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Clinical and angiographic outcome of patients with mild coronary lesions treated with balloon angioplasty or coronary stenting

N Mercado, W Maier, E Boersma, C Bucher, V de Valk, W.W O'Neill, B.J Gersh, B Meier, P.W Serruys, W Wijns
DOI: http://dx.doi.org/10.1016/S0195-668X(02)00422-0 541-551 First published online: 2 March 2003

Abstract

Aims To investigate the clinical and angiographic outcome of patients with mild coronary lesions treated with balloon angioplasty or coronary stenting (coronary plaque sealing, i.e. dilatation of angiographically non-significant lesions) compared to moderate and severe stenoses.

Methods and results Patients with chronic stable angina and a single de novo lesion in a native coronary vessel scheduled to undergo percutaneous coronary intervention (PCI) were selected from 14 different studies. Off-line analysis of angiographic outcomes was assessed in all patients using identical and standardised methods of data acquisition, analysis and definitions. Clinical endpoints were adjudicated by independent clinical events committees. All quantitative coronary angiographic (QCA) analyses were performed in the same core laboratory. Stenosis severity prior to PCI was categorised into three groups: <50% diameter stenosis (DS), 50–99%DS and >99%DS pre. A total of 3812 patients were included in this study; 1484 patients (39%) were successfully treated with balloon angioplasty (BA) only and stented angioplasty was performed in 2328 patients (61%).

One-year mortality and rate of non-fatal myocardial infarction (MI) (Kaplan–Meier) did not differ between BA and stented angioplasty for any of the stenosis severity categories. Following BA, the combined event rate (death and non-fatal MI) was 4.8, 4.6 and 0% in the <50, 50–99 and >99%DS categories, respectively. Following stented angioplasty, the combined event rate was 3.1, 4.4 and 4.8% in the same categories. The need for repeat revascularisation corrected for stenosis severity in the Cox proportional-hazards regression model was reduced by 20% after stented angioplasty (hazard ratio (HR) 0.80, 95%CI 0.69–0.93).

Conclusion The concept of plaque sealing is appealing from the theoretical point of view. However, with current technology, plaque sealing cannot prevent death and future non-fatal MIs in the long-term because 1-year event rates after PCI of non-significant stenoses remain unacceptably elevated when compared with the estimated 1-year probability of a non-fatal MI in lesions with a <50%DS. Moreover, major adverse cardiac events at 1-year after PCI are not directly related to the degree of pre-procedural stenosis severity.

  • Balloon angioplasty
  • Coronary stenting
  • Plaque sealing

1 Introduction

Revascularisation by percutaneous coronary intervention (PCI) is performed to relieve symptoms in patients with coronary artery disease and angiographically significant coronary stenosis. However, coronary stenoses vary in severity and even mild stenoses harbour an unpredictable risk of acute occlusion that may cause myocardial infarction (MI) and sudden death. Balloon angioplasty typically induces plaque splitting which engenders a tissular reaction covering the plaque. The smooth muscle-rich neointima later transforms into a collagen-rich layer, which results in plaque sealing. Thus, once the acute effect of vessel trauma with its inherent risk of abrupt occlusion has passed, the subsequent risk of acute occlusion of a sealed plaque should be markedly reduced thanks to the repaired fibrous cap, which has overgrown the inflicted wound.1,2

Therefore, plaque sealing by balloon angioplasty has been advocated to prevent acute coronary events in patients with angiographically non-significant coronary lesions.3

Endorsing this concept and recommending PCI for angiographically non-significant lesions would mean a potentially large increase in procedures that needs sound justification. So far, the plaque-sealing concept has not been tested in prospective randomised clinical trials. A few observational case series from single centre experiences4,5 have cautioned against the use of BA in non-significant lesions. We therefore aimed to investigate the clinical and angiographic outcome of coronary plaque sealing, i.e. dilatation of angiographically non-significant lesions compared to moderate and severe stenoses, selected from a large cohort of registries and clinical trials of patients undergoing PCI.

2 Methods

2.1 Patient selection

Patients with chronic stable angina and a single de novo lesion in a native coronary vessel scheduled to undergo PCI were selected from 14 different studies: two placebo-active randomised trials aimed at coronary restenosis prevention after balloon angioplasty (BA) alone or with additional stenting (FLARE6 and TRAPIST7), nine stent registries (BENESTENT-2 Pilot,8 WEST-1,9 WEST-2,10Wellstent Native,11 ROSE,12 DUET,13 EASI,14SOPHOS15 and MAGIC 5-L16), two randomised trials comparing coronary stenting against BA alone (BENESTENT-117 and BENESTENT-218) and the intravascular ultrasound (IVUS) substudy of a randomised clinical trial that evaluated the safety and efficacy of long-term treatment with an oral GP IIb/IIIa inhibitor in patients undergoing PCI(EXCITE19). A general description of these studies and the individual contribution of each clinical trial and registry, in terms of the number of single-lesion patients with chronic stable angina selected for this analysis is depicted in Table 1.

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Table 1

General overview of randomised clinical trials and device registries

Acronym-yearStudyType of studyTreatment for single-lesion patientsObjective
BACoronary stenting
BENESTENT-1—1994BElgian NEtherlands STENTRandomised PTCA vs Stent258262Evaluation of long-term angiographic and clinical outcomes of coronary stenting compared to standard PTCA
BENESTENT-2 Pilot—1996BElgian NEtherlands STENT-2 PilotStent registry1202Determine the safety of elective implantation of a heparin-coated Palmaz–Schatz stent in patients with a single de novo lesion in a native coronary artery
WEST-1—1997West European Stent TrialStent registry285Safety and efficacy of ACS Multi-Link coronary stenting in patients with chronic stable angina due to a single lesion in a native coronary artery
WEST-2—1998West European Stent Trial 2Stent registry0165Assess the use of aspirin alone following successful implantation of an ACS Multilink-Stent under IVUS and QCA guidance in patients with chronic stable or unstable angina
BENESTENT-2—1998BElgian NEtherlands STENT-2Randomised PTCA vs Stent379276Compare event-free survival in patients after heparin-coated stent implantation plus antiplatelet therapy with standard balloon angioplasty
FLARE—1999Fluvastatin Angiographic REstenosisRandomised active treatment vs placebo7130Evaluate the ability of Fluvastatin to reduce restenosis after successful PTCA
Wellstent Native—1999Wellstent native studyStent registry055Assess the safety and efficacy of the self-expanding Wallstent in patients with stable or unstable angina
ROSE—2000Registry for Optimal beStent EvaluationStent registry066Assess the procedural safety of beStent Brava implantation, 6-month angiographic and 12-month clinical outcomes of this population
DUET—2000Evaluation of the ACS-Multi-Link DUET coronary stent systemStent registry0113Assess the safety and efficacy of the ACS Multi-Link DUET coronary stainless steel balloon-expandable stent
SOPHOS—2000Study Of Phosphorylcholine coating On StentsStent registry0241Assess the safety and efficacy of the BiodivYsio stent
EXCITE—2000Evaluation of oral Xemilofiban in Controlling Thrombotic EventsRandomised active treatment vs placebo131430To evaluate whether long-term Administration of a glycoprotein IIb/IIIa receptor antagonist would provide sustained protection from death, MI, and the need for urgent revascularisation
EASI—2001European Antiplatelet Stent InvestigatorsStent registry0113Assess event-free survival after implantation of the Cordis coil cross-flex stent
MAGIC-5L—2001MAGIC—5L StudyStent registry0136Assess the safety and efficacy of 5 different lengths of the self-expanding Magic Wallstent
TRAPIST—2001Trapidil on restenosis after stentingRandomised active treatment vs placebo0184Assess the safety and efficacy of Trapidil (PDGF and Thromboxane A2 synthetase inhibitor) in restenosis prevention after coronary stenting

These studies are considered representative of the current practice of PCI but antedated the use of intracoronary brachytherapy and drug-eluting stents. Off-line analysis of angiographic outcomes was assessed in all patients using identical and standardised methods of data acquisition, analysis and definitions of the variables in the same core laboratory (Cardialysis, Rotterdam, TheNetherlands) using the Cardiovascular Angiography Analysis System II (CAAS II) (Pie Medical, Maastricht, The Netherlands).

Patients were included if they had threeadequate angiograms, one immediately before the intervention, one immediately after and one at 6-month follow-up. Patients with an unsuccessful procedure or patients with treated saphenous vein grafts were excluded.

2.2 Clinical endpoint definition

Clinical endpoints were uniformly defined across the different trials and registries as follows. Death was defined to include all deaths, regardless of cause. However, for the purposes of this study, only cardiac deaths were considered in the analysis of clinical events and any death was considered of cardiac origin unless unequivocally proven otherwise. Non-fatal MI was diagnosed if there were new pathologic Q waves (>0.04s) with a depth of more than one quarter of the corresponding R-waveamplitude in two or more contiguous leads considered by the investigator as not present at study inclusion20 or if there was an increase in serum creatine kinase (CK) to more than twice the normal value, together with a pathological increase in muscle brain creatine kinase (CK-MB) iso-enzyme. If CK-MB data were not available, CK values were accepted as sufficient evidence of MI. These enzymes were measured per protocol at screening, 6h before and 12h after intervention. Repeat revascularisations (by CABG or repeat PCI) were defined as those involving a previously treated vessel between the initial procedure (considered complete when the guiding catheter was removed from the arterial sheath) and 1-year.

The primary clinical endpoint of this study was cardiac death and the combined rate of death and non-fatal MI. Secondary combined endpoint included the rate of repeat revascularisation.

2.3 QCA analysis and angiographic endpoints

The standard definitions used in this study for QCA variables: vessel size, pre-procedural minimal luminal diameter (MLD pre), post-procedural minimal luminal diameter (MLD post), minimal luminal diameter at 6-month follow-up (MLD f-up), diameter stenosis greater than 50% at 6-month follow-up (DS >50% at 6-month), acute gain, late loss and loss index have been described elsewhere.21,22 The pre-procedural reference diameter (RD pre) was the diameter obtained by an interpolated method and the lesion length was defined by the curvature analysis.21

2.4 Data analysis

Data was divided into quintiles according to the degree of severity of pre-procedural diameter stenosis (DS pre) as assessed by QCA and based on the definitions used in the CASS registry study.23 Separate baseline, QCA and clinical endpoint analyses were performed in patients treated with balloon angioplasty only (BA group) and patients in whom coronary stents were implanted (stent group). Because the event rates for BA and stent groups were similar for patients in the middle three quintiles (50–69, 70–89 and 90–99%DS), we combined the middle three quintiles into a single group (50–99%DS). Therefore, stenosis severity was categorised into three groups as follows: <50, 50–99 and >99%DS pre.

The statistical analysis was performed using the SAS 8.0 software package (SAS Institute, Cary, NC). Quantitative values were given as median (25th, 75th percentiles) or mean±standard deviation. To test for differences in categorical variables the Fisher's exact test was applied and to test for differences in continuous baseline variables across the studies, the Kruskal–Wallis test was used.

Event rate curves were constructed by means of Kaplan–Meier methods, and event rate differences between the three groups of stenosis severity were compared with the use of the log-rank test.24 The Cox proportional-hazards regression model was used to examine the effect of coronary stenting on the primary and secondary clinical endpoints of this study, corrected for stenosis severity (<50, 50–99 and >99%DS pre). Statistical significance wasinferred at Math.

3 Results

A total of 3812 patients with chronic stable angina and a single coronary lesion in a native vessel were included in this study; 1484 patients (39%) were successfully treated with BA only and stentedangioplasty was performed in 2328 patients (61%). Comparisons between the three groups of stenosis severity (<50, 50–99 and >99%DS pre) were summarised for baseline characteristics, angiographic and clinical outcomes for BA and Stent groups in Tables 2–4and Figs. 1–3.

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Table 2

Baseline characteristics

Balloon angioplasty populationStent population
<50% DS preEmbedded Image50–99% DS preEmbedded Image>99% DS preEmbedded ImageP-value<50% DS preEmbedded Image)50–99% DS preEmbedded Image>99% DS preEmbedded ImageP-value
Age,60 (52, 68)60 (52, 67)59 (51,65)0.35660 (52, 69)60 (52, 66)59 (52, 67)0.689
Men, %7881850.4587880790.884
Height, cm170 (164, 175)170 (165, 176)170 (165, 180)0.355170 (164, 177)171 (165, 176)172 (166, 178)0.373
Weight, kg76 (69, 84)78 (70, 85)80 (74, 89)0.09677 (70, 85)78 (70, 86)80 (74, 90)0.073
History
Hypertension, %3736340.9143737340.888
Diabetes mellitus, %6.679.70.5931412110.760
MI, %4027340.0093029490.004
PVD, %7.45.64.80.6593.26.530.364
Angioplasty, %12.47.52.40.029111090.955
Bypass surgery, %2.43.400.2583.22.800.408
Smoking status, %
Current2628270.8353028230.486
Prior history4948460.8744148530.214
MVD, %2.583.60.0352623140.160
Vessel treated, %
RCA2627280.9362136420.056
LAD5247360.0866346330.002
LCx2126350.0611517240.414
  • Data presented are median (25th, 75th percentiles) or percentages.

    MI=prior history myocardial infarction; PVD=peripheral vascular disease; MVD=multiple vessel disease; DS pre=pre-procedural diameter stenosis.

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Table 3

Pre-procedural, post-procedural and 6-month follow-up QCA analysis of treated lesions

Balloon angioplasty populationStent population
<50% DS preEmbedded Image50–99% DS preEmbedded Image>99% DS preEmbedded ImageP-value<50% DS preEmbedded Image50–99% DS preEmbedded Image>99% DS preEmbedded ImageP-value
Vessel size, mm2.61 (2.3, 2.85)2.78 (2.47, 3.14)2.47 (2.23, 2.79)<0.00012.75 (2.52, 3.14)2.91 (2.64, 3.25)2.96 (2.7, 3.37)0.006
Lesion length, mm6.89 (5.59, 8.03)7.48 (6.01, 9.48)7.86 (6.33, 9.79)0.0096.74 (5.55, 8.81)8.15 (6.48, 10.3)17.4 (12, 25.8)<0.0001
MLD pre, mm1.4 (1.24, 1.62)1.01 (0.85, 1.18)0 (0, 0)<0.00011.53 (1.36, 1.68)1.01 (0.86, 1.18)0 (0, 0)<0.0001
MLD post, mm1.86 (1.61, 2.16)1.93 (1.68, 2.22)1.7 (1.47, 1.89)<0.00012.62 (2.3, 2.93)2.64 (2.39, 2.91)2.46 (2.2, 2.7)0.0002
MLD f-up, mm1.7 (1.35, 2)1.62 (1.25, 1.98)1.24 (0.73, 1.73)<0.00011.89 (1.52, 2.37)1.88 (1.44, 2.27)1.6 (1, 1.98)<0.0001
DS >50% at 6-month f-up, %2430440.0081921320.005
Acute gain0.45 (0.29, 0.6)0.9 (0.67, 1.14)1.7 (1.47, 1.89)<0.00011.1 (0.88, 1.28)1.6 (1.35, 1.86)2.46 (2.2, 2.69)<0.0001
Late loss0.19 (−0.09, 0.5)0.25 (−0.02, 0.6)0.41 (0.04, 1.03)0.0020.69 (0.42, 1.1)0.74 (0.42, 1.1)0.9 (0.54, 1.34)0.024
Loss index0.44 (−0.1 5, 1.07)0.28 (−0.02, 0.67)0.25 (0.02, 0.58)0.1710.59 (0.42, 1.01)0.46 (0.26, 0.72)0.37 (0.21, 0.5)<0.0001
  • Data presented are median (25th, 75th percentiles) or mean±standard deviation.

    MLD pre=pre-procedural minimal luminal diameter; MLD post=post-procedural minimal luminal diameter; MLD f-up=minimal luminal diameter at 6-month follow-up; acute gain =MLD post-MLD pre; late loss=MLD post-MLD f-up; loss index=acute gain/late loss; DS pre=pre-procedural diameter stenosis.

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Table 4

Frequency of clinical end-points in descending order of severity

Balloon angioplasty populationStent population
<50%DS pre Embedded Image50–99%DS pre Embedded Image>99%DS pre Embedded Image<50%DS pre Embedded Image50–99%DS pre Embedded Image>99%DS pre Embedded Image
Cardiac death3 (2.4)12 (0.9)0 (0)0 (0)19 (0.9)1 (1)
Non-fatal MI3 (2.4)48 (3.8)0 (0)3 (3.1)79 (3.7)4 (3.8)
Repeat revascularisation (CABGor Re-PCI)23 (18.5)268 (20.7)28 (29.7)18 (18.7)308 (14.5)20 (19.2)
Cardiac death or non-fatal MI6 (4.8)59 (4.6)0 (0)3 (3.1)95 (4.4)5 (4.8)
Cardiac death, non-fatal MI orrepeat revascularisation26 (21)301 (24)28 (29.7)18 (18.7)365 (17)23 (22)
Any event29 (23)328 (26)28 (29.7)21 (22)406 (19)25 (24)
  • MI, acute myocardial infarction; repeat revascularisation includes coronary artery bypass graft (CABG) surgery and percutaneous coronary intervention (PCI). Log–Rank test comparing the three categories of stenosis severity at 1-year was: cardiac death (BA, 3.41; Embedded Image; stent, 0.78; Embedded Image); non-fatal MI (BA, 4.65; Embedded Image; stent, 0.01, Embedded Image) and cardiac death or non-fatal MI (BA, 4.97; Embedded Image; stent, 0.197; Embedded Image). DS pre=pre-procedural diameter stenosis.

Fig. 1

One-year event rate curves for patients treated with balloon angioplasty and varying degrees of stenosis severity measured by QCA. Left: event rate curves for repeat revascularisation (CABG or Re-PCI). Right: event rate curves for death, non-fatal MI or repeat revascularisation (CABG/Re-PCI). <50%DS pre=<50% pre-procedural diameter stenosis; 50–99%DS pre=50–99% pre-procedural diameter stenosis, >99%DS pre=>99% pre-procedural diameter stenosis. QCA=quantitative coronary angiography; MI=myocardial infarction; PCI=percutaneous coronary intervention; CABG=coronary artery bypass graft surgery.

Fig. 2

One-year event rate curves for patients treated with coronary stenting and varying degrees of stenosis severity measured by QCA. Left: event rate curves for repeat revascularisation (CABG or Re-PCI). Right: event rate curves for death, non-fatal MI or repeat revascularisation (CABG/Re-PCI). <50%DS pre=<50% pre-procedural diameter stenosis, 50–99%DS pre=50–99% pre-procedural diameter stenosis, 99%DS pre=>99% pre-procedural diameter stenosis. QCA=quantitative coronary angiography; MI=myocardial infarction; PCI= percutaneous coronary intervention; CABG=coronary artery bypass graft surgery.

Fig. 3

HR for clinical endpoints. HR are shown with 95% CI. HR with upper confidence limits that are less than 1 represent a benefit with the use of coronary stents. Point estimates and CI have been corrected for pre-procedural stenosis severity (<50, 50–99 and >99%DS pre).

3.1 Baseline clinical characteristics

3.1.1 BA group

The three groups of patients with varying degrees of stenosis severity were similar with regard to age, gender, height, weight, history of hypertension, diabetes mellitus, peripheral vascular disease, previous bypass surgery (CABG), smoking status and treated vessel.

Baseline comparisons between the three groups that were statistically different included: history of prior MI, previous PCI and multiple vessel disease (MVD). History of prior MI was more frequent in the <50%DS category, whereas MVD occurred more often in the intermediate and highest categories of stenosis severity. A significant decreasing trend in the percentage of patients with a previous angioplasty was observed in 12.4, 7.5 and 2.4% in the <50, 50–99 and >99%DS categories, respectively (Table 1).

3.1.2 Stent group

The three different groups of patients with varying degrees of stenosis severity were similar with regard to age, gender, height, weight, history of hypertension, diabetes mellitus, peripheral vascular disease, previous PCI, CABG, smoking status and treated vessel. Baseline comparisons between the three groups that were statistically different included: previous MI and a treated lesion located in the LAD. A previous MI was more frequent in the >99%DS category whereas mild lesions where most often treated while located in the LAD (Table 2).

3.2 Baseline, post-procedural and 6-month follow-up QCA

Several angiographic variables were highly correlated with the degree of stenosis severity (Table 3). Lumen and vessel dimensions were smaller as the stenosis severity progressed. The acute gain increases with increasing stenosis severity as does the late loss, but the loss index diminished with increased stenosis severity. A significant and direct relationship between stenosis severity, lesion length and DS>50% at 6-month follow-up was observed across the three categories (<50, 50–99 and >99%DS) for both BA and stented patients.

3.3 Clinical endpoints at 1 year

3.3.1 BA group

The incidence of cardiac death and non-fatal MI was not different between the <50, 50–99 and >99%DS groups (Table 4). Repeat revascularisation (CABG or Re-PCI) occurred in 18.5% of patients in the <50%DS group, 20.7% patients in the 50–99%DS group and 29.7% patients in the >99%DS group (Table 4).

3.3.2 Stent population

The incidence of cardiac death and non-fatal MI did not differ with stenosis severity (Table 4). Repeat revascularisation (CABG or Re-PCI) occurred in 18.7% of patients in the <50%DS group, 14.5% patients in the 50–99%DS group and 19.2% patients in the >99%DS group (Table 4).

3.3.3 Event-rate analysis for BA and stent populations

The log–rank test did not reveal a statistically significant difference in the event-rates over time among the subgroups of increasing stenosis severity (Table 4, Figs. 1 and 2). The primary event rate (cardiac death, death or MI) following BA or stenting of angiographically non-significant stenoses was equivalent to the event rate observed after BA or stenting of angiographically significant stenoses. Irrespective of stenosis severity, death or non-fatal MI at 1 year occurred in nearly 5% of both BA and stent cases. A significant difference (Fig. 3) in favour of coronary stenting (corrected for stenosis severity) was observed with respect to the need for repeat revascularisation (HR 0.80; 95% CI 0.69–0.93) and the combined clinical end-point of cardiac death, non-fatal infarction or repeat revascularisation (HR 0.83; 95% CI 0.72–0.96).

4 Discussion

Our findings indicate that event rate at 1 year is substantial (over 20%) when angiographically non-significant stenoses (<50%DS) are treated by BA or stenting. In fact, the event rate after PCI was not related to stenosis severity. Originally, the concept of plaque sealing was intended to be applied with BA, which is no longer realistic since current practice involves stent implantation in over 70% of PCI procedures.25 Therefore, the concept was extended to the use of stents, hoping this would improve the outcome. Even after implantation of currently available stainless steel stents, the event rate remained as high as 22% at 1 year. The present data argue against the performance of PCI on angiographically non-significant stenoses because high short-term event rates outweigh any hypothetical long-term benefit that might be derived from this type of intervention.

Similar conclusions could be drawn from previously published studies. Based on the Coronary Artery Surgery Study (CASS) registry data,23 the estimated 1-year probability of an anterior MI in LAD lesions with a <50%DS is 0.6% and 2.2% in lesions between 50 and 70%DS. In the present study, the observed non-fatal MI rate after PCI of non-significant stenoses was four- to fivefold greater than the estimated spontaneous risk in the first and two-fold in the latter group.

The first report of BA in mild lesions waspublished 19 years ago by Ischinger et al.4 Patients with chronic stable angina pectoris poorly controlled by previous medical treatment in whom <60%DS were dilated Math were compared with a random sample of patients in whom >60%DS were dilated. After a mean follow-up of 7 months, these investigators cautioned against the application of BA in patients with mildly diseased vessels due to the high incidence of periprocedural MI (6.2% vs 0% in >60%DS, Math) and restenosis (29%).

A decade later, data from Hamon et al.5 provided additional evidence for this point of view. Angiographic outcome from 26 patients in whom dilated lesions were <50%DS Math was disappointing compared to lesions >50%DS Math. When mild stenoses were treated by BA, the DS at follow-up (40%) was the same as the DS prior to BA (42%). No net angiographic benefit was obtained because some non-significant lesions became significant at 6 months.

In the DEFER trial,26 patients with chest pain and an angiographic stenosis but without objective documentation of ischaemia by non-invasive testing, were randomised to deferral or performance of PCI based on the results of the fractional flow reserve (FFR) of the target lesion prior to intervention. Two-year event rates for death, non-fatal MI, and repeat revascularisation were 1.1, 3.3 and 7.8% in the perform group, which was not different from 2.2, 0 and 5.6% in the defer groups. This proved that there is no clinical benefit of PCI for non-significant stenoses at 2 years. It remains possible that a benefit will develop later and that deferred intervention needs to be performed subsequently, thereby reducing the percentage of patients spared the procedure.

The incidence of hard endpoints (cardiac death and MI) is comparable between our series and the performance group of the DEFER trial. The increased rate of repeat revascularisation in our series is due to the fact that protocol-driven angiography was applied in all patients at 6 months.27 This is obvious from Figs. 1 and 2 in which most revascularisation events occurred at 6 months. It has been well documented that when repeatangiography is guided by clinical symptoms rather than per protocol, the rates of repeat revascularisation decrease.18

4.1 Limitations

It should be stressed that the present results were gathered from multiple, high-performance, international sites and that the data collection was performed under rigorous control (common definitions, use of individual case record forms, independent data monitoring and source verification). The observed event rates may still represent a biased underestimation of the results obtainable in the ‘real world’.

In this retrospective analysis, event rates were limited to a 1-year follow-up period. We also lack data from a control group, patients with <50% DS medically treated and followed over time. Furthermore, all these studies were conducted before the introduction of glycoprotein IIb-IIIa inhibitors, which could have decreased event rates in the study groups.

We realize that any potential benefit of plaque sealing will only become evident in the long-term. However, the trade-off between high short-term event rates and long-term benefit appears to be unfavourable. This balance may be reverted with improved procedural and short-term results. The introduction of glycoprotein IIb-IIIa inhibitors has significantly decreased the incidence of non-fatal periprocedural MI.28 Likewise, restenosis could be virtually eliminated in the near future with the use of drug-eluting stents, as suggested by recently published data.29 The evaluation of plaque vulnerability by IVUS imaging30 or temperature measurements31 may help to identify which patients are at increased risk and may benefit the most from mechanical plaque sealing.32 When this new therapeutic armamentarium is at hand, the concept of plaque sealing will need to be revisited and may become clinically viable. Until such evidence eventually becomes available, one should refrain from dilating non-significant stenoses.

5 Conclusion

The concept of plaque sealing is appealing from the theoretical point of view. However, with the currently available technology, its clinical goals (prevention of death and MI in the long-term)cannot be reached because 1-year event rates after PCI of non-significant stenoses still are unacceptably high.

References

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