Cardiovascular Revascularization Medicine, 2018-07-01, Volume 19, Issue 5, Pages 480-486, Copyright © 2017 Elsevier Inc. Abstract Background The association of postprocedural high-sensitivity troponin T (hs-TnT) with prognosis of non-ST-segment elevation myocardial infarction (NSTEMI) patients is incompletely investigated. Aim To assess the prognostic value of hs-TnT in NSTEMI patients undergoing early percutaneous coronary intervention (PCI). Methods This study included 3783 patients with NSTEMI undergoing early PCI. Preprocedural and peak postprocedural hs-TnT was measured. Patients were divided into 3 groups: a group with postprocedural hs-TnT in the 1st tertile (hs-TnT < 105 ng/L; n = 1264), a group with postprocedural hs-TnT in the 2nd tertile (hs-TnT ≥ 105 ng/L to 470 ng/L; n = 1258) and a group with postprocedural hs-TnT in the 3rd tertile (hs-TnT > 470 ng/L; n = 1261). The primary outcome was 1-year all-cause mortality. Results Overall, there were 299 deaths: 59 (5.5%), 98 (8.2%) and 142 deaths (12.6%) among patients of the 1st, 2nd and 3rd postprocedural hs-TnT tertiles (unadjusted hazard ratio [HR] = 1.65, 95% confidence interval [CI] 1.20 to 2.67; P = 0.002 for tertile 2 vs tertile 1 and unadjusted HR = 2.41 [1.79–3.25]; P < 0.001 for tertile 3 vs tertile 1). After adjustment postprocedural hs-TnT was independently associated with the risk of all-cause mortality (adjusted [HR] = 1.22 [1.13–1.33], P < 0.001 for 1 unit higher log hs-TnT). Postprocedural hs-TnT improved the risk prediction of the model of all-cause mortality (the C statistic of the model without [with baseline variables only] and with incorporation of postprocedural hs-TnT was 0.759 [0.732–0.782] and 0.772 [0.746–0.794], respectively; P < 0.001). Conclusions In patients with NSTEMI undergoing early PCI, postprocedural hs-TnT is independently associated with increased risk of mortality up to 1 year after PCI. Highlights Post-procedural high-sensitivity cardiac troponin T (hs-TnT) was associated with 1-year mortality in patients with NSTEMI after PCI. An increase in the post-procedural hs-TnT of > 70xthe 99th percentile URL correlated with the increased risk of mortality. hs-TnT improved the discriminatory power of the multivariable models regarding prediction of mortality. 1 Introduction Acute coronary syndromes (ACS) remain a leading cause of morbidity and mortality worldwide . Among patients presenting with ACS, an increase in the proportion of non-ST-segment elevation myocardial infarction (NSTEMI) has been reported over the last 2 decades with NSTEMI accounting for 60–75% of all infarctions in current practice . Although mortality in patients with NSTEMI has been reduced mostly due to increased use of invasive treatment strategies , long-term mortality remains a concern and risk stratification of these patients remains suboptimal . Cardiac troponins are the gold-standard biomarker for the diagnosis of patients with ACS. The implementation of high-sensitivity troponin assays, including high-sensitivity troponin T (hs-TnT), has increased the proportion of patients with NSTEMI among patients presenting with ACS and has helped to improve clinical management by defining the most beneficial therapies . Postprocedural troponin reflects the extent of ischemic damage and myocardial damage due to procedure-related factors (distal thrombus embolization, side-branch occlusion, no-reflow or complex procedure with the use of multiple stents) and seems to be useful for risk-stratification of patients with NSTEMI treated by percutaneous coronary intervention (PCI). Several studies have used cardiac troponins for the risk stratification of patients with non-ST-segment ACS, yet the prognostic value of post-PCI cardiac troponins following PCI in patients with non-ST-segment elevation ACS remains controversial . Many prior studies have been performed in the conventional troponin era or have included patient groups that were inhomogeneous in terms of presentation (stable disease and ACS), ACS type (unstable angina and NSTEMI) or therapy (invasive and noninvasive medical therapy). These conditions differ with respect to their association with the patient prognosis. Given this background, we conducted this study with the aim to assess the prognostic value of postprocedural hs-TnT in a large series of patients with NSTEMI treated with an early invasive strategy. 2 Methods 2.1 Patients This was a retrospective study of 3783 patients with NSTEMI treated with an early PCI in 2 hospitals: Deutsches Herzzentrum München (between October 2009 and December 2014) and Bern University Hospital, Switzerland (between September 2010 and June 2014). NSTEMI was diagnosed in the presence of clinical symptoms suggestive of myocardial ischemia and elevation of hs-TnT exceeding the 99th upper reference limit (URL). The diagnosis was confirmed by angiography in all patients. Patients whose pre- or postprocedural hs-TnT data were not available for analysis were excluded (n = 23). The study was conducted in accordance with the Helsinki Declaration. 2.2 PCI procedure and definitions PCI was performed as per standard practice. An early (< 24-hour) invasive strategy consisting of PCI immediately following the diagnosis of NSTEMI was pursued. Commercially available balloon, bare-metal stents, drug-eluting stents, and bioresorbable vascular scaffolds were used. Unfractionated heparin or bivalirudin was used as an anticoagulant. Dual antiplatelet therapy consisting of aspirin and a P2Y 12 inhibitor was initiated before, at the time, or immediately after the procedure. Glycoprotein IIb/IIIa inhibitors were used at the discretion of the operator. Following PCI, chronic dual antiplatelet therapy with oral aspirin (continued indefinitely) and a P2Y 12 inhibitor (mostly clopidogrel continued for at least 12 months) was prescribed in all patients. Other cardiac medications were at the discretion of treating physicians. Cardiovascular risk factors (including diabetes, arterial hypertension, hypercholesterolemia and current smoking) were defined using the accepted criteria. Baseline and postprocedural epicardial blood flow was graded using the Thrombolysis in Myocardial Infarction (TIMI) group angiographic criteria. Left ventricular ejection fraction was calculated using the area-length method on left ventricular angiography. Body mass index was calculated by using patient's weight and height measured during the hospital course. Glomerular filtration rate was calculated using the Cockcroft-Gault equation. 2.3 Biochemical measurements Blood samples were collected in tubes containing a lithium-heparin anticoagulant. Blood samples for hs-TnT measurements were obtained before procedure and within 12 h after PCI. In case of an increase in postprocedural hs-TnT, repetitive measurements over 48 h were obtained. The peak postprocedural hs-TnT level was defined as the highest in-hospital concentration. Within 30 min, the blood was centrifuged at room temperature and the plasma supernatant was separated. The plasma concentration of hs-TnT was measured with a high-sensitivity assay (fourth generation Elecsys troponin T assay; Roche Diagnostics, Mannheim, Germany). The limit of blank for this assay, the concentration below which analyte-free samples are found with a probability of 95%, is ≤ 3 ng/L. The functional sensitivity, i.e., the lowest analyte concentration that can be reproducibly measured with a coefficient of variation ≤ 10% is ≤ 13 ng/L. The 99th URL is 14 ng/L. 2.4 Study outcome and follow-up The primary outcome was all-cause mortality up to 1 year after PCI. Follow-up was performed by phone interview at 1, 6, and 12 months after PCI. Data on mortality were obtained from hospital charts, death certificates, telephone contact with relatives of the patient or family physicians, insurance companies, or the registration of address office. Cardiac deaths were defined according to the Academic Research Consortium criteria . Medical personnel unaware of patient clinical or laboratory data performed follow-up and adjudication of events. 2.5 Statistical analysis Continuous variables are presented as median with 25th–75th percentiles and compared using the Kruskal-Wallis rank sum test. Categorical variables are presented as counts or proportions (percentage) and compared using chi-squared test. Survival analysis was performed using the Kaplan-Meier method and differences between groups were quantified by univariable Cox proportional hazards model. Landmark analysis with a prespecified landmark at 1 month was performed to assess early and late relative risk of death associated with postprocedural hs-TnT. The multiple linear regression model was used to assess variables that were independently associated with elevated postprocedural hs-TnT level. Cox proportional hazard model was used to identify the independent correlates of all-cause and cardiac mortality. All baseline and procedural variables of Tables 1 and S1 were entered into the multivariable models applied to obtain correlates of postprocedural hs-TnT or mortality. In lesion-based analyses, the unit was lesion and the generalized estimating equation method was used to take into account potential cluster effects of multiple lesions in a single patient. Multicollinearity was assessed by calculating the variance inflation factor (VIF) for each predictor. A VIF between 5 and 10 indicates high correlation between predictors . Baseline and postprocedural hs-TnT were entered into the model after logarithmic transformation because of its skewed distribution. Variables with incomplete data were included in the models after imputing missing data using multiple imputation by chained equations method. The discriminatory power of the multivariable models without (baseline variables only) and with baseline variables plus hs-TnT was assessed by calculating the Harrell's c statistic and the integrated discrimination improvement (IDI) . The same variables as for the Cox model of mortality were entered into the models used to calculate the C statistic and IDI. Bootstrapping (400 samples) was used to calculate the confidence interval of the C statistic and IDI and to enable the comparison of C statistics and IDIs of the models without and with hs-TnT. The statistical analysis was performed using the R 3.1.1 Statistical Package (The R foundation for Statistical Computing, Vienna, Austria). A two-sided P < 0.05 was considered to indicate statistical significance. Table 1 Patient characteristics. CharacteristicsHigh-sensitivity troponin T tertilesP value 1 (n = 1264)2 (n = 1258)3 (n = 1261) Age (years) 72.7 [64.7–79.0] 72.4 [62.9–80.0] 71.4 [61.2–80.0] 0.100 Female sex 313/1264 (24.8) 348/1258 (27.7) 334/1261 (26.5) 0.250 Diabetes mellitus 450/1264 (35.6) 389/1257 (30.9) 321/1255 (25.6) < 0.001 Insulin therapy 170/1264 (13.4) 162/1258 (12.9) 106/1261 (8.4) < 0.001 Body mass index (kg/m 2 ) 27.3 [24.5–30.7] 26.6 [21.1–30.0] 26.5 [24.2–29.4] < 0.001 Arterial hypertension 954/1263 (75.5) 900/1254 (71.8) 795/1252 (63.5) < 0.001 Current smoker 227/1260 (18.0) 276/1244 (22.2) 310/1244 (24.9) < 0.001 Hypercholesterolemia 922/1264 (72.9) 863/1253 (68.9) 769/1250 (61.5) < 0.001 Prior myocardial infarction 365/1264 (28.9) 275/1256 (21.9) 242/1254 (19.3) < 0.001 Prior CABG 187/1264 (14.8) 170/1257 (13.5) 140/1255 (11.1) 0.023 Baseline hs-TnT (ng/L) 30 [20–50] 108 [45–199] 504 [150–1190] < 0.001 Peak postprocedural hs-TnT (ng/L) 50 [32–73] 215 [150–320] 1290 [740–2560] < 0.001 Glomerular filtration rate (mL/min) 71.6 [52.7–100.1] 73.1 [51.3–103.5] 74.4 [51.3–105.9] 0.400 Extent of coronary artery disease < 0.001 1-Vessel disease 389/1264 (30.8) 467/1258 (37.1) 539/1261 (42.7) 2-Vessel disease 299/1264 (23.7) 301/1258 (23.9) 333/1261 (26.4) 3-Vessel disease 576/1264 (45.5) 490/1258 (39.0) 389/1261 (30.9) Multivessel disease 875/1264 (69.2) 791/1258 (62.9) 772/1261 (57.3) < 0.001 LVEF (%) 57.0 [47.0–62.0] 55.0 [43.0–60.0] 50.0 [40.0–60.0] < 0.001 Data are shown as medians [25th–75th percentiles] or number of patients (%). CABG = coronary artery bypass grafting; hs-TnT = high-sensitivity troponin T; LVEF = left ventricular ejection fraction; 3 Results 3.1 Baseline characteristics The study included 3783 patients with NSTEMI. Patients were divided according to the tertiles of postprocedural hs-TnT: 1st tertile (hs-TnT < 105 ng/L; n = 1264 patients), 2nd tertile (hs-TnT ≥ 105 ng/L to 470 ng/L; n = 1258 patients) and 3rd tertile (hs-TnT > 470 ng/L; n = 1261 patients). Baseline clinical characteristics are shown in Table 1 . The proportion of patients with diabetes, arterial hypertension, hypercholesterolemia, previous myocardial infarction or coronary artery bypass surgery decreased from lowest to highest postprocedural hs-cTnT tertiles. Procedural characteristics are shown in Table S1. Drug-eluting stents were implanted in 91.9% of lesions in patients in the 1st, 92.4% of lesions in patients in the 2nd, and 91.0% of lesions in patients in the 3rd tertiles of postprocedural hs-TnT. Multiple lesions were present in 47% of the patients. The multiple linear regression model showed that lower body mass index (P < 0.001), arterial hypertension (P = 0.007), diabetes (P = 0.018), multivessel disease (P = 0.009), higher baseline troponin level (P < 0.001), restenotic lesion (inverse association; P < 0.001), total stented length (P = 0.006) and lower baseline TIMI flow grade (P < 0.001) were independently associated with higher postprocedural hs-TnT levels. There was a trend for an association between lower postprocedural TIMI flow grade and postprocedural hs-TnT (P = 0.070). 3.2 Postprocedural hs-TnT and 1-year prognosis The median follow-up was 1.1 [1.0–1.7] years. Overall there were 299 deaths during the follow-up. Postprocedural hs-TnT (median with 25th–75th percentiles) was 204 [70–691] ng/L in survivors and 393 [138–1445] ng/L in nonsurvivors (P < 0.001). There were 59 deaths in patients in the 1st, 98 deaths in patients in the 2nd and 142 deaths in patients in the 3rd tertiles of postprocedural hs-TnT (Kaplan-Meier estimates of 1-year mortality, 5.5%, 8.2% and 12.6%; unadjusted hazard ratio [HR] = 1.65, 95% confidence interval [CI] 1.20 to 2.67; P = 0.002 for tertile 2 vs tertile 1 and unadjusted HR = 2.41 [1.79–3.25]; P < 0.001 for tertile 3 vs tertile 1; Fig. 1 ). Cardiac deaths occurred in 173 patients (58% of deaths): 31 deaths in patients in the 1st, 61 deaths in patients in the 2nd and 81 deaths in patients in the 3rd postprocedural hs-TnT tertiles (Kaplan-Meier estimates of 1-year cardiac mortality, 2.9%, 5.5% and 7.2%; unadjusted HR = 1.90 [1.25–2.90]; P = 0.003 for tertile 2 vs tertile 1 and unadjusted HR = 2.56 [1.71–3.83]; P < 0.001 for tertile 3 vs tertile 1; Fig. 1 ). The landmark analysis showed that postprocedural hs-TnT was associated with the risk of early (30-day) as well as late (30-day to 1 year) all-cause and cardiac mortality (Supplementary material; Fig. S1). Preprocedural hs-TnT was also associated with 1-year mortality (Supplementary material; Fig. S2). Fig. 1 Kaplan-Meier curves of all-cause and cardiac mortality in patient groups according to the tertile values of postprocedural high-sensitivity troponin T (hs-TnT) levels. The curves are hierarchically ordered according to the order of numbers of patients at risk. HR = hazard ratio. The association between postprocedural and preprocedural hs-TnT with all-cause or cardiac mortality was adjusted in the Cox proportional hazards model. The variables entered into the multivariable model showed a VIF < 2.31, excluding any relevant multicollinearity. Postprocedural hs-TnT was independently associated with the risk for all-cause (adjusted hazard ratio [HR] = 1.22, 95% confidence interval [CI] 1.13 to 1.33, P < 0.001) and cardiac (HR = 1.14 [1.04–1.27], P = 0.010) mortality, with both risk estimates calculated per unit of log hs-TnT ( Table 2 ). After inclusion of preprocedural hs-TnT in the model, the association between postprocedural hs-TnT and all-cause mortality remained significant (HR = 1.22 [1.08–1.37], P = 0.001) whereas the association with cardiac mortality was attenuated (HR = 1.14 [0.97–1.35], P = 0.116) with both risk estimates calculated per 1 unit of log postprocedural hs-TnT. Table 2 Results of multivariable Cox proportional hazards model applied to assess predictors of mortality with peak postprocedural high-sensitivity troponin in the model. CharacteristicsHazard ratio [95% confidence interval] Cardiac mortalityAll-cause mortality Peak postprocedural hs-TnT (for 1 unit log hs-TnT) 1.14 [1.04–1.27] 1.22 [1.13–1.33] Age (for 10-year older age) 1.59 [1.22–2.08] 1.50 [1.23–1.82] Female sex 0.91 [0.58–1.44] 0.94 [0.67–1.31] Diabetes mellitus 1.60 [1.07–2.39] 1.55 [1.16–2.07] Arterial hypertension 0.47 [0.34–0.66] 0.45 [0.36–0.61] Hypercholesterolemia 0.67 [0.47–0.96] 0.68 [0.52–0.89] Previous myocardial infarction 1.22 [0.82–1.80] 1.02 [0.75–1.38] Previous coronary bypass graft surgery 0.88 [0.49–1.58] 1.35 [0.89–2.04] Body mass index (for 5 kg/m 2 higher) 1.00 [0.96–1.06] 1.02 [0.83–1.25] Current smoker 0.90 [0.53–1.50] 1.16 [0.80–1.69] Multivessel disease 0.98 [0.65–1.48] 0.96 [0.69–1.33] Glomerular filtration rate (for 30 mL/min lower) 1.00 [0.98–1.01] 1.30 [1.01–1.67] Target vessel: left main coronary artery 1.43 [0.84–2.43] 1.40 [0.96–2.05] Restenotic lesions 0.51 [0.23–1.15] 0.81 [0.50–1.30] Bifurcational lesion 0.77 [0.52–1.15] 0.84 [0.63–1.13] Complex lesions (AHA B2/C class) 1.51 [1.07–2.17] 0.90 [0.67–1.19] Balloon diameter (for 0.5 mm greater diameter) 0.98 [0.78–1.23] 1.06 [0.96–1.15] Total stented length (for 10 mm longer length) 1.00 [0.98–1.01] 1.00 [0.94–1.06] Preprocedural TIMI flow grade (for 1 grade higher) 0.94 [0.80–1.10] 0.98 [0.87–1.12] Postprocedural TIMI flow grade (for 1 grade higher) 1.05 [0.46–2.44] 1.03 [0.59–1.81] Left ventricular ejection fraction (for 10% lower) 1.43 [1.26–1.64] 1.26 [1.13–1.40] AHA = American Heart Association; hs-TnT = high-sensitivity troponin T; TIMI = Thrombolysis in Myocardial Infarction. Preprocedural hs-TnT was also independently associated with the risk of 1-year mortality (see Supplementary material, Table S2). 3.3 Prognostic value of various cutoffs of postprocedural hs-TnT elevation The association between postprocedural hs-TnT level and all-cause and cardiac mortality was assessed over several multiples of 99th percentile URL cutoffs. The results of this analysis are shown in Fig. 2 . Notably, only patients with an increase in postprocedural hs-TnT > 70 × the 99th percentile URL cutoff had an increased risk of all-cause mortality compared with patients who had no increase in hs-TnT after procedure. Fig. 2 All-cause and cardiac mortality according to different cut-offs of elevation of postprocedural high-sensitivity troponin T (hs-TnT). Percentages represent Kaplan-Meier estimates of mortality. Risk estimates represent univariable hazard ratios calculated with univariable Cox proportional hazards model. PCI = percutaneous coronary intervention; URL = upper reference limit. *Not further elevated after PCI compared to the preprocedural level. 3.4 Discriminative prognostic value of hs-TnT The discrimination of the risk prediction models of all-cause mortality was assessed by calculating the C-statistic and IDI of the models without (with baseline variables only) and with inclusion of postprocedural hs-TnT alongside baseline variables. Results are shown in Table 3 . Addition of postprocedural hs-TnT alongside baseline data in multivariable model improved the discriminatory power of the model as regards the prediction of 1-year mortality. The inclusion of preprocedural hs-TnT did not attenuate the discriminatory power of postprocedural hs-TnT as regards prediction of all-cause mortality. The difference in C statistics (delta C statistic) of the model with both preprocedural and postprocedural hs-TnT versus the model with postprocedural hs-TnT only was 0.003 [− 0.0005 to 0.002 CI], P = 0.620. Delta IDI was 0.0006 [− 0.0002 to 0.003 CI], P = 0.355. Table 3 The discrimination of the risk prediction models of all-cause mortality without and with preprocedural and postprocedural high-sensitivity troponin T. ModelC statisticIDIDelta C statistic a Delta IDI a P1P2 Baseline variables 0.759 [0.732–0.782] 0.114 [0.085–0.147] … … … … Baseline variables plus preprocedural hs-TnT 0.765 [0.740–0.789] 0.121 [0.092–0.154] 0.006 [0.001–0.017] 0.007 [0.001–0.017] 0.005 0.005 Baseline variables plus postprocedural hs-TnT 0.772 [0.746–0.794] 0.127 [0.098–0.162] 0.012 [0.005–0.022] 0.013 [0.004–0.025] < 0.001 < 0.001 Baseline variables plus pre- and postprocedural hs-TnT 0.772 [0.745–0.794 0.127 [0.99–0.162] 0.013 [0.005–0.223] 0.014 [0.004–0.025] < 0.001 < 0.001 Numbers in brackets show 95% confidence interval of the C statistic and the integrated discrimination improvement (IDI). P1 shows difference in C statistics between the models without and with inclusion of hs-TnT. P2 shows difference in IDI between the models without and with inclusion of hs-TnT. a Difference of the C-statistic and IDI of the model with preprocedural or postprocedural high-sensitivity troponin T (hs-TnT) or both biomarkers with the model with baseline variables only b . b See Methods section (statistical analysis) for the list of baseline variables entered into the model. 4 Discussion The main findings of this study can be summarized as follows: First, in patients with NSTEMI treated with early PCI, postprocedural hs-TnT was an independent correlate of increased risk of mortality up to 1 year following the PCI procedure. Second, the relationship between postprocedural hs-TnT and mortality was not linear; only patients with an increase in the post-procedural hs-TnT of > 70 × the 99th percentile URL showed an increased risk of all-cause mortality compared with patients who had no increase in hs-TnT after procedure. Third, hs-TnT improved the discriminatory power of the multivariable models as regards prediction of mortality indicating that prognostic information provided by hs-TnT is incremental and beyond that provided by baseline cardiovascular risk factors, angiographic coronary artery disease (CAD) and indexes of epicardial reperfusion. Previous studies used cardiac troponins for risk stratification of patients with non-ST-segment elevation ACS but the results are controversial . There were, however, striking differences across the studies in terms of troponin assay used (conventional or high-sensitivity assay), ACS type (unstable angina and NSTEMI), and therapy received (invasive vs. conservative therapy). Although these differences make inter-study comparison difficult, in principle, they may help to explain the discordant results across the studies. The high-sensitivity troponin assays, such as hs-TnT used in current study, enable detection of minuscule myocardial damage and have markedly increased the proportion of patients with NSTEMI among patients presenting with ACS . One consequence of the use of high-sensitivity cardiac troponin assays is a marked reduction of the proportion of patients with unstable angina. As stated by Braunwald and Morrow it remains unclear whether acute coronary syndrome events can occur without some increase in circulating troponin measured by a high-sensitivity assay. Thus in the era of high-sensitivity troponin assays unstable angina is likely to be further marginalized. High-sensitivity cardiac troponin assays have also helped to guide therapy of patients presenting with ACS with no increase in hospital resource utilization . Unstable angina and NSTEMI, grouped together as non-ST-segment elevation ACS, differ markedly with regard to prognosis . Finally, an early invasive treatment strategy has been shown to improve the outcome of patients with non-ST-segment elevation ACS and is recommended by current guidelines . The current study differs from the above studies in several aspects. The study included only patients with NSTEMI and all patients were treated with a contemporary invasive strategy consisting of early PCI, predominantly with new-generation drug-eluting stents. Furthermore, a high-sensitivity troponin assay (hs-TnT) was used for the diagnosis of NSTEMI and risk stratification in all patients. The main finding of current study was that elevated postprocedural hs-TnT was associated with increased risk of all-cause and cardiac mortality up to 1 year after PCI. The risk was more pronounced in the early phase following PCI, but persisted beyond 30 days in landmark analyses. Furthermore, the study showed that postprocedural hs-TnT provides prognostic information that is incremental to the information provided by conventional risk factors, relevant clinical variables and indexes of successful reperfusion (postprocedural TIMI flow grade). Reasons why postprocedural hs-TnT is associated with an increased risk of mortality in patients with NSTEMI but not in patients with stable CAD undergoing elective PCI remain unknown. In patients with NSTEMI treated with early PCI, postprocedural hs-TnT includes 3 fractions with potential to impact on prognosis. A fraction of post-procedural hs-TnT may reflect cardiovascular risk factors, more extensive CAD and comorbidities known to be particularly prevalent among patients with NSTEMI . These factors may increase circulating troponin via increased cardiometabolic stress on myocardium . Another fraction of postprocedural hs-TnT reflects continuation of hs-TnT elevation due to spontaneous ischemic event in the post-PCI time interval. Prior studies have shown a close correlation between cardiac troponin and scintigraphic infarct size . On the other hand it is widely accepted that infarct size is a predictor of increased risk of mortality . The third fraction of postprocedural hs-TnT is PCI-related. The procedure-related hs-TnT elevation may be more relevant as regards the association with prognosis in patients with NSTEMI compared with stable patients undergoing elective PCI. Since coronary thrombus is highly prevalent in patients with NSTEMI, distal thrombus embolization and side-branch occlusion may be more frequent and may lead to more myocardial damage and troponin release in patients with NSTEMI compared with stable patients undergoing elective PCI. As recently shown by Pride et al. , the incidence of intraprocedural complications is high in patients with non-ST-segment elevation ACS and they are associated with worse clinical outcomes independent of epicardial and myocardial perfusion. Prior studies and a recent study from our group have shown that postprocedural troponin was not associated with prognosis following elective PCI. Other studies have demonstrated a strong association between baseline hs-TnT level and prognosis after elective PCI . There are at least 2 reasons why the prognostic performance of postprocedural hs-TnT may differ in patients with NSTEMI versus those with stable CAD. First, contrary to patients with stable CAD who have stable troponin levels at the time of elective PCI, patients with NSTEMI have an acute ischemic event and unstable levels of biomarker at the time of PCI. As recently shown by Tricoci et al. 41% of patients presenting with non-ST-segment elevation ACS have rising troponin levels at the time of PCI. Thus, in patients with NSTEMI, continuation of increase of preprocedural troponin which reflects the extent of spontaneous ischemic damage contributes to elevation of postprocedural troponin and conveys in it the prognostic information it bears. Conversely, stable patients are supposed to have stable levels of the biomarker which are not related to an acute ischemic event at the time of PCI. Second, cardiovascular risk profile and procedure-related complications (particularly those related to coronary thrombus) may make a greater contribution to troponin elevation after PCI and to prognosis in patients with NSTEMI compared to patients with stable CAD undergoing elective PCI. One study that included patients with stable angina and ACS showed that postprocedural troponin was associated with adverse outcomes in patients with ACS but not in those with stable CAD . The study has limitations. First, due to pursuing a strategy of early intervention following diagnosis of NSTEMI, serial testing of hs-TnT before PCI was not performed. Consequently, we could not discriminate between spontaneous and procedure-related elevations of postprocedural hs-TnT. Second information on the time interval from symptom onset to PCI and preprocedural or postprocedural hs-TnT measurement was not available. Third, information on drug therapy prescribed at discharge was not systematically recorded and is therefore not reported. Fourth, these data are obtained using the hs-TnT assay and may not be extrapolated to assess the performance of other troponin assays. Fifth, the reason why only postprocedural hs-TnT elevation in excess of 70 × 99th percentile URL was associated with the risk of mortality remains partially explainable. However, the occurrence of undocumented PCI-related complications that may have led to a large post-procedural hs-TnT elevation and have incurred a negative impact on prognosis in this subgroup of patients cannot be excluded. Finally, in the current study only early peak values of hs-TnT were assessed. However, it has been reported that a single 96-hour cardiac TnT value provides an accurate estimate of absolute infarct mass in patients with myocardial infarction . In conclusion, in patients with NSTEMI undergoing early PCI, elevated postprocedural level of hs-TnT is associated with increased risk of all-cause and cardiac mortality up to 1 year after intervention. Patients with an increase in postprocedural hs-TnT of > 70 × 99th percentile URL cutoff had an increased risk of mortality compared with patients with no increase in hs-TnT after procedure. Postprocedural hs-TnT improves the discriminatory power of multivariable models of mortality by providing prognostic information that is incremental to and beyond that provided by conventional cardiovascular risk factors, angiographic CAD and indexes of epicardial reperfusion. Conflicts of interest None declared. Funding sources None.