Cardioprotective effect of boswellic acids against doxorubicin induced myocardial infarction in rats.

The aim of the present study was to evaluate the cardioprotective activity of boswellic acids in doxorubicin (DOX) induced cardiotoxicity. DOX (2.5mg/kg) was used intraperitoneally in rats to induce cardiotoxicity in six divided doses every alternate day over a period of two weeks. Dexrazoxane (10:1) was used as a standard drug. Boswellic acids (250, 500 and 750 mg/kg) were orally administered to rats for 14 days. After 14 days, rats were sacrificed, and blood was withdrawn through cardiac puncture. The blood lipid profile and cardiac biomarkers including LDH, CK-MB, CPK, SGOT and troponin T were measured. The heart of rats was isolated for histopathological studies. Graphpad Prism was used for statistical analysis. There was a significant increase in the level of cardiac enzymes and complete lipid profile parameters in diseased group as compared to control group. Pre-treatment with boswellic acids decreased level of all the measured parameters and decreased the severity of myocardial damage as supported by histopathological studies. It was concluded that boswellic acids possess cardioprotective potential by lowering cardiac biomarkers and blood lipid profile. Thus, boswellic acids might act as cardioprotective agent against doxorubicin induced cardiotoxicity.

Molecular biomarkers of cantharidin-induced cardiotoxicity in Sprague-Dawley rats: Troponin T, vascular endothelial growth factor and hypoxia inducible factor-1α.

Early diagnosis of cantharidin-induced myocardial injury is the key to reduce the fatality rate in clinical practice. The purpose of the present study was to explore biomarkers that can be used for the prediction and diagnosis of cantharidin-induced myocardial injury. Of 65 male Sprague-Dawley rats weighing 200-230 g, 25 rats were divided into five groups according to the administration dose of cantharidin (0, 1.34, 2.67, 4 and 5.34 mg/kg; n = 5 per group) and the other 40 rats were treated with 2.67 mg/kg cantharidin and divided into nine groups according to the administration time (0, 1, 2, 4, 6, 8, 12, 24, 48 and 72 hours; n = 4 per group). Pathological changes of hypoxia, necrosis and inflammation were confirmed in heart samples that were exposed to cantharidin by hematoxylin-eosin staining and overall scores of pathological changes among heart samples in cantharidin exposure groups showed an increasing trend compared with in the control group. Coexpression of vascular endothelial growth factor (VEGF), hypoxia inducible factor-1α (HIF-1α) and caspase9 was shown in the myocardium by immunofluorescence staining. Western blotting results showed that expression of VEGF, HIF-1α and caspase9 in cantharidin-treated rat hearts showed an increasing trend compared with in the control group. Results of enzyme-linked immunosorbent assay suggested that plasma levels of troponin T (TN-T), VEGF and HIF-1α were elevated at different intervals after cantharidin administration, and VEGF and HIF-1α had a significant linear relationship with TN-T that was verified by multiple linear regression analysis. Preliminary results serve to illustrate that TN-T, VEGF and HIF-1α might be valuable molecular markers in cantharidin-induced myocardial injury and that diagnostic accuracy needs to be studied further.

Carvedilol and Cardiac Biomarkers in Dialysis Patients: Secondary Analysis of a Randomized Controlled Trial.

BACKGROUND/AIMS: Cardiac biomarkers are associated with cardiac abnormalities and adverse outcomes in dialysis patients. Our aim was to report the effect of the beta-blocker carvedilol on cardiac biomarkers in adult dialysis patients. METHODS: The Beta-Blocker to Lower Cardiovascular Dialysis Events Feasibility Study was a randomized controlled trial comparing carvedilol to placebo. Serum and plasma were collected before the run-in, then 6 and 12 months post-randomization to measure B-type Natriuretic Peptide (BNP), N-terminal BNP (NT-ProBNP), high-sensitivity cardiac troponins I (hs-TnI) and T (hs-TnT), and galectin-3. Left ventricular global longitudinal strain (GLS) was measured by echocardiography at baseline. RESULTS: Seventy-two participants were recruited of whom 49 completed the run-in and were randomized to carvedilol (n=26) or placebo (n=23). Baseline echocardiography demonstrated median (inter-quartile range) GLS of -14.27% (-16.63 to -11.93). NTproBNP and hs-TnT correlated with GLS (Spearman's rho=0.34 [p=0.018] and rho=0.28 [p=0.049], respectively). Median change scores from baseline to 12 months did not differ significantly between participants with complete biomarker data randomized to carvedilol (n=15) or placebo (n=16) for any biomarkers. CONCLUSIONS: NT-proBNP and hs-TnT were associated with GLS. However, changes in levels of the biomarkers from baseline to 12 months were not different between groups randomized to carvedilol and placebo.

Early anthracycline-induced cardiotoxicity monitored by echocardiographic Doppler parameters combined with serum hs-cTnT.

PURPOSE: As growing numbers of long-term cancer survivors faced with the cardiac side effects by anthracycline treatment, it is necessary to explore the optimal monitoring method for the early detection of cardiac toxicity. METHODS: We conducted a retrospective analysis of 82 consecutive patients with diffuse large B-cell lymphoma treated with chemotherapy. Echocardiographic Doppler imaging-derived Tei index and mitral annular peak systolic velocity (Sm) measured by tissue Doppler imaging TDI, serum high-sensitivity cardiac troponin T (hs-cTnT) levels, and left ventricular ejection fraction (LVEF) by multigated radionuclide angiography (MUGA) were obtained before, after 2-4, and after 6-8 chemotherapy cycles. Cardiotoxicity was defined as a relative reduction of LVEF ≥10% from the baseline or LVEF <50% as measured by MUGA. RESULTS: Following chemotherapy, 24 (29.3%) patients developed detectable cardiac abnormality during the treatment. Five (6.1%) patients' cardiac function changed from normal baseline LVEF to <50% after the chemotherapy. Echocardiographic pulse wave Doppler Tei index (PW Tei index) (baseline 0.347 ± 0.115 vs 2-4 cycles 0.459 ± 0.161 vs 6-8 cycles 0.424 ± 0.139, P = .000) inversely correlated with systolic (P < .001) and diastolic dysfunction (P < .001). Serum hs-cTnT levels increased significantly following chemotherapy after 2-4 cycles of chemotherapy with anthracycline. The increase in PW Tei index of 0.095 [sensitivity, 69.2%; specificity, 64.5%; area under the curve (AUC) = 0.697; P = .005] and the Sm < 13.65 cm/s (sensitivity, 66.7%; specificity, 71%; AUC = 0.682; P = .009) combined with elevation of serum hs-cTnT level of 0.0075 ng/mL (sensitivity, 69.2%; specificity, 83.9%; AUC = 0.790; P < .001) after 2-4 chemotherapy cycles from the baseline values can reliably predict cardiotoxicity. CONCLUSIONS: We demonstrated that echocardiographic PW Doppler-derived Tei index, and TDI-derived Sm, combined with serum hs-cTnT level can be obtained in outpatient settings to monitor early cardiac toxicity induced by anthracycline therapy.

Sevoflurane Versus Total Intravenous Anesthesia for Isolated Coronary Artery Bypass Surgery With Cardiopulmonary Bypass: A Randomized Trial.

OBJECTIVE: Several studies have suggested that the cardioprotective effects of halogenated anesthetics in cardiac surgery result in reduced cardiac biomarker release compared with total intravenous anesthesia (TIVA). These findings came from relatively small randomized clinical trials and meta-analyses. The authors of this study hypothesized that the beneficial effects of volatile anesthetics translate into a reduced length of hospital stay after coronary artery bypass grafting surgery (CABG) with cardiopulmonary bypass. DESIGN: A randomized controlled trial. SETTING: Two university hospitals. PARTICIPANTS: Adult patients undergoing elective CABG surgery with cardiopulmonary bypass. INTERVENTIONS: Patients were assigned randomly to 2 following groups: propofol-based TIVA group (n = 431) and sevoflurane group (n = 437). MEASUREMENTS AND MAIN RESULTS: The primary endpoint was hospital length of stay, and the secondary endpoint included postoperative troponin T and N-terminal pro-brain natriuretic peptide release and mortality. In the sevoflurane group, a reduced length of hospital stay was observed compared with the propofol-based TIVA group (10 [9-11] days v 14 [10-16], p<0.001) as were reductions in cardiac troponin T release (0.18 ng/mL v 0.57 ng/mL at 24 hours, p<0.001), in N-terminal pro-brain natriuretic peptide release (633 pg/mL v 878 pg/mL at 24 hours, p<0.001; 482 pg/mL v 1,036 pg/mL at 48 hours, p<0.001), and in mortality at 1-year follow up (17.8% v 24.8%, p = 0.03). CONCLUSIONS: Anesthesia with sevoflurane reduced cardiac biomarker release and length of hospital stay after CABG with cardiopulmonary bypass surgery compared with propofol-based TIVA with a possible reduction in 1-year mortality.

Allopurinol prevents cardiac and skeletal muscle damage in professional soccer players.

Xanthine oxidase (XO), a free radical-generating enzyme, is involved in tissue damage produced during exhaustive exercise. Our aim was to test whether allopurinol, a powerful inhibitor of XO, may be effective in preventing exercise-induced tissue damage in soccer players. Twelve soccer players were randomized into two experimental groups. One received allopurinol, before a match of the premier Spanish Football League, and the other placebo. Allopurinol prevented the exercise-induced increase in all the markers of skeletal muscle damage analyzed: creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and myoglobin. Creatine kinase-MB isoenzyme and highly sensitive troponin T, specific biomarkers of myocardial injury, increased significantly in the placebo but not in the allopurinol-treated group after the football match. We also found that the exercise-induced lipid peroxidation, as reflected by malondialdehyde measurements, was prevented after allopurinol administration. However, inhibition of XO did not prevent the increment in the activity of alanine aminotransferase found after the match. No changes in the serum gamma glutamyltransferase activity was found after the match on either the placebo and the allopurinol groups. These two enzymes were determined as biomarkers of liver injury. Allopurinol represents an effective and inexpensive pharmacological agent to prevent tissue damage in soccer players.

Tirasemtiv amplifies skeletal muscle response to nerve activation in humans.

INTRODUCTION: In this study we tested the hypothesis that tirasemtiv, a selective fast skeletal muscle troponin activator that sensitizes the sarcomere to calcium, could amplify the response of muscle to neuromuscular input in humans. METHODS: Healthy men received tirasemtiv and placebo in a randomized, double-blind, 4-period, crossover design. The deep fibular nerve was stimulated transcutaneously to activate the tibialis anterior muscle and produce dorsiflexion of the foot. The force-frequency relationship of tibialis anterior dorsiflexion was assessed after dosing. RESULTS: Tirasemtiv increased force produced by the tibialis anterior in a dose-, concentration-, and frequency-dependent manner with the largest increases [up to 24.5% (SE 3.1), P < 0.0001] produced at subtetanic nerve stimulation frequencies (10 Hz). CONCLUSIONS: The data confirm that tirasemtiv amplifies the response of skeletal muscle to nerve input in humans. This outcome provides support for further studies of tirasemtiv as a potential therapy in conditions marked by diminished neuromuscular input.

The anesthesia in abdominal aortic surgery (ABSENT) study: a prospective, randomized, controlled trial comparing troponin T release with fentanyl-sevoflurane and propofol-remifentanil anesthesia in major vascular surgery.

BACKGROUND: On the basis of data indicating that volatile anesthetics induce cardioprotection in cardiac surgery, current guidelines recommend volatile anesthetics for maintenance of general anesthesia during noncardiac surgery in hemodynamic stable patients at risk for perioperative myocardial ischemia. The aim of the current study was to compare increased troponin T (TnT) values in patients receiving sevoflurane-based anesthesia or total intravenous anesthesia in elective abdominal aortic surgery. METHODS: A prospective, randomized, open, parallel-group trial comparing sevoflurane-based anesthesia (group S) and total intravenous anesthesia (group T) with regard to cardioprotection in 193 patients scheduled for elective abdominal aortic surgery. Increased TnT level on the first postoperative day was the primary endpoint. Secondary endpoints were postoperative complications, nonfatal coronary events and mortality. RESULTS: On the first postoperative day increased TnT values (>13 ng/l) were found in 43 (44%) patients in group S versus 41 (43%) in group T (P = 0.999), with no significant differences in TnT levels between the groups at any time point. Although underpowered, the authors found no differences in postoperative complications, nonfatal coronary events or mortality between the groups. CONCLUSIONS: In elective abdominal aortic surgery sevoflurane-based anesthesia did not reduce myocardial injury, evaluated by TnT release, compared with total intravenous anesthesia. These data indicate that potential cardioprotective effects of volatile anesthetics found in cardiac surgery are less obvious in major vascular surgery.

REstoration of COronary flow in patients with no-reflow after primary coronary interVEntion of acute myocaRdial infarction (RECOVER).

BACKGROUND: No randomized trial has been conducted to compare different vasodilators for treating no-reflow during primary percutaneous coronary intervention (PCI) for ST-segment elevation acute myocardial infarction. METHODS: The prospective, randomized, 2-center trial was designed to compare the effect of 3 different vasodilators on coronary no-reflow. A total of 102 patients with no-reflow in primary PCI were randomized to receive intracoronary infusion of diltiazem, verapamil, or nitroglycerin (n = 34 in each group) through selective microcatheter. The primary end point was coronary flow improvement in corrected thrombolysis in myocardial infarction frame count (CTFC) after administration of the drug. RESULTS: Compared with that of the nitroglycerin group, there was a significant improvement of CTFC after drug infusion in the diltiazem and verapamil groups (42.4 frames vs 28.1 and 28.4 frames, P < .001). The improvement in CTFC was similar between the diltiazem and verapamil groups (P = .9). Compared with the nitroglycerin group, the diltiazem and verapamil groups had more complete ST-segment resolution at 3 hours after PCI, lower peak troponin T level, and lower N-terminal pro-B-type natriuretic peptide levels at 1 and 30 days after PCI. After drug infusion, the drop of heart rate and systolic blood pressure in the verapamil group was greater than that in the diltiazem and nitroglycerin groups. CONCLUSION: Intracoronary infusion of diltiazem or verapamil can reverse no-reflow more effectively than nitroglycerin during primary PCI for acute myocardial infarction. The efficacy of diltiazem and verapamil is similar, and diltiazem seems safer.

The cardioprotective effects of a combination of quercetin and α-tocopherol on isoproterenol-induced myocardial infarcted rats.

The present study aims to evaluate the combined protective effects of quercetin and α-tocopherol on isoproterenol-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with a combination of quercetin (10 mg/kg) and α-tocopherol (10 mg/kg) daily for 14 days. After the pretreatment, rats were injected isoproterenol (100 mg/kg) to induce myocardial infarction. Isoproterenol-treated rats showed increased levels of serum troponins and increased intensities of serum lactate dehydrogenase-1 and -2 isoenzyme bands. Isoproterenol treatment also showed significant decreased levels of antioxidant system and significant increased levels of plasma lipid peroxidation, plasma uric acid, and the heart calcium. Furthermore, isoproterenol-treated rat's electrocardiogram showed elevated ST segments. Combined pretreatment with quercetin and α-tocopherol normalized all the biochemical parameters and minimized the alterations in electrocardiogram. Histopathology of myocardium also confirmed the cardioprotective effects of quercetin and α-tocopherol. In vitro studies confirmed the mechanism of action of quercetin and α-tocopherol. Thus, quercetin and α-tocopherol exhibited cardioprotective effects against isoproterenol-induced cardiotoxicity due to their scavenging free radicals, improving antioxidants and maintaining Ca(2+) levels. Our study also showed that combined pretreatment (quercetin and α-tocopherol) was highly effective than single pretreatment (quercetin or α-tocopherol).

Comparison of S-(+)-ketamine- with sufentanil-based anaesthesia for elective coronary artery bypass graft surgery: effect on troponin T levels.

BACKGROUND: S-(+)-ketamine anaesthesia carries potential benefits for the cardiovascularly compromised patient. However, the use of S-(+)-ketamine in ischaemic coronary artery disease is controversial. In a prospective, randomized, clinical trial, we have investigated whether an S-(+)-ketamine-based anaesthetic protocol leads to increased cardiac troponin T levels (cTnT) after coronary artery bypass grafting (CABG). METHODS: Two hundred and nine patients undergoing elective CABG were randomized to receive either i.v. anaesthesia with sufentanil-midazolam-propofol (SMP; n=108) or S-(+)-ketamine-midazolam-propofol (KMP; n=101). Haemodynamic variables were maintained within the normal range. Invasive haemodynamic monitoring was performed using a pulmonary artery catheter. Plasma cTnT levels were sampled before induction and 1, 6, and 24 h after aortic unclamping. Cardiovascular adverse events, such as electrocardiographic signs of ischaemia, perioperative myocardial infarction, and death, were recorded. RESULTS: Patient characteristics, cardiac profile, intraoperative management, and the incidence of cardiovascular adverse events were comparable between the groups. Plasma cTnT levels increased after operation in both groups. cTnT levels were significantly lower in the KMP group 6 h after aortic unclamping compared with the SMP group (P=0.004), but did not differ 24 h after aortic unclamping [median (range): SMP 0.4 (0.01-3.9) vs KMP 0.4 (0.07-6.6) microg litre(-1), P=0.338]. CONCLUSIONS: S-(+)-ketamine does not accentuate postoperative cTNT rises in haemodynamically stable elective CABG patients.

Alprostadil attenuates myocardial ischemia/reperfusion injury by promoting antioxidant activity and eNOS activation in rats.

PURPOSE: To investigate the effect of alprostadil on myocardial ischemia/reperfusion (I/R) in rats. METHODS: Rats were subjected to myocardial ischemia for 30 min followed by 24h reperfusion. Alprostadil (4 or 8 µg/kg) was intravenously administered at the time of reperfusion and myocardial infarct size, levels of troponin T, and the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were measured. Antioxidative parameters, nitric oxide (NO) content and phosphorylated endothelial nitric oxide synthase 3 (p-eNOS) expression in the left ventricles were also measured. Histopathological examinations of the left ventricles were also performed. RESULTS: Alprostadil treatment significantly reduced myocardial infarct size, serum troponin T levels, and CK-MB and LDH activity (P<0.05). Furthermore, treatment with alprostadil significantly decreased malondialdehyde (MDA) content (P<0.05) and markedly reduced myonecrosis, edema and infiltration of inflammatory cells. Superoxide dismutase and catalase activities (P<0.05), NO level (P<0.01) and p-eNOS (P<0.05) were significantly increased in rats treated with alprostadil compared with control rats. CONCLUSION: These results indicate that alprostadil protects against myocardial I/R injury and that these protective effects are achieved, at least in part, via the promotion of antioxidant activity and activation of eNOS.

The effect of acetylsalicylic acid resistance on prognosis of patients who have developed acute coronary syndrome during acetylsalicylic acid therapy.

AIM: The relationships between clinical events and acetylsalicylic acid resistance (AR), as well as its frequency, have been established in stable patients with coronary artery disease (CAD). Although acute coronary syndrome (ACS) patients taking acetylsalicylic acid have been accepted as a high-risk population, the role of AR has not been investigated in these patient groups. Thus, in the present study, the impact of AR was investigated in patients with ACS who were taking acetylsalicylic acid. METHODS: Between January 2001 and February 2003, 140 ACS patients were included in the present prospective study. All patients had ACS while taking acetylsalicylic acid. Coronary angiographic scores for severity and extent of CAD were determined for all patients. The effect of acetylsalicylic acid on platelet function was assessed by the platelet function analyzer PFA-100 (Dade Behring, USA). The primary end point was the composite of death, myocardial infarction, cerebrovascular accident and revascularization. The mean follow-up period was 20 months. RESULTS: Patients with AR were older than patients without AR (63.8+/-10.8 years versus 58.3+/-11.2 years; P=0.005). Moreover, myocardial damage was higher in patients with AR according to cardiac troponin T values (1.11+/-1.3 mug/L versus 0.41+/-0.5 mug/L; P=0.01). The composite end point of death, myocardial infarction, cerebrovascular accident or revascularization was present in 16 of 45 patients (35%) with AR and in 13 of 79 patients (16%) without AR (hazard ratio 2.46, 95% CI 1.18 to 5.13; P=0.016). After adjustment for age, platelet count, cardiac troponin T value and CAD severity score, AR remained an independent predictor for long-term adverse events (hazard ratio 3.03, 95% CI 1.06 to 8.62; P=0.038). CONCLUSIONS: The clinical event rate was found to be higher in ACS patients with AR than in those without AR. Thus, it may be concluded that there is a strong correlation between a worse prognosis and AR in these patients.

Nicorandil reduces the incidence of minor cardiac marker elevation after coronary stenting.

BACKGROUND: Minor cardiac marker elevation after percutaneous coronary intervention has long-term prognostic significance. We examined whether nicorandil, a nicotinamide-nitrate ester, reduces the incidence of minor cardiac marker elevation after coronary stenting. METHODS: Patients (n=192) undergoing coronary stenting were randomly assigned to receive nicorandil (nicorandil group, n=91) or vehicle (control group, n=101). Nicorandil (2 mug/kg/min, intravenously) was administered immediately after the patients were transferred into the catheterization laboratory and continued for 6 h. We measured the serum concentrations of creatine kinase isoenzyme MB (CK-MB) before, immediately after, and 6, 12, and 24 h after the procedure, and those of cardiac troponin T (cTnT) 24 h after the procedure. RESULTS: There was no significant difference in clinical background between the 2 groups. The nicorandil group showed a significantly lower incidence of CK-MB elevation (>1x upper limit of control range, 20 IU/l) than the control group (8.8% vs 21.8%, p<0.05). The levels of serum CK-MB in the nicorandil group were significantly lower than those in the control group (13.4+/-5.7 vs 16.5+/-9.7 IU/l, p<0.01). Similarly, the nicorandil group showed a significantly lower incidence of cTnT elevation [>1x (0.1 ng/ml) or >2x (0.2 ng/ml)] upper limit of control range than the control group (14.3% vs 26.7%, p<0.05, or 7.7% vs 17.8%, p<0.05). Serum cTnT levels were also significantly lower in the nicorandil group than in the control group (0.05+/-0.10 vs 0.15+/-0.36 ng/ml, p<0.05). CONCLUSIONS: The results demonstrated that nicorandil reduces minor cardiac marker elevation after coronary stenting.

Application of C1-esterase inhibitor during reperfusion of ischemic myocardium: dose-related beneficial versus detrimental effects.

BACKGROUND: Complement activation during reperfusion of ischemic myocardium augments myocardial injury, and complement inhibition with C1-esterase inhibitor (C1-INH) at the time of reperfusion exerts marked cardioprotective effects in experimental studies. Application of C1-INH in newborns, however, was recently reported to have dangerous and even lethal side effects. This study addresses the essential role of dosage in studies using C1-INH. METHODS AND RESULTS: Cardioprotection by C1-INH was examined in a pig model with 60 minutes of coronary occlusion followed by 120 minutes of reperfusion. C1-INH was administered intravenously 5 to 10 minutes before coronary reperfusion without heparin at a dose of 40, 100, and 200 IU/kg body wt. Compared with the NaCl controls, C1-INH 40 IU/kg reduced myocardial injury (44.1+/-13.8% versus 76.7+/-4.6% necrosis of area at risk, P/=100 IU/kg) of C1-INH will provoke detrimental side effects, probably via its procoagulatory action.

Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients.

OBJECTIVES: Our primary objective was to examine the prognostic relationship between baseline quantitative ST-segment depression (ST) and cardiac troponin T (cTnT) elevation. The secondary objectives were to: 1) examine whether ST provided additional insight into therapeutic efficacy of glycoprotein IIb/IIIa therapy similar to that demonstrated by cTnT; and 2) explore whether the time to evaluation impacted on each marker's relative prognostic utility. BACKGROUND: The relationship between the baseline electrocardiogram (ECG) and cTnT measurements in risk-stratifying patients presenting with acute coronary syndromes (ACS) has not been evaluated comprehensively. METHODS: The study population consisted of 959 patients enrolled in the cTnT substudy of the Platelet IIb/IIIa Antagonism for the Reduction of Acute coronary syndrome events in a Global Organization Network (PARAGON)-B trial. Patients were classified as having no ST (n = 387), 1 mm ST (n = 433), and ST > or =2 mm (n = 139). Forty-percent (n = 381) were classified as cTnT-positive based on a definition of > or =0.1 ng/ml. RESULTS: Six-month death/(re)myocardial infarction rates were 8.4% among cTnT-negative patients with no ST and 26.8% among cTnT-positive patients with ST > or =2 mm. On ECGs done after 6 h of symptom onset, ST > or =2 mm was associated with higher risk compared to its presence on ECGs done earlier (odds ratio [OR] 7.3 vs. 2.1). In contrast, the presence of elevated cTnT within 6 h of symptom was associated with a higher risk of adverse events compared with elevations after 6 h (OR 2.4 vs. 1.5). CONCLUSIONS: Quantitative ST and cTnT status are complementary in assessing risk among ACS patients and both should be employed to determine prognosis and assist in medical decision making.