2016
Diagnosis of Myocardial Infarction Using a High-Sensitivity Troponin I 1-Hour Algorithm
Abstract: Patients with possible AMI can be triaged within 1 hour after admission with no loss of safety compared with a 3-hour approach, when a low and sensitive cutoff is applied. This concept enables safe discharge or rapid treatment initiation after 1 hour.
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Cited by 233 publications
(160 citation statements)
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Utility of S100A12 as an Early Biomarker in Patients With ST-Segment Elevation Myocardial Infarction
Abstract
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“…S100A12 is endogenously expressed by cells closely linked to vascular disease including granulocytes, myeloid cells and macrophages (14,15). Consistent with the findings from previous studies, the immunohistochemistry and immunofluorescence findings from the present study in acutely aspirated coronary thrombi and autopsy specimens from patients with STEMI suggests that the increase in plasma S100A12 in STEMI derives from its acute release from CD68+ macrophages in ruptured plaques, a mechanism quite different than the elevation of biomarkers derived from myocardial necrosis such as CK-MB and hscTnT (16). Plasma S100A12 was slightly increased in patients with non-plaque related chest pain, such as PTE and AD, possibly due to systemic or focal inflammation.…”
Section: Discussion
supporting
confidence: 92%
Utility of S100A12 as an Early Biomarker in Patients With ST-Segment Elevation Myocardial Infarction
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…S100A12 is endogenously expressed by cells closely linked to vascular disease including granulocytes, myeloid cells and macrophages (14,15). Consistent with the findings from previous studies, the immunohistochemistry and immunofluorescence findings from the present study in acutely aspirated coronary thrombi and autopsy specimens from patients with STEMI suggests that the increase in plasma S100A12 in STEMI derives from its acute release from CD68+ macrophages in ruptured plaques, a mechanism quite different than the elevation of biomarkers derived from myocardial necrosis such as CK-MB and hscTnT (16). Plasma S100A12 was slightly increased in patients with non-plaque related chest pain, such as PTE and AD, possibly due to systemic or focal inflammation.…”
Section: Discussion
supporting
confidence: 92%
Biomarkers-in-Cardiology 8 RE-VISITED—Consistent Safety of Early Discharge with a Dual Marker Strategy Combining a Normal hs-cTnT with a Normal Copeptin in Low-to-Intermediate Risk Patients with Suspected Acute Coronary Syndrome—A Secondary Analysis of the Randomized Biomarkers-in-Cardiology 8 Trial
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“…However, our findings are in line with established evidence that the use of hs-cTn instead of cTn improves risk stratification since more sensitive assays allow for the detection of prognostically adverse myocardial injury that would have been undetected with less sensitive assay generations [ 27 , 28 , 29 ]. Our findings are consistent with other observational studies that calculated future risk for MACE post-discharge based on risk modeling using different biomarker thresholds for hs-cTn [ 11 , 12 , 13 ]. The vast majority of these trials managed patients according to standard processes and not based on the optimal decision thresholds for rule-out or rule-in.…”
Section: Discussion
supporting
confidence: 92%
Abstract
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“…The results of the present study are in line with previous results of mainly lower-risk cohorts describing negative predictive values for rule-out of MI of the 1-hour troponin algorithm of above 99% 13 14 16 24. The negative predictive value of 99.8% in this cohort is remarkable since the much higher pretest probability could have negatively affected this result.…”
Section: Discussion
supporting
confidence: 92%
