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Giuseppe G.L. Biondi-Zoccai, Pierfrancesco Agostoni, Giuseppe M. Sangiorgi, Flavio Airoldi, John Cosgrave, Alaide Chieffo, Rossella Barbagallo, Corrado Tamburino, Guido Vittori, Elena Falchetti, Massimo Margheri, Carlo Briguori, Enrico Remigi, Ioannis Iakovou, Antonio Colombo, on behalf of the RECIPE (Real-world Eluting-stent Comparative Italian retrosPective Evaluation) Study Investigators, Incidence, predictors, and outcomes of coronary dissections left untreated after drug-eluting stent implantation, European Heart Journal, Volume 27, Issue 5, March 2006, Pages 540–546, https://doi.org/10.1093/eurheartj/ehi618
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Abstract
Aims Coronary dissections left untreated after percutaneous coronary intervention are associated with unfavourable outcomes. However, their role after drug-eluting stent (DES) implantation is still undescribed. We assessed incidence, predictors, and outcomes of residual dissections in DES-treated lesions.
Methods and results Consecutive patients undergoing DES implantation were enrolled in four Italian centres, with baseline, procedural, and outcome data entered into a dedicated database. Residual dissections were classified according to the National Heart Lung and Blood Institute criteria. End-points of interest were in-hospital, 1-month, and 6-month major adverse cardiovascular events (MACE, i.e. death, myocardial infarction, or target vessel revascularization), and stent thrombosis (ST). Among the 2418 included patients (4630 lesions), a total of 77 (1.7%) final dissections occurred in 67 (2.8%) subjects. Dissections were more frequent in longer and complex lesions and in the left anterior descending, and were associated with increased rates of in-hospital (11.9 vs. 5.2%, P=0.017) and 1-month MACE (13.4 vs. 6.0%, P=0.013), with similar 6-month trends. Cumulative ST was also greater in patients with dissections (6.3 vs. 1.3%, P=0.011). Even non-obstructive dissections with thrombolysis in myocardial infarction 3 flow conferred a significantly worse prognosis.
Conclusion This study, reporting for the first time on incidence, predictors, and outcomes of residual dissections in DES-treated coronary lesions, demonstrates their adverse clinical impact and supports the pursuit of a strategy of sealing dissection flaps with other DES.
See page 503 for the editorial comment on this article (doi:10.1093/eurheartj/ehi681)
Introduction
Residual final dissections left untreated after percutaneous coronary interventions (PCI) are significantly associated with increased short-term risk of major adverse cardiovascular events (MACE).1 This holds true for balloon-only angioplasty, as well as for debulking devices, and bare-metal stents (BMS).1–3 Indeed, flow-limiting dissections occurring during or at the end of the procedure and persisting post-procedurally may be a consequence of extensive vessel trauma and/or lesion complexity and can provide a prothrombotic milieu leading to abrupt vessel closure, thrombosis, with ensuing myocardial ischaemia and necrosis.1 However, the adverse role of minor and non-obstructive post-procedural dissections have been questioned for both in-hospital and mid-to-long term events, including target lesion revascularizations.4–6
In the last few years, drug-eluting stents (DES) have been widely adopted as the most effective antirestenotic strategy in patients undergoing PCI.7 However, doubts have been raised regarding the safety of these devices, especially in the light of anedoctal reports of increased thrombogenicity.8,9 Although the occurrence of final residual dissections may have been reduced in the DES era,10 thanks to gentler pre-dilation techniques, more limited use of debulking devices, and the strategy of deploying the DES ‘from normal to normal’, there is uncertainty on the real impact of such post-procedural dissections after deployment of DES.
Aim of this study was thus to assess incidence, predictors, and outcomes of final dissections after DES implantation.
Methods
Study design, patients, and procedures
The Real-world Eluting-stent Comparative Italian retrosPective Evaluation (RECIPE) was a multicentre retrospective study enrolling all consecutive patients undergoing successful DES implantation at four Italian tertiary care centres between April 2002 and May 2004, including both elective and acute admissions, without any exclusion. By design, the RECIPE study employed dedicated databases for data entry, explicit definitions for baseline and procedural characteristics, independent clinical-event committee-based end-point adjudication, and on-site qualitative and quantitative angiographic analysis. The decision to implant a DES was liberal and at the operator's discretion, although, conversely, patients over 75 years old with acute myocardial infarction (MI) were not treated with DES in any of the participating centres and were thus not enrolled in the study.
At the beginning of the procedure, a bolus of unfractionated heparin was administered at a dose of 70 IU/kg to achieve an activated clotting time ≥250 s. Glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors were used electively or as bail-out at the discretion of the operator. Patients were on life-long aspirin (≥100 mg per day) and were started on oral thienopyridines ≥3 days before elective procedures, with a 300-mg clopidogrel loading dose administered in non-pre-treated patients. All subjects provided written informed consent, the study complied with the Declaration of Helsinki, and explicit Ethics Committee approval was waived at the participating institutions given the non-experimental design of the study. Patients were discharged after the procedure on oral thienopyridines for 6–12 months plus aspirin indefinitely.
Coronary angioplasty and stenting were performed with the aim to fully cover the diseased segment and to accomplish adequate stent expansion.11 In the case of dissection after stent deployment, the recommended management strategy was either to refrain from further percutaneous manoeuvres because the dissection was not associated with impaired epicardial flow or myocardial ischaemia, or to try manage it percutaneously. In this case, operators either tried to deploy further stents to cover the intimal flaps or to perform prolonged balloon inflations for dissection sealing. Whenever dissections were resistant to balloon inflations and stenting approaches were not feasible for lesion characteristics (e.g. due to very distal lesion, calcifications, or vessel tortuosity) or for the impossibility of tracking other DES in place (e.g. bifurcation), dissections were left in place and managed conservatively.
Patients were followed-up by direct check of hospital charts (e.g. in the case of urgent re-hospitalization or elective follow-up angiography), direct patient visit, phone interview, or contact with referring physicians.
Angiographic analysis
Dissections occurring proximally or distally to the deployed DES were adjudicated off-line by an experienced angiographer working in a core angiographic laboratory of the respective participating centre and distinguished as occurring before vs. after stent implantation and/or post-dilation. Guidelines for dissection adjudication were spelled out in the steering phase of the RECIPE study, before the beginning of angiographic analysis and data collection. Only dissections occurring either before or after stent implantation but persisting after the last balloon inflation were adjudicated as ‘final dissections’ and thus assigned to the final dissection group. Conversely, dissections sealed with stents or balloon inflations were considered as non-persistent dissections and were assigned to the no final dissection group.
Residual final dissections were classified according to the National Heart Lung and Blood Institute (NHLBI) criteria: (i) minor radiolucent areas within the coronary lumen during contrast injection, with little or no persistence of contrast after the dye has cleared, (ii) parallel tracts or a double lumen separated by a radiolucent area during contrast injection, with minimal or no persistence after dye clearance, (iii) contrast outside the coronary lumen with persistence of contrast after dye has cleared from the lumen, (iv) spiral luminal filling defects, (v) appearance of a new, persistent filling defects within the coronary lumen, and (vi) dissections leading to total occlusion of the coronary lumen without distal antegrade flow.1,2 Final distal coronary flow was assessed according to the epicardial thrombolysis in myocardial infarction (TIMI) flow classification (from 0 to 3) in patients without persistent dissections and in those with dissections type A–E. Quantitative coronary angiography analysis was performed at baseline and for patients with available angiographic follow-up according to established standards and was conducted in each participating centre in a fashion similar to dissection adjudication and according to pre-specified criteria.12
Follow-up angiography was performed when clinically indicated (i.e. in patients with signs or symptoms of recurrent myocardial ischaemia) or routinely between 4 and 9 months in specified high-risk subsets (unprotected left main, chronic total occlusion, in-stent restenosis).
Clinical end-points
The primary end-point of the analysis was the 1-month hierarchical rate of MACE [i.e. the composite of death, MI, or target vessel revascularization (TVR)]. The secondary end-points were the individual rates of 1-month adverse events, as well as the hierarchical rate of MACE and of its individual components at 6 months. In-hospital MI was assessed in patients without acute MI as admitting diagnosis and distinguished as Q-wave (defined as new pathological Q-waves in ≥2 contiguous ECG leads) vs. non-Q-wave (peak CK>2 times the upper limit of normal together with increased CK-MB mass). We finally assessed the early and mid-term rate of stent thrombosis (ST). Specifically, ST was adjudicated only in the case of angiographically documented intraluminal filling defect within the stent resulting in TIMI grade 0 or 1 anterograde flow associated with clinical symptoms or signs of ischaemia and distinguished as intraprocedural (occurring during the stenting procedure or after sheath removal but before leaving the catheterization laboratory), subacute (occurring ≤30 days but after leaving the catheterization laboratory), or late (>30 days after PCI). All the events were assessed by an independent clinical event committee.
Statistical analysis
Continuous variables are presented as mean±standard deviation, categorical variables as n/N (%), odds ratios as OR, and pertinent 95% confidence intervals as CI. Student's t, Mann–Whitney U, χ2, and Fisher exact tests were computed when appropriate. Exploratory multivariable logistic regression analysis by means of a backward stepwise algorithm (cut-off for entry 0.05, for removal 0.10) was performed to select independent predictors of dissections and to test the adjusted prognostic role of dissections for 1-month MACE (including the variables associated with the occurrence of final dissection at univariate analysis, including direct stenting, final maximum device length, American College of Cardiology/American Heart Association (ACC/AHA) lesion type, chronic total occlusion, calcific lesion, intraprocedural dissection, bifurcation with balloon-only dilation of the side branch, use of GpIIb/IIIa inhibitors, and vessel site). Model assumptions (including linearity of logits and absence of collinearity) were checked by means of graphical inspection and correlation matrixes, respectively, and found to be satisfied. Goodness of fit of the final logistic regression models was assessed with the Hosmer–Lemeshow statistic.13 Internal validation of predictors generated by multivariable logistic regression analysis was performed by means of bootstrapping techniques, with 1000 cycles and generation of OR and bias-corrected 95% CI.14 SPSS 11.0 (SPSS, Chicago, IL, USA), StatsDirect 2.4.4 (StatsDirect, Sale, UK), and Epi-Info 5 (CDC, Atlanta, GA, USA) were used for these calculations. Significance for hypothesis testing was set at the 0.05 two-tailed level.
Results
Among the 2418 patients included in the study, undergoing percutaneous coronary intervention in 4630 lesions, with 1.1±0.5 DES implanted per lesion, a total of 77 (1.7% of all lesions) final persistent dissections occurred in 67 (2.8% of all patients) subjects. Tables 1 and 2 show major baseline and procedural characteristics in patients with vs. those without residual dissections. Dissection type was A in 23 (29.9%) cases, B in 32 (41.6%), C in 11 (14.3%), D in 5 (6.5%), E in 1 (1.3%), and F in 5 (6.5%). Moreover, they were proximal to the DES in 24 (31.7%) cases and distal in 47 (61.0%). Normal distal epicardial flow (i.e. TIMI 3) was present in 61 (80.2%) dissections. Specific reasons for leaving uncovered final dissections as reported by the operators were limited dye staining in the target lesion with normal distal flow (n=42, 54.5%), side branch dissection after balloon-only angioplasty for optimization of bifurcation treatment with provisional T-stenting technique (n=6, 7.8%), or undeliverability of further stents because of distal location or major vessel tortuosity (n=29, 37.7%).
Predictors of final dissections
Overall, final dissections occurred with increased frequency, as expected, in longer and more complex lesions, in the left anterior descending territory, and whenever side branch dilation by means of balloon-only angioplasty was performed. A thorough list of factors associated with the presence of residual dissections is available in Tables 1 and 2. Furthermore, the development of dissection before stenting was strictly associated with a persistent post-procedural dissection (P<0.001) and reduced final TIMI flow (i.e. <3, P<0.001).
Early and mid-term outcomes
One-month follow-up had been completed in 2386 (98.7%) patients and 6-month follow-up in 2342 (96.9%). Angiographic follow-up had been performed in 946 (40.2%) patients, 32 of whom with dissections and 914 without.
Residual dissections were associated with significantly increased rates of in-hospital MACE (11.9 vs. 5.2%, P=0.017) as well as 1-month MACE (13.4 vs. 6.0%, P=0.013), coronary artery bypass grafting (CABG, 3.0 vs. 0.1%, P=0.004), and TVR (4.5 vs. 0.9%, P=0.029). Six-month adverse events also tended to be more frequent in patients with residual dissections, with 18.5 vs. 11.2% MACE (P=0.069). In particular, death rate was three-fold and significantly higher in patients with final dissections (6.0 vs. 2.0%, P=0.043), with angiographically adjudicated subacute ST occurring in one patient and non-sudden cardiac ischaemic death accounting for the remaining three cases. Given the lack of post-mortem assessment, ST was not adjudicated, despite being quite plausible. Conversely, the occurrence of dissections did not seem to exert a detrimental effect on the antirestenotic action of implanted DES, as TVR were similar in the two groups (6.0 vs. 5.2%, P=0.777). Further details are available in Table 3.
The ominous impact of final dissections was demonstrated by a significant increase in the cumulative rate of ST (6.3% in patients with dissections vs. 1.3% in those without, P=0.011), with all of the excess ST occurring either intraprocedurally or within 1 month.
Patients with dissections occurring proximal or distal to the stent had similar rates of adverse events both in-hospital and 1-month follow-up (P>0.05 for all comparisons). The reasons for leaving uncovered final dissections, as reported by the operators, were not significantly associated with in-hospital or post-discharge adverse events (P>0.05), probably because of the relative small sample for this subgroup analysis (with the inherent risk of alpha error).
Finally, even non-obstructive dissections with normal (i.e. TIMI 3) distal flow carried an enhanced risk of adverse events, as testified by the comparison of the 49 patients with such apparently benign final dissections vs. those without dissections (1-month MACE 12.2 vs. 5.2%, P=0.043 and cumulative ST 8.1 vs. 0.9%, P=0.001). Similar findings were disclosed by subgroup analysis restricted to patients with type A or B final dissections in large vessels with normal flow (n=42), as such dissections were also associated with strong trends towards increased 1-month rates of major adverse events [5 (11.9%) vs. 142 (6.0%), P=0.11] and TLR [2 (5.0%) vs. 20 (0.9%), P=0.055]. The small number of events with the ensuing limited statistical power, however, limits the robustness of these results.
Angiographic follow-up [available for 38 (49.4%) of the 77 original final dissections] disclosed complete healing in 24 (63.2%), improvement of dissections in 7 (18.4%), and persistence in 6 (15.8%), with only one case (2.6%) of late worsening. Indeed, this was a patient with post-rotablator dissection in a mid-right coronary artery, persisting at the distal edge of a Cypher stent as a type C dissection. At angiographic follow-up after 9 months, performed for atypical chest pain in the absence of major adverse events, the dissection was still apparent and was graded as type E. Results of this angiographic follow-up subanalysis should however be viewed with caution, given low rate of angiographic follow-up and the lack of intravascular ultrasound (IVUS) assessment.
Exploratory multivariable analysis
Multivariable logistic regression analysis identified the presence of moderate-to-severe coronary calcification (OR=1.93, 95% CI=1.06–3.5, P=0.032) and maximum balloon length, a proxy for lesion length and atherosclerotic burden (related to the presence of diffuse disease or tandem lesions) (OR=1.03, CI=1.01–1.05, P<0.001 for each millimetre), as independent predictors of the occurrence of final dissections.
Logistic regression to test the independent predictive role of final dissections on the occurrence of 1-month MACE, and including in the backwards stepwise algorithm target vessel, revascularization technique (stenting vs. balloon-only), stenting technique (direct vs. with pre-dilation), maximum balloon length, occurrence of dissection before stenting, American College of Cardiology/American Heart Association lesion type, use of GpIIb/IIIa inhibitors, and whether the lesion was calcific or a chronic total occlusion, showed that the presence of a residual final dissection maintained an independent predictor ability for early events (OR=2.9, CI=1.36–6.1, P=0.005). Internal validation of such multivariable analysis by means of bootstrapping, including the same variables of the standard logistic regression model, further confirmed the significant predictive of final dissections (bootstrap OR=2.9, 95% bias-corrected 95% CI=1.09–5.6). Finally, both logistic regression models appeared in adequate fit with the data, as testified by Hosmer–Lemeshow statistics (P=0.791 and P=0.921, respectively).
Discussion
This study, reporting for the first time on the incidence, occurrence, and outcomes of final residual dissections after DES implantation, confirms the detrimental clinical impact of this procedural complication, as testified by the significantly increased rate of early and mid-term adverse events. Thus, it provides compelling data in support of a strategy of managing residual dissections until they are completely sealed, e.g. by prolonged balloon inflations or additional stent implantation.
Coronary dissections occur frequently after balloon dilation of coronary atherosclerotic plaques (e.g. in 32.4% of 2133 procedures performed in the pre-stent era)15 and should be considered not only as a complication,16 but also as part of the therapeutic mechanism of coronary angioplasty.17 Indeed, plaque fracture and tearing are critical in plaque redistribution and reduction of elastic recoil, as well as in later positive coronary remodelling.18 However, plaque disruption with exposure of its prothrombotic milieu and concomitant intimal flaps may promote thrombosis and distal embolization or even impair distal flow directly when large dissections are present. These pathophysiological data underlie the association between angiographically evident coronary dissections and adverse clinical outcomes. This relationship has been well known since the beginning of interventional cardiology and holds true in the balloon-only era as well in the BMS and debulking device era, even if mechanisms and impact of dissections vary obviously according to the ethiological mechanism.16,19,20 In fact, persistent dissections after BMS are significantly associated (OR=3.8, CI=1.9–7.7) with the occurrence of subacute ST.20 Dissections do not seem, conversely, to increase restenosis after PCI, and Cappelletti et al.6 showed that benign non-occlusive (type A–D) dissections after balloon-only angioplasty were associated with a significantly decreased risk of restenosis (P<0.001) and apparently favourable clinical outcomes. IVUS also demonstrated that minor dissections occurring at the edge of BMS do not seem to increase the risk of restenosis.4,5 However, the detrimental clinical role of final dissections on major adverse thrombotic events such as ST has been confirmed by systematic IVUS studies in the BMS era, even in the presence of optimal antiplatelet therapy.21
Coronary dissections in the DES era
The occurrence of dissections after DES implantation is incompletely characterized, and to date, no study has reported specific data concerning their incidence, predictors, or prognosis. Any comparison to other evidence-based data is thus impossible. Nonetheless, residual dissections next to implanted DES have the potential to cause slow or turbulent flow and platelet activation, thus predisposing to ST, with its ominous consequences.22 Some preliminary reports have provided insights into the increased occurrence of ST in the DES era, both acutely and in the mid-to-long term.8,9,23
Although the interplay between the potential prothrombotic role of DES and dissections is still unclear, several studies have investigated the presence and outcome of dissections in coronary lesions treated with brachytherapy. Indeed, coronary radiation therapy for the prevention or treatment of restenosis may provide important information on the natural history of coronary dissections in lesions where repair and scarring mechanisms are impaired similar to DES-treated lesions. Specifically, Kay et al.24 have shown that after intracoronary beta radiation, healing of coronary dissections is impaired in certain individuals (from 16 post-procedural dissections to eight unhealed dissections at 6-month follow-up). McClean et al.25 also provided anecdotic evidence of delayed healing of a dissection after intracoronary radiation at 6-month angiographic follow-up, which yielded to significant restenosis 14 months after the index procedure. These data have been largely discussed and might provide, at least in part, an explanation for the persistent long-term risk of ST after coronary brachytherapy.
The extent to which delayed healing and re-endothelialization affect also post-DES coronary dissections is however unclear and should be the specific focus of future pathological and IVUS studies. Intriguingly, delayed re-endothelialization of stent struts and local inflammatory reactions after DES implantation have been described and might have a synergistic detrimental effect with the prothrombotic role of intimal flaps.26,27
Given the previous evidence on the role of dissections in the bare-metal and brachytherapy era, our findings appear broadly concordant with previous evidence on their clinical detrimental role. Dissections in BMS were associated with ST with an OR of 3.8, quite similar to the 2.9 OR for 1-month MACE found in the present analysis.20 However, other factors may as well be considered of relevance in the DES era. Despite the improvements in adjunctive medical therapy (i.e. GpIIb/IIIa inhibition and long-term thienopyridine use), the pattern of patients undergoing coronary revascularization has dramatically changed. This is testified by the inclusion of complex lesion and patient subsets in the present study, including unprotected left main, acute MI, and chronic total occlusions, among the others. Indeed, our findings show that final dissections in DES-treated lesions are associated with unfavourable events both early and at mid-term follow-up. Such adverse events are likely to stem from coronary thrombosis, either in-stent or peri-stent, eventually leading to death, non-fatal MI, urgent TVR, or bypass grafting. This detrimental impact of final dissections is probably due to the greater patient and lesion complexity pattern in the DES era. However, given the non-experimental design and the inherent risk of confounding, the clustering of several unfavourable risk factors in the same patients experiencing final dissections cannot be excluded. Indeed, patients with coronary dissections represent a small but very high-risk group of subjects, with many additional problems and risk-factors, both present and acquired during the procedure, which may contribute to the increased adverse event rate and likely to complicate any mechanistic analysis.
Management strategies for coronary dissections have not been a specific aim of controlled clinical studies, to date, and thus any recommendation can only be based on indirect evidence or expert opinion. However, many authorities have suggested that whenever a dissection cannot be sealed by means of stents or prolonged balloon inflations, maximal medical therapy should be enforced (including GpIIb/IIIa inhibitors and/or anticoagulants) and CABG be considered in the case of impaired TIMI flow in a proximal lesion or refractory myocardial ischaemia.1 Such recommendations probably hold true even in the DES era. Nonetheless, considering the propensity for edge (<5 mm) or more distal restenosis near deployed DES whenever lesions are treated with balloon-only angioplasty, and the high risk of ST if thienopyridines are withheld in the case of CABG, we suggest that every effort should be enforced to deploy further DES in order to completely seal a coronary dissection occurring in or near a DES-treated lesion, and to prolong double antiplatelet treatment for several months (>6) after discharge. Nonetheless, other potentially useful interventions to be considered in the light of the individual risk-benefit balance include double-dose clopidogrel and/or additional antiplatelet treatment with trapidil in addition to bailout GpIIb/IIIa inhibitors.
Finally, the role of IVUS in better defining the management of dissections should not be dismissed. Although angiography has a very limited discriminatory power in identifying low-risk dissections, an IVUS cross-sectional area >4.5 mm2 or >70% of the reference vessel cross-sectional area should be considered a reliable hint that the index dissection is not likely to bear adverse consequences.28 Unfortunately, cost and logistic hurdles obviously limit the scientific testing and clinical application of this strategy.
Limitations of the present study
Drawbacks of this work are inherent to any non-experimental and retrospective study and include selection bias, adjudication bias, and confounding.29 While we tried to address these potential sources of systematic error by systematic data entry, independent event adjudication, and thorough univariate and multivariable analyses, the risk of persistent underlying bias should be borne in mind. However, dissections are quite uncommon and logistic, technical, but especially ethical issues would likely make unfeasible any randomized controlled trial concerning their optimal management. Moreover, the non-systematic angiographic follow-up and the inherent risk of overestimating restenosis undermine the relevance of the 6-month quantitative angiographic analysis, which should be viewed with caution and as exploratory only. Concerning the specific limitations of internal validation of predictive models, we have tried to confirm the reliability of our analysis by means of bootstrap resampling.14 However, the limitations of this approach should be borne in mind while awaiting further independent external validating studies.30
Conclusions
Dissections left untreated after DES implantation may have a major adverse clinical impact at both early and mid-term follow-up. Thus, given that more and more complex lesions, with their inherent risk of thrombosis, are currently being treated with DES, and the continuing difficulty for angiography to well evaluate if a dissection is benign or not, while awaiting further prospective and validation studies, these novel findings should prompt interventionalists to pursue a strategy of managing residual dissections in DES-treated lesions by completely covering intimal flaps with additional stents.
Acknowledgement
Funding for the overall RECIPE study was provided by Cordis Italia, Milan, Italy.
Conflict of interest: none declared.
This study was presented as an abstract at the 2005 Congress of the Italian Society of Invasive Cardiology, Genoa, Italy, where G.G.L.B.-Z. won the 1st Young Investigator Award.
Baseline and clinical characteristicsa
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patient | n=67 | n=2351 | |
| Age (years) | 62.3±9.9 | 62.6±10.5 | 0.811 |
| Male (%) | 61 (91.0) | 1949 (82.9) | 0.079 |
| Diabetes mellitus (%) | 17 (25.3) | 647 (27.5) | 0.405 |
| Hypertension (%) | 42 (62.7) | 1470 (62.5) | 0.979 |
| Dyslipidaemia (%) | 41 (61.2) | 1421 (60.4) | 0.901 |
| Current smoke (%) | 11 (16.4) | 469 (19.9) | 0.475 |
| Previous MI (%) | 32 (47.8) | 1023 (43.5) | 0.489 |
| Previous bypass surgery (%) | 7 (10.4) | 400 (17.0) | 0.157 |
| Previous PCI (%) | 11 (16.4) | 506 (21.5) | 0.315 |
| Stable angina (%) | 26 (38.8) | 852 (36.2) | 0.667 |
| Multivessel disease (%) | 48 (71.6) | 1702 (72.4) | 0.892 |
| Ejection fraction (%) | 50.3±11.6 | 52.2±10.2 | 0.174 |
| Target vessel (%) | 0.011 | ||
| LAD (%) | 47 (70.1) | 1162 (49.4) | |
| LCX (%) | 9 (13.4) | 489 (20.8) | |
| RCA (%) | 10 (14.9) | 462 (19.7) | |
| GpIIb/IIIa inhibitors (%) | 26 (38.8) | 570 (24.2) | 0.007 |
| Elective (%) | 17 (25.4) | 543 (23.1) | 0.663 |
| Bailout (%) | 9 (13.4) | 27 (1.1) | <0.001 |
| Double antiplatelet therapy at discharge (%) | 66 (98.5) | 2341 (99.6) | 0.266 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patient | n=67 | n=2351 | |
| Age (years) | 62.3±9.9 | 62.6±10.5 | 0.811 |
| Male (%) | 61 (91.0) | 1949 (82.9) | 0.079 |
| Diabetes mellitus (%) | 17 (25.3) | 647 (27.5) | 0.405 |
| Hypertension (%) | 42 (62.7) | 1470 (62.5) | 0.979 |
| Dyslipidaemia (%) | 41 (61.2) | 1421 (60.4) | 0.901 |
| Current smoke (%) | 11 (16.4) | 469 (19.9) | 0.475 |
| Previous MI (%) | 32 (47.8) | 1023 (43.5) | 0.489 |
| Previous bypass surgery (%) | 7 (10.4) | 400 (17.0) | 0.157 |
| Previous PCI (%) | 11 (16.4) | 506 (21.5) | 0.315 |
| Stable angina (%) | 26 (38.8) | 852 (36.2) | 0.667 |
| Multivessel disease (%) | 48 (71.6) | 1702 (72.4) | 0.892 |
| Ejection fraction (%) | 50.3±11.6 | 52.2±10.2 | 0.174 |
| Target vessel (%) | 0.011 | ||
| LAD (%) | 47 (70.1) | 1162 (49.4) | |
| LCX (%) | 9 (13.4) | 489 (20.8) | |
| RCA (%) | 10 (14.9) | 462 (19.7) | |
| GpIIb/IIIa inhibitors (%) | 26 (38.8) | 570 (24.2) | 0.007 |
| Elective (%) | 17 (25.4) | 543 (23.1) | 0.663 |
| Bailout (%) | 9 (13.4) | 27 (1.1) | <0.001 |
| Double antiplatelet therapy at discharge (%) | 66 (98.5) | 2341 (99.6) | 0.266 |
LAD, left anterior descending; LCX, left circumflex; RCA, right coronary artery.
aExpressed as n (%) or mean±standard deviation.
Baseline and clinical characteristicsa
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patient | n=67 | n=2351 | |
| Age (years) | 62.3±9.9 | 62.6±10.5 | 0.811 |
| Male (%) | 61 (91.0) | 1949 (82.9) | 0.079 |
| Diabetes mellitus (%) | 17 (25.3) | 647 (27.5) | 0.405 |
| Hypertension (%) | 42 (62.7) | 1470 (62.5) | 0.979 |
| Dyslipidaemia (%) | 41 (61.2) | 1421 (60.4) | 0.901 |
| Current smoke (%) | 11 (16.4) | 469 (19.9) | 0.475 |
| Previous MI (%) | 32 (47.8) | 1023 (43.5) | 0.489 |
| Previous bypass surgery (%) | 7 (10.4) | 400 (17.0) | 0.157 |
| Previous PCI (%) | 11 (16.4) | 506 (21.5) | 0.315 |
| Stable angina (%) | 26 (38.8) | 852 (36.2) | 0.667 |
| Multivessel disease (%) | 48 (71.6) | 1702 (72.4) | 0.892 |
| Ejection fraction (%) | 50.3±11.6 | 52.2±10.2 | 0.174 |
| Target vessel (%) | 0.011 | ||
| LAD (%) | 47 (70.1) | 1162 (49.4) | |
| LCX (%) | 9 (13.4) | 489 (20.8) | |
| RCA (%) | 10 (14.9) | 462 (19.7) | |
| GpIIb/IIIa inhibitors (%) | 26 (38.8) | 570 (24.2) | 0.007 |
| Elective (%) | 17 (25.4) | 543 (23.1) | 0.663 |
| Bailout (%) | 9 (13.4) | 27 (1.1) | <0.001 |
| Double antiplatelet therapy at discharge (%) | 66 (98.5) | 2341 (99.6) | 0.266 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patient | n=67 | n=2351 | |
| Age (years) | 62.3±9.9 | 62.6±10.5 | 0.811 |
| Male (%) | 61 (91.0) | 1949 (82.9) | 0.079 |
| Diabetes mellitus (%) | 17 (25.3) | 647 (27.5) | 0.405 |
| Hypertension (%) | 42 (62.7) | 1470 (62.5) | 0.979 |
| Dyslipidaemia (%) | 41 (61.2) | 1421 (60.4) | 0.901 |
| Current smoke (%) | 11 (16.4) | 469 (19.9) | 0.475 |
| Previous MI (%) | 32 (47.8) | 1023 (43.5) | 0.489 |
| Previous bypass surgery (%) | 7 (10.4) | 400 (17.0) | 0.157 |
| Previous PCI (%) | 11 (16.4) | 506 (21.5) | 0.315 |
| Stable angina (%) | 26 (38.8) | 852 (36.2) | 0.667 |
| Multivessel disease (%) | 48 (71.6) | 1702 (72.4) | 0.892 |
| Ejection fraction (%) | 50.3±11.6 | 52.2±10.2 | 0.174 |
| Target vessel (%) | 0.011 | ||
| LAD (%) | 47 (70.1) | 1162 (49.4) | |
| LCX (%) | 9 (13.4) | 489 (20.8) | |
| RCA (%) | 10 (14.9) | 462 (19.7) | |
| GpIIb/IIIa inhibitors (%) | 26 (38.8) | 570 (24.2) | 0.007 |
| Elective (%) | 17 (25.4) | 543 (23.1) | 0.663 |
| Bailout (%) | 9 (13.4) | 27 (1.1) | <0.001 |
| Double antiplatelet therapy at discharge (%) | 66 (98.5) | 2341 (99.6) | 0.266 |
LAD, left anterior descending; LCX, left circumflex; RCA, right coronary artery.
aExpressed as n (%) or mean±standard deviation.
Procedural and angiographic characteristics according to the presence vs. absence of post-procedural coronary dissectiona
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Lesions | n=77 | n=4630 | |
| In-stent restenosis (%) | 9 (11.7) | 451 (9.7) | 0.568 |
| Chronic total occlusion (%) | 11 (14.3) | 242 (5.2) | <0.001 |
| Calcification (%) | 20 (30.0) | 632 (13.7) | 0.002 |
| Thrombus (%) | 6 (7.8) | 303 (6.5) | 0.661 |
| Bifurcation (%) | 19 (24.7) | 1074 (23.2) | 0.761 |
| ACC/AHA lesion type B2 or C (%) | 34 (44.2) | 1309 (28.3) | 0.002 |
| Maximum dilation pressure (ATM) | 14.5±3.1 | 15.0±3.4 | 0.247 |
| Maximum balloon diameter (mm)b | 2.86±0.41 | 2.94±0.41 | 0.094 |
| Maximum balloon length (mm) | 28.6±13.7 | 23.6±10.0 | <0.001 |
| Directional atherectomy (%) | 0 | 50 (1.1) | 1.0 |
| Cutting balloon (%) | 1 (1.3) | 25 (0.5) | 0.350 |
| Direct stenting (%) | 4 (5.2) | 700 (15.1) | 0.015 |
| Post-dilation (%) | 9 (11.7) | 792 (17.1) | 0.210 |
| Sirolimus eluting stent (%) | 42 (54.5) | 2368 (51.1) | 0.714 |
| Paclitaxel eluting stent (%) | 29 (37.7) | 2063 (44.6) | 0.151 |
| Side-branch lesion with balloon-only dilation (%) | 6 (7.8) | 199 (4.3) | 0.019 |
| Intravascular ultrasound (%) | 7 (9.1) | 427 (9.2) | 0.968 |
| Dissection before stenting (%) | 50 (64.9) | 97 (2.1) | <0.001 |
| Final NHLBI dissection type | |||
| A (%) | 23 (29.9 | — | |
| B (%) | 32 (41.6) | — | |
| C (%) | 11 (14.3) | — | |
| D (%) | 5 (6.5) | — | |
| E (%) | 1 (1.3) | — | |
| F (%) | 5 (6.5) | — | |
| Final TIMI flow <3 (%) | 16 (20.8) | 65 (1.4) | <0.001 |
| Pre-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.60±0.54 | 2.69±0.55 | 0.230 |
| Minimum lumen diameter (mm) | 0.61±0.53 | 0.87±0.50 | 0.001 |
| Diameter stenosis (%) | 79±17 | 71±17 | <0.001 |
| Lesion length (mm) | 19.0±14.4 | 16.1±11.1 | 0.041 |
| Post-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.94±0.46 | 3.03±0.52 | 0.260 |
| Minimum lumen diameter (mm) | 2.59±0.46 | 2.71±0.52 | 0.075 |
| Diameter stenosis (mm) | 13±10 | 11±8 | 0.193 |
| 6-month angiographic follow-upc | |||
| Reference vessel diameter (mm) | 3.02±0.43 | 3.12±0.58 | 0.527 |
| Minimum lumen diameter (mm) | 2.01±1.18 | 2.33±1.10 | 0.257 |
| Diameter stenosis (%) | 34±36 | 27±26 | 0.307 |
| Binary angiographic restenosis (%) | 7 (21.9) | 177 (19.4) | 0.724 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Lesions | n=77 | n=4630 | |
| In-stent restenosis (%) | 9 (11.7) | 451 (9.7) | 0.568 |
| Chronic total occlusion (%) | 11 (14.3) | 242 (5.2) | <0.001 |
| Calcification (%) | 20 (30.0) | 632 (13.7) | 0.002 |
| Thrombus (%) | 6 (7.8) | 303 (6.5) | 0.661 |
| Bifurcation (%) | 19 (24.7) | 1074 (23.2) | 0.761 |
| ACC/AHA lesion type B2 or C (%) | 34 (44.2) | 1309 (28.3) | 0.002 |
| Maximum dilation pressure (ATM) | 14.5±3.1 | 15.0±3.4 | 0.247 |
| Maximum balloon diameter (mm)b | 2.86±0.41 | 2.94±0.41 | 0.094 |
| Maximum balloon length (mm) | 28.6±13.7 | 23.6±10.0 | <0.001 |
| Directional atherectomy (%) | 0 | 50 (1.1) | 1.0 |
| Cutting balloon (%) | 1 (1.3) | 25 (0.5) | 0.350 |
| Direct stenting (%) | 4 (5.2) | 700 (15.1) | 0.015 |
| Post-dilation (%) | 9 (11.7) | 792 (17.1) | 0.210 |
| Sirolimus eluting stent (%) | 42 (54.5) | 2368 (51.1) | 0.714 |
| Paclitaxel eluting stent (%) | 29 (37.7) | 2063 (44.6) | 0.151 |
| Side-branch lesion with balloon-only dilation (%) | 6 (7.8) | 199 (4.3) | 0.019 |
| Intravascular ultrasound (%) | 7 (9.1) | 427 (9.2) | 0.968 |
| Dissection before stenting (%) | 50 (64.9) | 97 (2.1) | <0.001 |
| Final NHLBI dissection type | |||
| A (%) | 23 (29.9 | — | |
| B (%) | 32 (41.6) | — | |
| C (%) | 11 (14.3) | — | |
| D (%) | 5 (6.5) | — | |
| E (%) | 1 (1.3) | — | |
| F (%) | 5 (6.5) | — | |
| Final TIMI flow <3 (%) | 16 (20.8) | 65 (1.4) | <0.001 |
| Pre-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.60±0.54 | 2.69±0.55 | 0.230 |
| Minimum lumen diameter (mm) | 0.61±0.53 | 0.87±0.50 | 0.001 |
| Diameter stenosis (%) | 79±17 | 71±17 | <0.001 |
| Lesion length (mm) | 19.0±14.4 | 16.1±11.1 | 0.041 |
| Post-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.94±0.46 | 3.03±0.52 | 0.260 |
| Minimum lumen diameter (mm) | 2.59±0.46 | 2.71±0.52 | 0.075 |
| Diameter stenosis (mm) | 13±10 | 11±8 | 0.193 |
| 6-month angiographic follow-upc | |||
| Reference vessel diameter (mm) | 3.02±0.43 | 3.12±0.58 | 0.527 |
| Minimum lumen diameter (mm) | 2.01±1.18 | 2.33±1.10 | 0.257 |
| Diameter stenosis (%) | 34±36 | 27±26 | 0.307 |
| Binary angiographic restenosis (%) | 7 (21.9) | 177 (19.4) | 0.724 |
QCA, quantitative coronary angiography.
aExpressed as n (%) or mean±standard deviation.
bFor the balloon-expandable stent system or the post-dilation balloon (when applicable).
cGiven the non-systematic angiographic follow-up and the inherent risk of overestimating restenosis, the 6-month angiographic analysis is merely comparative and absolute figures should be viewed with caution.
Procedural and angiographic characteristics according to the presence vs. absence of post-procedural coronary dissectiona
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Lesions | n=77 | n=4630 | |
| In-stent restenosis (%) | 9 (11.7) | 451 (9.7) | 0.568 |
| Chronic total occlusion (%) | 11 (14.3) | 242 (5.2) | <0.001 |
| Calcification (%) | 20 (30.0) | 632 (13.7) | 0.002 |
| Thrombus (%) | 6 (7.8) | 303 (6.5) | 0.661 |
| Bifurcation (%) | 19 (24.7) | 1074 (23.2) | 0.761 |
| ACC/AHA lesion type B2 or C (%) | 34 (44.2) | 1309 (28.3) | 0.002 |
| Maximum dilation pressure (ATM) | 14.5±3.1 | 15.0±3.4 | 0.247 |
| Maximum balloon diameter (mm)b | 2.86±0.41 | 2.94±0.41 | 0.094 |
| Maximum balloon length (mm) | 28.6±13.7 | 23.6±10.0 | <0.001 |
| Directional atherectomy (%) | 0 | 50 (1.1) | 1.0 |
| Cutting balloon (%) | 1 (1.3) | 25 (0.5) | 0.350 |
| Direct stenting (%) | 4 (5.2) | 700 (15.1) | 0.015 |
| Post-dilation (%) | 9 (11.7) | 792 (17.1) | 0.210 |
| Sirolimus eluting stent (%) | 42 (54.5) | 2368 (51.1) | 0.714 |
| Paclitaxel eluting stent (%) | 29 (37.7) | 2063 (44.6) | 0.151 |
| Side-branch lesion with balloon-only dilation (%) | 6 (7.8) | 199 (4.3) | 0.019 |
| Intravascular ultrasound (%) | 7 (9.1) | 427 (9.2) | 0.968 |
| Dissection before stenting (%) | 50 (64.9) | 97 (2.1) | <0.001 |
| Final NHLBI dissection type | |||
| A (%) | 23 (29.9 | — | |
| B (%) | 32 (41.6) | — | |
| C (%) | 11 (14.3) | — | |
| D (%) | 5 (6.5) | — | |
| E (%) | 1 (1.3) | — | |
| F (%) | 5 (6.5) | — | |
| Final TIMI flow <3 (%) | 16 (20.8) | 65 (1.4) | <0.001 |
| Pre-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.60±0.54 | 2.69±0.55 | 0.230 |
| Minimum lumen diameter (mm) | 0.61±0.53 | 0.87±0.50 | 0.001 |
| Diameter stenosis (%) | 79±17 | 71±17 | <0.001 |
| Lesion length (mm) | 19.0±14.4 | 16.1±11.1 | 0.041 |
| Post-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.94±0.46 | 3.03±0.52 | 0.260 |
| Minimum lumen diameter (mm) | 2.59±0.46 | 2.71±0.52 | 0.075 |
| Diameter stenosis (mm) | 13±10 | 11±8 | 0.193 |
| 6-month angiographic follow-upc | |||
| Reference vessel diameter (mm) | 3.02±0.43 | 3.12±0.58 | 0.527 |
| Minimum lumen diameter (mm) | 2.01±1.18 | 2.33±1.10 | 0.257 |
| Diameter stenosis (%) | 34±36 | 27±26 | 0.307 |
| Binary angiographic restenosis (%) | 7 (21.9) | 177 (19.4) | 0.724 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Lesions | n=77 | n=4630 | |
| In-stent restenosis (%) | 9 (11.7) | 451 (9.7) | 0.568 |
| Chronic total occlusion (%) | 11 (14.3) | 242 (5.2) | <0.001 |
| Calcification (%) | 20 (30.0) | 632 (13.7) | 0.002 |
| Thrombus (%) | 6 (7.8) | 303 (6.5) | 0.661 |
| Bifurcation (%) | 19 (24.7) | 1074 (23.2) | 0.761 |
| ACC/AHA lesion type B2 or C (%) | 34 (44.2) | 1309 (28.3) | 0.002 |
| Maximum dilation pressure (ATM) | 14.5±3.1 | 15.0±3.4 | 0.247 |
| Maximum balloon diameter (mm)b | 2.86±0.41 | 2.94±0.41 | 0.094 |
| Maximum balloon length (mm) | 28.6±13.7 | 23.6±10.0 | <0.001 |
| Directional atherectomy (%) | 0 | 50 (1.1) | 1.0 |
| Cutting balloon (%) | 1 (1.3) | 25 (0.5) | 0.350 |
| Direct stenting (%) | 4 (5.2) | 700 (15.1) | 0.015 |
| Post-dilation (%) | 9 (11.7) | 792 (17.1) | 0.210 |
| Sirolimus eluting stent (%) | 42 (54.5) | 2368 (51.1) | 0.714 |
| Paclitaxel eluting stent (%) | 29 (37.7) | 2063 (44.6) | 0.151 |
| Side-branch lesion with balloon-only dilation (%) | 6 (7.8) | 199 (4.3) | 0.019 |
| Intravascular ultrasound (%) | 7 (9.1) | 427 (9.2) | 0.968 |
| Dissection before stenting (%) | 50 (64.9) | 97 (2.1) | <0.001 |
| Final NHLBI dissection type | |||
| A (%) | 23 (29.9 | — | |
| B (%) | 32 (41.6) | — | |
| C (%) | 11 (14.3) | — | |
| D (%) | 5 (6.5) | — | |
| E (%) | 1 (1.3) | — | |
| F (%) | 5 (6.5) | — | |
| Final TIMI flow <3 (%) | 16 (20.8) | 65 (1.4) | <0.001 |
| Pre-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.60±0.54 | 2.69±0.55 | 0.230 |
| Minimum lumen diameter (mm) | 0.61±0.53 | 0.87±0.50 | 0.001 |
| Diameter stenosis (%) | 79±17 | 71±17 | <0.001 |
| Lesion length (mm) | 19.0±14.4 | 16.1±11.1 | 0.041 |
| Post-procedural QCA analysis | |||
| Reference vessel diameter (mm) | 2.94±0.46 | 3.03±0.52 | 0.260 |
| Minimum lumen diameter (mm) | 2.59±0.46 | 2.71±0.52 | 0.075 |
| Diameter stenosis (mm) | 13±10 | 11±8 | 0.193 |
| 6-month angiographic follow-upc | |||
| Reference vessel diameter (mm) | 3.02±0.43 | 3.12±0.58 | 0.527 |
| Minimum lumen diameter (mm) | 2.01±1.18 | 2.33±1.10 | 0.257 |
| Diameter stenosis (%) | 34±36 | 27±26 | 0.307 |
| Binary angiographic restenosis (%) | 7 (21.9) | 177 (19.4) | 0.724 |
QCA, quantitative coronary angiography.
aExpressed as n (%) or mean±standard deviation.
bFor the balloon-expandable stent system or the post-dilation balloon (when applicable).
cGiven the non-systematic angiographic follow-up and the inherent risk of overestimating restenosis, the 6-month angiographic analysis is merely comparative and absolute figures should be viewed with caution.
Univariate analysis of in-hospital, 1-month, and 6-month events according to the presence vs. absence of post-procedural coronary dissection.a
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patients | n=67 | n=2351 | |
| In-hospital events | |||
| Major adverse cardiovascular events (%) | 8 (11.9) | 123 (5.2) | 0.017 |
| Death (%) | 2 (3.0) | 13 (0.6) | 0.063 |
| Myocardial infarction (%) | 4 (6.0) | 102 (4.4) | 0.536 |
| Q-wave (%) | 0 | 2 (0.1) | 1.0 |
| Non-Q-wave (%) | 4 (6.0) | 100 (4.3) | 0.521 |
| Coronary artery bypass grafting | 2 (3.0) | 1 (0.1) | 0.002 |
| Repeat percutaneous revascularization (%) | 1 (0.6) | 14 (0.6) | 0.345 |
| 1-month follow-up | |||
| Major adverse cardiovascular events (%) | 9 (13.4) | 142 (6.0) | 0.013 |
| Death (%) | 2 (3.0) | 26 (1.1) | 0.176 |
| Myocardial infarction (%) | 4 (6.0) | 109 (4.6) | 0.552 |
| Q-wave (%) | 0 | 7 (0.3) | 1.00 |
| Non-Q-wave (%) | 4 (6.0) | 102 (4.3) | 0.536 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 2 (0.1) | 0.004 |
| Target vessel revascularization (%) | 3 (4.5) | 22 (0.9) | 0.029 |
| 6-month follow-up | |||
| Major adverse cardiovascular events (%) | 12 (18.5) | 255 (11.2) | 0.069 |
| Death (%) | 4 (6.3) | 45 (2.0) | 0.043 |
| Myocardial infarction (%) | 6 (9.0) | 116 (4.9) | 0.140 |
| Q-wave (%) | 1 (1.5) | 9 (0.4) | 0.245 |
| Non-Q-wave (%) | 5 (7.5) | 107 (4.6) | 0.236 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 12 (0.5) | 0.054 |
| Target vessel revascularization (%) | 4 (6.2) | 124 (5.5) | 0.779 |
| Stent thrombosis | |||
| Intraprocedural (%) | 2 (3.0) | 8 (0.3) | 0.030 |
| Subacute (%) | 2 (3.1) | 13 (0.6) | 0.062 |
| Late (%) | 0 | 7 (0.3) | 1.0 |
| Cumulative 6-month rate (%) | 4 (6.3) | 28 (1.3) | 0.011 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patients | n=67 | n=2351 | |
| In-hospital events | |||
| Major adverse cardiovascular events (%) | 8 (11.9) | 123 (5.2) | 0.017 |
| Death (%) | 2 (3.0) | 13 (0.6) | 0.063 |
| Myocardial infarction (%) | 4 (6.0) | 102 (4.4) | 0.536 |
| Q-wave (%) | 0 | 2 (0.1) | 1.0 |
| Non-Q-wave (%) | 4 (6.0) | 100 (4.3) | 0.521 |
| Coronary artery bypass grafting | 2 (3.0) | 1 (0.1) | 0.002 |
| Repeat percutaneous revascularization (%) | 1 (0.6) | 14 (0.6) | 0.345 |
| 1-month follow-up | |||
| Major adverse cardiovascular events (%) | 9 (13.4) | 142 (6.0) | 0.013 |
| Death (%) | 2 (3.0) | 26 (1.1) | 0.176 |
| Myocardial infarction (%) | 4 (6.0) | 109 (4.6) | 0.552 |
| Q-wave (%) | 0 | 7 (0.3) | 1.00 |
| Non-Q-wave (%) | 4 (6.0) | 102 (4.3) | 0.536 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 2 (0.1) | 0.004 |
| Target vessel revascularization (%) | 3 (4.5) | 22 (0.9) | 0.029 |
| 6-month follow-up | |||
| Major adverse cardiovascular events (%) | 12 (18.5) | 255 (11.2) | 0.069 |
| Death (%) | 4 (6.3) | 45 (2.0) | 0.043 |
| Myocardial infarction (%) | 6 (9.0) | 116 (4.9) | 0.140 |
| Q-wave (%) | 1 (1.5) | 9 (0.4) | 0.245 |
| Non-Q-wave (%) | 5 (7.5) | 107 (4.6) | 0.236 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 12 (0.5) | 0.054 |
| Target vessel revascularization (%) | 4 (6.2) | 124 (5.5) | 0.779 |
| Stent thrombosis | |||
| Intraprocedural (%) | 2 (3.0) | 8 (0.3) | 0.030 |
| Subacute (%) | 2 (3.1) | 13 (0.6) | 0.062 |
| Late (%) | 0 | 7 (0.3) | 1.0 |
| Cumulative 6-month rate (%) | 4 (6.3) | 28 (1.3) | 0.011 |
aExpressed as n (%).
Univariate analysis of in-hospital, 1-month, and 6-month events according to the presence vs. absence of post-procedural coronary dissection.a
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patients | n=67 | n=2351 | |
| In-hospital events | |||
| Major adverse cardiovascular events (%) | 8 (11.9) | 123 (5.2) | 0.017 |
| Death (%) | 2 (3.0) | 13 (0.6) | 0.063 |
| Myocardial infarction (%) | 4 (6.0) | 102 (4.4) | 0.536 |
| Q-wave (%) | 0 | 2 (0.1) | 1.0 |
| Non-Q-wave (%) | 4 (6.0) | 100 (4.3) | 0.521 |
| Coronary artery bypass grafting | 2 (3.0) | 1 (0.1) | 0.002 |
| Repeat percutaneous revascularization (%) | 1 (0.6) | 14 (0.6) | 0.345 |
| 1-month follow-up | |||
| Major adverse cardiovascular events (%) | 9 (13.4) | 142 (6.0) | 0.013 |
| Death (%) | 2 (3.0) | 26 (1.1) | 0.176 |
| Myocardial infarction (%) | 4 (6.0) | 109 (4.6) | 0.552 |
| Q-wave (%) | 0 | 7 (0.3) | 1.00 |
| Non-Q-wave (%) | 4 (6.0) | 102 (4.3) | 0.536 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 2 (0.1) | 0.004 |
| Target vessel revascularization (%) | 3 (4.5) | 22 (0.9) | 0.029 |
| 6-month follow-up | |||
| Major adverse cardiovascular events (%) | 12 (18.5) | 255 (11.2) | 0.069 |
| Death (%) | 4 (6.3) | 45 (2.0) | 0.043 |
| Myocardial infarction (%) | 6 (9.0) | 116 (4.9) | 0.140 |
| Q-wave (%) | 1 (1.5) | 9 (0.4) | 0.245 |
| Non-Q-wave (%) | 5 (7.5) | 107 (4.6) | 0.236 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 12 (0.5) | 0.054 |
| Target vessel revascularization (%) | 4 (6.2) | 124 (5.5) | 0.779 |
| Stent thrombosis | |||
| Intraprocedural (%) | 2 (3.0) | 8 (0.3) | 0.030 |
| Subacute (%) | 2 (3.1) | 13 (0.6) | 0.062 |
| Late (%) | 0 | 7 (0.3) | 1.0 |
| Cumulative 6-month rate (%) | 4 (6.3) | 28 (1.3) | 0.011 |
| . | Final dissection . | No final dissection . | P . |
|---|---|---|---|
| Patients | n=67 | n=2351 | |
| In-hospital events | |||
| Major adverse cardiovascular events (%) | 8 (11.9) | 123 (5.2) | 0.017 |
| Death (%) | 2 (3.0) | 13 (0.6) | 0.063 |
| Myocardial infarction (%) | 4 (6.0) | 102 (4.4) | 0.536 |
| Q-wave (%) | 0 | 2 (0.1) | 1.0 |
| Non-Q-wave (%) | 4 (6.0) | 100 (4.3) | 0.521 |
| Coronary artery bypass grafting | 2 (3.0) | 1 (0.1) | 0.002 |
| Repeat percutaneous revascularization (%) | 1 (0.6) | 14 (0.6) | 0.345 |
| 1-month follow-up | |||
| Major adverse cardiovascular events (%) | 9 (13.4) | 142 (6.0) | 0.013 |
| Death (%) | 2 (3.0) | 26 (1.1) | 0.176 |
| Myocardial infarction (%) | 4 (6.0) | 109 (4.6) | 0.552 |
| Q-wave (%) | 0 | 7 (0.3) | 1.00 |
| Non-Q-wave (%) | 4 (6.0) | 102 (4.3) | 0.536 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 2 (0.1) | 0.004 |
| Target vessel revascularization (%) | 3 (4.5) | 22 (0.9) | 0.029 |
| 6-month follow-up | |||
| Major adverse cardiovascular events (%) | 12 (18.5) | 255 (11.2) | 0.069 |
| Death (%) | 4 (6.3) | 45 (2.0) | 0.043 |
| Myocardial infarction (%) | 6 (9.0) | 116 (4.9) | 0.140 |
| Q-wave (%) | 1 (1.5) | 9 (0.4) | 0.245 |
| Non-Q-wave (%) | 5 (7.5) | 107 (4.6) | 0.236 |
| Coronary artery bypass grafting (%) | 2 (3.0) | 12 (0.5) | 0.054 |
| Target vessel revascularization (%) | 4 (6.2) | 124 (5.5) | 0.779 |
| Stent thrombosis | |||
| Intraprocedural (%) | 2 (3.0) | 8 (0.3) | 0.030 |
| Subacute (%) | 2 (3.1) | 13 (0.6) | 0.062 |
| Late (%) | 0 | 7 (0.3) | 1.0 |
| Cumulative 6-month rate (%) | 4 (6.3) | 28 (1.3) | 0.011 |
aExpressed as n (%).
References
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Sharma SK, Israel DH, Kamean JL, Bodian CA, Ambrose JA. Clinical, angiographic, and procedural determinants of major and minor coronary dissection during angioplasty.
Hong MK, Park SW, Lee NH, Nah DY, Lee CW, Kang DH, Song JK, Kim JJ, Park SJ. Long-term outcomes of minor dissections at the edge of stents detected with intravascular ultrasound.
Nishida T, Colombo A, Briguori C, Stankovic G, Albiero R, Corvaja N, Finci L, Di Mario C, Tobis JM. Outcome of nonobstructive residual dissections detected by intravascular ultrasound following percutaneous coronary intervention.
Cappelletti A, Margonato A, Rosano G, Mailhac A, Veglia F, Colombo A, Chierchia SL. Short- and long-term evolution of unstented nonocclusive coronary dissection after coronary angioplasty.
Hill RA, Dundar Y, Bakhai A, Dickson R, Walley T. Drug-eluting stents: an early systematic review to inform policy.
Chieffo A, Bonizzoni E, Orlic D, Stankovic G, Rogacka R, Airoldi F, Mikhail GW, Montorfano M, Michev I, Carlino M, Colombo A. Intraprocedural stent thrombosis during implantation of sirolimus-eluting stents.
McFadden EP, Stabile E, Regar E, Cheneau E, Ong AT, Kinnaird T, Suddath WO, Weissman NJ, Torguson R, Kent KM, Pichard AD, Satler LF, Waksman R, Serruys PW. Late thrombosis in drug-eluting stents after discontinuation of antiplatelet therapy.
Stankovic G, Chieffo A, Iakovou I, Orlic D, Corvaja N, Sangiorgi G, Airoldi F, Colombo A. Creatine kinase-myocardial band isoenzyme elevation after percutaneous coronary interventions using sirolimus-eluting stents.
Colombo A, Hall P, Nakamura S, Almagor Y, Maiello L, Martini G, Gaglione A, Goldberg SL, Tobis JM. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance.
Reimers B, Di Mario C, Di Francesco L, Moussa I, Blengino S, Martini G, Reiber JH, Colombo A. New approach to quantitative angiographic assessment after stent implantation.
Hosmer DW, Lemeshow S.
Steyerberg EW, Harrell FE Jr, Borsboom GJJM, Eijkemans MJCR, Vergouwe Y, Habbema JDF. Internal validation of predictive models: efficiency of some procedures for logistic regression analysis.
Huber MS, Mooney JF, Madison J, Mooney MR. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty.
Hermans WR, Foley DP, Rensing BJ, Rutsch W, Heyndrickx GR, Danchin N, Mast G, Hanet C, Lablanche JM, Rafflenbeul W. Usefulness of quantitative and qualitative angiographic lesion morphology, and clinical characteristics in predicting major adverse cardiac events during and after native coronary balloon angioplasty.
Hermans WR, Rensing BJ, Foley DP, Deckers JW, Rutsch W, Emanuelsson H, Danchin N, Wijns W, Chappuis F, Serruys PW. Therapeutic dissection after successful coronary balloon angioplasty: no influence on restenosis or on clinical outcome in 693 patients. The MERCATOR Study Group.
Costa MA, Kozuma K, Gaster AL, van Der Giessen WJ, Sabate M, Foley DP, Kay IP, Ligthart JM, Thayssen P, van Den Brand MJ, de Feyter PJ, Serruys PW. Three dimensional intravascular ultrasonic assessment of the local mechanism of restenosis after balloon angioplasty.
Agarwal R, Kaul U, Dev V, Sharma S, Venugopal P. The morphology of coronary arterial dissection occurring subsequent to angioplasty and its influence on acute complications.
Cutlip DE, Baim DS, Ho KK, Popma JJ, Lansky AJ, Cohen DJ, Carrozza JP Jr, Chauhan MS, Rodriguez O, Kuntz RE. Stent thrombosis in the modern era. A pooled analysis of multicenter coronary stent clinical trials.
Cheneau E, Leborgne L, Mintz GS, Kotani J, Pichard AD, Satler LF, Canos D, Castagna M, Weissman NJ, Waksman R. Predictors of subacute stent thrombosis: results of a systematic intravascular ultrasound study.
Kereiakes DJ, Choo JK, Young JJ, Broderick TM. Thrombosis and drug-eluting stents: a critical appraisal.
Jeremias A, Sylvia B, Bridges J, Kirtane AJ, Bigelow B, Pinto DS, Ho KK, Cohen DJ, Garcia LA, Cutlip DE, Carrozza JP Jr. Stent thrombosis after successful sirolimus-eluting stent implantation.
Kay IP, Sabate M, Van Langenhove G, Costa MA, Wardeh AJ, Gijzel AL, Deshpande NV, Carlier SG, Coen VL, Levendag PC, Van der Giessen W, de Feyter PJ, Serruys PW. Outcome of balloon induced coronary dissection after intracoronary beta radiation.
McClean DR, Thomas MR. Non-flow limiting dissection leading to late coronary restenosis following intracoronary brachytherapy.
Guagliumi G, Virmani R, Musumeci G, Motta T, Valsecchi O, Bonaldi G, Saino A, Tespili M, Greco N, Farb A. Drug-eluting versus bare-metal coronary stents: long-term human pathology. Findings from different coronary arteries in the same patient.
Virmani R, Guagliumi G, Farb A, Musumeci G, Grieco N, Motta T, Mihalcsik L, Tespili M, Valsecchi O, Kolodgie FD. Localized hypersensitivity and late coronary thrombosis secondary to a sirolimus-eluting stent. Should we be cautious?
Colombo A, De Gregorio J, Moussa I, Kobayashi Y, Karvouni E, Di Mario C, Albiero R, Finci L, Moses J. Intravascular ultrasound-guided percutaneous transluminal coronary angioplasty with provisional spot stenting for treatment of long coronary lesions.
Biondi-Zoccai GGL, Agostoni P, Abbate A. Parallel hierarchy of scientific studies in cardiovascular medicine.
