Cutoff For Myocardial Infarction Research Articles

Diagnostic and prognostic value of the sex-specific 99th percentile of four high-sensitivity cardiac troponin assays in patients with suspected myocardial infarction.

High-sensitivity cardiac troponin (hs-cTn) assays are used for detection of myocardial infarction (MI). Ninety-ninth percentiles show wide inter-assay variation. The use of sex-specific cut-offs is recommended as definitory cut-off for MI. We compared diagnostic performance and prognostic value of sex-specific 99th percentiles of four hs-cTn assays in patients with suspected MI. Concentrations of four hs-cTn assays were measured at presentation and after 3 h in patients with suspected MI. Final diagnoses were adjudicated according to the 4th Universal Definition of MI. Unisex and sex-specific 99th percentiles were evaluated as diagnostic cut-offs following the ESC 0/3 h algorithm. These cut-offs were used in Cox-regression analyses to investigate the association with a composite endpoint of MI, revascularization, cardiac rehospitalization, and death. Non-ST-elevation MI was diagnosed in 368 of 2718 patients. Applying the unisex 99th percentile, Elecsys hs-cTnT provided highest negative predictive value (NPV) of 99.7 and a positive predictive value (PPV) of 75.9. The analysed hs-cTnI assays showed slightly lower NPVs and comparable PPVs [Architect (NPV 98.0, PPV of 71.4); Atellica (NPV 97.7, PPV of 76.1); Pathfast (NPV 97.7, PPV of 66.6)]. Application of sex-specific 99th percentiles did not significantly affect diagnostic performance. Concentrations above 99th percentile were independent predictors for impaired long-term outcome (hazard ratios 1.2-1.5, P < 0.001). We describe a good diagnostic accuracy of four hs-cTn assays using the assay-specific 99th percentile for detection of MI. Application of sex-specific 99th percentiles did neither affect diagnostic performance nor prognostic value significantly. Finally, values above the 99th percentile were associated with poor long-term outcome.

Rapid Detection of Myocardial Infarction With a Sensitive Troponin Test

Rapid identification and treatment of patients with a myocardial infarction (MI) is mandatory. We studied the diagnostic capacities of a sensitive troponin assay for detection of MI in emergency department patients within 2 hours after arrival. The study included 157 patients suspected of having non-ST-elevation acute coronary syndrome. Blood was drawn on arrival (T0) and 2 (T2), 6, and 12 hours later. At T2, a troponin concentration above the MI cutoff is 87% sensitive and 100% specific for MI detection (positive predictive value [PPV], 100%; negative predictive value [NPV], 96%). If a difference of more than 30% between the troponin measurements at T0 and T2 in the absence of an absolute troponin increase above the 99th percentile of a reference population is also considered indicative of MI, the sensitivity increases to 100% and specificity decreases to 87% (PPV, 70%; NPV, 100%). Sensitivity and specificity of creatine kinase-MB and myoglobin are lower than those of troponin. By using a sensitive troponin assay and simple algorithms, the diagnosis of MI can be determined within 2 hours after arrival at the emergency department. Measurement of myoglobin and creatine kinase-MB has no added value.

Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study.

BackgroundThe aetiology and clinical significance of troponin release following endurance exercise is unclear but may be due to transient myocardial inflammation. Cardiovascular magnetic resonance (CMR) affords us the opportunity to evaluate the presence of myocardial inflammation and focal fibrosis and is the ideal imaging modality to study this hypothesis. We sought to correlate the relationship between acute bouts of ultra endurance exercise leading to cardiac biomarkers elevation and the presence of myocardial inflammation and fibrosis using CMR.Methods17 recreation athletes (33.5 +/- 6.5 years) were studied before and after a marathon run with troponin, NTproBNP, and CMR. Specific imaging parameters to look for inflammation included T2 weighted images, and T1 weighted spin-echo images before and after an intravenous gadolinium-DTPA to detect myocardial hyperemia secondary to inflammation. Late gadolinium imaging was performed (LGE) to detect any focal regions of replacement fibrosis.ResultsEleven of the 17 participant had elevations of TnI above levels of cut off for myocardial infarction 6 hrs after the marathon (0.075 +/- 0.02, p = 0.007). Left ventricular volumes were reduced post marathon and a small increase in ejection fraction was noted (64+/- 1% pre, 67+/- 1.2% post, P = 0.014). Right ventricular volumes, stroke volume, and ejection fraction were unchanged post marathon. No athlete fulfilled criteria for myocardial inflammation based on current criteria. No regions of focal fibrosis were seen in any of the participants.ConclusionExercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.

Troponin Levels after Cardiac Electrophysiology Procedures: Review of the Literature

Cardiac-specific Troponins (cTn) I and T have become markers of choice for myocardial injury. We reviewed the literature in order to understand the expected postprocedure cTn rise after electrophysiology procedures. A total of 34 studies and 1,608 patients were included. After external monophasic cardioversion, seven of 442 patients (1.6%) had minimal increase in cTnI (0.1-0.9 ng/mL), and only one of 368 (0.3%) had increase in cTnT (0.11 ng/mL). After internal cardioversion, 17 of 105 (16%) had increase in cTnI (0.7-2.4 ng/mL) but only three (2.9%) were above the cutoff for myocardial infarction (MI) (1.5 ng/mL). During implantable cardioverter-defibrillator (ICD) installation with a mean of 2-7 ICD shocks, 12 of 74 (16%) patients had cTnI >or=1.5 ng/mL (range 1.7-5.5 ng/mL) and 20 of 64 (32%) had cTnT >or=0.1 ng/mL (range 0.26-6.46 ng/mL) considered in the range of clinical MI. Radio frequency ablation (RFA) (n = 496) resulted in significant cTn elevation in 25-100% of patients with ventricular > atrial and linear > focal lesions. Average postprocedure peak cTnI ranged from 0.13 to 6 ng/mL (median: 2.36 ng/mL, max: 15 ng/mL) and cTnT 0.2 to 2.41 ng/mL (median: 0.44 ng/mL, max: 9 ng/mL). Early cTn peak at 2-8 hours was noted after RFA. External cardioversion should not cause a significant increase in cTn; RFA and ICD implantation with shocks often result in an increase in cTn. Interpretation of these markers can be difficult if acute coronary syndrome is suspected in the postprocedure period.

Assessment Of Cardiac Inflammation And Injury Following Prolonged Exercise Using Cardiovascular Magnetic Resonance (CMR) Imaging

PURPOSE: Myocardial inflammation may be a potential mechanism for the release of troponin and NTproBNP following a Marathon. CMR has not been previously used to detect and quantify myocardial inflammation and fibrosis pre- and post-Marathon. METHODS: CMR was performed in 18 athletes 24hrs pre and 6 hours post a Marathon run. Each scan was performed on a 1.5T Siemens Avanto scanner using a 4 channel body array coil. Myocardial structure and function was assessed using breath hold SSFP cine imaging in long and short axis views. The presence of myocardial inflammation and oedema was assessed using STIR imaging and a 3-4 minute spin echo sequence immediately post 0.1mmol intravenous gadolinium-DTPA to assess relative gadolinium enhancement. Inversion recovery segmented-FLASH imaging with TI adjusted to null normal myocardium to highlight regions of fibrosis was used to image delayed enhancement. Each participant had bloods drawn for TnI, NT-proBNP, and CRP at baseline, immediately post and 6 hours after the run. Each CMR scan was analyzed for wall thickness per segment, volumes and function, myocardial oedema. Delayed enhancement images were analysed using Medis software. RESULTS: Biventricular volumes, stroke volume, ejection fraction, and mass were unchanged pre and 6 hrs post marathon. The majority of subjects were found to have a rise in BTproBNP levels immediately and 6 hours after the race as well as elevations in TnI above the level of cut off for myocardial infarction (P=0.001). There were no focal regions of visual signal increase on the STIR images in any of the 18 subjects. Global myocardial oedema was predefined using a cut off ratio of 1.9 comparing SI of myocardium to skeletal muscle on STIR imaging, and a relative 45% increase in the SI myocardium/skeletal muscle immediately post intravenous gadolinium on relative gadolinium enhancement imaging (rGE). No subject reached these cut off values. None had any visual myocardial fibrosis on late enhancement imaging or using automated software. CONCLUSIONS: Serum markers of myocardial cell damage post ultra endurance exercise are not associated with CMR detectable levels of myocardial oedema, inflammation or scarring, suggesting lower degrees of myocardial damage than in patients with acute myocardial infarction, inspite of similar levels of troponin elevation.

Minor elevations in troponin T values enhance risk assessment in emergency department patients with suspected myocardial ischemia: analysis of novel troponin T cut-off values

Background: A consensus document developed by a joint committee of the European Society of Cardiology and the American College of Cardiology redefines myocardial infarction (MI) using an increase of troponin I or T as compared to a reference control population (i.e., troponin T (TnT) of 0.01 μg/l). A clinical problem arises when an arbitrary cut-off point is selected for determination of MI (i.e., TnT≥0.1 μg/l), as minor elevations of troponin are associated with increased cardiovascular risk in selected patients with acute coronary syndromes. Methods: We prospectively studied 420 unselected patients being evaluated for suspected myocardial ischemia in the emergency department (ED). We compared a 99th percentile MI cut-off limit for TnT, determined by constructing a standard receiver operator curve from our ED population in whom an acute coronary syndrome was excluded, to a standard MI cut-off limit of 0.1 μg/l in assessing cardiovascular risk. We also assessed the prognostic value of detectable TnT concentrations below this 99th percentile MI cut-off, but above the upper reference limit of healthy controls. Results: The diagnosis of acute coronary syndromes (ACS) was more frequent in groups with higher TnT concentrations: 16.8% with a normal TnT (<0.03 μg/l), 29.5% with detectable TnT below the 99th percentile MI limit (0.03–0.066 μg/l), 64.3% with detectable TnT between the 99th percentile and standard MI cut-offs (0.067–0.099 μg/l), and 85.4% with TnT≥0.1 μg/l ( p<0.001 for the trend). Thirty-day cardiovascular event rates increased for any detectable concentration of troponin: 1.3% with normal TnT, 4.8% with detectable TnT below the 99th percentile MI limit, 15.4% with TnT between the 99th percentile and standard MI cut-off limits, and 12.5% with TnT≥0.1 μg/l ( p<0.01 for the trend). Conclusion: Using an MI cut-off concentration for TnT from a “non-ACS reference” improves risk stratification, but fails to detect a positive TnT in 11.7% of subjects with an acute coronary syndrome.

Prognostic value of cardiac troponin-I levels following catheter-based coronary interventions

This study has examined the prognostic significance of troponin-I (Tn-I) levels after catheter-based coronary interventions in coronary arteries and saphenous vein grafts lesions. Tn-I and creatine kinase-MB (CK-MB) fraction levels were measured at 6 and 18 to 24 hours after catheter-based coronary intervention in 1,129 consecutive patients with normal preintervention plasma levels of Tn-I, and CK-MB levels below the cutoff for myocardial infarction. Patients were stratified according to maximal postangioplasty Tn-I levels. Group I (n = 784) had no elevated Tn-I (<0.15 ng/ml), group II (n = 170) had Tn-I at 0.15 to 0.45 ng/ml, and group III (n = 175) had Tn-I elevation >0.45 ng/ml. Major in-hospital complications (death, Q-wave infarction, and emergent coronary bypass grafting) and out-of-hospital intermediate-term (8 months) outcomes were compared between the 3 groups. Tn-I elevation >0.45 ng/ml was associated with increased risk of mortality (group III, 1.6%; group II, 0.6%; and group I, 0.1%; p = 0.019) and major in-hospital complications (3.2%, 1.7%, and 0.5%; p = 0.004). There was no difference in death (1.8%, 3.2%, and 2.4%; p = 0.74), Q-wave infarction (0.6%, 0%, and 0.3%; p = 0.66), or target lesion revascularization (10.1%, 9.0%, and 9.3%; p = 0.86) between the 3 groups at follow-up. Cardiac event-free survival was similar between groups (p = 0.3). By multivariate analysis, Tn-I >0.45 ng/ml was an independent predictor for major in-hospital complications (odds ratio 2.1, 95% confidence interval 1.2 to 3.9, p = 0.01). The degree of risk was also associated with the conjoint elevation of Tn-I and CK-MB levels (odds ratio 1.1, 95% confidence interval 1.02 to 1.2, p = 0.01). We conclude that Tn-I levels >3 times the normal limit and conjoint elevation of Tn-I and CK-MB levels after coronary angioplasty are associated with increased risk of major in-hospital complications, but have no incremental risk of adverse intermediate-term (8 months) clinical outcomes.

False-positive troponin I in the MEIA due to the presence of rheumatoid factors in serum. Elimination of this interference by using a polyclonal antisera against rheumatoid factors.

We report false-positive cardiac troponin (cTn) I results in the microparticle enzyme immunoassay (MEIA) using the AxSYM analyzer. We studied serum samples from 12 patients with positive rheumatoid factor but with no indication of myocardial infarction (MI); 2 also had positive antinuclear antibody (ANA) titers. Serum samples from 7 patients with positive ANA titers and negative rheumatoid factors also were studied. Total creatine kinase (CK) was run using a Hitachi 747 analyzer, cTnT using an Elecsys 2010 analyzer, and cTnI and CK-MB using an AxSYM analyzer. We observed no measurable cTnI and cTnT concentrations in 12 control samples or in specimens with positive ANA titers and negative rheumatoid factors. In contrast, samples from 7 of 12 patients containing rheumatoid factors had measurable cTnI concentrations. Four specimens showed cTnI concentrations more than 2.0 micrograms/L, the suggested diagnostic cutoff for MI. None of the specimens showed detectable cTnT. The concentrations of total CK and CK-MB were within normal ranges in all specimens. False-positive results were observed only with the MEIA for cTnI. This interference can be eliminated by using a polyclonal antisera against rheumatoid factor. The chemiluminescent assay for cTnI showed no detectable cTnI concentration in any specimen.