Abstract
Background
Data on the relevance of the location of coronary bifurcation lesions treated by crush stenting with outcomes were limited.
Hypothesis
We hypothesized that the location of the bifurcation lesion correlated with clinical outcome.
Method
A total of 212 patients with 230 true bifurcation lesions treated by crush stenting with drug‐eluting stents (DES) were assessed prospectively. Surveillance quantitative angiographies were indexed at 8 months after procedure. Primary endpoint was major adverse cardiac events (MACE), defined as cardiac death, myocardial infarction, and target lesion revascularization (TLR).
Results
Patients in the distal right coronary artery (RCAd) group were characterized by higher proportions of prior myocardial infarction and very tortuous lesions. However, lesions in the RCAd group, compared to those of other groups, had the lowest late lumen loss, with resultant lowest incidence of MACE at a mean follow‐up of 268±35 days. Independent predictors of MACE included unsatisfied kissing (KUS; hazard ratio [HR]: 12.14, 95% confidence interval [CI]: 4.01–12.10, P = .001) and non‐RCA lesion (HR: 20.69, 95% CI: 5.05–22.38, P = .001), while those of TLR were KUS (HR: 10.21, 95% CI: 0.01–0.34, P = .002), bifurcation angle (HR: 4.728, 95% CI: 2.541–4.109, P = .001), and non‐RCA lesion (HR: 16.05, 95%CI: 1.01–4.83, P = .001).
Conclusions
Classical crush stenting with drug‐eluting stents is associated with significantly better outcomes in RCAd. Quality of kissing inflation is mandatory to improve outcome. Copyright © 2009 Wiley Periodicals, Inc.
Introduction
Drug‐eluting stents (DES), compared to bare‐metal stents (BMS), are effective in decreasing restenosis, target‐lesion revascularization (TLR), and cumulative major adverse cardiac event (MACE) rates after percutaneous coronary intervention (PCI).1, 2, 3 This benefit extends to the main vessel of bifurcation lesions, but the stented side branch remains problematic because of high ostial restenosis incidences.4, 5, 6 Even with the classical crush technique,7 which was developed to ensure entire ostial side branch coverage, there is room for improvement in terms of ostial restenosis incidence. To this end, studies have reported that final kissing balloon inflation (FKBI) is mandatory to improve clinical outcomes.8, 9, 10
We had previously reported11 that FKBI is easily performed if bifurcation lesions involve the ostium of either the left anterior descending (LAD) and diagonal (D) coronary arteries, or the left circumflex (LCX) coronary arteries. Therefore, this study is aimed at gaining insight into the possibility that different coronary bifurcation lesion locations (ie, distal left‐main trunk [LMTd]; LAD‐diagonal [D]; LCX‐obtuse marginal [OM]; and distal right coronary artery [RCAd]) might be associated with differential clinical outcomes post‐crush stenting.
Methods
Study Population
True coronary bifurcation lesions by the Lefevre classification6 were treated by crush stenting between February 1, 2004 and September 30, 2006 from 9 centers. Patients were excluded if they had the following: liver dysfunction, renal insufficiency, cerebrovascular event within 6 months, expected survival < 1 year, or allergy to aspirin, clopidogrel, or DES. Lesions completely covered by no more than 2 overlapped stents were included if: main vessel diameter > 2.5 mm and side branch diameter ≥ 2.0 mm. No more than 1 bifurcation lesion per vessel was permitted. The choice of DES was up to the operator's discretion and no BMS were allowed. Only paclitaxel‐eluting (PES; Taxus, Boston Scientific, Natick, MA) and sirolimus‐eluting (SES; Cypher, Cordis, Johnson & Johnson, Miami Lakes, FL) stents were used in this study.
Procedure
The classical crush technique has been described previously.7 Briefly, it involves first delivering the side branch stent with the proximal 3–5 mm protruding into the main vessel; the protruding segment is then crushed by the main vessel stent.
Clinical and Angiographic Definitions
Myocardial infarction was defined as creatine kinase‐MB (CK‐MB) enzyme elevation ≥ 3 times the upper limit of the normal value, with or without new Q‐wave appearance. TLR was defined as repeat revascularization with a diameter stenosis ≥ 50% (within the stent or in the 5 mm distal or proximal segments adjacent to the stents) and ischemic symptoms. Target‐vessel revascularization (TVR) was defined as repeat revascularization within the treated vessel. Stent thrombosis was defined as an acute coronary syndrome with angiographic documentation of vessel occlusion by thrombus either within or adjacent to a previously successfully stented vessel. In the absence of angiographic confirmation, either acute myocardial infarction (AMI) in the distribution of the treated vessel or death not clearly attributable to other causes was also considered stent thrombosis. Bifurcation angle was defined as the angle between the axis of the post‐bifurcation segments of the main vessel and the axis of the side branch at its origin. Quality of FKBI was defined as satisfactory kissing (KS; no waist at the ostium of side branch balloon during FKBI) or unsatisfactory kissing (KUS; waist with ≥ 20% diameter stenosis of side branch balloon during FKBI). Plasma levels of CK‐MB, troponin I, and creatinine were monitored immediately before, and at 8 and 24 hours post‐PCI. Clinical follow‐up was done monthly by telephone or clinic visit.
Quantitative Coronary Angiography Analysis
Angiographic follow‐up was completed at 8 months after the procedure unless clinically indicated earlier. Three orthogonal views were required for the left coronary artery and 2 for the right coronary artery. A validated computer‐based edge detection system (CAAS II, Amsterdam Netherlands) was used for quantitative coronary angiography (QCA) analysis, with the dye‐filled catheter as a reference. Reference vessel diameter (RVD), lesion length, and minimum lumen diameter (MLD) were measured before and after PCI, and at the time of follow‐up angiography, and calculated from an average of 2 angiographic projections. Angiographic success was defined as the achievement of thrombolysis in myocardial infarction (TIMI) grade 3 flow in both vessels. Procedural success was defined as the achievement of angiographic success in the absence of any in‐hospital MACE.
Bifurcation lesions were divided into 3 segments: pre‐bifurcation segment of the main vessel (pre‐MV, including the stented segment and 5 mm proximal to it), post‐bifurcation segment of the main vessel (post‐MV, including the stented segments and 5 mm distal to it), and side branch segment (including the stented segments and 5 mm distal to it).
Statistics and Data Management
Continuous variables are expressed as mean ± SD and compared using the analysis of variance (ANOVA) test. Categorical variables (expressed as percentage frequencies) were compared with χ2 statistics or Fisher's exact test. Clinical variables were analyzed by the Kaplan‐Meier method and log‐rank test. Cox regression models were used to identify the TLR predictors at 8 months. A P value <.05 was considered to be significant. Data analysis was performed using the SPSS (version 16.0, SPSS Inc. Chicago Il).
Results
Baseline Clinical, Lesion, and Procedural Characteristics
There were around 65% of patients who presented with unstable angina, with 64% of lesions involving the left anterior descending artery (LAD)‐(D1) first diagnosis (Table 1). There were no significant differences among groups regarding age, gender, left ventricular systolic function, and other risk factors. More patients with acute myocardial infarction were included in the RCAd group (P = .005).
Table 1.
Baseline Characteristics in Patients With Different Lesion Locations
| LMTd (n = 31) | LAD‐D1 (n = 135) | LCX‐OM (n = 29) | RCAd (n = 17) | |
|---|---|---|---|---|
| Male, n (%) | 20 (64.5) | 105 (77.8) | 17 (58.6) | 14 (82.4) |
| Smoker, n (%) | 7 (22.6) | 54 (40.0) | 10 (34.5) | 7 (41.2) |
| EHP, n (%) | 19 (61.3) | 110 (81.5) | 20 (69.0) | 13 (76.5) |
| HL, n (%) | 21 (67.7) | 83 (61.5) | 23 (79.3) | 12 (70.6) |
| DM, n (%) | 7 (22.6) | 13 (9.6) | 49 (13.8) | 5 (29.4) |
| OMI, n (%) | 6 (19.4) | 14 (10.4) | 1 (3.4) | 1 (5.9) |
| Pre‐PCI, n (%) | 2 (6.5) | 15 (11.1) | 4 (13.8) | 1 (5.9) |
| UAP, n (%) | 21 (67.7) | 98 (72.6) | 19 (65.5) | 10 (58.8) |
| AMI, n (%) | 2 (6.5) | 21 (15.6) | 5 (17.2) | 6 (35.3)a |
| LVEF, % | 62.83 ± 11.15 | 62.31 ± 9.40 | 63.21 ± 8.50 | 61.20 ± 9.70 |
Abbreviations: AMI, acute myocardial infarction; D1, first diagonal; DM, diabetic mellitus; EHP, essential hypertension; HL, hyperlipidemia; LAD, left anterior descending; LCX, left circumflex; LMTd, distal left‐main trunk; LVEF, left ventricular ejection fraction; OM, obtuse marginal; OMI, old myocardial infarction; PCI, percutaneous coronary intervention; RCAd, distal right coronary artery; UAP, unstable angina pectoris.
P = .005
There were no differences in terms of number of balloons used and procedural times among groups. Patients in the LCX‐OM group had shorter lesion length in the main vessel (P = .005), with resultant shorter stent length (P = .005) and shorter total stent length in main vessels (P = .025). Interestingly, compared to the other 3 groups (Table 2), patients in the LMTd group had longer side stent lengths (P = .005). More contrast volume was needed in the RCAd group. A total of 97% in the LMTd group were treated by FKBI (P = .005). The RCAd group had the lowest incidence of KUS (15.4%, P = .005).
Table 2.
Lesion and Procedural Characteristics in Patients With Different Lesion Locations
| LMTd (n = 33) | LAD‐D1 (n = 138) | LCX‐OM (n = 34) | RCAd (n = 25) | |
|---|---|---|---|---|
| Thrombus‐containing, n (%) | 1 (3.2) | 4 (3.0) | 0 | 1 (5.9) |
| Severe calcification, n (%) | 0 | 1 (0.7) | 0 | 0 |
| Very tortuous, n (%) | 2 (6.5) | 15 (11.2) | 7 (25.0) | 10 (58.8)b |
| Restenotic lesions, n (%) | 1 (3.2) | 7 (5.2) | 2 (7.1) | 0 |
| CTO, n (%) | 1 (3.2) | 8 (6.0) | 0 | 1 (5.9) |
| Bifurcation angle (°) | 75.59 ± 24.11a | 48.23 ± 20.11 | 51.10 ± 20.73 | 56.94 ± 20.35 |
| Main vessel | ||||
| Lesion length (mm) | 19.89 ± 11.45 | 21.19 ± 10.46 | 15.79 ± 6.54d | 25.67 ± 12.04 |
| Stent number (n) | 1.13 ± 0.34 | 1.16 ± 0.42 | 1.07 ± 0.26 | 1.24 ± 0.43 |
| Stent length (mm) | 26.94 ± 10.94 | 28.73 ± 13.27 | 22.79 ± 8.08d | 30.06 ± 13.44 |
| Stent diameter (mm) | 3.74 ± 0.67a | 3.32 ± 0.45 | 3.17 ± 0.49 | 3.28 ± 0.71 |
| Maximal pressure (atm) | 16.32 ± 3.03 | 16.82 ± 2.79 | 16.37 ± 2.38 | 16.18 ± 2.22 |
| Max balloon dia. (mm) | 3.90 ± 0.68a | 3.44 ± 0.49 | 3.39 ± 0.50 | 3.32 ± 0.56 |
| Stent overlapping, n (%) | 4 (12.9) | 19 (14.2) | 2 (7.1) | 4 (23.5) |
| Side branch | ||||
| Lesion length (mm) | 12.38 ± 8.79 | 10.19 ± 6.37 | 9.45 ± 6.85 | 9.82 ± 7.56 |
| Stent number (n) | 1.10 ± 0.30 | 1.01 ± 0.08 | 1.04 ± 0.18 | 1.06 ± 0.24 |
| Stent length (mm) | 21.4 ± 9.79b | 17.20 ± 5.41 | 16.82 ± 5.26 | 16.06 ± 6.59 |
| Stent diameter (mm) | 3.25 ± 0.56c | 2.67 ± 0.32 | 2.67 ± 0.29 | 2.49 ± 0.24 |
| Maximal pressure (atm) | 10.04 ± 2.74 | 9.84 ± 2.70 | 9.84 ± 2.52 | 11.18 ± 2.78 |
| Max balloon dia. (mm) | 3.24 ± 0.63c | 2.66 ± 0.42 | 2.68 ± 0.41 | 2.47 ± 0.28 |
| Stent overlapping, n (%) | 3 (9.7) | 1 (0.7) | 1 (3.6) | 1 (5.9) |
| Procedural time (min.) | 43.39 ± 28.37 | 38.24 ± 19.87 | 42.07 ± 23.45 | 46.06 ± 25.95 |
| Contrast volume (ml) | 141.2 ± 99.81 | 109.02 ± 64.70 | 114.63 ± 61.81 | 163.13 ± 102.48e |
| Total stent length (mm) | 48.35 ± 17.24 | 45.93 ± 14.96 | 39.61 ± 8.82d | 46.12 ± 16.93 |
| Balloon number (n) | 2.44 ± 0.91 | 2.32 ± 0.68 | 2.35 ± 0.71 | 2.50 ± 0.22 |
| PES, n (%) | 24 (77.4) | 102 (75.6) | 22 (75.9) | 15 (88.2) |
| FKBI, % | 97b | 74 | 72 | 76 |
| KUS, n (%) | 7 (23.3) | 32 (27.8) | 5 (22.7) | 2 (15.4)b |
Abbreviations: CTO, chronic total occlusion; D1, first diagonal; FKBI, final kissing balloon inflation; KUS, kissing unsatisfied; LAD, left anterior descending; LCX, left circumflex; LMTd, distal left‐main trunk; OM, obtuse marginal; PES, paclitaxel‐eluting stent; RCAd, distal right coronary artery.
P = .001.
P = .005.
P < .001.
P = .025, compared with other 3 groups.
P = .005, compared to LAD‐D and LCX‐OM group
Angiographic Analysis
Pre‐Bifurcation Segments of the Main Vessels (Pre‐MV)
Angiographic follow‐up was available in 181 patients (86%) with 198 lesions at an average of 268±35 days (Table 3). Compared to the other 3 groups, patients in the RCAd group had the lowest late lumen loss at 8 month follow‐up (P <.001), without difference regarding restenosis rates among the 4 groups.
Table 3.
QCA in Pre‐MV Segments
| LMTd (n = 28) | LAD‐D1 (n = 126) | LCX‐OM (n = 23) | RCAd (n = 21) | |
|---|---|---|---|---|
| Baselinea | ||||
| RVD (mm) | 4.26 ± 0.82a | 3.53 ± 0.57 | 3.26 ± 0.65 | 3.31 ± 0.68 |
| % DS | 46.55 ± 7.91 | 45.22 ± 8.39 | 48.54 ± 5.31 | 51.47 ± 7.13 |
| MLD (mm) | 2.24 ± 0.31b | 1.92 ± 0.38 | 1.86 ± 0.41 | 1.67 ± 0.42 |
| Post‐PCI | ||||
| RVD (mm) | 4.44 ± 0.82a | 3.62 ± 0.51 | 3.39 ± 0.56 | 3.43 ± 0.58 |
| % DS | 13.90 ± 5.97 | 14.88 ± 7.12 | 16.21 ± 7.63 | 19.82 ± 7.41 |
| MLD (mm) | 3.83 ± 0.77b | 3.08 ± 0.51 | 2.85 ± 0.58 | 2.74 ± 0.51 |
| Acute gain (mm) | 1.65 ± 0.48b | 1.19 ± 0.43 | 1.13 ± 0.43 | 1.20 ± 0.39 |
| At 8 mo | ||||
| RVD (mm) | 3.92 ± 0.66b | 3.41 ± 0.61 | 3.09 ± 0.53 | 3.32 ± 0.52 |
| % DS | 23.15±14.86 | 31.65±18.00 | 31.72±15.03 | 34.82±14.70 |
| MLD (mm) | 3.03 ± 0.74b | 2.36 ± 0.81 | 2.11 ± 0.53 | 2.17 ± 0.17 |
| Late loss (mm) | 0.81 ± 0.27 | 0.74 ± 0.26 | 0.72 ± 0.26 | 0.51 ± 0.29c |
| Restenosis (%) | 3.8 | 5.1 | 2.0 | 1.2 |
Abbreviations: D1, first diagonal; DS, diameter stenosis; LAD, left anterior descending; LCX, left circumflex; LMTd, distal left‐main trunk; MLD, minimal lumen diameter; MV, main vessel; OM, obtuse marginal; QCA, quantitative coronary angiography; RCAd, distal right coronary artery; RVD, reference vessel diameter.
P = .001.
P = .005, comparing with patients in LAD‐D1, LCX‐OM, and RCAd groups.
P < .001, comparing with patients in LMTd, LAD‐D, and LCX‐OM groups
Post‐Bifurcation Segments of the Main Vessels (Post‐MV)
Late lumen loss in the RCAd group was also lower than in the other 3 groups (P = .001, Table 4). Compared to the other 3 groups, restenosis rates in both pre‐MV and whole main vessel segments in the RCAd group were lower although the differences did not achieve statistical significance (P >.05).
Table 4.
QCA in Post‐MV Segments
| LMTd (n = 28) | LAD‐D1 (n = 126) | LCX‐OM (n = 23) | RCAd (n = 21) | |
|---|---|---|---|---|
| Baselinea | ||||
| RVD (mm) | 3.49 ± 0.91b | 2.92 ± 0.61 | 2.88 ± 0.67 | 2.86 ± 0.67 |
| % DS | 63.57 ± 11.00 | 63.29 ± 11.33 | 68.54 ± 10.89 | 65.24 ± 14.14 |
| MLD (mm) | 1.44 ± 0.32 | 1.46 ± 0.33 | 1.39 ± 0.34 | 1.34 ± 0.32 |
| Post‐PCI | ||||
| RVD (mm) | 3.36 ± 0.81b | 2.84 ± 0.44 | 2.79 ± 0.55 | 2.67 ± 0.49 |
| % DS | 11.90 ± 2.42 | 10.61 ± 3.43 | 10.89 ± 5.29 | 11.35 ± 1.78 |
| MLD (mm) | 2.95 ± 0.83b | 2.56 ± 0.44 | 2.33 ± 0.56 | 2.34 ± 0.62 |
| Acute gain (mm) | 1.57 ± 0.23b | 1.20 ± 0.27 | 1.15 ± 0.37 | 1.19 ± 0.32 |
| At 8 mo | ||||
| RVD (mm) | 3.17 ± 0.64b | 2.72 ± 0.51 | 2.53 ± 0.39 | 2.66 ± 0.49 |
| % DS | 30.15 ± 13.16 | 32.16 ± 15.46 | 36.20 ± 19.48 | 39.82 ± 26.26 |
| MLD (mm) | 2.24 ± 0.68b | 1.85 ± 0.57 | 1.63 ± 0.59 | 1.61 ± 0.84 |
| Late loss (mm) | 0.57 ± 0.10 | 0.54 ± 0.16 | 0.58 ± 0.59 | 0.28 ± 0.42a |
| Restenosis (%) | ||||
| Post‐MV | 5.4 | 3.3 | 5.0 | 2.3 |
| Pre‐MV+Post‐MV | 7.6 | 8.1 | 6.0 | 2.5 |
Abbreviations: D1, first diagonal; DS, diameter stenosis; LAD, left anterior descending artery; LCX, left circumflex; LMTd, distal left‐main trunk; MLD, minimal lumen diameter; MV, main vessel; OM, obtuse marginal; QCA, quantitative coronary angiography; RCAd, distal right coronary artery; RVD, reference vessel diameter.
P = .001, comparing with other 3 groups.
P = .005
Side‐Branch Segments
Similar to the main vessel segments, there were significant differences regarding RVD, MLD, and acute gain among the 4 groups (Table 5). Patients in the RCAd group had the lowest late lumen loss and restenosis rates in either side branch or side branch with any 1 segment of main vessel (P = .005), compared to the LMTd and LCX‐OM group. The restenosis rate in the LAD‐D group tended to be lower compared to those in the LMTd and LCX‐OM groups, although differences did not achieve statistical significance.
Table 5.
QCA in Side Branches
| LMTd (n = 28) | LAD‐D1 (n = 126) | LCX‐OM (n = 23) | RCAd (n = 21) | |
|---|---|---|---|---|
| Baselinea | ||||
| RVD (mm) | 3.15 ± 0.68a | 2.49 ± 0.37 | 2.53 ± 0.44 | 2.42 ± 0.45 |
| % DS | 67.00 ± 17.13 | 66.24 ± 18.57 | 69.81 ± 17.45 | 65.36 ± 14.79 |
| MLD (mm) | 1.12 ± 0.24 | 1.15 ± 0.26 | 1.11 ± 0.24 | 1.12 ± 0.25 |
| Post‐PCI | ||||
| RVD (mm) | 2.88 ± 0.64b | 2.37 ± 0.34 | 2.46 ± 0.36 | 2.29 ± 0.33 |
| % DS | 11.76 ± 8.65 | 14.51 ± 9.54 | 13.00 ± 9.87 | 13.76 ± 10.61 |
| MLD (mm) | 2.57 ± 0.31b | 2.09 ± 0.38 | 2.11 ± 0.40 | 2.16 ± 0.34 |
| Acute gain (mm) | 1.47 ± 0.29b | 1.04 ± 0.27 | 1.03 ± 0.29 | 1.10 ± 0.30 |
| At 8 mo | ||||
| RVD (mm) | 2.87 ± 0.49b | 2.29 ± 0.36 | 2.32 ± 0.38 | 2.19 ± 0.28 |
| % DS | 37.38 ± 18.49 | 36.67 ± 19.45 | 43.68 ± 21.02 | 24.36 ± 17.33 |
| MLD (mm) | 1.81 ± 0.61b | 1.45 ± 0.52 | 1.32 ± 0.56 | 1.61 ± 0.37 |
| Late loss (mm) | 0.68 ± 0.15 | 0.64 ± 0.18 | 0.67 ± 0.21 | 0.49 ± 0.27b |
| Restenosis, (%) | ||||
| SB only | 23.1 | 18.1 | 25.0 | 13.3d |
| SB+MVc | 30.1 | 23.5 | 29.4 | 18.2d |
Abbreviations: D1, first diagonal; DS, diameter stenosis; LAD, left anterior descending; LCX, left circumflex; LMTd, distal left‐main trunk; MLD, minimal lumen diameter; MV, main vessel; OM, obtuse marginal; QCA, quantitative coronary angiography; RCAd, distal right coronary artery; RVD, reference vessel diameter.
P = .001.
P = .005, compared to other 3 groups.
Indicated side branch with any segment (pre‐MV or post‐MV) of main vessel.
P = .005, compared to side branches in LMTd and LCX‐OM groups
Clinical Follow‐Up
Clinical follow‐up was completed in all patients (100%). One patient in the LMTd group died from in‐hospital myocardial infarction. There were no significant differences in in‐hospital cumulative MACE rates among the 4 groups. At 8 months, there were no significant differences regarding myocardial infarction and cardiac death. Stent thrombosis rates were 3% to 4% in the non‐RCA groups, with 0% in the RCAd group. Two patients each in the LAD‐D1 and LCX‐OM groups died from myocardial infarction. TLR was frequently found in both the LMTd (26%) and LCX‐OM (25%) groups (Table 6), significantly higher than those in the LAD‐D1 (15%) and RCAd (6%, P <.001) groups.
Table 6.
Clinical Characteristics at 8 Month Follow‐up
| LMTd (n = 31) | LAD‐D1 (n = 135) | LCX‐OM (n = 29) | RCAd (n = 17) | |
|---|---|---|---|---|
| In‐hospital, n (%) | ||||
| Non Q‐wave MI | 3 (10.00) | 4 (3.00) | 3 (11.00) | 1 (6.00) |
| Q‐wave MI | 0 | 5 (4.00) | 0 | 1 (6.00) |
| Cardiac death | 1 (4.00) | 0 | 0 | 0 |
| TLR | 0 | 1 (1.00) | 0 | 0 |
| TVR | 0 | 1 (1.00) | 1 (4.00) | 0 |
| Cumulative MACE | 4 (13.00) | 10 (8.00) | 4 (14.00) | 2 (12.00) |
| Stent thrombosis | 0 | 0 | 0 | 0 |
| At 8 mo | ||||
| Non Q‐wave MI | 3 (10.00) | 5 (4.00) | 3 (11.00) | 1 (6.00) |
| Q‐wave MI | 1 (4.00) | 6 (5.00) | 1 (4.00) | 1 (6.00) |
| Cardiac death | 1 (4.00) | 1 (1.00) | 1 (4.00) | 0 |
| TLR | 8 (26.00) | 18 (15.00)b | 7 (25.00) | 1 (6.00)a |
| TVR | 9 (29.00)c | 21 (16.00) | 5 (20.00) | 3 (18.00) |
| Cumulative MACE | 12 (39.00)c | 29 (22.00) | 11 (38.00)c | 3 (18.00) |
| Stent thrombosis | 1 (4.00) | 3 (3.00) | 1 (4.00) | 0 |
Abbreviations: D1, first diagonal; LAD, left anterior descending; LCX, left circumflex; LMTd, distal left main trunk; MACE, major adverse cardiac event; MI, myocardial infarction; OM, obtuse marginal; RCAd, distal right coronary artery; TLR, target lesion revascularization; TVR, target‐vessel revascularization.
P < .001, compared to LMTd and LCX‐OM groups.
P = .025, compared to RCAd group.
P = .005, compared to LAD‐D and RCAd groups
By Cox regression analysis, KUS (hazard ratio [HR]: 12.14, 95% confidence interval [CI]: 4.01–12.10, P = .001) and non‐RCA lesion (HR: 20.69, 95% CI: 5.05–22.38, P = .001) were 2 independent MACE predictors. Independent TLR predictors were KUS (HR: 10.21, 95% CI: 0.01–0.34, P = .002), bifurcation angle (HR: 4.728, 95% CI: 2.541–4.109, P = .001), and non‐RCA lesion (HR: 16.05, 95% CI: 1.01–4.83, P = .001).
By Kaplan‐Meier analysis, TLR‐free rates in the LMTd (74%) and LCX‐OM (75%) groups were significantly lower from those in the LAD‐D (85%, P = .001) and RCAd (94%, P <.001) groups (Figure).
Figure 1.
Cumulative survival rate free from TLR at 8 months was 94% in the RCAd group and 85% in the LAD‐D group, significantly higher than that in the LMTd (74%) and LCX‐OM (75%) groups, respectively.
Discussion
The Nordic Bifurcation Study12 suggested that clinical outcomes were similar between single‐stent and double‐stent treated groups with very low 6 month MACE rates (2.9% vs 3.4% in single‐stent vs double‐stent groups, respectively); however, the side branch restenosis rate (19.2%) was still high when utilizing the single‐stent strategy. Hoye et al13 reported that the TLR in 9.7%; MACE in 16.5%; possible stent thrombosis in 4.3%; and side branch restenosis in 25.3%, at 9 months after classical crush stenting. Moussa et al 9 revealed that TLR at 6 months after classical stent was 11.3%. As a result, the most effective strategy to treat bifurcation lesions is still unknown.14, 15
To our knowledge, this is the first study that assesses clinical outcomes in patients treated with classical crush stenting at different bifurcation lesion locations. Similar to previous studies, bifurcation lesions commonly involve the LAD and the diagonal branch, and this preponderance would determine clinical outcome for the entire cohort of patients. The present study revealed that although baseline clinical, lesion, procedural, and QCA characteristics were similar between patients with LAD‐D1 and LCX‐OM lesions, there were significant differences in TLR rates between these 2 treated groups, with a resultant increased cumulative MACE rate in the LCX‐OM group. The mechanisms underlying this result are unknown, and the difference may be partially attributed to a trend that did not achieve statistical significance towards increased side branch restenosis in the LCX‐OM group.
Lesions involving the RCA, usually at the distal bifurcated segment, were more often very tortuous in the proximal and/or middle segments. This would make FKBI more procedurally difficult, thereby increasing contrast volume needed and procedural times. Significantly, the RCAd group had longer lesion lengths in the main vessel, compared to those in the LCX‐OM group, with resultant longer stent length. Furthermore, the lowest late lumen loss was found in the RCAd group, and fewer restenosis especially in the side branch was detected at 8 month follow‐up, mainly due to lower incidence of KUS. These features probably underlie the lower TLR during follow‐up. The question of why there was a lower incidence of KUS in the RCAd group remained undetermined. Another explanation of lower rate of MACE in the RCAd group was probably the possibility that there was small amount of myocardium supplied by RCA.
Stenting distal left‐main bifurcation lesions are a high risk subset for restenosis and TLR.16, 17 Stenting strategies remain a hot topic of debate.18 After a median follow‐up of 587 days, Valgimigli et al19 reported that cumulative MACE incidences were similar between single‐stenting and double‐stenting groups. In a study by Price et al,20 TLR after SES implantation was 38% due to a higher rate of restenosis within the side branch ostium. Clinical outcomes of left‐main bifurcation lesions vary depending upon the stenting technique used. Previously, we reported11 that FKBI was performed successfully in 36 of 37 patients (97.3%), a proportion similar to the present study. However, a TLR‐free survival rate of less than 50% was reported in that study. Because of the matched baseline clinical, lesion, and procedural characteristics among the 4 comparison groups, including similar lesion lengths (compared with the LAD‐D group) and KUS rates, bifurcation angle was left as the only factor influencing clinical outcomes in the LMTd group, similar to the study by Dzavik et al.21 In that study, MACE‐free survival rate was lower in high‐angle patients with FKBI vs low‐angle patients. A high angle indicates increased turbulent flow that is further exacerbated by suboptimal treatment of the crushed side branch stent,22 as indicated by Ormiston et al.23 These studies all supported the hypothesis that a greater bifurcation angle might associate with suboptimal clinical outcomes.
Conclusions
Several conclusions could be reached from this study: (1) the side branch remains a limiting factor in the improvement of clinical outcomes post‐classical crush stenting; (2) FKBI immediately post‐crush stenting did not improve clinical prognosis in patients with distal left‐main bifurcation; (3) RCAd had better outcomes post‐classical crush stenting; (4) bifurcation angle is associated with worse outcomes.
Limitations
This study had an open design, which introduces selection biases. The small patient sample size lacks the statistical power to assess differences in the rates of rare events. Also, intravascular ultrasound and glycoprotein IIb/IIIa inhibitors were not uniformly used.
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