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Background: The frequency and prognostic value of coronary no-reflow (CNR) was investigated in studies that have used an outdated reperfusion therapy in terms of stent technology and antithrombotic drugs. We assessed the association of CNR with adverse outcomes in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES) and newer antithrombotic drugs, ticagrelor or prasugrel. Methods: This study included 3100 patients with AMI who underwent PCI with current DES and third-generation P2Y12 inhibitors. CNR was defined as Thrombolysis in Myocardial Infarction (TIMI) blood flow grade ≤ 2 at the end of PCI. The primary end point was 1-year incidence of net adverse clinical and cerebral events—a composite end point of death of any cause, myocardial infarction, stroke or major bleeding. Results: CNR was diagnosed in 130 patients (4.2%). The primary end point occurred in 28 patients in the CNR group and 354 patients in the reflow group (cumulative incidence 23.2% and 12.8%; adjusted hazard ratio = 1.53, 95% confidence interval 1.01–2.33; P = 0.049). The 1-year incidences of death or myocardial infarction (14.6% vs. 7.6%; P = 0.003), myocardial infarction (8.8% vs. 3.9%; P = 0.007) and major bleeding (10.9% vs. 5.6%; P = 0.008) were significantly higher in patients with CNR than patients with reflow. The risk of adverse events in patients with CNR was highest within the first 30 days after PCI. Conclusion: In patients with AMI undergoing PCI with current DES and third generation P2Y12 receptor inhibitors, CNR was associated with a higher risk of adverse outcomes at 1 year. [ABSTRACT FROM AUTHOR]

Background: The association of aspartate aminotransferase to alanine aminotransferase ratio (De Ritis ratio) with clinical outcomes in patients with chronic coronary syndromes (CCS) remains unclear. This study aims to assess the association of De Ritis ratio with adverse cardiovascular events in patients with CCS. Materials and Methods: The study included 5020 patients with CCS undergoing percutaneous coronary intervention. Patients were categorized into groups according to tertiles of the De Ritis ratio: tertile 1 (De Ritis ratio: <.75; n = 1688 patients), tertile 2 (De Ritis ratio:.75–1.08; n = 1666 patients) and tertile 3 (De Ritis ratio: >1.08; n = 1666 patients). The primary endpoint was 3‐year mortality. Results: At 3 years, there were 384 deaths, 176 myocardial infarctions and 61 strokes. In groups with De Ritis in the 1st, 2nd and 3rd tertiles, deaths occurred in 5.0%, 7.5% and 14.5% of the patients, respectively (adjusted hazard ratio = 1.09, 95% confidence interval [1.06–1.12], p <.001); myocardial infarctions occurred in 2.6%, 3.5% and 5.1% of the patients, respectively (p <.001); strokes occurred in 1.0%, 1.2% and 1.9% of the patients, respectively (p =.030); bleeding at 30 days (n = 112) occurred in 1.4%, 1.6% and 3.7% of the patients, respectively (p <.001). The C‐statistic of the Cox proportional hazards model for all‐cause mortality with baseline data without the De Ritis ratio was.815 [.794–.836] and.818 [.797–.838] after the inclusion of the De Ritis ratio (delta C‐statistic =.003; p =.005). Conclusions: In patients with CCS undergoing percutaneous coronary intervention, an elevated De Ritis ratio was associated with long‐term major adverse cardiovascular events. [ABSTRACT FROM AUTHOR]

• Elevated De Ritis ratio with AST and ALT activity in the reference range has prognostic value. • De Ritis ratio with AST and ALT activity in the reference range predicts 3-year all-cause, cardiac and noncardiac mortality. • De Ritis ratio provides prognostic information on top of cardiovascular risk factors. Whether aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio (De Ritis ratio) with AST and ALT activities within the reference range has prognostic value is unknown. This study included 3392 patients with stable coronary artery disease and AST and ALT activities within the reference range. Patients are categorized in groups according to tertiles of the De Ritis ratio: a group with De Ritis ratio in the 1st tertile (De Ritis ratio: 0.22 to 0.81; n = 1131), a group with De Ritis ratio in the 2nd tertile (De Ritis ratio: >0.81 to 1.09; n = 1130) and a group with De Ritis ratio in the 3rd tertile (De Ritis ratio: >1.09 to 3.40; n = 1131). The primary endpoint was 3-year mortality. The mean value of De Ritis ratio was 1.00 ± 0.39 (range: 0.22–3.40). Overall, there were 234 deaths at 3 years: 43 deaths in patients of 1st tertile, 75 deaths in patients of 2nd tertile and 116 deaths in patients of 3rd tertile of De Ritis ratio (Kaplan-Meier estimates of 3-year mortality, 4.4 %, 7.8 % and 12.5 %, respectively; (adjusted hazard ratio = 1.24, 95 % confidence interval 1.12 to 1.38; P < 0.001 for 1 unit higher De Ritis ratio). The C-statistic of the risk prediction model for mortality with baseline demographical and clinical variables without De Ritis ratio was 0.803 [0.774–0.832] and it increased to 0.810 [0.782–0.839] after inclusion of De Ritis ratio into the model (P = 0.038). An elevated De Ritis ratio with aminotransferase levels within the reference range was associated with the increased risk of mortality. [ABSTRACT FROM AUTHOR]

• De Ritis ratio predicts 3-year all-cause mortality after acute myocardial infarction. • De Ritis ratio predicts 3-year cardiac mortality after acute myocardial infarction. • De Ritis ratio predicts 30-day risk of bleeding after percutaneous coronary intervention. • De Ritis ratio has a moderate sensitivity regarding prediction of mortality. The association between aspartate aminotransferase to alanine aminotransferase ratio (De Ritis ratio) and prognosis of patients with acute myocardial infarction (AMI) remains poorly investigated. This study included 3000 patients with AMI undergoing percutaneous coronary intervention. Patients were categorized in groups according to tertiles of the De Ritis ratio: tertile 1 (De Ritis ratio < 1.11; 905 patients), tertile 2 (De Ritis ratio 1.11 to 1.95; 1003 patients) and tertile 3 (De Ritis ratio > 1.95; 1002 patients). The primary endpoint was 3-year all-cause mortality. At 3 years, all-cause deaths occurred in 487 patients: 119 deaths (13.2%) in patients of 1st tertile, 164 deaths (17.8%) in patients of 2nd tertile and 204 deaths (21.9%) in patients of 3rd tertile of the De Ritis ratio (adjusted hazard ratio [HR] = 1.16, 95% confidence interval [CI] 1.02 to 1.31], P = 0.023 per unit increment in the logarithmic scale of the De Ritis ratio); cardiac deaths occurred in 328 patients: 76 deaths (8.2%) in patients of 1st tertile, 110 deaths (12.0%) in patients of 2nd tertile and 142 deaths (15.4%) in patients of 3rd tertile of the De Ritis ratio (adjusted HR = 1.20 [1.04–1.40], P = 0.014 per unit increment in the logarithmic scale of De Ritis ratio). The C-statistic of the multivariable model(s) with baseline data without and with De Ritis ratio was 0.822 [0.805–0.839] and 0.823 [0.805–0.840], (P = 0.419) for all-cause mortality and 0.831[0.811–0.852] and 0.832 [0.811–0.853], P = 0.621) for cardiac mortality. In patients with AMI, elevated De Ritis ratio was associated with increased risk of 3-year mortality. [ABSTRACT FROM AUTHOR]

Background: The prognostic value of in‐hospital haemoglobin drop in patients with acute coronary syndrome (ACS) undergoing invasive therapy remains insufficiently investigated. Materials and Methods: This observational study included 3838 patients with ACS with admission and in‐hospital nadir haemoglobin values available. Haemoglobin drop was defined as a positive difference between admission and nadir haemoglobin values. The primary endpoint was one‐year all‐cause mortality. Results: In‐hospital haemoglobin drop occurred in 3142 patients (82%). Patients were categorized into 4 groups: no haemoglobin drop (n = 696 patients), <3 g/dl haemoglobin drop (n = 2703 patients), 3 to <5 g/dl haemoglobin drop (n = 344 patients) and ≥5 g/dl haemoglobin drop (n = 95 patients). The primary endpoint occurred in 156 patients: 17 patients (2.5%) in the group with no haemoglobin drop, 81 patients (3.0%) in the group with <3g/dl haemoglobin drop, 37 patients (10.9%) in the group with 3 to <5 g/dl haemoglobin drop and 21 patients (22.2%) in the group with ≥5 g/dl haemoglobin (adjusted hazard ratio [HR] = 1.30, 95% confidence interval 1.17 to 1.45; p <.001 for one g/dl haemoglobin drop). The association of haemoglobin drop with one‐year mortality remained significant after exclusion of patients with in‐hospital overt bleeding (adjusted HR = 1.27 [1.11–1.46]; p <.001 for one g/dl haemoglobin drop). The lowest haemoglobin drop associated with mortality was 1.23 g/dl in all patients (HR = 1.03 [1.02–1.04]) and 1.13 g/dl in patients without overt bleeding (HR = 1.03 [1.01–1.04]). Conclusions: In patients with ACS, in‐hospital haemoglobin drop was associated with higher risk of one‐year mortality even in the absence of overt bleeding. [ABSTRACT FROM AUTHOR]

Background and Aims: Evidence on the association between aspartate aminotransferase (AST) activity and mortality of patients with ischemic heart disease (IHD) is limited. We investigated whether there is an association between AST activity and mortality in IHD patients.Methods and Results: The study included 6857 patients with coronary angiography-proven IHD and AST activity within the reference range. AST activity measurements were available in all patients. The primary outcome was 3-year cardiac mortality. Patients were categorized in groups according to the AST activity tertiles: a group with AST within the 1st tertile (AST < 17.0 U/L), a group with AST within the 2nd tertile (AST > 17-24.5 U/L) and a group with AST within the 3rd tertile (AST > 24.5 U/L). Cardiac death (n = 297) occurred in 109, 69 and 119 patients in the 1st to 3rd AST tertiles (Kaplan-Meier estimates of mortality: 5.3%, 3.6% and 5.9%; univariable hazard ratio [HR] = 1.75, 95% confidence interval [CI] 1.30-2.36, P < 0.001 for tertile 3 vs. 2; HR = 1.13 [0.87-1.46], P = 0.370 for tertile 3 vs. 1; and HR = 0.65 [0.48-0.87], P = 0.004 for tertile 2 vs. 1). The association between AST and cardiac mortality was U-shaped. AST values <15 U/L (HR = 1.118 [1.009-1.238]) and >23 U/L (HR = 1.029 [1.003-1.056]) were associated with higher cardiac mortality compared with the reference value (21 U/L). After adjustment, the association between AST and cardiac mortality was attenuated (P = 0.133) but remained non-linear (P = 0.047).Conclusions: In patients with IHD, AST activity was associated with the risk of cardiac mortality with a U-shaped relationship. After adjustment, the association between AST and mortality was attenuated. [ABSTRACT FROM AUTHOR]

Data regarding the association between alanine aminotransferase (ALT) and prognosis of patients with coronary artery disease (CAD) are limited. The aim of this study was to assess the association of ALT with the prognosis of patients with CAD. The study included 9523 patients with angiography-proven CAD who underwent percutaneous coronary intervention. Baseline ALT activity measurements were available for analysis in all patients. The primary outcome was 3-year cardiac mortality. Patients were divided into three groups: a group with ALT within the 1st tertile (ALT 2.0 U/L to ≤17.0 U/L; n = 3276 patients), a group with ALT within the 2nd tertile (ALT >17.0 U/L to ≤26.0 U/L; n = 3075 patients) and a group with ALT within 3rd tertile (>26 U/L to ≤50.0 U/L; n = 3172 patients). Cardiac death (primary outcome) occurred in 441 patients: 201 (7.1%), 126 (4.7%) and 114 (4.0%) of these occurring in patients in the 1st, 2nd and 3rd ALT tertiles, respectively (with percentages representing Kaplan–Meier estimates of 3-year cardiac mortality); adjusted hazard ratio = 1.43, 95% confidence interval 1.11 to 1.85, P = 0.006 calculated for 1 unit decrement in the logarithmic scale of ALT. The multivariable model for cardiac mortality with baseline variables without ALT had a C-statistic of 0.827 [0.801–0.853], P < 0.001, which increased to 0.832 [0.806–0.857], P < 0.001 after incorporation of ALT (P = 0.020). In patients with CAD, ALT was inversely and independently associated with the risk of 3-year cardiac mortality. Low ALT may reflect cardiovascular risk that is poorly mediated by traditional cardiovascular risk factors. • Alanine aminotransferase (ALT) is inversely associated with 3-year cardiac mortality • ALT improves the risk prediction for cardiac mortality • Low ALT mediates cardiovascular risk poorly presented by cardiovascular risk factors [ABSTRACT FROM AUTHOR]

Background Evidence on the use of high-sensitivity cardiac troponins (hs-cTn) to risk-stratify patients with ST-segment elevation myocardial infarction (STEMI) is limited. Methods We assessed the prognostic value of preprocedural (admission) and peak postprocedural hs-cTnT in 818 patients with STEMI treated with primary percutaneous coronary intervention (PPCI). Preprocedural and peak postprocedural hs-cTnT was measured. The primary outcome was 3-year all-cause mortality. Results The median values of preprocedural and peak postprocedural hs-cTnT were 153 ng/L and 1980 ng/L. Overall, 134 patients died during the follow-up. There were 85 deaths in patients with preprocedural hs-cTnT >median value and 49 deaths in patients with preprocedural hs-cTnT ≤median value [Kaplan–Meier estimates of mortality, 22.2% and 13.5%; unadjusted hazard ratio (HR) = 1.88, 95% confidence interval (CI) 1.32–2.67, p < 0.001]. According to peak postprocedural hs-cTnT, there were 84 deaths in patients with postprocedural hs-cTnT >median value and 50 deaths in patients with postprocedural hs-cTnT ≤median value [Kaplan–Meier estimates of mortality, 22.3% and 13.4%; unadjusted HR = 1.82 (1.28–2.59), p < 0.001]. After adjustment, preprocedural [adjusted HR = 1.08 (1.03–1.12), p < 0.001] and peak postprocedural hs-cTnT value [adjusted HR = 1.06 (1.04–1.08), p < 0.001] were independently associated with 3-year mortality (with risk estimates calculated per 70 × 99th upper reference limit of hs-cTnT). The C statistic of multivariable model increased from 0.868 (0.841–0.895) to 0.872 (0.845–0.898) after incorporation of preprocedural hs-cTnT ( p = 0.050) and to 0.874 (0.846–0.899) after incorporation of the postprocedural hs-cTnT into the model ( p = 0.035). Conclusions In conclusion, admission or peak postprocedural hs-cTnT is independently associated with the risk for 3-year mortality in patients with STEMI undergoing PPCI. [ABSTRACT FROM AUTHOR]

Objectives The objective of the study was to investigate the association between alkaline phosphatase (AP) activity and prognosis of patients with acute coronary syndrome (ACS). Design and methods The study included 2134 patients with ACS undergoing percutaneous coronary intervention. All included patients had baseline AP measurements available. The receiver operating characteristic curve analysis showed that the best cut-off of AP for mortality prediction was 98.0 U/L. Using this cut-off, patients were divided into two groups: a group with AP > 98.0 U/L ( n = 493) and a group with AP ≤ 98.0 U/L ( n = 1641). The primary endpoint was 3-year mortality. Results Overall, there were 229 deaths over the follow-up: 90 deaths among patients with an AP > 98.0 U/L and 139 deaths among patients with an AP ≤ 98.0 U/L (Kaplan-Meier estimates of 3-year total mortality, 19.5% and 9.3%, respectively; adjusted hazard ratio [HR] = 1.37, 95% confidence interval [CI] 1.10–1.70, P = 0.004 for each unit higher log AP). Cardiac deaths occurred in 157 patients: 66 deaths among patients with an AP > 98.0 U/L and 91 deaths among patients with an AP ≤ 98.0 U/L (Kaplan-Meier estimates of 3-year cardiac mortality, 14.3% and 6.0%, respectively; adjusted HR = 1.32 [1.02–1.70], P = 0.033, for each unit higher log AP). The C-statistic of the multivariable model with baseline variables was 0.836 [0.807–0.866] and it increased to 0.842 [0.814–0.874] after inclusion of AP ( P = 0.045). Conclusions In patients presenting with an ACS and treated with percutaneous coronary intervention, elevated AP activity is associated with increased risk of subsequent mortality. [ABSTRACT FROM AUTHOR]

Background The evidence on the association between alkaline phosphatase ( ALP) and prognosis of patients with coronary artery disease ( CAD) is limited. The aim of this study was to assess the association of ALP with the risk of mortality or coronary events in patients with CAD. Materials and methods The study included 5540 patients with angiography-proven CAD treated with catheter-based coronary revascularization. Baseline ALP measurements were available for analysis in all patients. Patients were divided into three groups: a group with an ALP activity in the 1st tertile (ALP ≤ 65·5 U/L; n = 1855), a group with an ALP activity in the 2nd tertile (ALP > 65·5 to 85·7 U/L; n = 1839) and a group with an ALP in the 3rd tertile (ALP > 85·7 U/L; n = 1846). The primary outcome was all-cause mortality at 3-year follow-up. Results All-cause deaths (number [Kaplan-Meier estimates]) occurred in 443 patients: 117 (7·2%), 130 (8·1%) and 196 deaths (11·8%) among patients of the 1st, 2nd and 3rd ALP tertiles (unadjusted hazard ratio [HR] = 1·33, 95% confidence interval [ CI]: 1·19 to 1·50; P < 0·001, calculated per tertile increment in the ALP activity). After adjustment in multivariable Cox proportional hazards model, ALP was independently associated with the risk of all-cause mortality (adjusted HR = 1·33 [1·18-1·51], P < 0·001, calculated per unit increment in log ALP). The multivariable model for all-cause mortality with baseline variables without ALP had a C statistic of 0·820 [0·797-0·843] which increased to 0·825 [0·804-0·849] after ALP inclusion; delta C statistic 0·005 [0·001-0·011]; P < 0·001. Conclusions In patients with CAD, elevated ALP activity was independently associated with the risk of 3-year all-cause mortality. [ABSTRACT FROM AUTHOR]

Background: The prognostic value of high-sensitivity troponin T (hs-TnT) elevation after elective percutaneous coronary intervention (PCI) in patients with or without raised baseline hs-TnT levels is unclear.Objectives: The goal of this study was to assess whether the prognostic value of post-procedural hs-TnT level after elective PCI depends on the baseline hs-TnT level.Methods: This study included 5,626 patients undergoing elective PCI who had baseline and peak post-procedural hs-TnT measurements available. The primary outcome was 3-year mortality (with risk estimates calculated per SD increase of the log hs-TnT scale).Results: Patients were divided into 4 groups: nonelevated baseline and post-procedural hs-TnT levels (hs-TnT ≤0.014 μg/l; n = 742); nonelevated baseline but elevated post-procedural hs-TnT levels (peak post-procedural hs-TnT >0.014 μg/l; n = 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 μg/l) with no further rise post-procedure (n = 516); and elevated baseline hs-TnT levels with a further rise post-procedure (n = 1,647). A total of 265 deaths occurred: 6 (1.6%) in patients with nonelevated baseline and post-procedural hs-TnT levels; 54 (3.8%) in patients with nonelevated baseline but elevated post-procedural hs-TnT levels; 50 (16.0%) in patients with elevated baseline hs-TnT levels with no further rise post-procedure; and 155 (18.2%) in patients with elevated baseline hs-TnT levels with a further rise post-procedure (p < 0.001). After adjustment, baseline hs-TnT levels (hazard ratio [HR]: 1.22; 95% confidence interval [CI]: 1.09 to 1.38; p < 0.001) but not peak post-procedural hs-TnT levels (HR: 1.04; 95% CI: 0.85 to 1.28; p = 0.679) were associated with an increased risk of mortality. Peak post-procedural hs-TnT findings were not associated with mortality in patients with nonelevated (HR: 0.93; 95% CI: 0.69 to 1.25; p = 0.653) or elevated (HR: 1.24; 95% CI: 0.91 to 1.69; p = 0.165) baseline hs-TnT levels.Conclusions: In patients with coronary artery disease undergoing elective PCI, an increase in post-procedural hs-TnT level did not offer prognostic information beyond that provided by the baseline level of the biomarker. [ABSTRACT FROM AUTHOR]

Objectives The aim of the study was to investigate the association between gamma-glutamyl transferase (GGT) activity and mortality in patients with diabetes mellitus and coronary artery disease (CAD). Design and methods The study included 1448 patients with diabetes and angiography-proven CAD who underwent percutaneous coronary intervention (PCI). Baseline GGT measurements were available in all patients. The primary outcome was 3-year mortality. Results Patients were divided into 3 groups: a group consisting of patients with a GGT activity in the 1st tertile (GGT ≤ 29.4 U/L; n = 487), a group consisting of patients with a GGT activity in the 2nd tertile (GGT > 29.4–52.5 U/L; n = 479) and a group consisting of patients with GGT in the 3rd tertile (GGT > 52.5 U/L; n = 482). Overall, there were 179 deaths: 46 (11.9%), 49 (12.1%) and 84 deaths (21.4%) among patients of the 1st, 2nd and 3rd GGT tertiles, respectively (adjusted hazard ratio [HR] = 1.25, 95% confidence interval [CI] 1.05–1.49, P = 0.011). Cardiac death occurred in 101 patients: 22 (5.8%), 30 (7.2%) and 49 deaths (12.9%) among patients of the 1st, 2nd and 3rd GGT tertiles, respectively (adjusted HR = 1.23 [0.96–1.58], P = 0.104, with risk estimates calculated per standard deviation increase in the logarithmic scale of GGT). GGT improved the risk prediction of models of all-cause (P = 0.020) but not cardiac (P = 0.135) mortality (P values show the difference in C-statistics between the models without and with GGT). Conclusion In patients with diabetes and CAD treated with PCI, elevated GGT was independently associated with the risk of 3-year all-cause mortality. [ABSTRACT FROM AUTHOR]

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Background The association between gamma-glutamyl transferase (GGT) activity and outcome of patients with coronary artery disease (CAD) remains poorly investigated. Methods The study included 5501 patients with CAD treated with percutaneous coronary intervention and GGT measurements available. The primary outcome was 3-year mortality. Results GGT activity tertiles were: 1st tertile (GGT < 28.10 U/L; n = 1866), 2nd tertile (GGT ≥ 28.10 U/L to 49.50 U/L; n = 1804) and 3rd tertile (GG > 49.50 U/L; n = 1831). There were 110 deaths in the 1st, 111 deaths in the 2nd and 216 deaths in the 3rd GGT tertile (mortality estimates, 7.1%, 7.2% and 13.9%; P < 0.001). GGT was independently associated with the increased risk of 3-year all-cause (adjusted hazard ratio [HR] = 1.30, 95% confidence interval [CI] 1.18 to 1.44, P < 0.001), cardiac (HR = 1.21 [1.06–1.39], P = 0.005) and non-cardiac (HR = 1.42 [1.23–1.63], P < 0.001) mortality (all risk estimates calculated per standard deviation increase in the log GGT activity). GGT improved prediction of all-cause (P < 0.001) and non-cardiac mortality (P < 0.001) but not cardiac mortality (P = 0.155). Conclusions In patients with CAD, elevated GGT activity is associated with increased risk of 3-year all-cause, cardiac and non-cardiac mortality. GGT provided incremental prognostic information on top of cardiovascular and metabolic risk factors for prediction of all-cause and non-cardiac mortality but not cardiac mortality. [ABSTRACT FROM AUTHOR]

Background & objectives: The comparative prognostic value of C-reactive protein (CRP) and fibrinogen for cardiovascular events has been inconclusively investigated. this study was carried out to compare the prognostic value of CRP versus fibrinogen in patients with coronary artery disease (CAD). Methods: The study included 13,100 patients with coronary angiography-confirmed CAD. Plasma CRP and fibrinogen levels were measured before angiography in all patients. The levels of CRP>3 mg/l and fibrinogen>350 mg/dl were considered as elevated. The primary outcome was 1-year all-cause mortality. Results: Patients were divided into four groups: patients with CRP≤3 mg/l and fibrinogen ≤350 mg/dl (n=4206); patients with CRP≤3 mg/l and fibrinogen >350 mg/dl (n=3132); patients with CRP>3 mg/l and fibrinogen ≤ 350 mg/dl (n=1273) and CRP >3 mg/l and patients with fibrinogen >350 mg/dl (n=4489). There were 634 deaths: 75 deaths in patients with CRP ≤3 mg/l and fibrinogen ≤350 mg/dl, 91 deaths in patients with CRP =3 mg/l and fibrinogen >350 mg/dl, 87 deaths in patients with CRP >3 mg/l and fibrinogen ≤350 mg/dl and 381 deaths in patients with CRP >3 mg/l and fibrinogen >350 mg/dl (Kaplan-Meier estimates of all-cause mortality, 1.8, 3.0, 7.0 and 8.7 %, log-rank test P<0.001). The multivariate analysis showed that CRP [adjusted hazard ratio (HR)=1.31, 95% confidence interval (CI) 1.18-1.45, for each standard deviation increase in the logarithmic scale] but not fibrinogen [adjusted HR=0.99 (0.90-1.09), for each standard deviation increase in the logarithmic scale] was an independent correlate of mortality. Interpretation & conclusions: The findings indicated that in patients with CAD, CRP was a better predictor of mortality than fibrinogen and offered prognostic information beyond that provided by the conventional cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Abstract: Background: Sex-based differences in the association between C-reactive protein (CRP) and cardiovascular events in patients with coronary artery disease (CAD) are incompletely investigated. We investigated whether there are gender differences in the association between CRP and outcome in patients with CAD after percutaneous coronary intervention (PCI). Methods: This study included 13,170 consecutive patients with CAD: 10,098 men and 3072 women. CRP was measured on admission in all patients. The primary outcome was 1-year mortality. Results: CRP level (median [25th–75th percentiles]) was higher in women than in men (3.08 [1.30–8.37] mg/L vs 2.30 [0.92–6.47] mg/L; P<0.001). CRP was >3mg/L in 4250 men (42.1%) and 1554 women (50.6%; P<0.001). One-year mortality was 4.9% (n=641 deaths). Deaths occurred in 318 men with CRP >3mg/L and 122 men with CRP ≤3mg/L (mortality estimates 7.7% and 2.1%, P<0.001) and in 154 women with CRP >3mg/L and 47 women with CRP ≤3mg/L (mortality estimates 10.1% and 3.2%, P<0.001). After adjustment in the Cox model, CRP was associated with increased risk of mortality in women (adjusted hazard ratio [HR]=1.03, 95% confidence interval [CI] 1.01–1.04, P<0.001 for each 5mg/L increase) and in men (adjusted HR=1.02 [1.01–1.03], P<0.001, for each 5mg/L increase). CRP predicted mortality with an area under the receiver-operating characteristic curve =0.721, [0.683–0.760] in women and 0.732, [0.707–0.757] in men (P=0.659). Conclusions: Elevated CRP levels provide similar prognostic information in men and women with CAD after PCI which is independent and supplementary to that provided by conventional cardiovascular risk factors. [Copyright &y& Elsevier]

Current guidelines recommend troponin T (TnT) as the biomarker of choice in the diagnosis of myocardial infarction. In patients with ST-elevation myocardial infarction (STEMI) however, its role in providing a measurement of infarct size and its association with survival is less well established. We sought to assess the correlation of TnT and creatine kinase-MB (CK-MB) with scintigraphically determined infarct size and to assess the predictive value of all 3 parameters on 12-month mortality. Patients presenting with STEMI managed with primary percutaneous intervention underwent serial TnT and CK-MB measurements at admission and for ≥72 hours after presentation. Before hospital discharge patients underwent assessment of infarct size by technetium-99m sestamibi single-photon emission computed tomographic (SPECT) scan. Clinical follow-up was performed up to 1 year. Data were available for 1,237 patients. Mean age was 62.9 ± 12.9 years. Infarct location was anterior in 509 patients (41%); 75 (6.1%) had cardiogenic shock. Median admission and peak TnT were 0.74 μg/L (0.10 to 2.70) and 3.70 μg/L (1.69 to 6.99), respectively. Corresponding values for CK-MB were 44.1 U/L (21.0 to 108.8) and 160.0 U/L (69.0 to 301.0), respectively. Median infarct size on SPECT scan was 12.0% (3.0 to 25.0) of the left ventricle. Peak TnT and CK-MB demonstrated similar moderate correlation with final infarct size (r = 0.45, p <0.001, and r = 0.41, p <0.001 respectively). This correlation was not affected by Thrombolysis In Myocardial Infarction flow grade after intervention. At 1 year, 47 patients (3.8%) had died. Final infarct size at SPECT scanning better predicted mortality than peak TnT or CK-MB. In conclusion, this study is the largest investigation on the value of cardiac troponin for assessment of infarct size in acute STEMI. Compared to peak CK-MB, peak TnT shows similar correlation with scintigraphic infarct size, although scintigraphic infarct size remains a better correlate of 1-year mortality than either biomarker. [Copyright &y& Elsevier]

We investigated whether N-terminal pro-brain natriuretic peptide (NT–pro-BNP) that was measured on admission in patients with acute myocardial infarction (AMI) predicts the efficacy of reperfusion or whether NT–pro-BNP provides prognostic information independent of infarct size as estimated by single-photon emission computed tomographic scintigraphy. The study included 174 patients with ST-segment elevation AMI who were admitted within 24 hours of pain onset. NT–pro-BNP level was measured on admission. Paired scintigraphic studies (before and 7 to 14 days after reperfusion) were performed to assess infarct size and define myocardial salvage. One-year clinical follow-up was assessed. Patients were categorized into the high NT–pro-BNP group (57 patients in the upper tertile of NT–pro-BNP) and low NT–pro-BNP group (117 patients in the middle and lower tertiles of NT–pro-BNP). Initial median perfusion defect was 35.0% (interquartile rage 20.0 to 53.0%) of the left ventricle in the high NT–pro-BNP group versus 19.0% (interquartile range 10.0 to 32.2) of the left ventricle in the low NT–pro-BNP group (p <0.001). Median salvage index was 0.36 (interquartile range 0.16 to 0.86) in the high NT–pro-BNP group versus 0.53 (interquartile range 0.31 to 0.75) in the low NT–pro-BNP group (p = 0.22). After adjustment in Cox’s proportional hazards model, NT–pro-BNP remained an independent correlate of 1-year mortality (adjusted hazard ratio 2.31, 95% confidence interval 1.09 to 4.89, p = 0.03, high vs low NT–pro-BNP group). In conclusion, NT–pro-BNP measured on admission in patients with AMI correlates with scintigraphic area at risk and predicts prognosis but does not predict the efficacy of mechanical reperfusion by stenting or angioplasty. [Copyright &y& Elsevier]

Supplemental Digital Content is available in the text. Background: The magnitude of prognostically relevant myocardial injury after percutaneous coronary interventions remains poorly defined. The Society for Cardiovascular Angiography and Interventions (SCAI) proposed marked biomarker elevations to define periprocedural myocardial infarction (PMI). These consensus-based thresholds have not been validated in the era of high-sensitivity cardiac troponins. We sought to assess the prognostic impact of SCAI-defined PMI and explore optimal prognostic thresholds of high-sensitivity cardiac troponin T (hs-cTnT) after elective percutaneous coronary interventions. Methods and Results: We evaluated patients who underwent elective percutaneous coronary interventions at 2 tertiary care centers with serial hs-cTnT measurements. PMI was defined as peak postprocedural hs-cTnT >70× upper reference limit (URL) in patients with nonelevated (≤1× URL) baseline levels; or incremental increase >70× URL in patients with elevated baseline levels. The primary outcome was 1-year all-cause mortality. Of 8140 patients, 220 (2.7%) died within 1 year. In multivariable analyses, patients with SCAI-defined PMI (n=140; 1.7%) had a higher risk of 1-year mortality (12.9% versus 2.5%, adjusted hazard ratio 4.10, 95% CI 2.51–6.68; P <0.001) as well as cardiac mortality (11.4% versus 2.1%, adjusted hazard ratio 4.21, 95% CI 2.50–7.11; P <0.001). Based on receiver operating characteristics analysis, the optimal prognostic threshold of hs-cTnT was >10×URL, observed in 14.6% of patients. This threshold showed lower specificity (85.7% versus 98.4%) but higher sensitivity (25.4% versus 8.2%) and better overall performance for prediction of 1-year mortality compared with the SCAI-defined cutoff value of troponin. Conclusions: In patients undergoing elective percutaneous coronary interventions, SCAI-defined PMI emerged as an independent, highly specific, but insensitive predictor of 1-year mortality. Optimal trade-off between sensitivity and specificity was observed at a lower threshold of hs-cTnT (10× URL) in this cohort. [ABSTRACT FROM AUTHOR]

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 <105ng/L; n=1264), a group with postprocedural hs-TnT in the 2nd tertile (hs-TnT ≥105ng/L to 470ng/L; n=1258) and a group with postprocedural hs-TnT in the 3rd tertile (hs-TnT >470ng/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 1year after PCI. [ABSTRACT FROM AUTHOR]