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This is the first study assessing the impact of NSTE-ACS on clinical outcomes in a large sample of patients with coronary bifurcation lesions treated with drug-eluting stents. Our study demonstrated that NSTE-ACS was associated with an increased risk of MACE during a 2-year follow-up. Of patients with NSTE-ACS, however, those with NSTEMI had similar risks of MACE, cardiac death, MI, TLR, and stent thrombosis as did patients with UA. In addition, the rate of MACE was consistently higher in the FKB group than in the non-FKB group among several subgroups.
Figure 3. Subgroups analysis on FKB. Abbreviations: CI, confidence interval; FKB, final kissing ballooning; HR, hazard ratio; NSTE-ACS, non–ST-segment elevation acute coronary syndrome; NSTEMI, non–ST-segment elevation myocardial infarction.
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The increased risk of MACE in patients with NSTE-ACS is attributable in part to the coexistence of serious comorbidities and NSTE-ACS itself. Results of our study correspond with the results of earlier studies.4–6 In our study, the NSTE-ACS patients had a higher proportion of current smokers, a higher probability of dyslipidemia, and a lower left ventricular ejection fraction than did patients with stable angina. As a result, patients with NSTE-ACS had a significantly increased risk of adverse events, with 7.3% MACE. In contrast, stable angina patients had a relatively favorable clinical outcome, with 5.2% MACE.
We stratified patients with NSTE-ACS into those with NSTEMI and those with UA and analyzed clinical outcomes among the 2 subgroups. Against expectations, no differences were seen in 2-year MACE, including cardiac death, MI, TLR, and stent thrombosis between the patients with NSTEMI and the UA patients. Acute coronary syndrome is a heterogeneous condition that may be divided into UA, NSTEMI, and ST-segment elevation myocardial infarction. All forms of ACS, however, share a similar underlying pathophysiology, primarily the rupture of an atherosclerotic plaque resulting in an intracoronary thrombus.7 Thus, clinical prognosis might be similar between NSTEMI and UA patients. Moreover, improvements in revascularization techniques as well as new agents to address factors of the acute thrombotic process underlying ACS have resulted in considerable reductions in mortality and adverse clinical outcomes.
Interestingly, we found the rate of MACE was significantly higher in both the NSTE-ACS and stable angina groups by the time of FKB and no significant interaction between the NSTE-ACS or stable angina patient groups and MACE. And also, the FKB group had consistently worse outcomes across various subgroups. Final kissing ballooning was reported to be associated with a lower incidence of clinical events.8–10 These associations, however, have been studied mostly in 2-stent techniques, including mainly crush stenting techniques, so data on FKB in 1-stent techniques are limited. Considering that most lesions were treated with 1-stent techniques in our study (85.3% in NSTE-ACS patients and 81.8% in stable angina patients), the implications of FKB in our registry could be different from previous studies. Our COBIS investigation showed that FKB increased the long-term risk of TLR, most of which occurred in the main vessel, even after propensity score matching.11 In the present study, the rate of MACE was consistently higher in the FKB group among several subgroups. We propose that distortion of the main vessel stent might occur after opening a stent though the ostium of the side branch, but this distortion might not be corrected by FKB. In a previous intravascular ultrasound study on changes in the geometry of the main vessel stent following side branch ballooning and FKB, a reduction was observed in the cross-sectional area of the main vessel stent immediately distal to the side branch origin after side branch ballooning. However, the area did not return to its initial value after FKB.12 Decreased main vessel stent area, main vessel stent deformation, or polymer disruption of drug-eluting stent associated with side branch intervention may translate into increased restenosis and TLR in the main vessel. The Nordic-Baltic Bifurcation Study III also reported that a simple main vessel stenting technique without FKB provides excellent clinical results that are similar to those of the more complex strategy of main vessel stenting with FKB in patients with bifurcation lesions.13 However, as our study used post hoc analysis, the results should be interpreted carefully, and a well-powered, randomized trial is required to evaluate the role of FKB in the simple, 1-stent strategy.
We used a retrospective multicenter registry; therefore, our results were affected by limitations inherent to this type of study. First, it is a nonrandomized and observational study, so uncounted confounders may have influenced study outcomes. Second, the selection of treatment strategies, including FKB, was at the discretion of the operators. Even though rigorous statistical adjustments were made to adjust for potential confounding factors, we were not able to control all variables. Third, in the present study, it is clear that NSTE-ACS patients presented higher risk profiles and more complicated angiographic pictures than stable angina patients. Thus, the study populations may not be well matched to draw definitive conclusions. Fourth, systemic angiographic follow-up was not performed, and coronary angiography was analyzed qualitatively, not quantitatively. Detailed quantitative analysis of the angiographic data would be helpful for interpreting our findings. Another limitation is that patients with ST-segment elevation myocardial infarction were excluded in this registry, so we cannot offer a more comprehensive view of the ACS patients and elucidate differences in outcomes between patients with various types of ACS. Finally, our sample was not large enough to evaluate the incidence of MACE, especially in the NSTE-ACS cohort. This limitation might be the reason that no significant differences were seen in clinical outcomes between the NSTEMI and UA patient subgroups.