This study evaluated the risk factors of postprocedure cardiac troponin I (cTnI) increase and its effects on repeat revascularization and on overall clinical outcomes in patients with angina and normal preprocedural cTnI levels who underwent successful drug-eluting stent implantation. Postprocedure cTnI increase (≥0.5 ng/ml) was observed in 207 of 802 patients (25.8%). Patients with cTnI increase had more extensive coronary disease than patients without cTnI increase, which necessitated for the cTnI group more multilesion interventions and a longer total stent length. In multivariate analysis, total stent length (odds ratio 1.02, 1.01 to 1.03, p = 0.001) and use of glycoprotein IIb/IIIa inhibitors (3.07, 1.54 to 6.11, p <0.001) were identified as independent predictors of cTnI increase. During a median follow-up of 42 months, however, there were no significant between-group differences in Kaplan–Meier estimates of any repeat revascularization (24.8% vs 18.4%, hazard ratio 1.085, 0.723 to 1.627, p = 0.694) and major adverse cardiovascular events (27.0% vs 22.4%, 1.022, 0.703 to 1.485, p = 0.911). In conclusion, patients with postprocedure cTnI increase had more severe baseline coronary disease and received more complex interventional procedures. However, cTnI increase after successful drug-eluting stent implantation was not associated with an increased risk of repeat revascularization or of other adverse events.
Some studies have demonstrated that cardiac troponin I (cTnI) increase after percutaneous coronary intervention (PCI) in patients with stable coronary disease is significantly associated with adverse outcomes, predominantly in the form of repeat revascularization. Currently, drug-eluting stents (DESs) have shown superior results not only for repeat revascularization but also for major adverse cardiovascular events (MACEs) compared to bare-metal stents in various angiographic patient subsets. However, there have been few reports evaluating the clinical characteristics and prognostic significance of postprocedure cTnI increase after DES implantation. The aim of the present study was to identify the risk factors and effects of postprocedure cTnI increase on repeat revascularization and on overall clinical outcomes in patients who underwent elective PCI using DESs.
Methods
The analysis was conducted from a DES registry of Seoul National University Bundang Hospital. A total of 802 patients with angina and normal preprocedural cTnI levels who underwent successful DES implantation from January 2005 through December 2007 were included. We excluded patients who had serum and electrocardiographic evidence of acute and recent myocardial infarction (MI) or whose cTnI results were unavailable. Blood samples for cTnI were collected before the procedure and at 6 and 12 hours after the procedure. cTnI levels were measured by a sandwich enzyme immunoassay using Dimension RxL (Dade Behring, Deerfield, Illinois; reference range <0.5 ng/ml). This study was approved by the institutional review board of Seoul National University Bundang Hospital.
Coronary interventions were performed using conventional techniques. Choice of the stent, predilatation, poststent adjunctive balloon inflation, and use of glycoprotein IIb/IIIa inhibitors was left to the operators’ discretion. All patients were pretreated with aspirin and clopidogrel. Aspirin was maintained indefinitely and clopidogrel for ≥6 months. Successful PCI was defined as the achievement of Thrombolysis In Myocardial Infarction grade 3 flow in the treated vessel with a residual stenosis <30% in the absence of major (>1.5 mm) side branch occlusion or evident distal embolization. Clinical follow-up after PCI was recommended at 1 month, 6 months, and 1 year and then annually thereafter. Subjects who were lost to recommended follow-up were contacted by telephone at regular 12-month intervals. Outcome data were collected by independent nurses and researchers who had not participated in the management of the patients. MACEs were defined as a composite of death, nonfatal MI, and any repeat revascularization including target vessel revascularization and nontarget vessel revascularization. All deaths were considered cardiovascular unless a specific cause of death was demonstrated. MI was defined as the presence of ≥2 of the 3 following items: ischemic symptoms, cardiac enzyme concentration ≥2 times the upper limit of normal, and/or new electrocardiographic changes compatible with MI. Target vessel revascularization was defined as any repeat PCI or coronary artery bypass graft surgery of the target vessel.
Continuous variables, which are presented as mean ± SD, were compared by unpaired Student’s t test. Categorical variables, presented as frequency and percentage, were compared using chi-square test or Fisher’s exact test as appropriate. Event rates of interest were estimated using Kaplan–Meier methods and comparisons between groups were performed using log-rank statistics. Stepwise multivariate logistic regression analysis was performed to determine independent predictors of cTnI increase after PCI. Variables entered in multivariate analysis were selected using stepwise regression analysis with an entry criterion of a p value <0.10. Predictors identified through univariate analysis (p <0.10) and other variables considered likely to have important prognostic value were tested in a multivariable stepwise forward Cox proportional-hazards model for association with MACEs during the follow-up periods. All statistical analyses were performed using SPSS 17.0 (SPSS Inc., Chicago, Illinois).
Results
Of the 802 patients who underwent successful elective PCI with DESs, cTnI increase was detected in 207 (25.8%). Figure 1 shows the distribution of patients with increased cTnI. Baseline characteristics are listed in Table 1 .
| Characteristics | Postprocedure cTnI Increase | p Value | |
|---|---|---|---|
| Yes (n = 207) | No (n = 595) | ||
| Age (years) | 65.1 ± 10.6 | 64.4 ± 9.7 | 0.411 |
| Men | 130 (63%) | 407 (68%) | 0.145 |
| Initial clinical diagnosis | 0.628 | ||
| Stable angina pectoris | 106 (51%) | 317 (53%) | |
| Unstable angina pectoris | 101 (49%) | 278 (47%) | |
| Smoker | 110 (55%) | 337 (58%) | 0.408 |
| Diabetes mellitus | 77 (37%) | 226 (38%) | 0.868 |
| Hypertension ⁎ | 149 (72%) | 412 (69%) | 0.482 |
| Hypercholesterolemia † | 93 (45%) | 252 (42%) | 0.568 |
| Previous percutaneous coronary intervention | 20 (9.7%) | 85 (14.3%) | 0.095 |
| Previous coronary bypass | 10 (4.8%) | 21 (3.5%) | 0.406 |
| Creatinine (mg/dl) | 1.35 ± 1.26 | 1.27 ± 1.19 | 0.419 |
| Creatinine ≥2 mg/dl | 13 (6.3%) | 41 (6.9%) | 0.873 |
| Cholesterol (mg/dl) | 184.9 ± 40.9 | 182.5 ± 41.5 | 0.465 |
| Use of statin ‡ | 114 (55%) | 351 (59%) | 0.328 |
| Left ventricular ejection fraction (%) | 58.7 ± 10.1 | 60.0 ± 9.1 | 0.091 |
| Left ventricular ejection fraction <45% | 21 (10.1%) | 44 (7.4%) | 0.237 |
⁎ Blood pressure ≥140/90 mm Hg or use of antihypertensive medications.
† Total cholesterol level >200 mg/dl or previous use of lipid-lowering agents for a history of dyslipidemia at admission.
Patients with cTnI increase had more multivessel coronary involvement and received multilesion PCI more frequently than patients without cTnI increase. Furthermore, patients with cTnI increase had more type B2/C lesions and received more and longer stents per lesion. Consistent with having more extensive coronary artery disease with more complex lesions, patients with cTnI increase were likely to receive glycoprotein IIb/IIIa inhibitors more frequently than patients without cTnI increase ( Table 2 ). On multivariate logistic regression analysis, total stent length (odds ratio 1.02, 1.01 to 1.03, p = 0.001) and use of glycoprotein IIb/IIIa inhibitors (odds ratio 3.07, 1.54 to 6.11, p <0.001) were identified as independent predictors of postprocedure cTnI increase.
| Characteristics | Postprocedure cTnI Increase | p Value | |
|---|---|---|---|
| Yes (n = 207) | No (n = 595) | ||
| Left main coronary disease | 15 (7.2%) | 38 (6.4%) | 0.630 |
| Multivessel coronary disease | 161 (78%) | 399 (67%) | 0.004 |
| Multilesion coronary intervention | 95 (46%) | 175 (29%) | <0.001 |
| Use of glycoprotein IIb/IIIa inhibitor | 19 (9.2%) | 18 (3.0%) | 0.001 |
| Type of stent | 0.266 | ||
| Cypher | 95 (46%) | 306 (51%) | |
| Taxus | 49 (24%) | 149 (25%) | |
| Endeavor | 42 (20%) | 94 (16%) | |
| Mixed | 21 (10%) | 46 (8%) | |
| Stent number per patient | 2.22 ± 1.24 | 1.67 ± 0.90 | <0.001 |
| Total stent length (mm) | 53.9 ± 31.8 | 39.5 ± 23.7 | <0.001 |
| Target coronary vessel (n) | 310 | 774 | 0.200 |
| Left anterior descending | 138 (45%) | 404 (52%) | |
| Left circumflex | 83 (27%) | 164 (21%) | |
| Right | 76 (25%) | 173 (22%) | |
| Left main | 10 (3.2%) | 28 (3.6%) | |
| Saphenous vein graft | 3 (1.0%) | 4 (0.5%) | |
| Left internal mammary | 0 (0.0%) | 1 (0.1%) | |
| Lesion (n) | 332 | 802 | |
| American College of Cardiology/American Heart Association type B2/C lesion | 252 (76%) | 545 (68%) | 0.008 |
| Quantitative coronary angiography | |||
| Reference vessel (mm) | 2.77 ± 0.58 | 2.81 ± 0.53 | 0.348 |
| Minimal luminal diameter (mm) | 0.66 ± 0.42 | 0.71 ± 0.47 | 0.104 |
| Diameter stenosis (%) | 76.5 ± 13.8 | 74.8 ± 15.2 | 0.08 |
| Stent number per lesion | 1.37 ± 0.64 | 1.22 ± 0.47 | <0.001 |
| Stent length per lesion (mm) | 33.6 ± 18.1 | 29.1 ± 14.2 | <0.001 |
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