Association of accompanying dyspnoea with diagnosis and outcome of patients presenting with acute chest discomfort - Boeddinghaus, J.; Nestelberger, T.; Koechlin, L.; Lopez-Ayala, P.; Wussler, D.; Mais, M.; Zwimpfer, L.; Zimmermann, T.; Wildi, K.; Gimenez, M. R.; Strebel, I.; Miro, O.; et al. (Eur Heart J Acute Cardiovasc Care, 2023)
AIMS: The presence of accompanying dyspnoea is routinely assessed and common in patients presenting with acute chest pain/discomfort to the emergency department (ED). We aimed to assess the association of accompanying dyspnoea with differential diagnoses, diagnostic work-up, and outcome. METHODS AND RESULTS: We enrolled patients presenting to the ED with chest pain/discomfort. Final diagnoses were adjudicated by independent cardiologists using all information including cardiac imaging. The primary diagnostic endpoint was the final diagnosis. The secondary diagnostic endpoint was the performance of high-sensitivity cardiac troponin (hs-cTn) and the European Society of Cardiology (ESC) 0/1h-algorithms for the diagnosis of myocardial infarction (MI). The prognostic endpoints were cardiovascular and all-cause mortality at two years. Among 6045 patients, 2892/6045 (48%) had accompanying dyspnoea. The prevalence of acute coronary syndrome (ACS) in patients with vs. without dyspnoea was comparable (MI 22.4% vs. 21.9%, P = 0.60, unstable angina 8.7% vs. 7.9%, P = 0.29). In contrast, patients with dyspnoea more often had cardiac, non-coronary disease (15.3% vs. 10.2%, P < 0.001). Diagnostic accuracy of hs-cTnT/I concentrations was not affected by the presence of dyspnoea (area under the curve 0.89-0.91 in both groups), and the safety of the ESC 0/1h-algorithms was maintained with negative predictive values >99.4%. Accompanying dyspnoea was an independent predictor for cardiovascular and all-cause death at two years [hazard ratio 1.813 (95% confidence intervals, 1.453-2.261, P < 0.01)]. CONCLUSION: Accompanying dyspnoea was not associated with a higher prevalence of ACS but with cardiac, non-coronary disease. While the safety of the diagnostic work-up was not affected, accompanying dyspnoea was an independent predictor for cardiovascular and all-cause death. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT00470587, number NCT00470587.
Keywords: journalArticle; (P400PM_180828), the Swiss Heart Foundation, and the Women and Heart Foundation,; (P400PM_191037/1), the Swiss Heart Foundation (FF20079), the Prof. Dr. Max; *Acute Coronary Syndrome; *Myocardial Infarction/diagnosis; 0/1h-algorithm; Acon, Amgen, Astra Zeneca, Boehringer Ingelheim, Bayer, BMS, Idorsia, Novartis,; Biomarkers; Biomerieux, Idorsia, Novartis, Ortho Cinical Diagnostics, Quidel, Roche, Siemens,; Chest Pain/diagnosis/etiology; Clinical Diagnostics, and Orion Pharma, all outside the submitted work. L.K.; Cloetta Foundation, the Margarete und Walter Lichtenstein-Stiftung (3MS1038), the; Diagnosis of MI; Diagnostics, Ortho Clinical Diagnostics, and Quidel Corporation. T.N. has; Diagnostics. C.M. has received research support from the Swiss National Science; Division of Internal Medicine, the Swiss Academy of Medical Sciences, the; Dyspnea/diagnosis/epidemiology/etiology; Dyspnoea; Foundation (P500PM_206636), and speaker honoraria from Siemens, Roche; Foundation, the Swiss Heart Foundation, the KTI, the European Union, the; Gottfried and Julia Bangerter-Rhyner Foundation, and the Swiss National Science; High-sensitivity cardiac troponin; Hospital Foundation, and a PhD scholarship of the University of Queensland. T.Z.; Humans; J.B., T.N., L.K., P.L.-A., M.R.G., K.W., and C.M. had full access to all the data; M.R.G. received research grants from the Swiss National Science Foundation; Medical Sciences, and the Gottfried and Julia Bangerter-Rhyner Foundation, as; Osler, Roche, and Sanofi, outside of the submitted work. All other authors; Predictive Value of Tests; Prognosis; Singulex, and Sphingotec, as well as speaker honoraria/consulting honoraria from; The sponsors had no role in designing or conducting the study and no role in; Troponin T; University Basel, and the University Hospital Basel as well as speaker; University of Basel, the University Hospital Basel, Abbott, Beckman Coulter,; accessible websites or e-print servers. We disclose that J.B. received research; accuracy of the data analysis. All authors have read and approved the manuscript; and speaker honoraria from Abbott, Roche, Siemens, and Ortho Clinical; contents have not been published previously and are not being considered for; data, vouched for the data and analysis, wrote the paper, and decided to publish; decision to submit the manuscript for publication; declare that they have no conflict of interest with this study. The hs-cTn assays; gathering or analysing the data or writing the manuscript. The manuscript and its; grants from the University of Basel, the University Hospital of Basel, the; honoraria from Quidel, outside the submitted work, paid to the institution. K.W.; honoraria/consulting honoraria from Siemens, Beckman Coulter, Bayer, Ortho; in the study and take responsibility for the integrity of the data and the; investigated were donated by the manufacturers, who had no role in the design of; publications elsewhere in whole or in part in any language, including publicly; received a research grant from the 'Freiwillige Akademische Gesellschaft Basel',; received a research grant from the University of Basel, the Swiss Academy of; received research support from the 'Freiwillige Akademische Gesellschaft Basel'.; received research support from the Swiss National Science Foundation; research grants from the Swiss Heart Foundation (FF20079 and FF21103) and speaker; the Gottfried and Julia Bangerter-Rhyner Foundation, and the Prince Charles; the study, the analysis of the data, the preparation of the manuscript, or the; well as the 'Freiwillige Akademische Gesellschaft Basel'. P.L.-A. has received