Final Lumen Research Articles

Prognostic value of absolute versus relative measures of the procedural result after successful coronary stenting: Importance of vessel size in predicting long-term freedom from target vessel revascularization

Background The procedural result is a major determinant of the incidence of 6-month target vessel revascularization (TVR) after successful coronary stenting. However, the prognostic implications of the different measures of the procedural result or procedural end points have not been directly compared. In this study, we sought to assess and compare the impact of achieving different procedural end points on the long-term (2-year) incidence of TVR. Methods and Results We studied 234 patients in whom 1 or 2 stents were successfully deployed and ultrasound imaging performed after angiographic optimization. End points included a visually estimated angiographic residual stenosis <10% and ultrasound stent-to-mean reference lumen area ≥80%. After 2 years, TVR was required in 48 (20.5%) patients. Qualitative predictors of TVR were vein graft lesions, 3-vessel disease, and baseline TIMI flow grade <3. Quantitatively, reference diameter by quantitative coronary angiography (QCA), final minimum lumen diameter (MLD) by QCA, and in-stent minimum lumen area (MLA) by ultrasound were predictive of TVR. Stent-to-reference ratios were not significantly predictive of TVR. By multivariable analysis, vein graft location and MLA by ultrasound were the only significant predictors of TVR (relative risk, 2.9 [1.5, 5.4] and 0.72 [0.6, 0.9], respectively). Receiver operator curves for MLD by QCA and MLA by ultrasound were similar in predicting TVR. Neither was significantly superior to reference vessel diameter. Conclusions Commonly used angiographic and ultrasound stent-to-reference ratios do not predict the incidence of TVR. Absolute measures of the lumen size (MLA by ultrasound and MLD by QCA) were the most important quantitative predictors of TVR within 2 years. This emphasizes the role of the vessel size as the limiting factor in determining the long-term outcome of coronary stenting. (Am Heart J 2001;141:823-31.)

Stent thrombosis in the modern era: a pooled analysis of multicenter coronary stent clinical trials.

There are limited studies of stent thrombosis in the modern era of second-generation stents, high-pressure deployment, and current antithrombotic regimens. Six recently completed coronary stent trials and associated nonrandomized registries that enrolled 6186 patients (6219 treated vessels) treated with >/=1 coronary stent followed by antiplatelet therapy with aspirin and ticlopidine were pooled for this analysis. Within 30 days, clinical stent thrombosis developed in 53 patients (0.9%). The variables most significantly associated with the probability of stent thrombosis were persistent dissection NHLBI grade B or higher after stenting (OR, 3.7; 95% CI, 1.9 to 7.7), total stent length (OR, 1.3; 95% CI, 1.2 to 1.5 per 10 mm), and final minimal lumen diameter within the stent (OR, 0.4; 95% CI, 0.2 to 0.7 per 1 mm). Stent thrombosis was documented by angiography in 45 patients (0.7%). Clinical consequences of angiographic stent thrombosis included 64.4% incidence of death or myocardial infarction at the time of stent thrombosis and 8.9% 6-month mortality. Stent thrombosis occurred in <1.0% of patients undergoing stenting of native coronary artery lesions and receiving routine antiplatelet therapy with aspirin plus ticlopidine. Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis. Continued efforts to eliminate this complication are warranted given the serious clinical consequences.

Results of the study to determine rotablator and transluminal angioplasty strategy (STRATAS)

Rotational atherectomy is used to debulk calcified or complex coronary stenoses. Whether aggressive burr sizing with minimal balloon dilation (<1 atm) to limit deep wall arterial injury improves results is unknown. Patients being considered for elective rotational atherectomy were randomized to either an “aggressive” strategy (n = 249) (maximum burr/artery >0.70 alone, or with adjunctive balloon inflation ≤1 atm), or a “routine” strategy (n = 248) (maximum burr/artery ≤0.70 and routine balloon inflation ≥4 atm). Patient age was 62 ± 11 years. Fifty-nine percent routine and 60% aggressive strategy patients had class III to IV angina. Fifteen percent routine and 16% aggressive strategy patients had a restenotic lesion treated; lesion length was 13.6 versus 13.7 mm. Reference vessel diameter was 2.64 mm. Maximum burr size (1.8 vs 2.1 mm), burr/artery ratio (0.71 vs 0.82), and number of burrs used (1.9 vs 2.7) were greater for the aggressive strategy, p <0.0001. Final minimum lumen diameter and residual stenosis were 1.97 mm and 26% for the routine strategy versus 1.95 mm and 27% for the aggressive strategy. Clinical success was 93.5% for the routine strategy and 93.9% for the aggressive strategy. Creatine kinase-myocardial band (CK-MB) was >5 times normal in 7% of the routine versus 11% of the aggressive group. CK-MB elevation was associated with a decrease in rpm of >5,000 from baseline for a cumulative time >5 seconds, p = 0.002. At 6 months, 22% of the routine patients versus 31% of the aggressive strategy patients had target lesion revascularization. Angiographic follow-up (77%) showed minimum lumen diameter to be 1.26 mm in the routine group versus 1.16 mm in the aggressive group, and the loss index 0.54 versus 0.62. Dichotomous restenosis was 52% for the routine strategy versus 58% for the aggressive strategy. Multivariable analysis indicated that left anterior descending location (odds ratio 1.67, p = 0.02) and operator-reported excessive speed decrease >5,000 rpm (odds ratio 1.74, p = 0.01) were significantly associated with restenosis. Thus, the aggressive rotational atherectomy strategy offers no advantage over more routine burr sizing plus routine angioplasty. Operator technique reflected by an rpm decrease of >5,000 from baseline is associated with CK-MB elevation and restenosis.

A prospective evaluation of angiography-guided coronary stent implantation with high versus very high balloon inflation pressure

Background High inflation pressure (HP) after coronary stent deployment has become a standard approach because it has been associated with a decreased subacute stent thrombosis (SAT) rate. However, the impact of HP on long-term outcomes is still unclear. We compared the long-term results of a strategy of increasing HP (≥12 atm) until the achievement of angiographic success (<20% residual stenosis) with a prespecified very high inflation pressure (VHP) strategy of 20 atm without intermediate inflations. Methods and Results We conducted a parallel-group, nonrandomized study to evaluate the short- and long-term results in 136 consecutive eligible patients who underwent successful single Palmaz-Schatz stent implantation in vessels ≥3 mm. Major adverse cardiac events (MACE), that is, death, myocardial infarction, and target lesion revascularization (TLR), were monitored for a minimum of 6 months. No significant differences were observed between the two strategies in terms of final minimal lumen diameter (HP, 3.0 ± 0.5 vs VHP, 3.1 ± 0.5 mm) and acute gain (HP, 2.1 ± 0.7 vs VHP, 2.2 ± 0.6). The overall rate of subacute stent thrombosis was 0.7%. During a 405 ± 148-day follow-up, 21 (28.8%) patients in the VHP group and 6 (9.5%) in the HP group (P =.005) had MACE, with a TLR rate of 27.4% versus 7.9% (P =.009), respectively. By multivariate analysis, the use of VHP increased the odds of long-term MACE by a factor of 3.48 (P =.009). Among patients undergoing TLR, those treated with VHP had a greater lumen loss (HP, 1.83 ± 0.57 vs VHP, 2.15 ± 0.36 mm, P =.02) and a more frequent pattern of diffuse restenosis (71% vs 16%, P =.06). Conclusions In our study, the two strategies had similar acute and short-term results, but VHP was associated with a poorer long-term outcome. These data provide a rationale for a less aggressive strategy for stent deployment by optimizing rather than attempting to maximize inflation pressure and stent expansion. (Am Heart J 2000;140:804-12.)

Predictors of event-free survival after repeat intracoronary procedure for in-stent restenosis; study with angiographic and intravascular ultrasound imaging.

Lumen enlargement during repeat percutaneous coronary intervention for in-stent restenosis has been shown to be the result of both stent over-expansion and decrease in neointimal tissue. How these two different mechanisms of action may influence outcome and target lesion revascularization after repeat intervention for in-stent restenosis is unclear. Intravascular ultrasound guided repeat intervention for in-stent restenosis was carried out either with balloon angioplasty, or with a combination of rotational atherectomy plus balloon angioplasty. Clinical follow-up at 1 year, including death, myocardial infarction, or need for revascularization, was obtained. Seventy patients were included in this study; 40 were treated by balloon alone, and 30 by combination of rotational atherectomy plus balloon. Event-free survival probability was 76+/-5%. The mechanism of lumen enlargement, be it stent over-expansion or tissue removal, had no influence on long-term clinical evolution. The only independent predictor was the minimal lumen cross-sectional area at the end of the procedure, the larger the lumen cross-sectional area, the higher the event-free probability. The cut-off point of the lumen cross-sectional area was set at 4.7 mm(2)by discriminant analysis. Event-free survival was 69+/-15% in patients with <4.7 mm(2)lumen cross-sectional area and 91+/-8% in patients with >4.7 mm(2)lumen cross-sectional area (P=0. 008). This study showed that the only independent predictor of late clinical outcome after percutaneous re-intervention for in-stent restenosis was final lumen size, no matter which means were used to achieve it.

Comparison of debulking followed by stenting versus stenting alone for saphenous vein graft aortoostial lesions: immediate and one-year clinical outcomes

OBJECTIVESWe compared in-hospital and one-year clinical outcomes in patients undergoing debulking followed by stent implantation versus stenting alone for saphenous vein graft (SVG) aortoostial lesions.BACKGROUNDStent implantation in SVG aortoostial lesions may improve procedural and late clinical outcomes. However, the impact of debulking before stenting in this complex lesion subset is unknown.METHODSWe studied 320 consecutive patients (340 SVG aortoostial lesions) treated with Palmaz-Schatz stents. Debulking with excimer laser or atherectomy was performed in 133 patients (139 lesions) before stenting (group I), while 187 patients (201 lesions) underwent stent implantation without debulking (group II). Procedural success and late clinical outcomes were compared between the groups.RESULTSOverall procedural success (97.6%) was similar between the groups. Procedural complications were also similar (2.2% for group I and 2.6% for group II). At one-year follow-up, target lesion revascularization (TLR) was 19.4% for group I and 18.2% for group II (p = 0.47). There was no difference in cumulative death or Q wave myocardial infarction between the groups. Overall cardiac event-free survival was similar (69% for group I and 68% for group II). By Cox regression analysis, the independent predictors of late cardiac events were final lumen cross-sectional area (CSA) by intravascular ultrasound (IVUS) (p = 0.001) and restenotic lesions (p = 0.01). Similarly, final IVUS lumen CSA (p = 0.0001) and restenotic lesions (p = 0.006) were found to predict TLR at one year.CONCLUSIONSThese results suggest that, in most patients with SVG aortoostial lesions, debulking before stent implantation may not be necessary.

Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions : intravascular ultrasound study of 2256 patients.

Elevation of serum creatine kinase MB fraction (CK-MB) after percutaneous coronary interventions has been associated with early and late mortality; however, the pathogenesis of CK-MB elevation is still unknown. We hypothesized that CK-MB elevation was related to atherosclerotic plaque burden as assessed by preintervention intravascular ultrasound (IVUS). We studied 2256 consecutive patients who underwent intervention of 2780 native coronary lesions and had complete high-quality preintervention IVUS imaging in the era before routine use of platelet glycoprotein IIb/IIIa inhibitors. Patients were divided into 3 groups: CK-MB within normal range (1675 patients; 2061 lesions); CK-MB elevation 1 to 5 times upper limit of normal (292 patients; 355 lesions); and CK-MB elevation > or = 5 times upper limit of normal (289 patients; 364 lesions). Qualitative angiographic lesion morphology and quantitative analysis were similar among the 3 groups. On preintervention IVUS, progressively more reference segment and lesion site plaque burden and lesion site calcium occurred in the groups with CK-MB elevation. Positive remodeling was more common in lesions with CK-MB elevation. As levels of CK-MB increased, cross-sectional narrowing (percentage plaque burden) increased, both at the reference site (mean cross-sectional narrowing values were 45.1%, <49.3%, and <52.2% for normal CK-MB, 1 to 5 times upper limit of normal, and > or =5 times upper limit of normal groups, respectively; P=0.03) and at the lesion site (81.9%, <85.4%, and <87.1%, respectively; P=0.04). Multivariate analysis indicated that de novo lesions, atheroablative technique, plaque burden at the lesion and reference segments, and final minimal lumen diameter were independent predictors of CK-MB elevation. CK-MB elevation correlates with a greater atherosclerotic plaque burden. CK-MB elevation after intervention may be a marker of diffuse atherosclerotic disease or a consequence of catheter-based intervention in more diseased arteries or both.

Optimally deployed stents in the treatment of restenotic versus de novo lesions

Results from earlier trials performed before the implementation of optimal stent deployment techniques suggest that stenting for restenotic lesions may be associated with a higher risk of restenosis when compared with de novo lesions. The aim of this study was to compare the short- and long-term outcome of optimal stent deployment in restenotic versus de novo lesions. In all, 1,865 consecutive patients with 2,707 de novo lesions and 489 patients with 633 restenotic lesions underwent intravascular ultrasound-guided optimal stent deployment. In-hospital outcome was similar for both groups, except for a higher incidence of non–Q-wave myocardial infarction in the de novo group (14.6% vs 8.6%, p = 0.001). At 12-month follow-up, there was no statistical significant difference in the incidence of death or myocardial infarction, but event-free survival was better in the de novo lesion group of patients (74.5% vs 63.7%, p = 0.001). There was a higher incidence of target lesion revascularization in the restenosis group (25.1% vs 13.0%, p = 0.001). By multivariate analysis, restenotic lesions, vein graft lesions, and diabetes mellitus were strong determinants of repeat revascularization, whereas larger preprocedural reference vessel minimal lumen diameter and larger final minimal lumen diameter were associated with a reduced chance of restenosis and increased event-free survival. This study shows that optimal stent deployment for restenotic and de novo lesions has favorable short- and long-term outcome. However, the incidence of target lesion revascularization was significantly greater in restenotic lesions. Saphenous vein graft lesions and diabetes mellitus were confirmed as other independent risk factors for clinical restenosis.

Relation of coronary artery size to one-year clinical events after new device angioplasty of native coronary arteries (a New Approach to Coronary Intervention [NACI] Registry report)

The influence of vessel size on clinical and angiographic outcomes after new device angioplasty has not been well documented. We reviewed clinical and angiographic outcomes of 2,044 patients undergoing new device angioplasty of native vessels enrolled in the New Approaches to Coronary Interventions (NACI) Registry. Quantitative angiography was performed using standard methods. Patients were divided into 3 groups according to reference vessel diameter (RVD) (<2.75, 2.75 to 3.25, and >3.25 mm). Patients with the smallest vessels had a higher incidence of diabetes (26% vs 16%, p <0.01), multivessel disease (50% vs 45%, p <0.01), left anterior descending coronary artery disease (61% vs 39% p <0.01), and in general, more severe baseline lesion characteristics than patients with larger (>3.25 mm) vessels. Absolute baseline and final minimal lumen diameter (MLD) was also smaller in patients with RVD <2.75 mm despite similar final percent diameter stenosis. Although in-hospital events were similar, patients who underwent interventions in vessels <2.75 mm had an increased incidence of death (p <0.01), surgical revascularization (p <0.05), and target lesion revascularization (TLR) (p <0.01) at 1 year. Multivariate analysis by vessel size showed a stepwise increase in the risk of TLR by 1 year in patients with the smaller RVD (p = 0.0001) and the combined end point of 1 year death/Q wave-myocardial infarction/TLR (p = 0.02). Thus, despite similar early clinical events among patients undergoing new device angioplasty, patients who underwent treatment of smaller vessels had a significantly increased risk of major adverse clinical events and particularly TLR by 1 year after new device angioplasty of native coronary arteries.

Stent thrombosis: historical perspectives and current trends.

Coronary stents are now implanted in more than 70% of percutaneous coronary revascularization procedures. Early enthusiasm for improved acute angiographic results and limited restenosis was dampened initially by a high rate of stent thrombosis and later by the increased bleeding complications of aggressive and complex anticoagulation protocols designed to lower the stent thrombosis risk. More recently, routine high-pressure deployment strategies and anti-platelet drug regimens have lowered the incidence of stent thrombosis to approximately 1% without an increased bleeding risk. The timing of stent thrombosis has also changed from a median of 4-5 days to a median of 1 day after the stent procedure. Risk factors in earlier studies included stenting for threatened or abrupt closure, smaller vessels, longer lesions, and possibly left anterior descending artery lesion location. Modern studies have shown a slightly increased risk for multiple stent use, residual dissection, and smaller final lumen. Optimal therapy for stent thrombosis includes emergent revascularization and anti-thrombotic treatment, although the clinical consequences remain dire despite successful reperfusion. The use of platelet glycoprotein IIb/IIIa inhibitors, especially in high-risk situations may further reduce the incidence of stent thrombosis.

Acute and nine-month clinical outcomes after “suboptimal” coronary stenting: Results from the STent anti-thrombotic regimen study (STARS) registry

OBJECTIVESThis registry collected the 30-day and 9-month clinical outcomes of patients whose coronary stent implantation was suboptimal, and compared them with the cohort of patients with “optimal” stenting in the randomized portion of the STent Anti-thrombotic Regimen Study (STARS) trial.BACKGROUNDAlthough “optimal” stenting combined with an aspirin and ticlopidine regimen carries a low (0.5%) incidence of subacute stent thrombosis, only limited data are available for patients in whom stents are deployed suboptimally.METHODSIn the STARS, 312 (15.9%) of 1,965 patients enrolled were excluded from participation in the randomized trial based on a perceived “suboptimal” result of coronary stenting. Of these, 265 patients met prespecified criteria for suboptimal stenting, and were followed in a parallel registry, which was compared with the randomized STARS optimal stenting cohort. The primary end point was a 30-day composite of death, emergent target lesion revascularization, angiographic thrombosis of the target vessel without revascularization and nonfatal myocardial infarction (MI)unrelated to direct procedural complications.RESULTSRegistry patients had a similar frequency of the primary end point compared with the overall randomized cohort (3.0% vs. 2.2%), with this end point correlating to use of multiple stents, smaller final lumen diameter and absence of ticlopidine from the poststent regimen. Overall 30-day mortality (1.1% vs. 0.06%, p = 0.009) and periprocedural non-Q wave MI (8.7% vs. 4.2%, p = 0.003) were more frequent in registry patients, and appeared to be related to acute procedural complications. Clinical restenosis was significantly higher for registry patients (26.8% vs. 16.0%, p = 0.001), relating to greater prevalence of independent predictors such as smaller final lumen diameter and multiple stent use.CONCLUSIONSIn the STARS registry, the inability to perform optimal stenting correlated with smaller final lumen diameter and longer stent length. With ticlopidine-containing regimens, the acute clinical results of “suboptimal” stent deployment are clinically acceptable, although they are not quite as good as those of optimal stenting using similar drug therapy.

Role of nitric oxide in restenosis after experimental balloon angioplasty in the hypercholesterolemic rabbit: effects on neointimal hyperplasia and vascular remodeling

OBJECTIVESThe purpose of this study was to assess the effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on neointimal hyperplasia and vascular remodeling after balloon angioplasty in the hypercholesterolemic rabbit.BACKGROUNDRestenosis after balloon angioplasty is a consequence of both neointimal hyperplasia and vessel remodeling. Nitric oxide inhibits neointimal hyperplasia, but its effect on vessel remodeling is unknown.METHODSSix weeks after induction of bilateral iliac atherosclerosis, 48 rabbits underwent successful angioplasty in 75 vessels. Eight rabbits (acute group) were sacrificed immediately after angioplasty. The remaining animals received either placebo (chronic control group), or a diet supplemented with either L-arginine (1.5 g/kg/day), or L-NAME (15 mg/kg/day) for 4 weeks after angioplasty.RESULTSThe intimal area was significantly greater in the chronic control group compared to the acute group (2.60 ± 1.03 mm2vs. 1.35 ± 0.62 mm2). This increase in intimal area was lower in the L-arginine group (1.79 ± 0.61 mm2), and greater in the L-NAME group (3.23 ± 0.92 mm2). The area circumscribed by the internal elastic lamina (IEL) increased significantly in the control group compared to the acute group (from 2.52 ± 0.66 to 3.33 ± 0.85 mm2); a more marked increase occurred in the L-NAME group (3.90 ± 0.85 mm2). By contrast, IEL area was unchanged in the L-arginine group (2.41 ± 0.62 mm2). As a result, there was no significant difference in lumen area after 4 weeks in the chronic groups (control: 0.74 ± 0.38 mm2; L-arginine: 0.50 ± 0.43 mm2; L-NAME: 0.48 ± 0.42 mm2).CONCLUSIONSOur results demonstrate that L-arginine inhibits whereas L-NAME stimulates neointimal hyperplasia after experimental balloon angioplasty in the hypercholesterolemic rabbit. However, the lack of vessel enlargement in the L-arginine group resulted in a similar final lumen size in the L-NAME and L-arginine groups.

Intravascular ultrasound predictors of target lesion revascularization after stenting of protected left main coronary artery stenoses

We evaluated the predictors of late clinical outcomes after stenting of protected left main coronary artery (LMCA) stenoses. Intravascular ultrasound (IVUS) guided stenting of protected LMCA stenoses was performed in 87 consecutive patients between January 1994 and December 1996. Results were evaluated using conventional (clinical, angiographic, and IVUS) methodology. Late (12 month) clinical follow-up information was obtained in all patients. Initial procedural success was achieved in 86 patients (99%). There was 1 in-hospital death (in the 1 patient with a procedural failure). There were no other in-hospital complications, including Q-wave myocardial infarction, emergency bypass surgery, or repeat coronary angioplasty. The overall target lesion revascularization (TLR) rate was 13%. Using multivariate logistic regression analysis, the only independent predictor of TLR was the postintervention lumen area by IVUS. A final lumen area ≥7.0 mm 2 was obtained in 74 patients (86%); the TLR rate for these patients was 7%. This was compared with patients with a final lumen area <7.0 mm 2 in whom the TLR rate was 50% (p = 0.0011). Stenting of protected LMCA stenoses is safe and effective with acceptable long-term clinical outcomes. The most important factor determining long-term success was the postintervention lumen area by IVUS.

Angiographic and intravascular ultrasound predictors of in-stent restenosis.

This study was performed to determine predictors of in-stent restenosis from a high volume, single-center practice. Intracoronary stents have been shown to reduce the restenosis rate as compared with balloon angioplasty, but in-stent restenosis continues to be an important clinical problem. Between April 1993 and March 1997, 1,706 patients with 2,343 lesions were treated with a variety of intracoronary stents. The majority of stents were placed with high pressure balloon inflations and intravascular ultrasound (IVUS) guidance. Angiographic follow-up was obtained in 1,173 patients with 1,633 lesions (70%). Clinical, angiographic and IVUS variables were prospectively recorded and analyzed by univariate and multivariate models for the ability to predict the occurrence of in-stent restenosis defined as a diameter stenosis > or =50%. In-stent restenosis was angiographically documented in 282 patients with 409 lesions (25%). The restenosis group had a significantly longer total stent length, smaller reference lumen diameter, smaller final minimal lumen diameter (MLD) by angiography and smaller stent lumen cross-sectional area (CSA) by IVUS. In lesions where IVUS guidance was used, the restenosis rate was 24% as compared with 29% if IVUS was not used (p < 0.05). By multivariate logistic regression analysis, longer total stent length, smaller reference lumen diameter and smaller final MLD were strong predictors of in-stent restenosis. In lesions with IVUS guidance, IVUS stent lumen CSA was a better independent predictor than the angiographic measurements. Achieving an optimal stent lumen CSA by using IVUS guidance during the procedure and minimizing the total stent length may reduce in-stent restenosis.

Treatment of calcified coronary lesions with Palmaz-Schatz stents. An intravascular ultrasound study.

To evaluate the result of coronary stenting in calcified lesions and to find morphological and procedural factors influencing the final result. Three hundred and twenty three native coronary artery lesions in 303 patients (197 men, mean age 63.9 +/- 11.5 years) treated with Palmaz-Schatz stents were differentiated into four groups depending on their degree of circumferential calcification as defined by intravascular ultrasound [0-90 degrees (n=120), 91-180 degrees (n=58, 181-270$ (n=71) and 271-360 degrees n=74)]. In 117 lesions rotational atherectomy was used prior to stent placement. Intravascular ultrasound and quantitative angiography were performed prior to treatment and after stent placement to measure minimal and maximal lumen diameter and lumen cross-sectional area at the lesion site and the reference segments. Acute lumen gain and eccentricity index were calculated. Although higher balloon pressures were used than in the minimally calcified lesions. the final angiographic minimal lumen diameter decreased with increasing arc of calcification (3.01 +/- 0.47, 3.04 +/- 0.43, 2.85 +/- 0.53, 2.83 +/- 0.40 mm, respectively, P=0.0320) resulting in a decrease in acute diameter gain with increasing arc of calcification (2.06 +/- 0.51, 1.91 +/- 0.46, 1.81 +/- 0.56, 1.78 +/- 0.51 mm, respectively, P=0.0067). Adjunctive rotational atherectomy prior to stent placement resulted in a greater acute diameter and a greater lumen cross-sectional area gain, coupled with less final residual stenosis than pre-treatment with balloon angioplasty. Implantation of stents in calcified lesions results in less optimal stent expansion, especially in lesions with thick, eccentric calcific plaque layers. Use of adjunctive rotational atherectomy before stent placement may improve the procedural result.

Mechanisms of residual lumen stenosis after high-pressure stent implantation: a quantitative coronary angiography and intravascular ultrasound study.

Intravascular ultrasound (IVUS) studies have demonstrated that stents are frequently suboptimally expanded despite the use of high pressures for deployment. The purpose of this study was to identify the mechanisms responsible for such residual lumen stenosis. Fifty-seven lesions from 50 patients treated with high-pressure (median+/-interquartile range, 14+/-2 atm) elective (44 de novo, 13 restenotic lesions) stenting were prospectively studied (29 Wiktor, Medtronic; 28 Palmaz-Schatz, Cordis Corp). Balloon subexpansion was calculated as the difference between maximal and minimal balloon cross-sectional areas at peak pressure measured by automatic edge detection; elastic recoil was calculated as the difference between minimal measured balloon size and IVUS-derived minimal lumen area within the stent. Angiographic residual diameter stenosis was 10+/-13% (reference diameter, 3.1+/-0.7 mm; balloon to artery ratio, 1.12+/-0.23) and IVUS-derived stent expansion was 80+/-28%. However, although balloon nominal size was 9.6+/-1.3 mm2 and maximal balloon size measured inside the coronary lumen was 12.5+/-3.2 mm2, final stent minimal lumen area was only 7.1+/-2.2 mm2. Balloon subexpansion of 4.0+/-1.8 mm2 (33%) and elastic recoil of 1.6+/-2.3 mm2 (20%) (both P<0.0001) were the two mechanisms responsible for residual luminal stenosis. Wiktor stent and peak inflation pressure correlated with balloon subexpansion, whereas Wiktor stent, de novo lesion, and minimal lumen area at baseline correlated with elastic recoil. Despite high-pressure deployment, lumen dimensions after stenting are only 57% of maximal achievable. Inadequate balloon expansion and elastic recoil are responsible for residual lumen stenosis, suggesting that plaque characteristics and stent resistance deserve further investigation.

Intravascular Ultrasound Predictors of Angiographic Restenosis in Lesions Treated With Palmaz-Schatz Stents

Objectives. This study sought to evaluate the clinical, procedural, preinterventional and postinterventional quantitative coronary angiographic (QCA) and intravascular ultrasound (IVUS) predictors of restenosis after Palmaz-Schatz stent placement.Background. Although Palmaz-Schatz stent placement reduces restenosis compared with balloon angioplasty, in-stent restenosis remains a major clinical problem.Methods. QCA and IVUS studies were performed before and after intervention (after stent placement and high pressure adjunct balloon angioplasty) in 382 lesions in 291 patients treated with 476 Palmaz-Schatz stents for whom follow-up QCA data were available 5.5 ± 4.8 months (mean ± SD) later. Univariate and multivariate predictors of QCA restenosis (≥50% diameter stenosis at follow-up, follow-up percent diameter stenosis [DS] and follow-up minimal lumen diameter [MLD]) were determined.Results. Three variables were the most consistent predictors of the follow-up angiographic findings: ostial lesion location, IVUS preinterventional lesion site plaque burden (plaque/total arterial area) and IVUS assessment of final lumen dimensions (whether final lumen area or final MLD). All three variables predicted both the primary (binary restenosis) and secondary (follow-up MLD and follow-up DS) end points. In addition, a number of variables predicted one or more but not all the end points: 1) restenosis (IVUS preinterventional lumen and arterial area); 2) follow-up DS (QCA lesion length); and 3) follow-up MLD (QCA lesion length and preinterventional MLD and DS and IVUS preinterventional lumen and arterial area).Conclusions. Ostial lesion location and IVUS preinterventional plaque burden and postinterventional lumen dimensions were the most consistent predictors of angiographic in-stent restenosis.

Influence of coronary atherosclerotic remodeling on the mechanism of balloon angioplasty

Objectives Intracoronary ultrasonography was used to assess coronary arteries before and after balloon percutaneous transluminal coronary angioplasty (PTCA) to determine whether the mode of coronary atherosclerotic remodeling affects the mechanism of balloon dilation. Background Coronary arteries may enlarge or shrink in response to atherosclerotic plaque development. The effect of coronary remodeling on the mechanism of balloon PTCA has not yet been studied. Methods Forty-one patients with 47 native de novo coronary artery lesions were studied with a 30 MHz intracoronary ultrasound catheter before and after balloon PTCA. Images were analyzed at the lesion site and the adjacent reference segments. At each site the lumen, vessel, and plaque area and the percent area stenosis were measured. Lesions were separated into two groups based on relative vessel area (lesion vessel area/reference vessel area). A relative vessel area >1.0 defines adaptive enlargement (group 1, n = 25), whereas a relative vessel area ≤1.0 reflects coronary shrinkage (group 2, n = 22). Regression analysis examined whether elastic recoil and the PTCA balloon/vessel area ratio correlated. Results After balloon PTCA was performed, both the enlargement and shrinkage groups had similar gains in luminal area (2.3 ± 1.8 mm 2 [mean ± SD] vs 2.8 ± 1.7 mm 2, p = 0.32), reduction in percent stenosis (−19.2% ± 11.5% vs −14.4 ± 12.7, p = 0.18), and final lumen area (4.9 ± 1.7 mm 2 vs 4.7 ± 1.9 mm 2, p = 0.73). However, the mechanism of luminal enlargement was different in each group. Reduction in plaque area was significantly greater in the enlargement group (group 1, −2.0 ± 1.7 mm 2 vs group 2, 0.04 ± 2.2 mm 2 ; p = 0.001), whereas increased vessel area was more important in the shrinkage group (group 1, 0.8 ± 1.5 mm 2 vs group 2, 2.4 ± 2.3 mm 2; p = 0.009). Positive correlation was seen between elastic recoil and the balloon/vessel area ratio in lesions with vessel enlargement ( r = 0.80, p < 0.0001). No such correlation was observed in shrinkage vessels ( r = 0.28, p = 0.21). Conclusions The acute luminal gain after balloon PTCA is similar regardless of the type of coronary remodeling. However, the mode of remodeling affects the mechanism of balloon dilation such that enlargement vessels exhibit plaque compression, whereas shrinkage arteries demonstrate vessel stretch. The post-PTCA elastic recoil correlates linearly to the balloon/vessel area ratio in arteries that have undergone adaptive enlargement. (Am Heart J 1997;134:1099-106.)

Excimer Laser Coronary Angioplasty: The New Approaches to Coronary Intervention (NACI) Experience

In the New Approaches to Coronary Intervention (NACI) registry, 887 patients were electively treated with excimer laser coronary angioplasty (ELCA) for coronary artery disease. The Advanced Interventional System (AIS) system was used in 487 cases; the Spectranetics system, in 400. The mean age was 63.4 years. Most patients had unstable angina (60.3%); 43.7% had a prior myocardial infarction; and 18.6% were high risk or inoperable patients. Mean ejection fraction was 55.4%. A total of 1,000 lesions were treated in the 887 patients. Of the 1,000 lesions treated with ELCA in the 887 patients, 36% were in the right coronary artery; 33%, left anterior descending; 13%, circumflex; 3%, left main; and 16.6%, vein graft. By angiographic core laboratory analysis available for 752 (85%) patients with 839 lesions, lesions were 12.76 mm long. The minimum lumen diameter increased to 1.29 mm after the laser and finally to 1.95 mm after adjunctive percutaneous transluminal coronary angioplasty (PTCA) (which was performed in 93% of all lesions), with a final residual stenosis of 32.1% and Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in 95%. Dissections of grades B, C, or D were seen after 22.0% of initial laser attempts, and postlaser perforations were noted in 2.6%. Additional such dissections accumulated after adjunctive PTCA but the perforation rate remained low. Procedural success was achieved in 84% of patients, but 1.2% died, 0.7% experienced Q-wave myocardial infarction (MI), and 2.7% required emergency bypass surgery. Multiple logistic regression analysis could not identify any independent predictors of these in-hospital complications. One-year mortality was 5.7% and the cumulative incidence of Q-wave MI was 1.5%. Coronary artery bypass graft (CABG) surgery was performed in 15.0% of patients whereas 25.5% required repeat percutaneous intervention with a target lesion revascularization rate of 31%. Independent predictors of death, Q-wave MI, or target lesion revascularization (which, combined, occurred in 35.6% of patients) were the absence of prior MI, ELCA in the circumflex, perforation after the procedure, and small (<2 mm) final minimal lumen diameter. Considering the large number of patients with high-risk lesions, laser angioplasty was performed with excellent procedural success rates and a reasonable incidence of major complications.

Intravascular Ultrasound to Discern Device-Specific Effects and Mechanisms of Restenosis

Restenosis continues to be the “Achilles' heel” of transcatheter interventions. While attempts to reduce restenosis by inhibiting cellular proliferation through pharmacologic or mechanical means have been unsuccessful, stents, which inhibit acute recoil and chronic remodeling, have been shown convincingly to reduce restenosis in 2 randomized clinical trials. Intravascular ultrasound (IVUS) allows transmural, tomographic imaging of coronary arteries in humans in vivo to subdivide restenosis into the two basic underlying components: tissue proliferation and arterial remodeling. In studies performed at the Washington Hospital Center, in nonstented lesions 73% of late lumen loss was due to arterial remodeling (a decrease in arterial, or external elastic membrane cross-sectional area) and 27% was due to tissue growth (an increase in plaque plus media cross-sectional area). These findings were confirmed by 2 other studies: the Optimal Atherectomy Restenosis Study (OARS) and the Serial Ultrasound analysis of REstenosis (SURE) Trial. IVUS was also used to study the mechanisms by which stents reduce restenosis. Stents created a larger final lumen cross-sectional area and, for all practical purposes, abolished arterial remodeling to offset a stent-related increase in neointimal tissue accumulation. Neointimal hyperplasia is solely responsible for in-stent restenosis and therefore appears to be a pure model for studying strategies to limit tissue proliferation. (Am J Cardiol 1996;78(suppl 3A):18–22)