暂无摘要。

BACKGROUND: While the clinical importance of cardiac troponin is well-known in type 1 myocardial infarction (MI), evidence on this topic in type 2 MI is limited. We assessed the clinical and prognostic implications of high-sensitivity cardiac troponin (hs-cTnT) concentrations in a large sample of patients with type 2 MI.
METHODS: Retrospective registry-based cohort study (SWEDEHEART) including 4607 patients with type 2 MI and 43,405 patients with type 1 MI, used for comparisons. Patients with ST-elevation MI were excluded. Multivariable-adjusted regressions were applied to investigate the associations of hs-cTnT concentrations (highest measured value during each hospitalization) with clinical variables and prognosis during a median follow-up of up to 1.9 years.
RESULTS: Hs-cTnT concentrations (median 264 [25th, 75th percentiles 112-654] ng/L) were significantly associated with various cardiovascular risk factors and comorbidities in type 2 non-ST elevation MI (NSTEMI) but only weakly with the underlying triggering condition. Most of these findings including the magnitude of hs-cTn release were similar to type 1 NSTEMI. Hs-cTnT (ln) independently predicted all-cause mortality (hazard ratio 1.13 [95% confidence interval 1.09-1.17]) and major adverse events (hazard ratio 1.13 [95% confidence interval 1.10-1.17]) in type 2 NSTEMI, similar as for type 1 NSTEMI according to interaction analysis. The associations of hs-cTnT (ln) with poor prognosis tended to be stronger in type 2 NSTEMI patients without known cardiovascular disease.
CONCLUSIONS: Hs-cTnT concentrations independently predict adverse outcome in type 2 NSTEMI. The similarities to type 1 NSTEMI however, are striking and emphasize the difficulty to distinguish both MI types.

A 47-year-old woman presented with atypical chest pain and a troponin level of 30.15 ng/dl. A detailed diagnostic work-up did not detect an acute myocardial infarction but revealed the presence of heterophile antibodies. Laboratory values need to be interpreted in the context of the clinical picture when test results do not correspond to clinical findings. (Level of Difficulty: Beginner.).

We present the case of a female patient who developed persistently elevated levels of cardiac troponin (cTn) after a previous episode of clinically presumed myocarditis. Extensive investigation concluded that the presence of heterophile antibodies was causing false positive cTn elevation. (Level of Difficulty: Intermediate.).

BACKGROUND: High-sensitivity cardiac troponin I (hs-cTnI) assays have been developed that quantify lower cTnI concentrations with better precision versus earlier generation assays. hs-cTnI assays allow improved clinical utility for diagnosis and risk stratification in patients presenting to the emergency department with suspected acute myocardial infarction. We describe the High-Sensitivity Cardiac Troponin I Assays in the United States (HIGH-US) study design used to conduct studies for characterizing the analytical and clinical performance of hs-cTnI assays, as required by the US Food and Drug Administration for a 510(k) clearance application. This study was non-interventional and therefore it was not registered at clinicaltrials.gov.
METHODS: We conducted analytic studies utilizing Clinical and Laboratory Standards Institute guidance that included limit of blank, limit of detection, limit of quantitation, linearity, within-run and between run imprecision and reproducibility as well as potential interferences and high dose hook effect. A sample set collected from healthy females and males was used to determine the overall and sex-specific cTnI 99th percentile upper reference limits (URL). The total coefficient of variation at the female 99th percentile URL and a universally available American Association for Clinical Chemistry sample set (AACC Universal Sample Bank) from healthy females and males was used to examine high-sensitivity (hs) performance of the cTnI assays. Clinical diagnosis of enrolled subjects was adjudicated by expert cardiologists and emergency medicine physicians. Assessment of temporal diagnostic accuracy including sensitivity, specificity, positive predictive value, and negative predictive value were determined at presentation and collection times thereafter. The prognostic performance at one-year after presentation to the emergency department was also performed. This design is appropriate to describe analytical characterization and clinical performance, and allows for acute myocardial infarction diagnosis and risk assessment.

Chest pain accounts for approximately 6% of Emergency Department (ED) attendances and is the most common reason for emergency hospital admission. For many years, our approach to diagnosis has required patients to stay in hospital for at least 6-12 h to undergo serial biomarker testing. As less than one fifth of the patients undergoing investigation actually has an acute coronary syndrome (ACS), there is tremendous potential to reduce unnecessary hospital admissions. Recent advances in diagnostic technology have improved the efficiency of care pathways. Decision aids such as the Thrombolysis in Myocardial Infarction (TIMI) risk score and the History, Electrocardiogram, Age, Risk factors and Troponin (HEART) score enable rapid \'rule out\' of ACS within hours of patients arriving in the ED. With high sensitivity cardiac troponin (hs-cTn) assays, approximately one third of patients can have ACS \'ruled out\' with a single blood test, and up to two thirds could have an acute myocardial infarction \'ruled out\' with a second sample taken after as little as 1 h. Building on those recent advances, this paper presents an overview of the principles behind the development of the Troponin-only Manchester Acute Coronary Syndromes (T-MACS) decision aid. This clinical prediction model could be used to \'rule out\' and \'rule in\' ACS following a single blood test and to calculate the probability of ACS for every patient. The future potential of this approach is then addressed, including practical applications of artificial intelligence, shared decision making, near-patient testing and personalized medicine.

OBJECTIVE: High sensitivity cardiac troponin T and I (hs-cTnT and hs-cTnI) assays show analytical, diagnostic and prognostic improvement over contemporary sensitive cTn assays. However, given the importance of troponin in the diagnosis of myocardial infarction, implementing this test requires rigorous analytical and clinical verification across the total testing pathway. This was the aim of this study.
METHODS: Analytical verification included assessment of critical outlier frequency, for hs-cTnI and cTnI assays. Concordance for paired cTnI and hs-cTnI measurements (n=1096) was verified using 99th percentiles for both genders (cTnI: 30 ng/L, hs-cTnI: 25 ng/L) and for men and women separately (hs-cTnI: M: 34;F: 16 ng/L). Discordant data was correlated with clinical and laboratory information. Diagnosis of Acute Coronary Syndrome (ACS) or Non-ACS was adjudicated by two cardiologists independently.
RESULTS: The hs-cTnI assay showed a lower (10-fold) critical outlier rate (0.091%) and more detectable results above the limit of detection (LOD) (23.4%) and 99th percentile (2.4%), compared to cTnI. Analytical concordance between the two assays was high (94.5%) but decreased (91.7%) when gender-specific hs-cTnI cut-offs were used. The hs-cTnI assay gave fewer false negatives (up to 1.0%) but disproportionately more false positives (up to 6.7%) overall, which improved (3.9%) for serial measurements.
CONCLUSIONS: Laboratories should analytically and clinically verify hs-cTn assays before use, with attention to performance and the clinical and diagnostic algorithms that support appropriate testing and result interpretation. Work in the pre- and post-analytical phases is necessary to augment the analytical improvement in the new era of troponin testing.