We read the article by Çınar et al. [1] entitled “Prognostic significance of cardiac troponin level in Covid-19 patients without known cardiovascular risk factors” with great interest. Troponin measurement appears to be a misleading biomarker that incorrectly guides physicians to cardiac diagnosis in the period of COVID-19 [2]. First of all, we would like to thank the authors for addressing the non-cardiac importance of this biomarker [1].
COVID-19 has been in constant debate since its emergence in Wuhan Province, China in 2019, and it seems to remain on our agenda for a while [3,4]. The fact that SARS-CoV-2 disrupts not only the respiratory tract but various systems and this multisystemic involvement requires us to make a multidisciplinary evaluation of COVID-19 patients [[5], [6], [7], [8], [9]]. Since SARS-CoV-2 increases the risk of thrombosis, it comes to mind that it may cause cardiac effects in patients. Although the relationship of this disease with myocardial infarction is still unclear, the question of whether the patient has a myocardial infarction is constantly raised for every patient with high troponin levels [2].
This study shows to physicians who follow COVID-19 patients that we should follow patients with high troponin levels more closely. These patients have a higher risk of mortality. Another important point of this study is that patients with cardiovascular risk factors were excluded from the study. Although these patients were not included in the study, troponin values were found to be 89.6 ± 66.0 in the non-survivor group and 6.2 ± 9.6 in the survivor group. The difference between troponin levels in patient groups is remarkable [1].
The guidelines do not have a common recommendation for approaching myocardial infarction in COVID-19 patients if the patient is not ST elevation myocardial infarction. There is no clear answer to the question of what the troponin value is in COVID-19 patients, we should consider a non ST elevation myocardial infarction (NSTEMI). It is not clear what kind of medical treatment we should apply to these patients, let alone whether to make an intervention or not. Because this high troponin level may be secondary to infection, independent of vascular occlusion, or it may be due to a blockage at the level of large or small vessels [2,10]. If we consider COVID-19 patients with high troponin levels as NSTEMI, antiischemic medical therapy should definitely be initiated in these patients. These patients can also be followed up conservatively. This decision can be determined based on the patient's clinic and symptoms [2]. I have a question to the authors on this subject. I wonder if antiischemic therapy was initiated in patients with high troponin levels, especially in patients with high levels such as in the non-survivor group, or how the diagnosis of myocardial infarction was ruled out.
Funding
No funding was taken for the study.
Declaration of competing interest
The authors declare that they have no conflict of interest.
References
- 1.Çınar T., Hayıroğlu M.İ., Çiçek V., et al. Prognostic significance of cardiac troponin level in Covid-19 patients without known cardiovascular risk factors. Am J Emerg Med. 2020 Dec 18 doi: 10.1016/j.ajem.2020.12.033. S0735-6757(20)31152-9. [Epub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Aktoz M., Altay H., Aslanger E., et al. Türk Kardiyoloji Derneği Uzlaşı Raporu: COVID-19 Pandemisi ve Kardiyovasküler Hastalıklar Konusunda Bilinmesi Gerekenler (13 Mayıs 2020) [Turkish Cardiology Association Consensus Report: COVID-19 Pandemic and Cardiovascular Diseases (May 13, 2020)] Turk Kardiyol Dern Ars. 2020 May;48(Suppl. 1):1–87. doi: 10.5543/tkda.2020.36713. [Turkish] [DOI] [PubMed] [Google Scholar]
- 3.Bruoha S., Yosefy C., Gallego-Colon E., et al. Impact in total ischemic time and ST-segment elevation myocardial infarction admissions during COVID-19. Am J Emerg Med. 2021 Feb 18;45:7–10. doi: 10.1016/j.ajem.2021.02.020. [Epub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Siman-Tov M., Strugo R., Podolsky T., et al. An assessment of treatment, transport, and refusal incidence in a National EMS’s routine work during COVID-19. Am J Emerg Med. 2021 Jan 28;44:45–49. doi: 10.1016/j.ajem.2021.01.051. [Epub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Lamamri M., Chebbi A., Mamane J., et al. Priapism in a patient with coronavirus disease 2019 (COVID-19) Am J Emerg Med. 2021 Jan;39:251.e5–251.e7. doi: 10.1016/j.ajem.2020.06.027. [Epub 2020 Jun 18] [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Ufuk F., Bulgurcu E., Sari T. COVID-19-associated pancytopenia and typhlitis. Am J Emerg Med. 2021 Jan 4 doi: 10.1016/j.ajem.2020.12.049. S0735-6757(20)31169-4. [Epub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Fisher J., Monette D.L., Patel K.R., et al. COVID-19 associated parotitis. Am J Emerg Med. 2021 Jan;39:254.e1–254.e3. doi: 10.1016/j.ajem.2020.06.059. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Uzun Uslu P. Pandemia and insomnia. Eskisehir Med J. 2020;1(1):5–9. [Google Scholar]
- 9.Turgay Yıldırım Ö., Turgay A., Laflı Tunay D. COVID-19 pandemic and cardiovascular effects. J Cukurova Anesth Surg Sci. 2020;3(3):128–133. [Google Scholar]
- 10.Chieffo A., Stefanini G.G., Price S., et al. EAPCI position statement on invasive management of acute coronary syndromes during the COVID-19 pandemic. Eur Heart J. 2020 May 14;41(19):1839–1851. doi: 10.1093/eurheartj/ehaa381. [DOI] [PMC free article] [PubMed] [Google Scholar]