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Improving the Diagnosis of Acute Myocardial Infarction
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Improving the Diagnosis of Acute Myocardial Infarction

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 9774

Special Issue Editor

Dr. Maria Rubini Giménez

E-Mail Website
Guest Editor
Department of Cardiology, Heart Center Leipzig, Leipzig, Germany
Interests: acute coronary syndromes; high-sensitivity cardiac troponin; biomarkers; cardiogenic shock; sex-specific acute cardiac care

Special Issue Information

Dear Colleagues,

The introduction of high-sensitivity cardiac troponin (hs-cTn) in recent years has substantially increased the accuracy in rapidly identifying acute myocardial infarction (AMI) and has enabled the development and extensive validation of early hs-cTn-based diagnostic algorithms, which has substantially reduced the time required for the safe rule-out or rule-in of AMI.

Despite these great advances, there are still several interesting topics in the diagnosis of AMI using hs-cTn for further improvements. The differentiation of myocardial infarction vs. myocardial injury or differentiation between type 1 or 2 myocardial infarction and, consequently, the different therapeutic approaches still remain challenging today. In addition, the clinical benefit of using sex-specific reference values for hs-cTn remains controversial. Finally, the practicability of introducing rapid diagnostic algorithms (e.g., 0/1 h ESC algorithm) in different health care systems worldwide has also been recently questioned.

In this Special Issue, we welcome the submission of original research and review articles to deepen the latest evidence in the field of using hs-cTn for the diagnosis of AMI.

Dr. Maria Rubini Giménez
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • acute myocardial infarction
  • high-sensitivity cardiac troponin
  • myocardial injury
  • type 1 and type 2
  • sex-specific reference values

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Published Papers (4 papers)

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Research

12 pages, 446 KiB  
Article
Comparing Door-To-Balloon Time between ST-Elevation Myocardial Infarction Electrocardiogram and Its Equivalents
by Youngchul Choi, Kiwook Kim, Joo Suk Oh, Hyun Ho Jeong, Jung Taek Park, Yeon Young Kyong, Young Min Oh, Se Min Choi and Kyoung Ho Choi
J. Clin. Med. 2022, 11(19), 5547; https://doi.org/10.3390/jcm11195547 - 22 Sep 2022
Cited by 1 | Viewed by 1975
Abstract
Background: In patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (pPCI), longer door-to-balloon (DTB) time is known to be associated with an unfavorable outcome. A percentage of patients with acute coronary occlusion present with atypical electrocardiographic (ECG) findings, known as [...] Read more.
Background: In patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (pPCI), longer door-to-balloon (DTB) time is known to be associated with an unfavorable outcome. A percentage of patients with acute coronary occlusion present with atypical electrocardiographic (ECG) findings, known as STEMI-equivalents. We investigated whether DTB time for STEMI-equivalent patients was delayed. Methods: This is a retrospective study including patients arriving at an emergency department with the acute coronary syndrome in whom emergent pPCI was performed. ECGs were classified into STEMI and STEMI-equivalent groups. We compared DTB time, with its components, between the groups. We also investigated whether STEMI-equivalent ECG was an independent predictor of DTB time delayed for more than 90 min. Results: A total of 180 patients were included in the present study, and 23 patients (12.8%) presented with STEMI-equivalent ECGs. DTB time was significantly delayed in patients with STEMI-equivalent ECGs (89 (80–122) vs. 81 (70–88) min, p = 0.001). Multivariable logistic regression analysis showed that STEMI-equivalent ECG was an independent predictor of delayed DTB time (odds ratio: 4.692; 95% confidence interval: 1.632–13.490, p = 0.004). Conclusions: DTB time was significantly delayed in patients presenting with STEMI-equivalent ECGs. Prompt recognition of STEMI-equivalent ECGs by emergency physicians and interventional cardiologists might reduce DTB time and lead to a better clinical outcome. Full article
(This article belongs to the Special Issue Improving the Diagnosis of Acute Myocardial Infarction)
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12 pages, 1762 KiB  
Article
High-Sensitivity Cardiac Troponin T and the Diagnosis of Cardiovascular Disease in the Emergency Room: The Importance of Combining Cardiovascular Biomarkers with Clinical Data
by Michele Golino, Jacopo Marazzato, Federico Blasi, Matteo Morello, Valentina Chierchia, Cristina Cadonati, Federica Matteo, Claudio Licciardello, Martina Zappa, Walter Ageno, Alberto Passi, Fabio Angeli and Roberto De Ponti
J. Clin. Med. 2022, 11(13), 3798; https://doi.org/10.3390/jcm11133798 - 30 Jun 2022
Cited by 4 | Viewed by 2377
Abstract
Background. Nowadays, it is still not possible to clinically distinguish whether an increase in high-sensitivity cardiac troponin (hs-cTn) values is due to myocardial injury or an acute coronary syndrome (ACS). Moreover, predictive data regarding hs-cTnT in an emergency room (ER) setting are scarce. [...] Read more.
Background. Nowadays, it is still not possible to clinically distinguish whether an increase in high-sensitivity cardiac troponin (hs-cTn) values is due to myocardial injury or an acute coronary syndrome (ACS). Moreover, predictive data regarding hs-cTnT in an emergency room (ER) setting are scarce. This monocentric retrospective study aimed to improve the knowledge and interpretation of this cardiac biomarker in daily clinical practice. Methods. Consecutive adult patients presenting at the ER and hospitalized with a first abnormal hs-cTnT value (≥14 ng/L) were enrolled for 6 months. The baseline hs-cTnT value and the ensuing changes and variations were correlated with the clinical presentation and the type of diagnosis. Subsequently, multivariable models were built to assess which clinical/laboratory variables most influenced hospital admissions in the investigated population analyzed according to the final reason for hospitalization: (1) cardiovascular vs. non-cardiovascular diagnosis, and (2) ACS vs. non-ACS one. Results. A total of 4660 patients were considered, and, after a first screening, 4149 patients were enrolled. Out of 4129 patients, 1555 (37.5%) had a first hs-cTnT ≥14 ng/L, and 1007 (65%) were hospitalized with the following types of diagnosis: ACS (182; 18%), non-ACS cardiovascular disease (337; 34%) and non-cardiovascular disease (487; 48%). Higher hs-cTnT values and significant hs-cTnT variations were found in the ACS group (p < 0.01). The mean percentage of variation was higher in patients with ACS, intermediate in those with non-ACS cardiovascular disease, and low in those with non-cardiovascular disease (407.5%, 270.6% and 12.4%, respectively). Only syncope and CRP (OR: 0.08, 95% CI: 0.02–0.39, p < 0.01 and OR: 0.9988, 95% CI: 0.9979–0.9998, p = 0.02, respectively) or CRP (OR: 0.9948, 95% CI: 0.9908–0.9989, p = 0.01) and NT-proBNP (OR: 1.0002, 95% CI: 1.0000–1.0004, p = 0.02) were independent predictors of a cardiovascular disease diagnosis. On the other hand, only chest pain (OR: 22.91, 95% CI: 3.97–132.32, p < 0.01) and eGFR (OR: 1.04, 95% CI: 1.004–1.083, p = 0.03) were associated with the ACS diagnosis. Conclusions. Differently from the investigated biomarkers, in this study, only clinical variables predicted hospitalizations in different patients’ subgroups. Full article
(This article belongs to the Special Issue Improving the Diagnosis of Acute Myocardial Infarction)
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11 pages, 693 KiB  
Article
Clinical History and Detectable Troponin Concentrations below the 99th Percentile for Risk Stratification of Patients with Chest Pain and First Normal Troponin
by Agustín Fernández-Cisnal, Ernesto Valero, Sergio García-Blas, Vicente Pernias, Adela Pozo, Arturo Carratalá, Jessika González, José Noceda, Gema Miñana, Julio Núñez and Juan Sanchis
J. Clin. Med. 2021, 10(8), 1784; https://doi.org/10.3390/jcm10081784 - 20 Apr 2021
Cited by 4 | Viewed by 2169
Abstract
Decision-making is challenging in patients with chest pain and normal high-sensitivity cardiac troponin T (hs-cTnT; <99th percentile; <14 ng/L) at hospital arrival. Most of these patients might be discharged early. We investigated clinical data and hs-cTnT concentrations for risk stratification. This is a [...] Read more.
Decision-making is challenging in patients with chest pain and normal high-sensitivity cardiac troponin T (hs-cTnT; <99th percentile; <14 ng/L) at hospital arrival. Most of these patients might be discharged early. We investigated clinical data and hs-cTnT concentrations for risk stratification. This is a retrospective study including 4476 consecutive patients presenting to the emergency department with chest pain and first normal hs-cTnT. The primary endpoint was one-year death or acute myocardial infarction, and the secondary endpoint added urgent revascularization. The number of primary and secondary endpoints was 173 (3.9%) and 252 (5.6%). Mean hs-cTnT concentrations were 6.9 ± 2.5 ng/L. Undetectable (<5 ng/L) hs-cTnT (n = 1847, 41%) had optimal negative predictive value (99.1%) but suboptimal sensitivity (90.2%) and discrimination accuracy (AUC = 0.664) for the primary endpoint. Multivariable analysis was used to identify the predictive clinical variables. The clinical model showed good discrimination accuracy (AUC = 0.810). The addition of undetectable hs-cTnT (≥ or <5 ng/L; HR, hazard ratio = 3.80; 95% CI, confidence interval 2.27–6.35; p = 0.00001) outperformed the clinical model alone (AUC = 0.836, p = 0.002 compared to the clinical model). Measurable hs-cTnT concentrations (between detection limit and 99th percentile; per 0.1 ng/L, HR = 1.13; CI 1.06–1.20; p = 0.0001) provided further predictive information (AUC = 0.844; p = 0.05 compared to the clinical plus undetectable hs-cTnT model). The results were reproducible for the secondary endpoint and 30-day events. Clinical assessment, undetectable hs-cTnT and measurable hs-cTnT concentrations must be considered for decision-making after a single negative hs-cTnT result in patients presenting to the emergency department with acute chest pain. Full article
(This article belongs to the Special Issue Improving the Diagnosis of Acute Myocardial Infarction)
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13 pages, 630 KiB  
Article
Acute Phase Response and Non-Reproducible Elevated Concentrations with a High-Sensitivity Cardiac Troponin I Assay
by Peter A. Kavsak, Lorna Clark, Janet Martin, Ching-Tong Mark, Guillaume Paré, Shawn Mondoux, V. Tony Chetty, Craig Ainsworth and Andrew Worster
J. Clin. Med. 2021, 10(5), 1014; https://doi.org/10.3390/jcm10051014 - 2 Mar 2021
Cited by 16 | Viewed by 2352
Abstract
High-sensitivity cardiac troponin (hs-cTn) testing has enabled physicians to make earlier diagnostic and prognostic decisions in the hospital setting than previous cardiac troponin assays. Analytical improvements have permitted one to measure cardiac troponin precisely in the nanogram per litre (ng/L) range with hs-cTn [...] Read more.
High-sensitivity cardiac troponin (hs-cTn) testing has enabled physicians to make earlier diagnostic and prognostic decisions in the hospital setting than previous cardiac troponin assays. Analytical improvements have permitted one to measure cardiac troponin precisely in the nanogram per litre (ng/L) range with hs-cTn assays which has resulted in fast 0/1-h and 0/2-h algorithms for ruling-in and ruling-out myocardial infarction. Although analytical interferences that affect the reporting of hs-cTn are uncommon, not all hs-cTn assays are designed the same nor have undergone the same clinical and analytical validations. Here, after investigating an initial case of discrepant hs-cTnI results, we report that patients with an acute phase response (e.g., patients with inflammatory or infectious illnesses) can yield high and non-reproducible results with the Ortho Clinical Diagnostics hs-cTnI assay. Compared to Abbott Diagnostics hs-cTnI, Ortho Clinical Diagnostics hs-cTnI assay misclassifies biochemical injury in approximately 10% of the population being assessed for myocardial injury with imprecise results in approximately half of this population (i.e., 5%). In conclusion, caution is warranted in interpreting Ortho Clinical Diagnostics hs-cTnI alone in patients being evaluated for myocardial injury, especially in patients whose primary presentation is related to an acute phase response and not an acute coronary syndrome symptom. Full article
(This article belongs to the Special Issue Improving the Diagnosis of Acute Myocardial Infarction)
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