Key result
D-dimer-based nomogram models accurately discriminated acute aortic syndromes from NSTEMI during the troponin-blind period, achieving an AUC of 0.952 for symptom onset <2 hours and 0.974 for onset ≥2 hours.
Why the study?
Discriminating acute aortic syndromes from NSTEMI during the troponin-blind period (<2-3 h of symptom onset) had not been studied previously.
Does a nomogram based on routine biomarkers improve discrimination between acute aortic syndromes and NSTEMI during the troponin-blind period in patients with acute chest pain?
Cohort (n=638)
No
Does a nomogram based on routine biomarkers improve discrimination between acute aortic syndromes and NSTEMI during the troponin-blind period in patients with acute chest pain?
Nomogram models incorporating time-dependent D-dimer and other routine biomarkers can accurately discriminate acute aortic syndromes from NSTEMI during the early troponin-blind period.
May support biomarker-aided differentiation of AAS from early NSTEMI; leaves open prospective validation before any clinical adoption.
Background: elevation myocardial infarction (NSTEMI) during the troponin-blind period of <2-3 h of symptom onset have not been studied previously. We aimed to explore whether routine biomarkers might facilitate differential diagnosis. Methods: Data were retrospectively collected from 178 patients with AASs and 460 patients with NSTEMI within 3 h of onset. Differential risk factors related to AASs were identified by univariate and multivariate logistic regression analyses for patients with onset <2 h and onset ≥2 h, respectively, in the cardiac troponin (cTn) cohort. Nomograms were established in the cTn cohort as a training set and validated in the high-sensitivity cTn cohort. To assess the utility of the models in clinical practice, decision curve analyses were performed. Results: D-dimer, fibrinogen, and age were identified as differential risk factors for AASs with the onset of <2 h. D-dimer at an optimal cutoff level of 281 ng/mL for AASs had a sensitivity of 86.4% and a specificity of 91.3%. A nomogram was developed and validated with areas under the curve (AUC) of 0.934 (95% CI: 0.880-0.988) and 0.952 (95% CI: 0.874-1.000), respectively. D-dimer, neutrophil, bilirubin, and platelet were the differential risk factors for AASs with the onset of ≥2 h. D-dimer at an optimal cutoff level of 385 ng/mL has a sensitivity of 91.8% and a specificity of 91.3%. The AUC of the second nomogram in the training set and the validation set were 0.965 (95% CI: 0.942-0.988) and 0.974 (95% CI: 0.944-1.000), respectively. Conclusion: Time-dependent quality of D-dimer should be considered for discriminating AASs from NSTEMI. Both nomogram models may have a clinical utility for evaluating the probability of AASs.
No takes yet. Share an insight, caveat, or question.
Tong et al. (2023) conducted a cohort in Acute aortic syndromes and non-ST-elevation myocardial infarction (n=638). D-dimer-based nomogram models was evaluated on Discrimination between acute aortic syndromes and NSTEMI (AUC in validation set for <2h onset) (AUC 0.952, 95% CI 0.874-1.000). D-dimer-based nomogram models accurately discriminated acute aortic syndromes from NSTEMI during the troponin-blind period, achieving an AUC of 0.952 for symptom onset <2 hours and 0.974 for onset ≥2 hours.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: