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Background: The association of aspirin loading with the risk of coronary no‐reflow (CNR) after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) has not been investigated. We assessed the association of aspirin loading before PCI with CNR in patients with AMI. Materials and Methods: This study included 3100 patients with AMI undergoing PCI. Of them, 2812 patients received aspirin loading (a single oral [or chewed] or intravenous dose of 150–300 mg) and 288 patients did not receive aspirin loading before PCI. The primary endpoint was CNR, defined as Thrombolysis in Myocardial Infarction blood flow grade of <3 after the PCI. Results: CNR occurred in 130 patients: 127 patients in the group with aspirin loading and 3 patients in the group without aspirin loading before PCI (4.5% vs. 1.0%; odds ratio [OR] = 4.50, 95% confidence interval, [1.42–14.21], p = 0.005). After adjustment, the association between aspirin loading and CNR was significant (adjusted OR = 4.49 [1.56–12.92]; p < 0.001). There was no aspirin loading‐by‐P2Y12 inhibitor (ticagrelor or prasugrel) interaction (pint = 0.465) or aspirin loading‐by‐chronic aspirin therapy on admission (pint = 0.977) interaction with respect to the occurrence of CNR after PCI. Chronic low‐dose aspirin therapy on admission was not independently associated with higher risk of CNR after PCI (adjusted OR = 1.06 [0.65–1.72]; p = 0.824). Conclusion: In patients with AMI undergoing PCI, aspirin loading before the PCI procedure at the guideline‐recommended doses was associated with higher odds of developing CNR. However, due to the limited number of events, the findings should be considered as hypothesis generating. [ABSTRACT FROM AUTHOR]

Coronary no-reflow (CNR) is a frequent phenomenon that develops in patients with ST-segment elevation myocardial infarction (STEMI) following reperfusion therapy. CNR is highly dynamic, develops gradually (over hours) and persists for days to weeks after reperfusion. Microvascular obstruction (MVO) developing as a consequence of myocardial ischemia, distal embolization and reperfusion-related injury is the main pathophysiological mechanism of CNR. The frequency of CNR or MVO after primary PCI differs widely depending on the sensitivity of the tools used for diagnosis and timing of examination. Coronary angiography is readily available and most convenient to diagnose CNR but it is highly conservative and underestimates the true frequency of CNR. Cardiac magnetic resonance (CMR) imaging is the most sensitive method to diagnose MVO and CNR that provides information on the presence, localization and extent of MVO. CMR imaging detects intramyocardial hemorrhage and accurately estimates the infarct size. MVO and CNR markedly negate the benefits of reperfusion therapy and contribute to poor clinical outcomes including adverse remodeling of left ventricle, worsening or new congestive heart failure and reduced survival. Despite extensive research and the use of therapies that target almost all known pathophysiological mechanisms of CNR, no therapy has been found that prevents or reverses CNR and provides consistent clinical benefit in patients with STEMI undergoing reperfusion. Currently, the prevention or alleviation of MVO and CNR remain unmet goals in the therapy of STEMI that continue to be under intense research. [ABSTRACT FROM AUTHOR]

Background: The aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio (De Ritis ratio), obtained from AST and ALT activities in the healthy range, has not been studied in association with mortality. Methods: This study included 3392 patients with stable coronary heart disease and aminotransferase activity in the reference range. Patients are categorized into two groups: a group with AST and ALT activity in the healthy range (n = 1697), and a group with AST and/or ALT activity outside the healthy range but in the reference range (n = 1695). The primary endpoint was all-cause mortality at three years. Results: The De Ritis ratio (median 5th–95th percentile] was 0.94 [0.61–1.41] in patients with AST and ALT in the healthy range and 0.93 [0.45–1.96] in patients with AST and/or ALT outside the healthy range (p = 0.700). At three years, there were 86 deaths in patients with AST and ALT in the healthy range: 27 deaths (3.9%) in patients with a De Ritis ratio ≤median, and 59 deaths (8.2%) in patients with the De Ritis ratio >median (adjusted hazard ratio [HR] = 1.16, 95% confidence interval [CI] 0.94 to 1.42; p = 0.159); in patients with AST and/or ALT outside the healthy range, there were 148 deaths: 49 deaths (6.6%) in patients with a De Ritis ratio ≤median, and 99 deaths (14.1%) in patients with De Ritis ratio >median (adjusted HR = 1.27 [1.09–1.48], p = 0.002), with both HRs calculated per unit higher values of the De Ritis ratio. Conclusions: The De Ritis ratio obtained from AST and ALT activity in the healthy range was not independently associated with higher risk of mortality. The De Ritis ratio obtained from aminotransferase activity outside the healthy range (but still in the reference range) was independently associated with the risk of mortality. [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]

• ALP predicts 3-year mortality in patients with diabetes mellitus and ischemic heart disease. • Low and high ALP activity levels were associated with increased risk of mortality. • Impaired renal function and elevated C-reactive protein correlated with higher ALP activity. The association between alkaline phosphatase (ALP) and mortality in patients with diabetes mellitus (DM) and ischemic heart disease (IHD) remains poorly investigated. The study included 1426 patients with DM and IHD who underwent percutaneous coronary intervention. Patients were divided in groups according to tertiles of ALP activity: a group with ALP activity in 1st tertile (ALP activity: 20.8–65.0 U/L; n = 478), a group with ALP activity in 2nd tertile (ALP activity: 65.1–87.0 U/L; n = 473) and a group with ALP activity in 3rd tertile (ALP activity: 87.1–1520 U/L; n = 475). The primary endpoint was 3-year all-cause mortality. At 3 years, all-cause deaths occurred in 182 patients: 50 deaths (12.4%) in patients of 1st tertile, 47 deaths (11.7%) in patients of 2nd tertile and 85 deaths (20.8%) in patients of 3rd tertile of ALP activity (adjusted hazard ratio [HR] = 1.20, 95% confidence interval [CI] 1.02 to 1.42, P = 0.031); cardiac deaths occurred in 110 patients: 28 deaths (7.0%) in patients of 1st tertile, 30 deaths (7.6%) in patients of 2nd tertile and 52 deaths (12.7%) in patients of 3rd tertile of ALP activity (adjusted HR = 1.27 [1.04–1.56], P = 0.021, with both risk estimates calculated for unit increment in the log scale of ALP activity). The C-statistic of the multivariable model with baseline data without and with ALP was 0.787 [0.750–0.818] and 0.804 [0.757–0.851], (P = 0.575) for all-cause mortality and 0.832 [0.798–0.864] and 0.876 [0.833–0.918], (P = 0.115) for cardiac mortality. In patients with DM and IHD, elevated ALP activity was associated with increased risk of 3-year mortality. [ABSTRACT FROM AUTHOR]

• Cockcroft-Gault creatinine clearance and EKFC equations predict mortality better than MDRD-4 and CKD-EPI equations. • Cockcroft-Gault creatinine clearance and EKFC equations predict bleeding better than MDRD-4 and CKD-EPI equations. • All four eGFR equations failed to improve risk prediction for myocardial infarction. It remains unknown which equation used to assess the glomerular function is better for risk stratification in patients with acute coronary syndrome (ACS). This study included 3985 patients with ACS. Glomerular function was assessed using 4 equations: the Cockcroft-Gault creatinine clearance (C-G CrCl), Modification of Diet in Renal Disease-4 (MDRD-4), Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and European Kidney Function Consortium (EKFC) equations. The primary outcome was one-year all-cause mortality. For each 30 ml/min decrement, the adjusted hazard ratio [HR] with 95% confidence interval [CI] for one-year mortality was 1.67 [1.27–2.25] for C-G CrCl , 1.45 [1.16–1.81] for MDRD-4, 1.76 [1.35–2.30] for CKD-EPI and 1.94 [1.44–2.63] for EKFC equation. Area under the receiver operating characteristic curve (AUC) for one-year mortality was 0.748 [0.709–0.788] for C-G CrCl , 0.670 [0.621–0.718] for estimated glomerular filtration rate (eGFR) calculated by MDRD-4 equation, 0.725 [0.684–0.765] for eGFR calculated by CKD-EPI equation and 0.741 [0.703–0.779] for eGFR calculated by EKFC equation (P = 0.342 for C-G CrCl , vs. EKFC equation and P ≤ 0.009 for all other AUC comparisons). In patients with ACS, C-G CrCl and EKFC equations showed a similar discriminatory power regarding prediction of one-year mortality. Both equations were better than MDRD-4 and CKD-EPI equations for risk discrimination for mortality. Clinical Trial Registration: NCT01944800. [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]

The efficacy and safety of ticagrelor versus prasugrel according to smoking status in patients with acute coronary syndromes (ACS) are not known. We assessed the efficacy and safety of ticagrelor versus prasugrel according to smoking status in patients with ACS undergoing invasive management. This pre-specified analysis of the ISAR-REACT 5 trial included 1349 smokers and 2652 nonsmokers randomized to receive ticagrelor or prasugrel. The primary endpoint was the incidence of death, myocardial infarction, or stroke; the secondary endpoint was the incidence of Bleeding Academic Research Consortium (BARC) type 3 to 5 bleeding (both endpoints assessed at 12 months). There was no significant treatment arm-by-smoking status interaction regarding the efficacy outcome. The primary endpoint occurred in 47 patients (7.0%) in the ticagrelor group and 41 patients (6.2%) in the prasugrel group in smokers (hazard ratio [HR] = 1.15; 95% confidence interval [CI] 0.76–1.75; P = 0.510) and in 133 patients (10.2%) in the ticagrelor group and 94 patients (7.2%) in the prasugrel group in nonsmokers (HR = 1.44 [1.10–1.87]; P = 0.007; P for interaction = 0.378). The secondary endpoint occurred in 27 patients (4.6%) in the ticagrelor group and 33 patients (5.6%) in the prasugrel group in smokers (HR = 0.81 [0.49–1.35]; P = 0.412) and in 66 patients (6.0%) in the ticagrelor group and 46 patients (4.4%) in the prasugrel group in nonsmokers (HR = 1.38 [0.94–2.01]; P = 0.097). In patients with ACS undergoing an invasive management strategy, the smoking status did not significantly interact with the relative treatment effect of ticagrelor vs. prasugrel. NCT01944800 • In ACS patients, ticagrelor and prasugrel showed similar efficacy regardless of smoking status. • Bleeding risk was comparable between ticagrelor and prasugrel in smokers and nonsmokers. • Smoking status does not interfere with the relative treatment effect of ticagrelor vs. prasugrel. [ABSTRACT FROM AUTHOR]

Background: The association between elevated creatine kinase (CK) and bleeding in patients with acute coronary syndrome (ACS) remains incompletely investigated. We undertook this study to assess whether there is an association between elevated CK activity and the risk for bleeding in contemporary patients with ACS. Materials and Methods: This post hoc analysis of a randomized trial included 3368 patients with ACS undergoing percutaneous coronary intervention. CK was measured serially in all patients until hospital discharge. The main outcome was 30‐day incidence of major bleeding (type 3 to 5 bleeding according to the Bleeding Academic Research Consortium criteria). Results: Patients were categorized in groups according to the peak CK tertiles: 1st tertile (CK ≤259 U/L; n = 1127 patients), 2nd tertile (CK ≥260 to 990 U/L; n = 1119 patients), and 3rd tertile (CK ≥ 991 U/L; n = 1122 patients). Peak CK activity was higher in patients with bleeding than those without bleeding (771 [316‐1845] U/L vs. 496 [190‐1357] U/L; P <.001). Bleeding occurred in 26 patients (2.3%) with peak CK within 1st tertile, 39 patients (3.5%) with peak CK within 2nd tertile, and 54 patients (4.8%) with peak CK within 3rd tertile (univariable hazard ratio [HR]=1.39, 95% confidence interval [CI] 1.08 to 1.81, P =.012, per tertile increment in CK values). After adjustment, peak CK activity remained significantly associated with the 30‐day bleeding (HR = 1.67 [1.16‐2.41]; P =.006 per unit increment in logarithmic CK values). The C statistic of the multivariable model with CK activity was 0.807 [0.770‐0.842]. Conclusions: In patients with ACS, peak CK activity was independently associated with increased 30‐day incidence of bleeding. [ABSTRACT FROM AUTHOR]

Background: Data on the comparative efficacy and safety of ticagrelor versus prasugrel in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention are limited. We assessed the efficacy and safety of ticagrelor versus prasugrel in a head-to-head comparison in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention.Methods: In this prespecified subgroup analysis, we included 1653 patients with ST-segment-elevation myocardial infarction randomized to receive ticagrelor or prasugrel in the setting of the ISAR REACT-5 trial (Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment 5). The primary end point was the incidence of death, myocardial infarction, or stroke at 1 year after randomization. The secondary end point was the incidence of bleeding defined as BARC (Bleeding Academic Research Consortium) type 3 to 5 bleeding at 1 year after randomization.Results: The primary end point occurred in 83 patients (10.1%) in the ticagrelor group and in 64 patients (7.9%) in the prasugrel group (hazard ratio, 1.31 [95% CI, 0.95-1.82]; P=0.10). One-year incidence of all-cause death (4.9% versus 4.7%; P=0.83), stroke (1.3% versus 1.0%; P=0.46), and definite stent thrombosis (1.8% versus 1.0%; P=0.15) did not differ significantly in patients assigned to ticagrelor or prasugrel. One-year incidence of myocardial infarction (5.3% versus 2.8%; hazard ratio, 1.95 [95% CI, 1.18-3.23]; P=0.010) was higher with ticagrelor than with prasugrel. BARC type 3 to 5 bleeding occurred in 46 patients (6.1%) in the ticagrelor group and in 39 patients (5.1%) in the prasugrel group (hazard ratio, 1.22 [95% CI, 0.80-1.87]; P=0.36).Conclusions: In patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention, there was no significant difference in the primary end point between prasugrel and ticagrelor. Ticagrelor was associated with a significant increase in the risk for recurrent myocardial infarction. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01944800. [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]

The relationship between central pulse pressure (CPP) measured at the time of primary percutaneous coronary intervention (PPCI) and long-term prognosis after ST-segment elevation myocardial infarction (STEMI) has not been investigated. CPP measurements were performed in 1348 patients with STEMI (327 women; mean age 62.5 ± 12.1 years) undergoing PPCI. Aortic systolic and diastolic blood pressure was measured before intervention. The primary outcome was 8-year all-cause mortality. The median [25–75th percentile] CPP value was 55.0 [43.0–70.0] mmHg. CPP correlated negatively with heart rate (P < 0.001), body mass index (P = 0.007), Killip class (P < 0.001) and initial area at risk (P < 0.001) and positively with age (P < 0.001), female sex (P < 0.001), diabetes (P = 0.012), arterial hypertension (P < 0.001) and glomerular filtration rate (P = 0.004). There were 181 deaths over the follow-up. In patients with CPP within the 1st, 2nd and 3rd tertiles, the Kaplan–Meier estimates of mortality were 17.3%, 10.8% and 24.2%, respectively; univariable hazard ratio [HR] =1.52, 95% confidence interval [CI] 0.99 to 2.32; P = 0.055 for tertile 1 vs. tertile 2 and HR =2.09 [1.36–3.21]; P < 0.001 for tertile 3 vs. tertile 2. For CPP values lower than 35 mmHg and higher than 71 mmHg, the association between CPP and all-cause mortality was significant (HR =1.276 [1.004–1.621] for the 35 mmHg value and HR =1.289 [1.003–1.657] for the 71 mmHg value) compared with the CPP reference value (54 mmHg). After adjustment, the association between CPP and all-cause mortality was attenuated (P = 0.304). In patients with STEMI undergoing PPCI there is a U-shaped association between CPP and mortality up to 8 years after PPCI. [ABSTRACT FROM AUTHOR]

Myeloperoxidase (MPO) is a member of the superfamily of heme peroxidases that is mainly expressed in neutrophils and monocytes. MPO-derived reactive species play a key role in neutrophil antimicrobial activity and human defense against various pathogens primarily by participating in phagocytosis. Elevated MPO levels in circulation are associated with inflammation and increased oxidative stress. Multiple lines of evidence suggest an association between MPO and cardiovascular disease (CVD) including coronary artery disease, congestive heart failure, arterial hypertension, pulmonary arterial hypertension, peripheral arterial disease, myocardial ischemia/reperfusion-related injury, stroke, cardiac arrhythmia and venous thrombosis. Elevated MPO levels are associated with a poor prognosis including increased risk for overall and CVD-related mortality. Elevated MPO may signify an increased risk for CVD for at least 2 reasons. First, low-grade inflammation and increased oxidative stress coexist with many metabolic abnormalities and comorbidities and consequently an elevated MPO level may represent an increased cardiometabolic risk in general. Second, MPO produces a large number of highly reactive species which can attack, destroy or modify the function of every known cellular component. The most common MPO actions relevant to CVD are generation of dysfunctional lipoproteins with an increased atherogenicity potential, reduced NO availability, endothelial dysfunction, impaired vasoreactivity and atherosclerotic plaque instability. These actions strongly suggest that MPO is directly involved in the pathophysiology of CVD. In this regard MPO may be seen as a mediator or an instrument through which inflammation promotes CVD at molecular and cellular level. Clinical value of MPO therapeutic inhibition remains to be tested. • Myeloperoxidase is a marker and mediator of inflammation and oxidative stress. • Elevated myeloperoxidase level is associated with increased risk of cardiovascular disease. • Myeloperoxidase level correlates with prevalence and severity of cardiovascular disease. • Elevated myeloperoxidase predicts a poor prognosis in patients with cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: Whether there are sex differences in the outcome of patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI) remains controversial. We undertook this study to assess whether there are sex-related differences in the long-term mortality in a large series of patients with CAD after PCI.Methods: The study included 18,334 patients (4735 women and 13,599 men) with CAD treated with PCI. Propensity matching was performed to obtain a group of patients (3000 women and 3000 men) matched for all characteristics available in database. The primary outcome was a composite of cardiac mortality, myocardial infarction or stroke at 3 years of follow-up.Results: The primary outcome occurred in 660 women and 1440 men (Kaplan-Meier [KM] estimates, 15.2% in women and 11.6% in men, unadjusted hazard ratio [HR] = 1.35, 95% confidence interval [CI] 1.24 to 1.49; P < 0.001). Women were at higher risk of all-cause mortality (15.4% vs. 12.3%; P < 0.001), cardiac mortality (10.2% vs. 7.6%; P < 0.001) and stroke (2.6% vs. 1.4%; P < 0.001) than men. In matched patients, the primary outcome occurred in 371 women and 322 men (KM estimates, 13.4% vs. 11.6%, HR = 1.18 [1.01-1.36], P = 0.033). Women were at higher risk of myocardial infarction (4.2% vs. 3.1%; P = 0.044) but not cardiac (8.7% vs. 8.2%; P = 0.306) or all-cause death (12.5% vs. 12.9%; P = 0.991) or stroke (1.9% vs. 1.6%; P = 0.550) than men.Conclusions: After propensity matching, women remained at a higher risk of a composite of cardiac mortality, myocardial infarction or stroke up to 3 years after PCI than men. [ABSTRACT FROM AUTHOR]

Uric acid (UA) is an end product of purine metabolism in humans and great apes. UA acts as an antioxidant and it accounts for 50% of the total antioxidant capacity of biological fluids in humans. When present in cytoplasm of the cells or in acidic/hydrophobic milieu in atherosclerotic plaques, UA converts into a pro-oxidant agent and promotes oxidative stress and through this mechanism participates in the pathophysiology of human disease including cardiovascular disease (CVD). Most epidemiological studies but not all of them suggested the existence of an association between elevated serum UA level and CVD, including coronary heart disease (CHD), stroke, congestive heart failure, arterial hypertension and atrial fibrillation as well as an increased risk for mortality due to CVD in general population and subjects with confirmed CHD. Evidence available also suggests an association between elevated UA and traditional cardiovascular risk factors, metabolic syndrome, insulin resistance, obesity, non-alcoholic fatty liver disease and chronic kidney disease. Experimental and clinical studies have evidenced several mechanisms through which elevated UA level exerts deleterious effects on cardiovascular health including increased oxidative stress, reduced availability of nitric oxide and endothelial dysfunction, promotion of local and systemic inflammation, vasoconstriction and proliferation of vascular smooth muscle cells, insulin resistance and metabolic dysregulation. Although the causality in the relationship between UA and CVD remains unproven, UA may be pathogenic and participate in the pathophysiology of CVD by serving as a bridging mechanism mediating (enabling) or potentiating the deleterious effects of cardiovascular risk factors on vascular tissue and myocardium. [ABSTRACT FROM AUTHOR]

Gamma-glutamyl transferase (GGT) is a ubiquitous cell surface enzyme that cleaves extracellular glutathione (G-SH) or other gamma-glutamyl compounds. GGT serves to increase the availability of amino acids, primarily cysteine, for intracellular G-SH synthesis and plays a crucial role in maintaining G-SH homeostasis and defense against oxidative stress in organisms. Measurement of circulating GGT activity is widely used for the diagnosis of liver and obstructive biliary diseases and as an indicator of alcohol consumption. Epidemiological studies suggest an association between elevated GGT activity level and a risk of incident coronary heart disease (CHD) or CHD-related mortality. Elevated GGT activity level is associated with a plethora of cardio-metabolic risk factors, including traditional cardiovascular risk factors, metabolic syndrome, systemic inflammation, oxidative stress burden and various comorbidities that incur a negative impact on patient risk profile and prognosis. Experimental studies and studies of human atherosclerotic plaques have revealed not only the presence of catalytically active GGT in atherosclerotic plaques, but also a correlation between GGT activity and indices of plaque instability, suggesting direct involvement in the pathophysiology of atherosclerosis and related clinical events via promotion of pro-oxidant reactions by the enzyme. However, it remains unknown whether GGT plays a direct role in the pathophysiology of atherosclerosis and CHD or is merely a correlate of coexisting cardiovascular risk factors. The exact molecular mechanisms of GGT participation in atherosclerosis or CHD and assessment of GGT-lowering therapies, as well as their impact on clinical outcomes, remain to be investigated in longitudinal studies. [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]

The author talks about atherosclerosis and its clinical manifestation, ischaemic heart disease. Topics discussed include the history of atherosclerosis, the role of coronary thrombosis in causing myocardial infarction, and the concept of cardiovascular prevention pioneered by Paul Dudley White. Also mentioned is the role of cholesterol in atherosclerosis.

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]

The frequency and pattern of progression or regression of coronary atherosclerosis in contemporary patients with diabetes remain unknown. This study included 605 patients with coronary artery disease (CAD). Two coronary angiographic examinations at baseline and after 2 years were performed. The analysis focused on non-stented segments with diameter stenosis ≥25 %. Atherosclerosis progression (or regression) was defined as a decrease (or increase) in the mean minimal lumen diameter (MLD) in the 2-year angiogram compared to mean MLD in the baseline angiogram of >0.2 mm. Statins were prescribed in 576 patients (95.2 %). The primary outcome was atherosclerosis progression or regression in the 2-year angiogram. One hundred sixty-nine patients (28 %) had diabetes. Diabetic patients had greater reduction of mean MLD in the 24 angiogram compared to baseline angiogram than nondiabetic patients (0.11 ± 0.18 vs. −0.08 ± 0.15 mm, P < 0.001). Atherosclerosis progression was observed in 37 patients with diabetes and 16 nondiabetic patients (21.9 vs. 3.7 %; P < 0.001). Atherosclerosis regression was observed in two diabetic patients and 78 nondiabetic patients (1.2 vs. 17.9 %; P < 0.001). A progression pattern across all coronary segments was observed in 70 patients (41.4 %) with diabetes and 60 patients (13.8 %) without diabetes ( P < 0.001). Diabetic patients with a low-density lipoprotein cholesterol ≥70 mg/dl showed more atherosclerosis progression than diabetic patients with LDL cholesterol <70 mg/dl (delta-MLD: 0.12 ± 0.19 vs. 0.08 ± 0.16 mm; P = 0.04). In conclusion, in contemporary patients with CAD treated with moderate-intensity statin therapy, diabetes is associated with the increased risk of progression and decreased probability of regression of coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Background The association between gamma-glutamyl transferase (GGT) and atrial fibrillation (AF) in patients with coronary artery disease (CAD) is uncertain. Methods This study included 5501 consecutive patients with CAD, all of whom had baseline GGT measurements available. The primary endpoint was presence of AF. Results Overall 809 patients (14.7%) had AF on hospital admission. Patients with AF had significantly higher GGT activity compared with patients in sinus rhythm (median [25th–75th percentile]: 52.0 [32.9–96.0] U/L versus 34.8 [23.8–55.9] U/L, P < 0.001). The prevalence of AF increased from 8.6% of patients in the first GGT decile to 30.3% of patients in the tenth decile (P < 0.001). After multivariable adjustment, GGT activity remained independently associated with the probability of the presence of AF (adjusted adds ratio = 1.66, 95% confidence interval 1.53–1.81, P < 0.001 for each standard deviation increment in the GGT logarithmic scale). GGT predicted the probability of AF with an area under the receiver operating characteristic (ROC) curve of 0.6496, 95% confidence interval 0.6287 to 0.6705, P < 0.001 indicating moderate strength to discriminate between patients with and without AF. Conclusions In patients with CAD, elevated GGT activity is independently associated with the presence of AF. GGT may be a circulating marker of the risk for AF. [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]

The prognostic value of gamma-glutamyl transferase (GGT) in patients with acute coronary syndromes (ACS) has been incompletely investigated. We investigated this clinically relevant question in 2,534 consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). GGT activity was measured before PCI procedure in all patients. Statin therapy at hospital discharge was prescribed in 94% of the patients. The primary outcome was 3-year mortality. Patients were divided into 3 groups: the group with GGT in the first tertile (GGT <28 U/L; n = 848 patients), the group with GGT in the second tertile (GGT 28 to <50 U/L; n = 843 patients), and the group with GGT in the third tertile (GGT ≥50 U/L; n = 843 patients). The primary outcome (all-cause deaths) occurred in 250 patients: 70 deaths (9.7%) among patients of the first, 69 deaths (9.0%) among patients of the second, and 111 deaths (14.8%) among patients of the third GGT tertile (adjusted hazard ratio [HR] 1.24, 95% CI 1.08 to 1.42, p = 0.002) and cardiac and noncardiac deaths occurred in 157 (63%) and 93 patients (37%), respectively. GGT was associated with the increased risk of noncardiac mortality (adjusted HR 1.35 [1.09 to 1.66], p = 0.005) but not cardiac mortality (adjusted HR 1.16 [0.97 to 1.38], p = 0.098; all 3 risk estimates were calculated per SD increase in the logarithmic scale of GGT activity). In conclusion, in contemporary patients with ACS treated with PCI and on statin therapy, elevated GGT activity was associated with the increased risk of all-cause and noncardiac mortality but not with the risk of cardiac mortality. [ABSTRACT FROM AUTHOR]

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 Prognostic impact of procedure-related bleeding in patients with stable coronary artery disease ( CAD) undergoing elective percutaneous coronary intervention ( PCI) remains incompletely investigated. The aim of this study was to investigate the association between peri- PCI bleeding and 1-year outcome of patients with stable CAD. Materials and methods The study included 9035 patients with stable CAD who underwent elective PCI. Bleeding within 30 days of PCI was defined using the Bleeding Academic Research Consortium ( BARC) criteria. The primary outcome was 1-year mortality. Results Bleeding occurred in 844 patients (9·3%). Actionable bleeding ( BARC class ≥ 2) occurred in 442 patients (4·9%). There were 210 deaths (2·3%) at 1 year following PCI: 41 deaths among patients with bleeding and 169 deaths among patients without bleeding [Kaplan-Meier estimates of mortality, 4·9% and 2·1%; odds ratio = 2·41, 95% confidence interval ( CI) 1·73-3·36, P < 0·001]. The association between bleeding and mortality remained significant after adjustment for baseline risk variables (adjusted hazard ratio = 1·87, 95% CI 1·27-2·76, P = 0·002). Bleeding increased the discriminatory power of the model regarding prediction of 1-year mortality (absolute and relative integrated discrimination improvement, 0·006% and 16·3%, respectively, P = 0·001). Conclusions In patients with stable CAD undergoing elective PCI, the occurrence of bleeding within 30 days of the procedure was associated with increased risk of death at 1 year after PCI. These findings suggest that procedure-related bleeding may contribute to less than optimal results of PCI in terms of mortality reduction in patients with stable CAD. [ABSTRACT FROM AUTHOR]

The relation between body mass index (BMI) and bleeding after percutaneous coronary intervention (PCI) remains incompletely understood. This study aimed to assess the association between BMI and bleeding and mortality after PCI. The study included 14,178 patients with coronary artery disease treated by PCI. Bleeding within 30 days of PCI was defined using the Bleeding Academic Research Consortium criteria. The primary outcome was 1-year all-cause mortality. BMI quartiles were 14.1 to 24.8 kg/m² (first quartile [Q1]), >24.8 to 27.1 kg/m² (second quartile [Q2]), >27.1 to 29.8 kg/m² (third quartile [Q3]), and >29.8 to 56.3 kg/m² (fourth quartile [Q4]). In BMI Q1, Q2, Q3, and Q4, the frequency of bleeding was 13.8%, 10.1%, 10.8%, and 7.7%, respectively (odds ratio [OR] 1.90, 95% confidence interval [CI] 1.63 to 2.23, p <0.001, for Q1 vs Q4). Multiple logistic regression showed that BMI was independently associated with bleeding (adjusted OR 1.05,95% CI 1.04 to 1.07, p <0.001, for any bleeding; adjusted OR 1.07, 95% CI 1.04 to 1.09, p <0.001, for access site bleeding; and adjusted OR 1.03,95% CI 1.01 to 1.05, p = 0.039, for non-access site bleeding with all 3 risk estimates calculated per 1 kg/m² decrease in BMI). Analysis by sex showed an increase in the frequency of bleeding with the decrease in BMI for women and men (p for trend <0.001 for women and men) with no sex-by-BMI interaction (p = 0.90). The Cox proportional hazards model showed that bleeding (adjusted hazard ratio [HR] 2.17, 95% CI 1.67 to 2.82, p <0.001) and BMI (HR 1.03, 95% CI 1.01 to 1.06, p = 0.048, per 1 kg/m² decrease in the BMI) were independently associated with increased risk of 1-year mortality with no bleeding-by-BMI interaction (p = 0.81). In conclusion, BMI is inversely associated with the increased risk of bleeding and mortality after PCI. [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: The comparative prognostic value of low density lipoprotein-cholesterol (LDL-C) and C-reactive protein (CRP) in patients with stable coronary artery disease (CAD) treated with percutaneous coronary intervention (PCI) and statin therapy is poorly investigated. Methods: The study included 7595 patients with stable CAD treated with PCI. Based on a cut-off of 100mg/dl for LDL-C and 3mg/L for CRP, patients were divided into 4 groups: patients with LDL-C≤100mg/dl and CRP≤3mg/L (n=2795); patients with LDL-C>100mg/dl and CRP≤3mg/L (n=2091); patients with LDL-C≤100mg/dl and CRP>3mg/L (n=1296); and patients with LDL-C>100mg/dl and CRP>3mg/L (n=1413). Statins at discharge were prescribed in all patients. The primary outcome was 1-year all-cause mortality. Results: One-year mortality was 2.1% (160 deaths): 1.2% (33 deaths) among patients with LDL-C ≤100mg/dl and CRP≤3mg/L, 1.4% (28 deaths) among patients with LDL-C>100mg/dl and CRP≤3mg/L, 4.8% (60 deaths) among patients with LDL-C≤100mg/dl and CRP>3mg/L and 2.9% (39 deaths) among patients with LDL-C>100mg/dl and CRP>3mg/L (P<0.001). After adjustment, CRP (hazard ratio [HR]=1.64, 95% confidence interval [CI] 1.33–2.02, for 1 standard deviation increase in the logarithmic scale) but not LDL-C (HR=1.03 [0.90–1.17], for 30mg/dl increase) showed an independent association with 1-year mortality. CRP (P=0.045) but not LDL-C (P=0.294) increased the discriminatory power of multivariable model for prediction of mortality. Conclusion: In patients with stable CAD treated with PCI and statin therapy, CRP but not LDL-C was independently associated with increased risk of 1-year mortality. [Copyright &y& Elsevier]

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]

Evidence on the usefulness of fibrinogen for the risk stratification of patients with coronary artery disease remains inconclusive. The aims of this study were to investigate the association of fibrinogen with cardiovascular events and to assess whether this biomarker provides additional prognostic information on top of that provided by traditional cardiovascular risk factors. This study included 13,195 patients with angiography-proved coronary artery disease and fibrinogen measurements available. Receiver-operating characteristic curve analysis showed that the best fibrinogen cutoff for mortality prediction was 402.0 mg/dl. On the basis of this cutoff, patients were divided into 2 groups: the group with fibrinogen >402.0 mg/dl (n [ 5,198) and the group with fibrinogen £402.0 mg/dl (n [ 7,997). The primary outcome was 1-year mortality. All-cause deaths occurred in 393 patients with fibrinogen >402.0 mg/dl and in 246 patients with fibrinogen £402.0 mg/dl (Kaplan-Meier estimates of mortality 7.7% and 3.1%, log-rank test p <0.001). The relation between fibrinogen and mortality followed a J-shaped pattern, with lowest mortality in patients with fibrinogen concentrations of 295 to 369 mg/dl. After adjustment for cardiovascular risk factors and relevant clinical variables, fibrinogen remained an independent correlate of all-cause mortality (adjusted hazard ratio 1.07, 95% confidence interval 1.04 to 1.10, p <0.001, for each 50 mg/dl increase in fibrinogen level), but it did not improve the discriminatory power of the model for mortality prediction (integrated discrimination improvement 0.002, p [ 0.32). In conclusion, in patients with coronary artery disease, fibrinogen is an independent correlate of mortality, but it does not provide additional prognostic information on top of that provided by traditional cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Background The optimal uric acid ( UA) level associated with the lowest mortality and the strength of association between UA and mortality in various subgroups of patients with coronary artery disease ( CAD) are unknown. Materials and methods This study included 13 273 patients with angiographic confirmation of CAD and UA measurements available. The primary outcome analysis was 1-year mortality. Results Based on the receiver operating characteristic curve analysis, the best cut-off of UA for mortality prediction was 7·11 mg/dL. Using this cut-off, patients were divided into two groups: the group with UA ≤ 7·11 mg/dL ( n = 9075) and the group with UA > 7·11 mg/dL ( n = 4198). Cardiac mortality was 6·3% (256 deaths) in patients with UA > 7·11 mg/dL and 2·3% (201 deaths) in patients with UA ≤ 7·11 mg/dL [hazard ratio ( HR) = 2·82, 95% confidence interval ( CI) 2·36-3·36; P < 0·001]. After adjustment for cardiovascular risk factors, UA remained an independent correlate of cardiac mortality ( HR = 1·20, 95% CI 1·08-1·34; P = 0·001, for each standard deviation increase in the logarithmic scale of UA). The relationship between cardiac or all-cause mortality and UA showed a J-shaped pattern with lowest mortality in patients with UA between 5·17 and 6·76 mg/dL. UA predicted mortality across all subgroups of patients, with strongest association in women and patients without arterial hypertension. Conclusions UA predicted an increased risk of cardiac mortality across all subgroups of patients with CAD. The association between UA and cardiac or all-cause mortality had a 'J-shaped' pattern with lowest risk of death in patients with UA levels between 5·17 and < 6·76 mg/dL. [ABSTRACT FROM AUTHOR]

Abstract: Background: Statins have multiple effects in patients with coronary artery disease. No studies have investigated whether chronic statin pretreatment before percutaneous coronary intervention (PCI) has an impact on long-term mortality in patients with stable angina. Methods: The study included 8041 patients with stable angina. At the time of PCI, 5939 patients (73.8%) were receiving statins for ≥1month before procedure and 2102 patients (26.2%) were not receiving statins. The primary outcome analysis was 1-year mortality. Results: There were 192 deaths during the follow-up: 119 deaths among patients receiving statins and 73 deaths among patients not receiving statins (Kaplan–Meier estimates of 1-year mortality 2.06% and 3.59%; unadjusted hazards ratio [HR]=0.56, 95% confidence interval [CI] 0.42–0.75; P<0.001). Landmark analysis showed that almost all mortality benefit occurred in the first 30-days after PCI: 10 deaths among patients receiving statins and 22 deaths among patients not receiving statins (Kaplan–Meier estimates of 30-day death, 0.17% and 1.06%, respectively; HR=0.16, 95% CI 0.08–0.34, P<0.001). No significant difference in mortality according to statin pretreatment between 30days and 1year was observed (109 deaths among patients receiving statins vs 51 deaths among patients not receiving statins; Kaplan–Meier estimates 1.89% and 2.53%; HR=0.75, 95% CI 0.53–1.05, P=0.095). After adjustment in the Cox proportional hazards model, statin pretreatment was associated with a 35% reduction in the adjusted risk for 1-year mortality (adjusted HR=0.65, 95% CI 0.44–0.98, P=0.039). Conclusions: Pretreatment with statins before PCI was associated with a significant reduction of 1-year mortality in patients with stable angina. [Copyright &y& Elsevier]

Studies investigating the prognostic role of UA (uric acid) in patients with Type 2 diabetes mellitus have given conflicting findings. We undertook the present study to assess the association between UA and outcome in patients with Type 2 diabetes mellitus and CAD (coronary artery disease). The study included 3705 patients with diabetes mellitus and angiography-proven CAD. UA was measured before coronary angiography. The primary outcome was 1-year all-cause mortality. The UA concentration [median (25th-75th quartiles)] was 6.44 mg/dl (5.40-7.70 mg/dl). There were 264 deaths (7.1 %) during follow-up: 45 deaths in patients of the first UA quartile, 43 deaths in patients of the second UA quartile, 51 deaths in patients of the third UA quartile and 125 deaths in patients of the fourth UA quartile {Kaplan-Meier estimates of mortality, 5.1, 4.8, 5.6 and 14.0% respectively; unadjusted HR (hazard ratio), 2.81 [95% CI (confidence interval), 2.21-3.58]; P<0.001 for fourth quartile compared with first-third quartiles combined}. In the multivariable analysis, UA predicted all-cause mortality with an adjusted HR of 1.29 (95% CI, 1.12-1.48; P<0.001), for each S.D. increase in the logarithmic scale of UA level. The inclusion of UA in the multivariable model alongside known cardiovascular risk factors and other relevant variables increased the discriminatory power of the model regarding prediction of all-cause mortality [absolute and relative IDI (integrated discrimination improvement) 0.034 and 20.5% respectively; P<0.001]. In conclusion, in patients with Type 2 diabetes mellitus and confirmed CAD, elevated levels of UA predict mortality independently of known cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Objective To evaluate efficacy and safety of two zotarolimus-eluting stent generations versus other limuseluting stents (LES), and to compare Resolute zotarolimus-eluting stents (R-ZES) with Endeavor zotarolimus-eluting stents (E-ZES). Background The performance of zotarolimus-eluting stents versus other LES, and the possible improvements of R-ZES versus E-ZES still remain to be defined. Methods We undertook a meta-analysis of trials in which patients were randomly assigned to percutaneous coronary interventions (PCI) with R-ZES versus LES, or with E-ZES versus LES, as well as an indirect comparison of R-ZES versus E-ZES, with LES as common comparator. The primary efficacy endpoint was ischaemia-driven target vessel revascularisation (ID-TVR); the primary safety endpoints were myocardial infarction (MI), cardiac death and cumulative definite/probable stent thrombosis (ST). Results Overall, 13'709 patients were assigned to PCI with R-ZES versus LES (n¼7185) or with E-ZES versus LES (n¼6524). The risk of ID-TVR (OR (95% CI)¼1.06 (0.90 to 1.25), p¼0.47), MI (1.00 (0.81 to 1.25), p¼0.97), cardiac death (0.99 (0.69 to 1.42), p¼0.96) and ST (1.18 (0.68 to 2.03), p¼0.56) did not differ between RZES and LES. Patients receiving E-ZES were more likely to undergo ID-TVR as compared with those receiving LES (1.95 (1.40 to 2.73), p<0.0001). The risk of MI (0.91 (0.54 to 1.54), p¼0.73), cardiac death (1.02 (0.54 to 1.91), p¼0.96) and ST (1.10 (0.50 to 2.44), p¼0.81) was similar between E-ZES and LES. At indirect comparison, PCI with R-ZES versus E-ZES reduced the risk of ID-TVR (0.54 (0.37 to 0.78), p¼0.001), without increasing MI (1.09 (0.62 to 1.93), p¼0.74), cardiac death (0.97 (0.46 to 2.00), p¼0.93) and ST (1.07 (0.40 to 2.80), p¼0.88). Conclusions The antirestenotic efficacy of Resolute zotarolimus-eluting stents is superior to Endeavor zotarolimus-eluting stents and similar to other limuseluting stents. Endeavor zotarolimus-eluting stents increase the risk of reinterventions as compared with other limus-eluting stents. First and second-generation zotarolimus-eluting stents have similar thrombogenicity compared with other limus-eluting stents. [ABSTRACT FROM AUTHOR]

The association between uric acid and cardiovascular disease is incompletely understood. In particular, the prognostic value of uric acid in patients with acute coronary syndromes who undergo percutaneous coronary intervention has not been studied. This study included 5,124 patients with acute coronary syndromes who underwent percutaneous coronary intervention: 1,629 with acute ST-segment elevation myocardial infarction, 1,332 with acute non–ST-segment elevation myocardial infarction, and 2,163 with unstable angina. The primary end point was 1-year mortality. Patients were divided into quartiles according to uric acid level as follows: quartile 1, 1.3 to <5.3 mg/dl; quartile 2, 5.3 to <6.3 mg/dl; quartile 3, 6.3 to <7.5 mg/dl; and quartile 4, 7.5 to 18.4 mg/dl. There were 450 deaths during follow-up: 80 deaths in quartile 1, 77deaths in quartile 2, 72 deaths in quartile 3, and 221 deaths in quartile 4 of uric acid (Kaplan-Meier estimates of 1-year mortality 6.4%, 6.2%, 5.6%, and 17.4%, respectively; unadjusted hazard ratio 3.05, 95% confidence interval 2.54 to 3.67, p <0.001 for fourth vs first quartile of uric acid). After adjustment for traditional cardiovascular risk factors, renal function, and inflammatory status, the association between uric acid and mortality remained significant, with a 12% increase in the adjusted risk for 1-year mortality for every 1 mg/dl increase in the uric acid level. Uric acid improved the discriminatory power of the predictive model regarding 1-year mortality (absolute integrated discrimination improvement 0.008, p = 0.005). In conclusion, elevated levels of uric acid are an independent predictor of 1-year mortality across the whole spectrum of patients with acute coronary syndromes treated with percutaneous coronary intervention. [ABSTRACT FROM AUTHOR]

Background--The Bleeding Academic Research Consortium (BARC) has recently proposed a unified definition of bleeding in patients receiving antithrombotic therapy. We investigated the relationship between bleeding events as defined by BARC and 1-year mortality in patients undergoing percutaneous coronary intervention (PCI) and assessed whether the BARC bleeding definition is superior to existing bleeding definitions in regard to mortality prediction in patients after PCI procedures. Methods and Results--This study represents a patient-level pooled analysis of 12 459 patients recruited in 6 randomized trials of patients undergoing PCI. Bleeding events were assessed with the use of BARC, Thrombolysis in Myocardial Infarction (TIMI), and Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE-2) trial criteria. The primary outcome was I-year mortality. Bleeding occurred in 1233 patients (9.9%) according to BARC (679 patients or 5.4% with BARC class >2 bleeding), in 374 patients (3.0%) according to TIMI, and in 491 patients (3.9%) according to REPLACE-2 criteria. There were 340 deaths (2.7%) over the first year after PCI. BARC class >2 bleeding was associated with a significant increase in I-year mortality (adjusted hazard ratio 2.72; 95% confidence interval, 2.03-3.63). The predictivity of a multivariable model for 1-year mortality was significantly improved after inclusion of bleeding defined according to BARC to an extent comparable to that provided by TIMI and REPLACE-2 criteria. Conclusions--The present study demonstrated a close association between bleeding events defined according to BARC and 1-year mortality after PCI. [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2011; 41 (10): 1054-1062 Abstract Background High-sensitivity cardiac troponin (hs-TnT) and N-terminal probrain natriuretic peptide (NT-proBNP) are powerful predictors of mortality in patients with stable coronary artery disease. Whether their combined use may further improve mortality prediction in these patients is unknown. Materials and methods The study included 869 patients with stable coronary artery disease who underwent percutaneous coronary intervention. Hs-TnT and NT-proBNP were measured before angiography. Using median values of hs-TnT (0·008 μg L−1) and NT-proBNP (250·0 ng L−1) as cut-off points, patients were divided into four groups: low hs-TnT/low NT-proBNP group (293 patients with hs-TnT and NT-proBNP < median); low hs-TnT/high NT-proBNP group (142 patients with hs-TnT < median and NT-proBNP ≥ median); high hs-TnT/low NT-proBNP group (142 patients with hs-TnT ≥ median and NT-proBNP < median) and high hs-TnT/high NT-proBNP group (292 patients with hs-TnT and NT-proBNP ≥ median). The primary end point was all-cause mortality. Results The 4-year follow-up was complete in 90·7% of the patients. There were 76 deaths during the follow-up: seven in low hs-TnT/low NT-proBNP, 8 in low hs-TnT/high NT-proBNP, 10 in high hs-TnT/low NT-proBNP and 51 in high hs-TnT/high NT-proBNP groups (mortality estimates, 2·5%, 5·9%, 7·4% and 18·1%, respectively; odds ratio = 8·64, 95% confidence interval 3·85-19·4, P < 0·001 for high hs-TnT/high NT-proBNP vs. low hs-TnT/low NT-proBNP). Inclusion of hs-TnT and NT-proBNP in the multivariable model increased the discriminatory power of the model regarding mortality prediction compared with the model without biomarkers (absolute and relative integrated discrimination improvement 0·039 and 26·0%, P = 0·0015). Conclusions Combined use of hs-TnT and NT-proBNP improves long-term risk prediction of mortality in patients with stable coronary heart disease. [ABSTRACT FROM AUTHOR]

Aims: The present study attempts to develop an objective, statistically based set of criteria for activation time determination from unipolar electrograms (U-EGMs) using a standard of activation related to biophysical theory. Methods: A high-resolution assembly of U-EGMs obtained from the epicardial surface of the canine postinfarction heart were analyzed in order to achieve the best prediction of local versus distant activation. An activation time standard (ATS) consisted of three properties: (1) propagation of activation, evidenced by a linear temporal shift of waveforms from closely spaced U-EGMs with little or no decay in amplitude; (2) cycle length-dependent changes of those propagating waveforms; and (3) evidence of electrotonic deflections, seen as nonpropagating potentials having decaying amplitude with distance. Results: A number of U-EGM features were calculated and subjected to analysis by comparing their occurrence with the ATS. A discriminant function analysis incorporating multiple features (Voltage, −dV/dt and Ratio) of major U-EGM deflections improved prediction of activation time of complex fractionated EMGs from ischemic canine epicardium to 90%. Conclusion: A unique discriminant function based on sound biophysical principles markedly improved prediction of activation time of complex U-EGMs from ischemic canine epicardium. A computerized version of the algorithm could be developed to provide more accurate activation maps for both basic and clinical use. (PACE 2011; 34:1105-1115) [ABSTRACT FROM AUTHOR]

The association between circulating levels of cardiac troponins and angiographic severity of coronary artery disease (CAD) has not been studied. We investigated whether there is an association between the level of high-sensitivity troponin T (hs-TnT) and angiographic severity of CAD and whether this association is independent of conventional risk factors, N-terminal pro–brain natriuretic peptide (NT–pro-BNP) and C-reactive protein (CRP). This case–control study included 904 patients with stable CAD (cases) and 412 patients with chest pain but without significant CAD on coronary angiogram (controls). Diagnosis of CAD was confirmed or excluded by coronary angiography. Cardiac TnT was measured with conventional and high-sensitivity assays in parallel using the same plasma sample. In patients with no CAD and in those with 1-, 2-, or 3-vessel disease, hs-TnT levels (median, twenty-fifth to seventy-fifth percentiles) were 0.005 μg/L (<0.003 to 0.009), 0.006 μg/L (0.003 to 0.011), 0.008 μg/L (0.004 to 0.013), and 0.010 μg/L (0.006 to 0.017), respectively (p <0.001). In multivariable analysis adjusting for cardiovascular risk factors and clinical variables including NT–pro-BNP and CRP, hs-TnT was an independent predictor of presence of CAD (adjusted odds ratio 1.30, 95% confidence interval 1.07 to 1.59, p = 0.009). In conclusion, in patients with stable and angiographically proved CAD, hs-TnT level is increased compared to subjects without CAD and correlates with angiographic atherosclerotic extent and burden. The association between increased levels of hs-TnT and presence of CAD was independent of traditional cardiovascular risk factors, NT–pro-BNP, and CRP. [ABSTRACT FROM AUTHOR]

Abstract: Background: The impact of high-sensitivity troponin assays on risk stratification of patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS) is unknown. Methods: The study included 447 patients with NSTE-ACS. Cardiac troponin T (TnT) was measured with conventional and high-sensitivity assays, in parallel, using the same plasma sample. The primary end-point was 4-year mortality. Results: The use of cut-off of 0.014μg/L of high-sensitivity TnT (hs-TnT) instead of 0.01μg/L of the conventional (cTnT) increased proportion of non-ST-segment elevation myocardial infarction (NSTEMI) patients by 33% (from 201 to 268 patients). Re-classified patients from unstable angina to NSTEMI had similar 4-year mortality compared to patients with NSTEMI by both assays: 16 deaths (25.1%) among 67 re-classified patients versus 47 deaths (23.6%) among patients diagnosed with NSTEMI by both assays; odds ratio=1.03, 95% confidence interval [CI] 0.53–1.97; P=0.933). The Cox model identified hsTnT (hazard ratio=2.59, 95% CI 1.22–5.50; P=0.013 for hsTnT>0.014μg/L versus hsTnT≤0.014μg/L) as an independent correlate of 4-year mortality. hsTnT significantly improved prediction of the four-year mortality (relative integrated discrimination improvement 8.2%, P=0.005). Conclusions: The use of hsTnT instead of cTnT increased the proportion of patients with NSTEMI among patients with NSTE-ACS and significantly improved risk stratification regarding long-term mortality. [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]

Bleeding complications in patients undergoing percutaneous coronary interventions (PCIs) are associated with increased risk of subsequent mortality. We undertook this study to characterize the subset of patients with bleeding complications who are at an increased risk of death within the first year after a PCI procedure. The study included 331 patients with bleeding complications among 9 954 patients who underwent PCI. The primary outcome analysis was 1-year mortality. Within the first year following PCI there were 39 deaths among 331 patients (11.8%), with bleeding complications and 240 deaths among 9 623 patients without bleeding complications (Kaplan-Meier estimates of 1-year mortality; 11.8% vs 2.5%, odds ratio 5.09, 95% confidence interval 3.76–6.90, P < 0.001). Time to death (median [25th–75th percentiles]) was 38.5 [7.2–125.9] days in patients with bleeding complications vs 137.1 [68.3–234.0] days in patients without bleeding complications ( P < 0.001). Compared with survivors ( n = 292), nonsurvivors ( n = 39) had a significantly more adverse risk profile. The Cox proportional hazards model identified the elevated troponin level as the only independent correlate of 1-year mortality (hazard ratio = 2.35, 95% confidence interval 1.04–5.31, P = 0.039). In conclusion, patients with peri-PCI bleeding complications who die have a more adverse cardiovascular risk profile than patients with bleeding complications who survive the first year after PCI. Patients with bleeding complications and an elevated troponin level are at high risk of death within the first year following PCI. The majority of deaths in patients with peri-PCI bleeding occur within the first 3 months after PCI procedure. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this study was to investigate the impact of no-reflow phenomenon on 5-year mortality among patients with acute ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (PCI). This impact was also assessed in relation to infarct size. Background: The impact of no-reflow on long-term mortality in patients with STEMI has been insufficiently studied. Methods: This study included 1,406 patients with STEMI treated by primary PCI. No-reflow was diagnosed using angiographic criteria. Infarct size was measured with single-photon emission computed tomography imaging 7 to 14 days after the acute event. The primary outcome was 5-year mortality. Results: The no-reflow phenomenon was diagnosed in 410 patients (29%). Infarct size was 15.0% (6.0% to 29.0%) of the left ventricle in the no-reflow group versus 8.0% (2.0% to 21.0%) of the left ventricle in the reflow group (p < 0.001). There were 132 deaths during follow-up. Of them, 59 deaths occurred among patients with no-reflow and 73 deaths occurred among patients with reflow (Kaplan-Meier estimates of 5-year mortality 18.2% and 9.5%, respectively; odds ratio: 2.02; 95% confidence interval: 1.44 to 2.82; p < 0.001). The Cox proportional hazards model adjusting for infarct size among other variables identified the no-reflow phenomenon as an independent correlate of 5-year mortality (hazard ratio: 1.66; 95% confidence interval: 1.17 to 2.36; p = 0.004). Conclusions: In patients with STEMI treated by primary PCI, no-reflow phenomenon is a strong predictor of 5-year mortality. No-reflow phenomenon after PCI provides prognostic information that is independent of and beyond that provided by infarct size. [Copyright &y& Elsevier]

Compared to unfractionated heparin (UFH), bivalirudin decreases bleeding during percutaneous coronary interventions (PCIs). We sought to investigate the association between periprocedural bleeding and 1-year mortality as a function of antithrombotic therapy with bivalirudin or UFH. This analysis of the association between bleeding with bivalirudin or UFH and 1-year mortality included the 4,570 patients with negative biomarkers enrolled in the Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment (ISAR-REACT 3) trial. Major or minor bleeding occurred in 555 patients (12.1%): 225 patients treated with bivalirudin (9.8%) and 330 patients treated with UFH (14.5%, p <0.001). There were 82 deaths (1.8%) within the first year after PCI: 29 deaths occurred in patients who had bled, and 53 deaths occurred in patients who had not bled (Kaplan-Meier estimates of 1-year mortality 5.2% and 1.3%, odds ratio 4.12, 95% confidence interval 2.59 to 6.54, p <0.001). One year after PCI, there were 15 deaths in patients who bled with bivalirudin versus 14 deaths in patients who bled with UFH (Kaplan-Meier estimates of 1-year mortality 6.7% vs 4.2%, odds ratio 1.61, 95% confidence interval 0.76 to 3.40, p = 0.20). Major bleeding occurred in 70 patients (3.0%) treated with bivalirudin and 104 patients treated with UFH (4.5%, p = 0.008). One-year mortality was 11.4% (n = 8) in patients with major bleeding with bivalirudin versus 4.8% (n = 5) in patients with major bleeding with UFH (p = 0.10). In conclusion, these data suggest that in patients with negative biomarkers undergoing PCI, bivalirudin decreases bleeding after PCI compared to UFH, without affecting 1-year mortality in those who had bled. [Copyright &y& Elsevier]

Studies that have tested the relationship between body weight as assessed by body mass index (BMI) and clinical outcome after percutaneous coronary intervention (PCI) have given contradictory results. The aim of the study was to investigate the impact of BMI on clinical outcome and assess the impact of adjustment for other cardiovascular risk factors on the relationship between obesity and clinical outcome in patients with acute coronary syndromes (ACS) following PCI. This study included 9146 patients with ACS who underwent coronary angiography and PCI: 2610 patients with ST-segment elevation acute myocardial infarction, 2792 patients with non-ST-segment elevation acute myocardial infarction, and 3744 patients with unstable angina. The primary outcome of this analysis was 1-year mortality. Quartiles of BMI were: 12.8 to <24.3 (1st quartile), 24.3 to <26.4 (2nd quartile), 26.4 to <29.1 (3rd quartile), and >29.1 to 50.7 (4th quartile). Within the first year following PCI, there were 756 deaths: 228 deaths in the 1st BMI quartile, 209 deaths in the 2nd BMI quartile, 161 deaths in the 3rd BMI quartile and 158 deaths in the 4th BMI quartile (Kaplan-Meier estimates of mortality 10.3%, 9.1%, 7.2%, and 7.0%, respectively; odds ratio [OR] = 1.51, 95% confidence interval [CI] 1.22-1.86, P < 0.001 for 1st vs 4th BMI quartile). After adjustment in the Cox proportional hazards model, the association between BMI and 1-year mortality was attenuated to the level of statistical insignificance (hazards ratio [HR] = 1.25, 95% CI 0.94–1.64; P = 0.127 for 1st vs 4th BMI quartile). In conclusion, in patients with ACS undergoing PCI, obesity as assessed with BMI was not an independent correlate of 1-year mortality. [ABSTRACT FROM AUTHOR]