Treatment of In-Stent Restenosis With Excimer Laser Coronary Angioplasty
Mechanisms and Results Compared With PTCA Alone
Background This study determined the clinical safety, mechanisms, and 6-month results of excimer laser angioplasty (ELCA)+adjunct PTCA for the treatment of in-stent restenosis and (via lesion matching) compared the results of ELCA+PTCA to PTCA alone.
Methods and Results Using quantitative angiography (QCA) and intravascular ultrasound (IVUS), we studied 107 restenotic previously stented lesions in 98 patients before and after intervention. QCA measurements included minimum lumen diameter (MLD) and diameter stenosis (DS). IVUS measurements included stent, lumen, and intimal hyperplasia (IH=stent−lumen) cross-sectional areas (CSA) and volumes. In the 54 lesions treated with ELCA+PTCA, the MLD increased from 0.73±0.38 mm before ELCA to 2.10±0.47 mm after ELCA+PTCA (P<.0001); the DS decreased from 70±14% to 25±12% (P<.0001). By IVUS, the minimum lumen CSA increased from 1.58±0.78 mm2 before ELCA to 6.34±1.75 mm2 after ELCA+PTCA (P<.0001) as a result of an increase in minimum stent CSA from 7.70±2.41 to 9.10±2.60 mm2 (P<.0001) and a decrease in IH CSA from 5.25±2.84 to 2.63±1.41 mm2 (P<.0001). Volumetric analysis showed that tissue ablation (during ELCA) contributed 29±15%, tissue extrusion (during adjunct PTCA) contributed 31±14%, and additional stent expansion (during adjunct PTCA) contributed 40±16% to the overall lumen gain. There were no ELCA-related complications. Matched to lesions treated with PTCA alone, ELCA+PTCA resulted in greater lumen gain, more IH ablation/extrusion, larger final lumen CSA (IVUS), and a tendency for less frequent need for subsequent target vessel revascularization (TVR, 21% versus 38%, P=.0823).
Conclusions ELCA safely and effectively ablates in-stent neointimal tissue. Adjunct PTCA extrudes neointimal tissue out of the stent and also further expands the stent. Compared with PTCA alone, ELCA+PTCA achieves better short-term and, potentially, better long-term results.
Intracoronary stents reduce restenosis compared with PTCA.1 2 Because stent use has increased significantly, in-stent restenosis is now an important clinical problem. Previous postintervention and follow-up IVUS studies have shown that in-stent restenosis is secondary to IH.3 4 In-stent restenosis is most commonly treated with PTCA.5 Preintervention and postintervention IVUS studies have shown that (1) the mechanism of lumen enlargement during PTCA of in-stent restenosis is a combination of additional stent expansion and tissue extrusion out of the stent and (2) there is a relatively high residual stenosis, partly as a result of remaining in-stent neointimal tissue.6 The recurrence rate, especially after PTCA for diffuse in-stent restenosis, has been reported to be as high as 80%.7
The use of ELCA followed by adjunct PTCA has been proposed as an alternative approach to the treatment of in-stent restenosis in an effort to reduce the residual in-stent neointimal tissue, improve final lumen dimensions, and decrease subsequent clinical recurrence. IVUS permits detailed, high-quality cross-sectional imaging of the coronary arteries in vivo. The normal coronary artery architecture, the major components of the atherosclerotic plaque, and the changes that occur during atherogenesis, transcatheter therapy, and follow-up can be studied in a manner previously not possible. This includes the direct visualization of the intensely echoreflective (but relatively radiolucent) stainless steel stent struts.
The purpose of the present study was (1) to use sequential (preintervention and postintervention) QCA and IVUS to evaluate the safety and study the mechanisms and procedural results after ELCA+PTCA for the treatment of in-stent restenosis and (2) to compare the 6-month outcome with a case-matched group of patients treated with PTCA alone.
Patient and Lesion Population
Using preintervention and postintervention QCA and IVUS, we studied 107 lesions in 98 patients during the treatment of in-stent restenosis 5.4±3.2 months after implantation of Palmaz-Schatz stents. This represents a consecutive series of patients (69 men, 29 women; age, 61.8±10.1 years) with in-stent restenosis treated with PTCA alone or ELCA+adjunct PTCA and studied with IVUS before and after intervention.
Sixty-four lesions had been treated with a single Palmaz-Schatz stent, 41 lesions with two stents, and 2 lesions with three stents. There were 52 articulated “biliary” (PS204) and 100 “coronary” stents. Of the coronary stents, 46 were 3.0-mm, 38 were 3.5-mm, and 16 were 4.0-mm stents.
Lesion location was the saphenous vein graft in 45, left anterior descending coronary artery in 24, left circumflex artery in 11, right coronary artery in 22, left main in 4, and left internal mammary artery in 1. Twenty-one lesions were in the aorto-ostial location. Thirty patients had diabetes mellitus.
In 53 lesions with in-stent restenosis treated with PTCA alone, nominal balloon sizes ranged between 3.0 and 5.0 mm (mean, 3.68±0.66 mm), with a balloon-to-artery ratio of 1.33±0.17 and a maximum balloon pressure of 15.0±4.1 atm.
In the 54 lesions treated with ELCA (Spectranetics/Advanced Interventional Systems), the procedure was performed as described elsewhere.8 9 10 11 12 The largest laser fiber catheter used was a 1.4-mm catheter in 2, a 1.6-mm catheter in 4, a 1.7-mm catheter in 14, and a 2.0-mm catheter in 38; the average catheter size was 1.98±0.16 mm. Initially, selection of ELCA catheters intentionally favored smaller catheters because of safety concerns. Later, however, unless vessel tortuosity was prohibitive, either a 1.7-mm eccentric catheter (with multiple passes) or a 2.0-mm concentric catheter was preferentially used to maximize tissue ablation.
Energy densities ranged from 35 to 55 mJ/mm2 (mean, 45.7±5.5 mJ/mm2). A single-laser-pass technique was used in 58%; multiple passes were used in the rest. In all cases, the “saline flush” technique was used. Adjunct PTCA was performed in all lesions after ELCA. Nominal balloon size ranged between 3.0 and 5.0 mm (mean, 3.59±0.58 mm), with a balloon-to-artery ratio of 1.42±0.26 and a maximum balloon pressure of 16.5±3.1 atm.
QCA Analysis and Procedural Success
QCA was performed by an independent core angiographic laboratory blinded to the results of the IVUS analysis and clinical follow-up. QCA was performed with an automated edge-detection algorithm (ARTREK, Quantitative Cardiac Systems) with the contrast-filled catheter as the calibration standard. MLD, reference diameter, and percent DS before ELCA and after ELCA+PTCA were measured from multiple projections, and the results from the “worst” view were recorded. Ostial lesions began within 3 mm of the major coronary artery ostium. Lesion length was measured as the distance (in millimeters) from shoulder to shoulder in the projection that demonstrated the in-stent restenotic lesion with the least amount of foreshortening. These methods have been reported previously.13
Procedure success was a final DS <50% in the absence of major in-hospital complications (death, bypass surgery, or Q-wave MI). A non–Q-wave MI was defined as a peak postprocedure CK-MB >20.
IVUS Imaging Protocol
Studies were performed with one of three commercially available systems. The first system (CVIS/Inter Therapy Inc) incorporated a single-element 25-MHz transducer and an angled mirror mounted on the tip of a flexible shaft, which was rotated at 1800 rpm within a 3.9F short monorail polyethylene imaging sheath to form planar cross-sectional images in real time. With this system, the transducer was withdrawn automatically at 0.5 mm/s to perform the imaging sequence. The second system (Hewlett Packard and Boston Scientific Corp) incorporated a single-element 30-MHz beveled transducer rotated at 1800 rpm within a 3.5F short monorail imaging catheter; with this system, the catheter was withdrawn manually with fluoroscopic guidance to perform the imaging sequence. The third system (Cardiovascular Imaging Systems, Inc) used a single-element beveled transducer mounted on the end of flexible shaft and rotated at 1800 rpm within either a 2.9F long monorail/common distal lumen imaging sheath or within a 3.2F short monorail imaging sheath. With this system, the transducer was also withdrawn automatically at 0.5 mm/s to perform the imaging sequence.
IVUS imaging was performed after administration of 0.2 mg IC nitroglycerin. The ultrasound catheter was advanced ≈10 mm beyond the target lesion, and an imaging run (using automated transducer pullback at 0.5 mm/s or slow manual catheter pullback) was performed from beyond the target lesion to the aorto-ostial junction. Studies were recorded only during pullback onto 1/2-in high-resolution s-VHS for off-line analysis.
Patients were studied after giving written informed consent. IVUS imaging is performed as part of on-going protocols approved by the Institutional Review Board of the Washington Hospital Center.
Quantitative IVUS Measurements
CSA measurements by IVUS have been validated.14 15 16 17 18 19 20 21 Area measurements were performed with a commercially available program for computerized planimetry (TapeMeasure, Indec Systems). Five stent segments were identified and measured before ELCA and after adjunct PTCA: (1) proximal edge, (2) proximal body, (3) central articulation, (4) distal body, and (5) distal edge. The IH CSA was calculated as stent CSA minus lumen CSA. Stent CSA at the central articulation was the mean of the stent CSA just proximal and distal to the articulation. When the plaque encompassed the catheter, the lumen was assumed to be the physical size of the imaging catheter. The stent, lumen, and IH CSA of the five segments were then averaged per lesion and compared before ELCA versus after adjunct PTCA.
In studies performed with motorized transducer pullback, in-stent restenosis length was measured from number of seconds of videotape. At a pullback speed of 0.5 mm/s, 2 seconds of the videotape playback is equal to 1 mm axial stent length. This has been validated in vivo.22 In-stent restenosis length was defined as the axial length of the stent (in millimeters) in which IH CSA=75% stent CSA. If the restenotic lesion continued into the contiguous reference segment, then the length of the restenotic lesion included the length of the contiguous reference segment whose lumen CSA was <25% of the adjacent stent margin CSA.
Effectiveness of ELCA+PTCA
The smallest stent CSA and lumen CSA within each lesion were identified; the smallest lumen CSA was then compared with the average reference lumen CSA to calculate a percent area stenosis. The proximal and distal references were defined as the most normal-looking cross section (largest lumen with the least plaque) within 10 mm proximal and distal to the stent but (in native arteries) before side branches. If a stent was ostial in location, then only a distal reference was used.
Previous serial (postintervention and follow-up) IVUS studies have shown that stents do not recoil over time.4 23 Therefore, in the absence of prior treatment of in-stent restenosis (which would have altered stent dimensions), stent CSA at the time of follow-up is an accurate surrogate for lumen CSA at the time of initial stent implantation. Therefore, post-ELCA+PTCA lumen CSA was compared with pre-ELCA stent CSA to determine the percent lumen recovery during the treatment of in-stent restenosis. This comparison has been used to study results of PTCA alone for the treatment of in-stent restenosis.6
Mechanism of ELCA Versus Adjunct PTCA
To determine the relative contribution of ELCA versus adjunct PTCA to lumen enlargement during the treatment of in-stent restenosis, sequential (preintervention, post-ELCA, and post–adjunct PTCA) volumetric IVUS analysis was performed on a subset of 14 lesions (10 native coronary, 4 saphenous vein grafts). On playback of the recorded studies, an ultrasound image was selected every 1 mm of axial length and digitized. The stent, lumen, and IH CSAs were measured. Stent, lumen, and IH volumes were calculated by Simpson’s rule. These methods have been reported previously.3 4
ELCA+PTCA Versus PTCA Alone
To evaluate the impact of tissue ablation in the treatment of in-stent restenosis, we performed a case-matched comparison of lesions treated with ELCA+PTCA versus PTCA alone. Lesions were matched for preintervention reference lumen CSA (IVUS) and diameter (QCA); IVUS and QCA lesion length; IVUS lumen, stent, and IH CSA; and QCA MLD and DS. In general, the milder cases of in-stent restenosis (often with lumen CSAs larger than the laser catheter) were eliminated from the PTCA group; the more severe cases (including several with total occlusions) were removed from the ELCA+PTCA group. Therefore, only a subset of the 54 lesions treated with ELCA+PTCA (n=47) and a subset of the 53 lesions treated with PTCA alone (n=45) were compared.
After successful treatment of in-stent restenosis (ELCA+PTCA or PTCA alone), patients were contacted by telephone or office visit 1, 3, and 6 months after the procedure. The occurrence of major late clinical events (death, Q-wave MI, or the clinical need for late treatment site revascularization [coronary artery bypass surgery or repeat coronary intervention]) was recorded. Events were subsequently source-documented.
Statistical analysis was performed with StatView 4.02 (Abacus Concepts) or SAS (Statistical Analysis Systems). Categorical data were presented as frequencies. Comparison of categorical variables was performed with χ2 statistics. Continuous data were presented as mean±SD. Comparisons of continuous variables were performed with paired and unpaired t tests, factorial ANOVA, or ANOVA for repeated measures with post hoc analysis.
In the overall cohort of 54 lesions treated with ELCA+PTCA, QCA lesion length measured 12.67±9.00 mm; 52% were longer than 10 mm in length. The reference lumen diameter measured 2.63±0.50 mm. The MLD increased from 0.73±0.38 mm before ELCA to 2.10±0.47 mm after ELCA+PTCA (P<.0001). Conversely, the DS decreased from 70±14% before ELCA to 25±12% after ELCA+PTCA (P<.0001). Procedural success was 98%; one patient was referred to bypass surgery for distal edge dissections. There were two additional cases of minor post-ELCA dissections that resolved after adjunct PTCA. There were no perforations. Four patients had a postprocedure non–Q-wave MI.
During the follow-up period (9.1±0.9 months), there were 2 deaths, 1 Q-wave MI, and 17 episodes of repeat TVR.
In the overall cohort of 54 lesions treated with ELCA+PTCA, IVUS lesion length measured 19.6±13.6 mm. Reference lumen CSA measured 8.95±3.97 mm2. Overall, the minimum lumen CSA increased from 1.58±0.78 mm2 before ELCA to 6.34±1.75 mm2 after ELCA+PTCA (P<.0001) as a result of an increase in minimum stent CSA from 7.70±2.41 to 9.10±2.60 mm2 (P<.0001) and a decrease in mean IH CSA within the stent from 5.25±2.84 to 2.63±1.41 mm2 (P<.0001). This translated into a decrease in area stenosis from 80±12% to 39±17% (P<.0001). An example is shown in Fig 1⇓.
With the pre-ELCA stent CSA used as a surrogate for the final lumen CSA at the time of stent implantation, the minimum lumen CSA after ELCA+PTCA (6.34±1.75 mm2) was significantly smaller than the minimum stent CSA before ELCA (7.70±2.41 mm2, P<.0001). Thus, ELCA+PTCA was able to recover only 85±18% of the lumen CSA of the original stent implantation procedure. This was true throughout the length of the stent (Fig 2⇓).
Mechanisms of ELCA+PTCA (Planar IVUS Results)
In the overall cohort of 54 lesions treated with ELCA+PTCA, the overall gain in mean lumen CSA before ELCA versus after adjunct PTCA (4.05±2.03 mm2) came as a result of an increase in mean stent CSA of 1.45±0.84 mm2 and a decrease in mean in-stent IH CSA of 2.60±1.91 mm2. Thus, 59±23% of the gain in mean lumen CSA (before ELCA versus after adjunct PTCA) was the result of neointimal tissue ablation/extrusion out through the stent, and 41±23% was the result of additional stent expansion.
Mechanisms of ELCA Versus Adjunct PTCA (Volumetric IVUS Results)
In the subgroup of 14 lesions studied with motorized transducer pullback before ELCA, after ELCA, and after adjunct PTCA, volumetric IVUS analysis (Fig 3⇓) was used to separate the contribution to lumen enlargement from (1) IH ablation versus IH extrusion and (2) ELCA versus adjunct PTCA.
Lumen volume increased from 43.7±18.5 mm3 before ELCA to 62.8±14.2 mm3 after ELCA (P<.0001). IH volume decreased from 96.0±23.3 to 77.4±19.8 mm3 (P<.0001). There was no change in stent volume (139.7±24.8 versus 140.2±24.7 mm2). Thus, tissue ablation with ELCA (18.7±10.2 mm3) was responsible for all of the lumen increase before versus after ELCA.
Lumen volume increased from 62.8±14.2 mm3 after ELCA to 111.8±25.8 mm3 after adjunct PTCA (P<.0001) as a result of both tissue extrusion (additional decrease in IH volume from 77.4±19.8 to 54.5±10.8 mm3, P<.0001) and an increase in stent volume (from 140.2±24.7 to 166.3±26.4 mm3, P<.0001). Thus, both neointimal tissue extrusion out of the stent (22.8±15.6 mm3) and additional stent expansion (26.1±10.3 mm2) contributed importantly to lumen volume increase after ELCA versus after adjunct PTCA.
Thus, the various contributions to the overall increase in lumen volume were as follows: (1) tissue ablation (during ELCA), 29±15%; (2) tissue extrusion during adjunct PTCA, 31±14% (P=.7333 versus tissue ablation); and (3) additional stent expansion, 40±16%.
Forty-seven lesions treated with ELCA+PTCA were matched with 45 lesions treated with PTCA alone (Table 1⇑). Although lesions were well matched for lesion location and for preintervention QCA and IVUS measurements, lesions treated with ELCA+PTCA tended to be more complex: patients with diabetes mellitus, more previous in-stent restenosis, and lesion length (QCA) >10 mm.
Compared with lesions treated with PTCA alone, lesions treated with ELCA+PTCA had (1) greater acute lumen gain (Δmean lumen CSA), (2) more IH ablation/extrusion (Δmean IH CSA), and (3) larger final lumens by IVUS (although not by QCA). Procedural successes were similar; one patient (with one lesion each) in each group was referred for bypass surgery for distal edge dissections.
Six-month follow-up was available in all patients with lesions in the matched groups. There was a trend toward less frequent need for 6-month TVR in the ELCA+PTCA group (21%) than in the PTCA alone group (38%, P=.0823). There was one death in each group. There was one Q-wave MI in the ELCA+PTCA group.
In the treatment of in-stent restenosis, the present study shows that the use of ELCA for the treatment of in-stent restenosis was safe. ELCA+PTCA improved lumen dimensions by a combination of tissue ablation, tissue extrusion, and additional stent expansion. Final residual lumen dimensions were smaller than the (presumed) final lumen dimensions of the initial stent implantation procedure, and residual stenoses were high. Compared with a matched group treated with PTCA alone, ELCA+PTCA tended to have better long-term (6-month) results.
PTCA of In-Stent Restenosis
Using QCA, Gordon and coworkers5 concluded that lumen enlargement during PTCA of in-stent restenosis was entirely due to neointimal tissue compression or extrusion out of the stent, rather than to additional stent expansion. Because the metallic stainless steel stent struts are relatively radiolucent (but intensely echoreflective), QCA may be less accurate than IVUS in quantifying additional stent expansion. Alternatively, IVUS studies before and after the treatment of in-stent restenosis showed that tissue extrusion contributed 44% and additional stent expansion contributed 56% to lumen enlargement.6 In that study, (1) PTCA achieved only 85% of the minimum lumen CSA of the original stent implantation procedure, (2) after PTCA there was significant residual neointimal tissue within the stent (averaging 32% of the stent CSA), and (3) the residual stenosis by angiography (18%) was relatively high. These IVUS findings have recently been confirmed by two reports.24 25
Few studies have evaluated the long-term efficacy of PTCA for the treatment of in-stent restenosis. Baim et al26 reported 105 patients with in-stent restenosis treated with repeat PTCA. In the 50 patients who underwent angiographic follow-up, the restenosis rate was 54%. Yokoi et al7 reported a 37% angiographic restenosis rate in 82 patients; however, the restenosis rate was 85% after PTCA of diffuse in-stent restenosis. Sridhar et al27 reported a 22% TVR rate in 31 patients. Tan et al28 reported a 47% event rate in 47 patients. In the present study, the need for subsequent TVR in the PTCA group was 38% at 6 months. Thus, although the true efficacy of this therapeutic approach is not known, subsequent recurrence may be significant (especially in diffuse lesions), and alternative procedures are worth exploring.
Mechanisms of Lumen Enlargement During ELCA of In-Stent Restenosis
In the present study, neointimal tissue ablation from ELCA was responsible for 29% of overall lumen gain. In vitro or in vivo animal models originally suggested that excimer lasers precisely cut through atheroma, including calcium, without harmful thermal injury.29 30 31 32 Conversely, IVUS has indicated that the mechanism of lumen enlargement after ELCA of nonstented lesions was a combination of tissue ablation (76% of lumen enlargement) and vessel expansion (24% of lumen enlargement), with no evidence of calcium ablation.33 The in vivo IVUS findings in nonstented lesions were explained by other in vitro studies. Laser-induced shock waves caused the forceful expansion of vapor bubbles into tissue similar to the ELCA-induced vessel expansion seen on IVUS imaging.34 35 36
In the present study, volumetric IVUS analysis showed that all of the lumen enlargement from ELCA during the treatment of in-stent restenosis was the result of tissue ablation. This suggests that there may be enhanced tissue ablation compared with nonstented lesions. This improved laser ablation efficiency may be related to the absence of calcium and to the scaffolding effects of endovascular stents, which may limit laser-induced vessel expansion. Also, in contrast to previous reports,33 the absence of calcification may have limited the incidence of laser-induced dissections in the present series.
Mechanisms of Lumen Enlargement During Adjunct PTCA of In-Stent Restenosis
In the present study, adjunct PTCA was responsible for 71% of overall lumen gain. Volumetric IVUS analysis showed that extrusion of tissue out of the stents (during adjunct PTCA) contributed as much to lumen enlargement as did tissue ablation (during ELCA). However, additional stent expansion (during adjunct PTCA) was an important part of the treatment of in-stent restenosis during ELCA+PTCA, even though balloon-to-artery ratio during the original stent implantation procedure was 1.31±0.29, with inflation pressures of 14.5±4.4 atm. This finding of additional stent expansion is similar to stand-alone PTCA (Δstent CSA in Table 1⇑) and has been observed by others.37
Acute Procedural Results With ELCA+PTCA
The present study demonstrated the safety of using ELCA to treat in-stent restenosis. Clinical success was high. Post-ELCA dissections were observed in only three patients; two resolved after adjunct PTCA. There were no Q-wave MIs.
The present study also showed the limitations of ELCA+PTCA. First, the QCA residual DS measured 25±12%, and the IVUS residual area stenosis measured 39±17%. Second, ELCA+PTCA recovered only 85±18% of the pre-ELCA stent CSA, a surrogate for the lumen CSA at the time of initial stent implantation. (If ELCA+PTCA achieved the same acute results as the original stent implantation procedure, then the final lumen CSA should be similar to the pre-ELCA stent CSA.) Third, despite tissue ablation, after ELCA+PTCA there was significant residual neointimal tissue within the stent (25±8% of the stent CSA). Two explanations are possible. (1) The largest laser fiber catheter used was the 2.0-mm catheter (72% of patients), and 58% of procedures were intentionally performed with a single-pass technique. This might have limited the amount of tissue removal. (2) Peristent arterial structures (residual plaque, media and adventitia, or periadventitial tissue) may hamper optimization of final lumen dimensions by limiting extrusion of residual neointimal tissue or additional stent expansion during adjunct PTCA.
Comparison of Patients Treated With ELCA+PTCA Versus PTCA Alone
A subpopulation of 47 lesions treated with ELCA+PTCA were matched to a group of 45 lesions treated with PTCA alone. This necessitated excluding (1) patients with the most severe cases of in-stent restenosis, including six with total occlusions, who were preferentially treated with ELCA and (2) those with the more mild cases of in-stent restenosis, often with lumen dimensions larger than the available laser catheters, who were preferentially treated with PTCA alone. After matching (Table 1⇑), there was still a tendency for the ELCA+PTCA group to be more complex: diabetic patients with longer lesions and more previous in-stent restenosis. Nevertheless, lesions treated with ELCA+PTCA did better than lesions treated with PTCA alone.
The only independent predictors of subsequent TVR were aorto-ostial lesion location and the acute procedural decrease in in-stent IH CSA (whether from tissue ablation or extrusion), not the use of ELCA per se. IVUS studies have shown that PTCA alone has a limited ability to decrease in-stent neointimal tissue. The present study, therefore, supports the use of atheroablation in the treatment of in-stent restenosis. However, because it was the decrease in neointimal tissue (not the use of ELCA) that was predictive, improved long-term results may not be a unique property of ELCA but may be accomplished by other atheroablative devices as well.
(1) Only lesions treated with Palmaz-Schatz stents were included in this analysis. (2) This study was a retrospective analysis of lesions treated with ELCA+PTCA or PTCA; lesions were not randomized to the two treatment strategies. (3) Operators were not blinded to any of the IVUS imaging runs. (4) In general, longer and more diffuse narrowings were selected for ELCA, and shorter lesions with less severe lumen compromise were selected for stand-alone PTCA. (5) In more severe cases of in-stent restenosis, occasionally the IVUS catheter could not cross the lesion before intervention. These lesions were not included in the present analysis. (6) The methods used could not separate IH tissue compression from ablation/extrusion. However, liquids and solids are not compressible, and volumetric IVUS analysis of nonstented lesions before and after PTCA suggest that plaque compression does not occur. (7) Similarly, IVUS could not separate tissue ablation from tissue extrusion. (8) Larger laser catheters or eccentric laser catheters with multiple passes (potentially causing additional tissue ablation), rotational atherectomy (2.5-mm burrs are available), or directional coronary atherectomy might have improved the short- and long-term results.38 39 40 (9) Clinical follow-up in the matched cohorts was deliberately truncated at 6 months (all were followed for at least 6 months). Longer clinical follow-up is necessary to determine true TVR.
ELCA+PTCA was safe and appeared to be superior to PTCA alone for the treatment of in-stent restenosis. A prospective randomized trial comparing PTCA versus ELCA+PTCA (or other ablative techniques) is warranted, especially if targeted toward more diffuse in-stent restenosis with greater in-stent neointimal volumes.
Selected Abbreviations and Acronyms
|ELCA||=||excimer laser coronary angioplasty|
|MLD||=||minimum lumen diameter|
|PTCA||=||percutaneous transluminal coronary (balloon) angioplasty|
|QCA||=||quantitative coronary angiography|
|TVR||=||target vessel revascularization|
This study was supported in part by the Cardiology Research Foundation, Washington, DC.
- Received March 12, 1997.
- Revision received May 20, 1997.
- Accepted May 27, 1997.
- Copyright © 1997 by American Heart Association
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