] vs <50% [n = 17]), there was a greater decrease in lumen area (-1.12 +/- 0.81 vs -0.33 +/- 0.26 mm(2), p <0.001) and greater increases in SVG area (0.26 +/- 0.29 vs 0.09 +/- 0.09 mm(2), p = 0.027), plaque area (1.37 +/- 0.96 vs 0.42 +/- 0.30 mm(2), p <0.001), and plaque burden (8.2 +/- 5.6% vs. 2.8 +/- 1.6%, p <0.001) in segments with a plaque burden >50%. In conclusion, peri-stent reference segment SVG disease progression and lumen loss were more significant in segments with a greater postintervention plaque burden after implantation of a bare metal stent or drug-eluting stent.     

Intravascular ultrasonic analysis of atherosclerotic vessel remodeling and plaque distribution of stenotic left anterior descending coronary arterial bifurcation lesions upstream and downstream of the side branch

Bifurcation lesions remain a challenging lesion subset, even in the era of drug-eluting stents. The aim of this study was to investigate the longitudinal remodeling pattern and cross-sectional plaque location of bifurcation lesions. Seventy-four preintervention intravascular ultrasound studies of left anterior descending bifurcation lesions were analyzed, in which the lesion was located proximal (type A, n=32) or distal (type B, n=42) to the side branch. Vessel area and plaque area at the lesion (VAlesion and PAlesion) and at the reference site (VAreference and PAreference) were measured. The remodeling ratio was defined as VAlesion/VAreference, and the vessel compensation ratio was defined as (VAlesion-VAreference)/(PAlesion-PAreference). The geometric center of the lumen at the lesion site was identified, and the lesion site was divided into circumferential equal arcs to compare the cross-sectional distribution of percentage plaque area (100x[PAlesion/VAlesion]) between the 2 groups. The remodeling ratio (1.03+/-0.15 vs 0.94+/-0.14, p=0.01) and the vessel compensation ratio (0.0+/-0.36 vs -0.37+/-0.61, p<0.01) were significantly greater in type A than in type B lesions. The circumferential distribution pattern of percentage plaque area was significantly different between the groups (analysis of variance p<0.005), with greater percentage plaque area for the vessel wall opposite from the side branch in type B lesions (46.3+/-18.0% vs 54.6+/-15.4%, type A vs type B lesions, p<0.05). In conclusion, these results suggest that a major side branch may affect longitudinal lesion remodeling as well as the circumferential location of atherosclerotic plaque.     

Preintervention angiographic and intravascular ultrasound predictors for side branch compromise after a single-stent crossover technique

A single stent crossover technique is the most common approach to treating bifurcation lesions. In 90 bifurcation lesions with side branch (SB) angiographic diameter stenosis <75%, we assessed preintervention intravascular ultrasound (IVUS; of main branch [MB] and SB) predictors for SB compromise (fractional flow reserve [FFR] <0.80) after a single stent crossover. Minimal lumen area (MLA) was measured within each of 4 segments (MB just distal to the carina, polygon of confluence, MB just proximal to polygon of confluence, and SB ostium). All lesions showed Thrombolysis In Myocardial Infarction grade 3 flow in the SB after MB stenting. Although angiographic diameter stenosis at the SB ostium increased from 26 ± 15% before the procedure to 36 ± 21% after stenting (p = 0.001), FFR <0.80 was observed in only 16 patients (18%). Negative remodeling (remodeling index <1) was seen in 83 (92%) lesions but did not correlate with FFR after stenting. Independent predictors for FFR after stenting were maximal balloon pressure (p = 0.002) and MLA of SB ostium before percutaneous coronary intervention (p <0.001), MLA within the MB just distal to the carina (p = 0.025), and plaque burden at the SB ostium before percutaneous coronary intervention (p = 0.005), but not angiographic poststenting diameter stenosis or minimal lumen diameter. For prediction of FFR <0.80 after percutaneous coronary intervention, the best cutoff of MLA within the SB ostium before percutaneous coronary intervention was 2.4 mm(2) (sensitivity 94%, specificity 69%). Also, the cutoff of plaque burden within the SB ostium before percutaneous coronary intervention was ≥51% (sensitivity 75%, specificity 71%). In 67 lesions with an MLA ≥2.4 mm(2) or plaque burden <50% before percutaneous coronary intervention, 63 (94%) showed FFR ≥0.80. However, FFR <0.80 was seen in only 12 (52%) of 23 lesions with an MLA <2.4 mm(2) and plaque burden ≥50%. In conclusion, there do not appear to be reliable IVUS predictors of functional SB compromise after crossover stenting.     

Effect of stent implantation on upstream coronary artery compliance--a cause of late plaque rupture?

Stent implantation in the rabbit aorta has been shown to increase vessel wall compliance at the inflow to the stent, but it is uncertain whether similar effects might be seen in the coronary arteries of humans and whether this would have any significant clinical consequences. First, we measured vessel compliance (systolic lumen area--diastolic lumen area/pulse pressure) before, immediately after, and at the 6-month follow-up visit at a site 5 mm upstream of the proximal edge of an implanted coronary stent in patients undergoing coronary intervention using motorized pull-back intravascular ultrasound recordings. Compliance in the upstream segment increased significantly immediately after stenting (before 7.13 +/- 1.49 vs after 10.73 +/- 1.36 mm2/mm Hg, p = 0.03), an effect that was unchanged at 6 months of follow-up (11.84 +/- 2.11 mm2/mm Hg, p = 0.08 vs before stenting). Second, we examined the site of plaque rupture in all patients presenting with an acute coronary syndrome in whom the culprit lesion was in a vessel that had had a stent implanted >12 months previously (n = 31). Plaque rupture was statistically more likely at the inflow to the stent (n = 22) than at other sites within the culprit vessel (n = 9, p <0.01). We conclude that stenting causes an increase in vessel compliance immediately proximal to the stent, and that when a vessel has been previously stented, plaque rupture is most likely to occur at the stent inflow site.     

应用血管内超声探讨冠状动脉不同长度支架置入后对斑块重新分布的影响

目的 探讨冠状动脉支架置入后斑块的重新分布对支架边缘的影响及此影响是否与所置入支架长度有关.方法 47例行经皮冠状动脉介入治疗(PCI)的稳定性和不稳定性心绞痛患者,冠状动脉内共置人支架70枚,根据支架的长度分为两组,支架长度≤18 mm和>18 mm组.于支架置入前后的支架远端边缘(支架远端5 mm)、支架和支架近端边缘(支架近端5mm)进行血管内超声(IVUS)图像分析,测量冠状动脉横截面上的管腔面积(LA)、血管面积(VA).三段分析部位的LA和VA的平均值乘以三段的长度(即5 mm、支架长度和5 mm)即为三段的管腔体积(LV)和血管体积(VV).VV-LV=管壁体积(WV),支架两端移动斑块体积=支架置入后WV-支架置入前WV.结果 在支架长度≤18 mm组支架近远端分别检测到91%和93%斑块移位(P>0.05),在支架长度>18 mm组支架近远端分别检测到80%和91%的斑块移位(P<0.05).支架置入后支架长度≤18 mm组支架近远端和支架长度>18 mm组支架近端边缘,LV缩小、VV无变化、WV明显增加,即由于斑块的移位造成支架置入后即刻以上部位有明显的管腔缩小,但是支架长度>18 mm组支架远端边缘情况不同,LV和VV反而增加,WV有所增加,即在支架长度>18 mm组支架远端边缘斑块的移位并没有造成支架置入即刻管腔的缩小.结论 长、短支架置入后对支架近远端边缘斑块的移位和管腔的影响不同,短支架近远端和长支架近端边缘在支架置入后有斑块的移入和管腔的缩小,而长支架远端边缘虽有斑块的移入但无管腔的缩小.     

Relation between vascular morphologic changes during stent implantation and the magnitude of in-stent neointimal hyperplasia

Intimal hyperplasia usually occurs after balloon overstretch injury or wire coil stimuli to coronary arteries. We examined whether the degree of vessel wall stretch during coronary stent placement could predict the amount of in-stent neointimal hyperplasia after a 6-month follow-up. Serial (preintervention, postballooning, poststent implantation, and a follow-up after 6 months) intravascular ultrasound (IVUS) was used to study 457 consecutive cross-sectional areas in 28 patients. IVUS imaging, using a motorized pullback system at 0.5 mm/s, allowed 1-mm axial increment measurements of the total vascular, stent, and lumen cross-sectional areas. The mean total vascular area changed from 10.89 +/- 2.50 mm2 before to 11.27 +/- 2.49 mm2 after ballooning, to 12.80 +/- 2.59 mm2 after stenting, and to 12.58 +/- 2.41 mm2 at follow-up (p < 0.0001). The mean lumen area changed from 3.36 +/- 1.95 mm2 before to 4.21 +/- 1.65 mm2 after ballooning, to 5.16 +/- 1.09 mm2 after stenting, and to 3.57 +/- 1.23 mm2 at follow-up (p < 0.0001). The mean stent area decreased from 5.25 +/- 1.17 mm2 after stenting to 5.09 +/- 0.90 mm2 at follow-up (p < 0.0001). Stepwise logistic regression analysis showed that delta total vascular area (after stent implantation - before intervention) was a strong predictor of the amount of intimal hyperplasia (r = 0.57, p < 0.0001). Vascular overstretch caused by the stenting procedure promotes intimal hyperplasia in proportion to the degree of sectional vascular stretch.     

Longitudinal plaque redistribution during stent expansion

The purpose of this study was to clarify the 3-dimensional behavior of plaque during coronary stent expansion. Serial intravascular ultrasound (IVUS) studies, preintervention, and poststenting were evaluated in 32 patients treated with a single-balloon expandable tubular stent. External elastic membrane (EEM), lumen, stent, and plaque + media cross-sectional area were measured at 1-mm intervals through the entire stent as well as proximal and distal reference segments 5 mm from the stent edge. Volumetric calculations were based on Simpson's rule. Overall, the plaque + media volume through the entire lesion did not change during stent expansion (218 +/- 51 vs 217 +/- 47 mm3, p = 0.69). However, EEM and lumen volume increased significantly (EEM volume, 391 +/- 84 vs 448 +/- 87 mm3 [p < 0.0001]; lumen volume, 173 +/- 52 vs 231 +/- 54 mm3 [p < 0.0001]). The change in lumen volume correlated strongly with the change in EEM volume (r = 0.85, p < 0.0001), but poorly with the change in plaque + media volume (r = 0.37, p = 0.03). Plaque + media volume decreased in the midstent zone (59 +/- 14 vs 53 +/- 11 mm3, p = 0.0005), and increased in the distal stent zone (40 +/- 11 vs 44 +/- 9 mm3, p = 0.003), but did not change in either the proximal stent zone or reference segments. The mechanism of stent expansion is a combination of vessel stretch and plaque redistribution, translating disease accumulation from the midstent zone to the distal stent zone.     

Late vascular response at the edges of sirolimus analogous-eluting stents in diabetic patients: An intravascular ultrasound study.

INTRODUCTION: Vascular response at edges of drug-eluting stents is still not well established, particularly in diabetic patients who are prone to aggressive atherosclerosis progression. Recently, Biolimus and Zotarolimus have demonstrated potent antiproliferative effects. OBJECTIVE: To compare the vascular responses at edges of sirolimus analogous-eluting stents in patients with and without diabetes, using intravascular ultrasound (IVUS). METHODS: 306 edges were analyzed in 153 patients treated with drug-eluting stents and divided in: diabetics (122 edges) and nondiabetics (166 edges). IVUS was performed postintervention and at 6-month follow-up and included 5 mm distal and proximal to the stented segment. Vessel, lumen, and plaque volumes were calculated. Volume variation (follow-up minus basal) was also calculated. Edge restenosis was defined as obstruction >50%. RESULTS: Baseline characteristics were similar between groups. In both groups the entire lesion length was covered (stent length/lesion length ratio was 1.5 for both groups). There were no differences in edge volumes and restenosis rate between the groups. Among diabetics, there was no significant volume variation. However, in nondiabetic patients there was significant increase in vessel volume in proximal (from 67.1 +/- 22 mm(3) to 72.2 +/- 25 mm(3): P = 0.02) and distal (from 54.4 +/- 22 mm(3) to 59.8 +/- 22 mm(3): P = 0.001) edges. CONCLUSION: Nondiabetic patients showed a significant positive vascular remodeling in proximal and distal edges of sirolimus analogous-eluting stent. This vascular mechanism was not observed in diabetic patients. Although different vascular responses were observed, restenosis rates were equivalent between the 2 groups at 6-month follow-up.     

A synergistic approach to optimal stenting: directional coronary atherectomy prior to coronary artery stent implantation--the AtheroLink Registry. AtheroLink Study Group

OBJECTIVES: The AtheroLink registry sought to observe the effect of plaque burden reduction by directional coronary atherectomy (DCA) prior to stenting on acute lesion success rate, on the clinical success rate and on the incidence of in-stent restenosis six months after intervention. BACKGROUND: Although coronary stenting has reduced restenosis, its effect has been less favorable in complex lesions with a high plaque burden that results from suboptimal stent expansion. Therefore, plaque removal by DCA may improve the results of coronary stenting. METHODS: A total of 167 patients with >60% stenosis in a native coronary artery of 2.8 to 4.0 mm in diameter were enrolled in 10 study centers on an intention-to-treat basis. All patients underwent DCA aimed at an optimal result (residual diameter stenosis <20%) followed by stenting. Angiographic follow-up was performed in 120 (71.8%) patients at 5.3+/-2.8 months. RESULTS: Lesion success was achieved in 164/167 (98.2%) patients, and the clinical success rate was 95.2% (159/167 patients). The overall restenosis rate in the 120 patients with angiographic follow-up was 10.8% (13/120). Incidence of restenosis was lower (8.4%) in patients with optimal stent deployment following DCA compared to patients with a persisting caliber reduction >15% (restenosis rate 15.3.%) and restenosis occurred with a significantly higher frequency (p<0.04) in distal lesions (37.5%) compared to proximal stenoses (9.0%). CONCLUSIONS: This observational multicenter registry points to a potential reduction in restenosis by a synergistic approach of DCA and stenting performed under routinely accessible angiographic guidance. Therefore, multicenter-based randomized clinical trials are clearly warranted to finally clarify the validity of this complex approach versus conventional angioplasty plus stenting.     

Progression of dissection due to residual dissection after intracoronary stenting for spontaneous coronary dissection at bifurcation site of LAD and diagonal artery

A 34-year old male patient visited our hospital due to severe chest pain. Initial ECG showed ST elevation at precordial leads and all cardiac enzymes were markedly elevated. Coronary angiography showed a long, longitudinal coronary dissection with dissected flap extending from the proximal LAD to the mid segment of the vessel and proximal diagonal artery. IVUS showed dissected flap and false lumen communicating with true lumen from proximal to mid-LAD. We implanted two paclitaxel-eluting stents using crushing technique at bifurcation lesion and overlapped another paclitaxel-eluting stent at proximal LAD for full coverage of dissection. Final angiography showed good distal flow. However, despite of maximal pressure of post stent ballooning, a residual dissection was noted at proximal LAD. IVUS examination also showed encircling gap that was noted between stent and vessel wall at proximal LAD stent area. Because distal flow was good and there was no ischemic symptom and sign, the patient was discharged. Six months later from index procedure, routine follow-up angiography and IVUS examination were performed and revealed more progressed previous residual coronary dissection at proximal LAD which was extended to bifurcation site. Our case showed, although intracoronary stenting might be an attractive approach by closure of the inlet and the false lumen, complete resolution of dissection by stenting is very important for long-term prognosis.     

Effects of stenting on adjacent vascular distensibility and neointima formation: role of nitric oxide.

Intravascular stents increase long-term patency but their effects on the vascular mechanics of adjacent segments have not been studied. In this study, stents were deployed in the rabbit abdominal aorta after 1 week of normal diet, 1% cholesterol diet or 1% cholesterol diet with L-nitro arginine (L-NA 60 mg/l water). Intravascular ultrasound showed a small distal decrease in vessel distensibility (area/pressure * 100) before stenting. Distensibility was almost abolished by stenting (0.12 +/- 0.01, p < 0.001), but was increased proximal to the stent and decreased distal to the stent both acutely (proximal: 1.18 +/- 0.10 vs distal: 0.65 +/- 0.06, p < 0.001), and at 4 weeks (proximal: 1.05 +/- 0.08 vs distal: 0.37 +/- 0.07, p < 0.001). Nitric oxide (NO) activity was enhanced proximal to and within the stent, and remained constant distal to the stent, (versus control, proximal: 57 +/- 23%, stent: 136 +/- 35%, distal: 2 +/- 12%, p < 0.01). The I/M ratio was significantly higher proximal to and within the stent than in the distal segment (proximal: 0.40 +/- 0.10, stent: 0.37 +/- 0.12, distal: 0.12 +/- 0.11, p < 0.01). NO blockade with L-NA prevented hyperdistensibility proximally, and significantly increased the I/M ratio within the stent and distally (stent: 0.81 +/- 0.19, distal: 0.30 +/- 0.10, p < 0.05) but not proximally (0.38 +/- 0.09). In conclusion, aortic stenting increases proximal vascular distensibility and intimal lesion formation. Nitric oxide blockade augments intimal growth within but not proximal to the stent.     

Morphology and location of restenosis following bare metal coronary stenting

Restenosis following bare metal coronary stenting is common. The location and characteristics of restenotic lesions in patients who have undergone coronary stent implantation is not well described. The purpose of this study was to determine the location, type and temporal distribution of stent-related restenosis. We reviewed the clinical and angiographic characteristics of 203 consecutive patients with stent-related restenosis undergoing a repeat clinically-indicated coronary angiogram, 30 days to 1 year after the index procedure. All lesions within 10 mm of the proximal and distal margins of the stent were included in the analysis. An angiographic classification was developed based on lesion location. Class I lesions were those occurring within the stent, and Class II comprised those lesions occurring within 10 mm of the proximal and distal stent edge. We classified a total of 234 stent-related restenosis lesions. Class I lesions were found in 52% of patients, and Class II in 48%. Three-fifths of the patients who developed new lesions at a stent edge presented 1-3 months following the initial procedure, which was significantly earlier than other lesion types (p < 0.001). A substantial number of patients undergoing repeat angiography after stent placement have lesions proximate, but peripheral, to the stent. This may limit the effectiveness of stent-based efforts to reduce restenosis. The time interval between coronary stenting and symptom recurrence appears to vary according to lesion location.     

Predictors and implications of residual plaque burden after coronary stenting: an intravascular ultrasound study

Background Residual plaque burden after coronary stenting may be visualized by use of intravascular ultrasound. Determinants and implications of residual atherosclerotic plaque burden after coronary stenting are not well established. In particular, the implications of residual plaque burden, after adjusting for confounding factors, are still unknown. Methods Sixty-two consecutive patients (age 56 ± 9 years) undergoing coronary stenting under intravascular ultrasound imaging guidance were prospectively studied. A total of 616 slices were analyzed (every 2 mm of stent length) from motorized pull-back recordings. Residual plaque burden was calculated as residual plaque/vessel area × 100. Results In 565 slices (89%), both residual plaque area and stent area could be measured. Mean residual plaque burden was 46.5% ± 6%. By use of multiple regression analysis, lesion plaque area and reference segment plaque burden were identified as independent predictors of residual plaque burden after stenting. In addition, a significant correlation was found between residual plaque burden and most relevant angiographic parameters at follow-up (including minimal lumen diameter, percent diameter stenosis, and loss index), which persisted after adjustment. Furthermore, stents with a residual plaque burden ≥46% had higher a restenosis rate (relative risk [RR] 4.4, 95% CI 1.09-18.2, P = .03). On logistic regression analysis, residual plaque burden (RR 4.8, 95% CI 4.1-5.6, P = .01) and diabetes (RR 4.3, 95% CI 3.6-5.1, P = .03) emerged as the only independent predictors of restenosis. Conclusions The amount of residual plaque burden after coronary stenting plays an independent role on the late angiographic outcome of these patients. (Am Heart J 2003;145:254-61.)     

Comparison of the efficacy of direct coronary stenting with sirolimus-eluting stents versus stenting with predilation by intravascular ultrasound imaging (from the DIRECT trial)

A direct coronary stenting technique using drug-eluting stents may decrease drug-eluting stent efficacy due to possible damage to the surface coating of the stent. The DIRECT is a multicenter, prospective, nonrandomized trial designed to evaluate the direct stenting strategy for the sirolimus-eluting Bx-Velocity stent compared with the historical control (SIRIUS trial, stenting with predilation). Volumetric and cross-sectional intravascular ultrasound analyses at 8-month follow-up were performed in 115 patients (DIRECT n= 64, control n = 51). Patient and lesion characteristics were comparable between groups. The DIRECT group achieved an equivalent uniform expansion index, defined as minimum stent area/maximum stent area x 100, compared with the control group (65.9 +/- 11.7 vs 63.1 +/- 12.7, p = NS). At 8-month follow-up, vessel, stent, lumen, and neointimal volume index (volume in cubic millimeters/length in millimeters) and percent neointimal volume were similar between the DIRECT and control groups (vessel volume index 13.9 +/- 4.40 vs 15.0 +/- 3.83; stent volume index 6.83 +/- 2.02 vs 6.94 +/- 2.04; lumen volume index 6.71 +/- 2.04 vs 6.81 +/- 2.07; neointimal volume index 0.14 +/- 0.24 vs 0.16 +/- 0.23; percent neointimal volume 3.73 +/- 6.97 vs 3.14 +/- 5.32, p = NS for all). In addition, in-stent neointimal hyperplasia distribution was significantly smaller near the distal stent edge (0.22 vs 0.098 mm(3)/mm, p = 0.01 for an average neointimal volume index within 3 mm from the distal stent edge). In conclusion, direct coronary stenting with the sirolimus-eluting Bx-Velocity stent is equally effective in terms of uniform stent expansion and long-term quantitative intravascular ultrasound results compared with conventional stenting using predilation. This strategy appears to be associated with less neointimal hyperplasia near the distal stent edge.     

Relation between residual plaque burden after stenting and six-month angiographic restenosis

The degree of residual plaque burden outside of a stent might be correlated with the degree of intimal hyperplasia. However, the relation between residual plaque burden and angiographic restenosis are still unknown in a large number of patients. Therefore, we evaluated the effect of residual plaque burden after stenting on 6-month angiographic restenosis. Intravascular ultrasound (IVUS)-guided coronary stenting was successfully performed in 723 patients with 785 native coronary lesions. Six-month follow-up angiograms and evaluation of residual plaque burden by IVUS were available in 566 patients (78.3%) with 622 lesions (79.2%). Results were evaluated using conventional methods. The overall angiographic restenosis rate was 23.0% (143 of 622 lesions). There was no significant difference in residual plaque burden between the lesions with and without restenosis (52% vs 51%, respectively, p = 0.148). The angiographic restenosis rate was 20.8% (11 of 53 lesions), 21.6% (51 of 236 lesions), 22.0% (55 of 250 lesions), and 31.3% (26 of 83 lesions) in the lesions with residual plaque burden < 40%, between 40% and 50%, between 50% and 60%, and > 60%, respectively (p = 0.284). Using multivariate logistic regression analysis, the only independent predictor of angiographic restenosis was the IVUS stent area (odds ratio 0.807, 95% confidence intervals 0.69 to 0.95, p = 0.011). Furthermore, even in the lesions with residual plaque burden > 60%, the restenosis rate was 37.3% (23 of 61 lesions) versus 13.6% (3 of 22 lesions ) in IVUS stent areas of < 7 and > or =7 mm(2), respectively (p = 0.031). In conclusion, residual plaque burden outside the stent might not predict angiographic restenosis. IVUS stent area was the only independent predictor of angiographic restenosis.     

Relation of stent design and stent surface material to subsequent in-stent intimal hyperplasia in coronary arteries determined by intravascular ultrasound

A variety of different stent designs and coatings have become available. This study sought to determine the impact of stent design and gold-coating of stents on intimal hyperplasia (IH) in human atherosclerotic coronary arteries in relation to known predictors of restenosis. Angiographic and intravascular ultrasound (IVUS) studies were performed at 6-month follow-up on 311 native coronary lesions of 311 patients treated with 99 Multi-Link stents, 74 InFlow steel stents, 73 InFlow gold-coated stents, 41 Palmaz-Schatz stents, 12 NIR steel stents, and 12 gold-coated NIR Royal stents. Lumen and stent cross-sectional area (CSA) were measured at 1-mm axial increments. Mean IH CSA (stent CSA − lumen CSA) and mean IH thickness were calculated and averaged over the total stent length. IVUS demonstrated different levels of IH for the 6 stents. Mean IH thickness ranged from 0.20 ± 0.13 mm for Multi-Link stents to 0.43 ± 0.14 mm for InFlow goal-coated stents (p <0.001). Multivariate analysis proved non–Multi-Link stent design (odds ratio 3.45, 95% confidence intervals 1.13 to 11.11, p <0.034) and gold coating (odds ratio 3.78, 95% confidence intervals 1.88 to 7.54, p <0.001) to be the only independent predictors of IH thickness >0.3 mm. In conclusion, stent design and surface material have an important impact on the IH response to stents implanted in human coronary arteries. However, the differences in IH thickness between the analyzed stents were relatively small compared with the absolute lumen dimensions.     

Intravascular ultrasound predictors of restenosis after percutaneous transcatheter coronary revascularization

Objectives. This study sought to evaluate preintervention and postintervention intravascular ultrasound studies for potential predictors of angiographic restenosis and to use ultrasound predictors of restenosis to enhance our understanding of the pathophysiology of the restenosis disease process.

Background. Restenosis remains the major limitation of percutaneous transcatheter coronary revascularization. Although its mechanisms remain incompletely understood, numerous studies have identified some of the clinical, anatomic and procedural risk factors for restenosis. Intravascular ultrasound imaging of target lesions before and after catheter-based treatmetn consistently demonstrates more target lesion calcium, more extensive reference segment atherosclerosis, smaller final lumen dimensions, significant residual plaque burden and a greater degree of tissue trauma than is evident by angiography.

Methods. Intravascular ultrasound studies were performed in 360 nonstented native coronary artery lesions (final diameter stenosis 18 ± 11%) in 351 patients for whom follow-up angiographic data were available 6.4 ± 3.6 months later. Hospital charts were reviewed, and qualitative and quantitative coronary angiographic and intravascular ultrasound analyses were performed by independent core laboratories. Four dependent angiographic end points were tested: restenosis as a binary definition (50% diameter stenosis at follow-up) was the primary end point; follow-up diameter stenosis, late lumen loss and follow-up minimal lumen diameter were the secondary end points.

Results. Reference vessel size, the preintervention quantitative coronary angiographic assessment of lesion severity and the postintervention intravascular ultrasound cross-sectional measurements predicted the late angiographic results. In particular, the intravascular ultrasound postintervention cross-sectional narrowing (plaque plus media cross-sectional area divided by external elastic membrane cross-sectional area) predicted the primary end point (restenosi) and two of the three secondary end points (follow-up diameter stenosis and late lumen loss) and was therefore the most consistent predictor of restenosis.

Conclusions. Intravascular ultrasound variables are more powerful and consistent predictors of angiographic restenosis than currently accepted clinical or angiographic risk factors.