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. 2023 May 4;12(5):283-295.
doi: 10.1093/ehjacc/zuad026.

Association of accompanying dyspnoea with diagnosis and outcome of patients presenting with acute chest discomfort

Jasper Boeddinghaus  1   2   3 , Thomas Nestelberger  1   2 , Luca Koechlin  1   2   4 , Pedro Lopez-Ayala  1   2 , Desiree Wussler  1   2   5 , Maximilian Mais  1 , Luca Zwimpfer  1 , Tobias Zimmermann  1   2   6 , Karin Wildi  1   2   7 , Maria Rubini Giménez  1   2   8 , Ivo Strebel  1   2 , Òscar Miró  2   9 , F Javier Martin-Sanchez  2   10 , Jiri Parenica  11 , Dagmar I Keller  12 , Danielle M Gualandro  1   2 , Christian H Nickel  13 , Roland Bingisser  13 , Michael Christ  14 , Christian Mueller  1   2 ; APACE investigators
Affiliations

V体育ios版 - Association of accompanying dyspnoea with diagnosis and outcome of patients presenting with acute chest discomfort

Jasper Boeddinghaus et al. Eur Heart J Acute Cardiovasc Care. .

Abstract

Aims: The presence of accompanying dyspnoea is routinely assessed and common in patients presenting with acute chest pain/discomfort to the emergency department (ED) VSports手机版. 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 V体育安卓版. 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 V体育ios版. .

Clinical trial registration: https://clinicaltrials VSports最新版本. gov/ct2/show/NCT00470587, number NCT00470587. .

Keywords: 0/1h-algorithm; Diagnosis of MI; Dyspnoea; High-sensitivity cardiac troponin. V体育平台登录.

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Conflict of interest statement

Conflict of interest: The authors designed the study, gathered and analysed the data, vouched for the data and analysis, wrote the paper, and decided to publish. J. B. , T. N. , L. K. , P. L. -A. , M. R. G V体育官网入口. , K. W. , and C. M. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. All authors have read and approved the manuscript. The sponsors had no role in designing or conducting the study and no role in gathering or analysing the data or writing the manuscript. The manuscript and its contents have not been published previously and are not being considered for publications elsewhere in whole or in part in any language, including publicly accessible websites or e-print servers. We disclose that J. B. received research grants from the University of Basel, the University Hospital of Basel, the Division of Internal Medicine, the Swiss Academy of Medical Sciences, the Gottfried and Julia Bangerter-Rhyner Foundation, and the Swiss National Science Foundation (P500PM_206636), and speaker honoraria from Siemens, Roche Diagnostics, Ortho Clinical Diagnostics, and Quidel Corporation. T. N. has received research support from the Swiss National Science Foundation (P400PM_191037/1), the Swiss Heart Foundation (FF20079), the Prof. Dr. Max Cloëtta Foundation, the Margarete und Walter Lichtenstein-Stiftung (3MS1038), the University Basel, and the University Hospital Basel as well as speaker honoraria/consulting honoraria from Siemens, Beckman Coulter, Bayer, Ortho Clinical Diagnostics, and Orion Pharma, all outside the submitted work. L. K. received a research grant from the University of Basel, the Swiss Academy of Medical Sciences, and the Gottfried and Julia Bangerter-Rhyner Foundation, as well as the ‘Freiwillige Akademische Gesellschaft Basel’. P. L. -A. has received research grants from the Swiss Heart Foundation (FF20079 and FF21103) and speaker honoraria from Quidel, outside the submitted work, paid to the institution. K. W. received a research grant from the ‘Freiwillige Akademische Gesellschaft Basel’, the Gottfried and Julia Bangerter-Rhyner Foundation, and the Prince Charles Hospital Foundation, and a PhD scholarship of the University of Queensland. T. Z. received research support from the ‘Freiwillige Akademische Gesellschaft Basel’. M. R. G. received research grants from the Swiss National Science Foundation (P400PM_180828), the Swiss Heart Foundation, and the Women and Heart Foundation, and speaker honoraria from Abbott, Roche, Siemens, and Ortho Clinical Diagnostics. C. M. has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the KTI, the European Union, the University of Basel, the University Hospital Basel, Abbott, Beckman Coulter, Biomerieux, Idorsia, Novartis, Ortho Cinical Diagnostics, Quidel, Roche, Siemens, Singulex, and Sphingotec, as well as speaker honoraria/consulting honoraria from Acon, Amgen, Astra Zeneca, Boehringer Ingelheim, Bayer, BMS, Idorsia, Novartis, Osler, Roche, and Sanofi, outside of the submitted work. All other authors declare that they have no conflict of interest with this study. The hs-cTn assays investigated were donated by the manufacturers, who had no role in the design of the study, the analysis of the data, the preparation of the manuscript, or the decision to submit the manuscript for publication.

Figures

Graphical abstract
Graphical abstract
Figure 1
Figure 1
(A) Differential diagnoses according to the presence or absence of accompanying dyspnoea. AMI, acute myocardial infarction; UA, unstable angina. (B) Differential diagnoses of patients with cardiac non-coronary disease according to the presence or absence of accompanying dyspnoea. (C) Differential diagnoses of patients with non-cardiac disease according to the presence or absence of accompanying dyspnoea. COPD, chronic obstructive pulmonary disease.
Figure 2
Figure 2
(A) Boxplots showing hs-cTnT and hs-cTnI concentrations according to the presence of accompanying dyspnoea in patients with MI vs. those with other adjudicated diagnoses. Boxplots showing hs-cTnT concentrations (upper boxplots) and hs-cTnI concentrations (lower boxplots) at presentation according to final diagnoses (MI vs. non-MI) in patients with vs. without accompanying dyspnoea. MI, myocardial infarction. (B) Diagnostic accuracy of hs-cTnT and hs-cTnI concentrations at presentation for the diagnosis of NSTEMI according to the presence or absence of accompanying dyspnoea. Receiver-operating-characteristics curves indicating the diagnostic accuracy of hs-cTnT (left) and hs-cTnI (right) concentrations at presentation for the diagnosis of NSTEMI in patients with (red line) vs. without (black line) accompanying dyspnoea. Hs-cTn, high-sensitivity cardiac troponin; AUC, area under the curve; CI, confidence interval.
Figure 3
Figure 3
(A+B) Diagnostic performance of the ESC hs-cTnT 0/1h-algorithm. Diagnostic performance of the ESC hs-cTnT 0/1h-algorithm in (A) patients with and (B) patients without accompanying dyspnoea. *, if chest pain onset >3 h; Delta, unsigned change within the first hour; NSTEMI, non-ST-segment elevation myocardial infarction; Sens., sensitivity; NPV, negative predictive value; Prev., prevalence; Spec., specificity; PPV, positive predictive value; hs-cTnT, high-sensitivity cardiac troponin T. (C+D) Diagnostic performance of the ESC hs-cTnI 0/1h-algorithm. Diagnostic performance of the ESC hs-cTnI 0/1h-algorithm in (C) patients with and (D) patients without accompanying dyspnoea. *, if chest pain onset >3 h; Delta, unsigned change within the first hour; NSTEMI, non-ST-segment elevation myocardial infarction; Sens., sensitivity; NPV, negative predictive value; Prev., prevalence; Spec., specificity; PPV, positive predictive value; hs-cTnI, high-sensitivity cardiac troponin I.
Figure 3
Figure 3
(A+B) Diagnostic performance of the ESC hs-cTnT 0/1h-algorithm. Diagnostic performance of the ESC hs-cTnT 0/1h-algorithm in (A) patients with and (B) patients without accompanying dyspnoea. *, if chest pain onset >3 h; Delta, unsigned change within the first hour; NSTEMI, non-ST-segment elevation myocardial infarction; Sens., sensitivity; NPV, negative predictive value; Prev., prevalence; Spec., specificity; PPV, positive predictive value; hs-cTnT, high-sensitivity cardiac troponin T. (C+D) Diagnostic performance of the ESC hs-cTnI 0/1h-algorithm. Diagnostic performance of the ESC hs-cTnI 0/1h-algorithm in (C) patients with and (D) patients without accompanying dyspnoea. *, if chest pain onset >3 h; Delta, unsigned change within the first hour; NSTEMI, non-ST-segment elevation myocardial infarction; Sens., sensitivity; NPV, negative predictive value; Prev., prevalence; Spec., specificity; PPV, positive predictive value; hs-cTnI, high-sensitivity cardiac troponin I.
Figure 4
Figure 4
Forest plot showing adjusted hazard ratios from multivariable cox regression analysis. Hazard ratios from multivariable cox proportional hazard model for all-cause death at 2 years. HR, hazard ratio; CAD, coronary artery disease; eGFR, estimated glomerular filtration rate; hs-cTnT, high-sensitivity cardiac troponin T.
Figure 5
Figure 5
Cumulate death at 30 days and two years of follow-up in patients with vs. without accompanying dyspnoea. Kaplan–Meier curves indicating cumulative all-cause death at 30 days and two years of follow-up in patients without (black line) vs. with (red line) accompanying dyspnoea. Differences between survival rates were assessed using the log-rank test.
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