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Case Report
Open Access Peer-reviewed

Pharmaco-invasive Therapy for STEMI in a Patient with COVID-19: A Case Report

Pramod Theetha Kariyanna, Naseem A. Hossain, Apoorva Jayarangaiah, Nimrah.A. Hossain, Jonathan Christopher Francois, Jonathan D. Marmur, Moro O. Salifu, Samy. I. McFarlane
American Journal of Medical Case Reports. 2020, 8(7), 192-196. DOI: 10.12691/ajmcr-8-7-9
Received April 01, 2020; Revised April 18, 2020; Accepted April 22, 2020

Abstract

Coronavirus disease 2019 (COVID-19) is a pandemic that started in the Wuhan province of China in December 2019. It is associated with increased morbidity and mortality mainly due to severe acute respiratory syndrome 2 (SARS-Cov-2). Cardiac manifestations related to COVID-19 include demand ischemia, fulminant myocarditis, myocardial infarction and arrhythmias. In this report, we present a case of ST-segment elevation myocardial infarction (STEMI) in a 68-year-old man with COVID-19 who initially presented with chest pain and shortness of breath. Patient's STEMI was managed with pharmaco-invasive strategy with tissue plasminogen activator (t-PA). He then developed acute hypoxic respiratory failure that was managed in the intensive care unit (ICU), together with multi-organ failure from which the patient died 2 days after presentation. Although the pathophysiologic mechanisms of STEMI in COVID-19 patients has not been clearly established, we hypothesize that interrelated pathogenetic factors, that we highlight in this report, can play a role in the development of STEMI, including plaque rupture secondary to systemic inflammation, increased pro-coagulants, endothelial dysfunction, impaired fibrinolysis and impaired oxygen utilization leading to demand/ supply mismatch and myocardial ischemia.

1. Introduction

Coronavirus disease 2019 (COVID-19) is a pandemic encompassing the entire globe at this current time. Similar to previous coronaviruses and influenza epidemics, it has been observed that there has been increased morbidity and mortality in COVID-19 patients with pre-existing cardiovascular disease. 1 There also appears to be an association with myocardial injury. 2, 3 We aim to describe the case of a 68-year-old man with coronavirus who presented with ST elevation MI (STEMI).

2. Case Presentation

A 68-year-old male with a past medical history of lung cancer and asthma presented to the emergency department with severe shortness of breath and acute onset chest pain for the last 2 hours. The patient reportedly complained of subjective fevers, cough, dyspnea and diarrhea over the past few days. On arrival, vital signs revealed a blood pressure of 116/80 mmHg, heart rate of 120 beats per minute, oxygen saturation of 89% on room air, and a body temperature of 100.3 F. Physical examination was pertinent for tachypnea and inability to speak in complete sentences. Initial blood work was significant for leukocytosis of 20.36 K/uL, troponin of 75 ng/mL, C-reactive protein of 247 mg/dL, procalcitonin of 7.4 ng/mL and ferritin of 2634.1 ng/m. Complete laboratory test results are shown in (Table 1).

Chest X-ray (CXR) displayed bilateral airspace opacities, more predominant in the right lung (Figure 1). A 12-lead electrocardiogram (ECG) sinus tachycardia, Q waves with ST-elevation in leads III and aVF, ST segment elevation in leads II, V4, V5, V6 and ST segment depression in lead I and aVL (Figure 2). The patient received 325 mg of Aspirin, 600mg of Plavix and 100mg of tissue plasminogen activator (tPA). The patient was subsequently intubated for acute hypoxic respiratory failure. Within 12 hours, the patient suffered a cardiopulmonary arrest, advanced cardiovascular life support was initiated. Return of spontaneous circulation was obtained in 4 minutes. Thereafter, the patient was admitted to the intensive care unit however the patient expired the day after admission from multi-organ failure.

3. Discussion

The emergence of coronavirus disease 2019 (COVID-19) has become a pandemic since its discovery in Wuhan, China in late 2019. It is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). It is a single stranded enveloped RNA virus. 1 Infection occurs by the binding of the virus spike protein to the human angiotensin-converting enzyme 2 (ACE2) receptor. 4 ACE 2 is found in the type II pneumocyte in the lung, which is theorized to be the main point of entry of the virus. The ACE2 Receptor is also found in the heart, where it antagonizes the effects of angiotensin 2 in diseases where neurohormonal dysregulation is present. 5 6. This explains the observation of various studies done, which show that most of the clinical manifestations from COVID-19 infection are respiratory in nature, although severe cardiovascular events have been reported in the literature. 7

In a cohort study of 416 patients who tested positive for COVID, Shi et al. 3 described evidence of myocardial injury in 82 patients (19.7%), as evidenced by elevated high sensitivity troponin I (TnI) levels. These patients had a significantly elevated in-hospital mortality rate (42 of 82 [51.2%]) compared to those who did not have biochemical evidence of myocardial injury (15 of 335 [4.5%]). In the group with myocardial injury, greater degrees of troponin elevation were associated with increased mortality.

A study by Guo et al. 2 reported that 27.8% of patients in a cohort of 187 patients. A significant difference within in-hospital mortality for patients with elevated troponin T levels (59.6%) as compared with patients with normal TnT (8.9%). The highest mortality rate was observed in the cohort with pre-existing cardiac disease and elevated troponin (25 of 36 [69.4%]). It was also found that elevated C-reactive protein, procalcitonin and N-terminal-pro-B-type natriuretic peptide (NT-proBNP) were linked with elevated troponin t levels, suggesting a close interaction between inflammation and myocardial stress. 2

Studies from previous influenza and coronavirus epidemics have shown an association with viral infections and adverse cardiac outcomes, including acute coronary syndromes 8, arrhythmias 9 and exacerbation of heart failure 10. The mechanism of myocardial injury during COVID-19 infection has been theorized to be multifactorial. Direct toxicity of the virus to cardiac myocytes, systemic inflammatory responses, destabilization of pre-existing coronary plaque and aggravated hypoxia are some of the predominating ideas behind mechanism of injury. 2 It can be extrapolated that diffuse endothelial injury and impaired fibrinolysis are likely additional factors. Impaired myocardial oxygen utilization in the setting of elevated inflammatory cytokine levels may further contribute to cardiac ischemia.

In China, where the outbreak of COVID-19 initially started, there have been reports of COVID associated disseminated intravascular coagulation (DIC). Wang YD, et al 11 describes two cases of COVID-19 infection complicated by DIC. Acute myocardial infarction can be attributed to DIC, due to dysregulation and dysfunction in the coagulation cascade. 12, 13 Coagulopathy has also been seen in the dysregulated immune state seen in severe COVID-19 infections. Currently, early stage observation studies have shown some benefit in anticoagulation with heparin. 14, 15 (Figure 3).

To date, this case report may be the first documented case of COVID-19 associated ST segment elevation myocardial infarction (STEMI). Due to the novel nature of this virus, we feel that surveillance for STEMI associated with the virus is warranted. As of this point, there is not a clear pathophysiological mechanism to account for STEMI, only theorized mechanisms derived from past coronavirus and influenza epidemics. We hope that further case reports, cohort studies and autopsy data can further our understanding of this disease.

Emergency intravenous thrombolysis (pharmaco-invasive strategy) is indicated as the first line management of STEMI patients who are COVID-19 positive. Our management was consistent with the updated American College of Cardiology guidelines however the patient’s clinical condition deteriorated rapidly. This case reflects the staggering mortality rate associated with COVID-19 infection in patients with myocardial involvement, as reported in previous cases in China. Given the various mechanisms at play and a limited window for intervention, an ideal approach is yet to be determined; however, for now, thrombolytic therapy remains the recommended approach in COVID-19 confirmed cases.

4. Conclusion

COVID-19 is a disease that can present with severe pulmonary, cardiovascular, hematologic and immunologic manifestations. We believe that all of these interrelated systems can play a role in the development of ST segment elevation myocardial infarction. Further studies and autopsy data will be needed to truly assess the impact of COVID-19 and its relationship to the development of STEMI.

Acknowledgements

This work is supported, in part, by the efforts of Dr. Moro O. Salifu M.D., M.P.H., M.B.A., M.A.C.P., Professor and Chairman of Medicine through NIH Grant number S21MD012474.

References

[1]  Clerkin KJ, Fried JA, Raikhelkar J, et al. Coronavirus Disease 2019 (COVID-19) and Cardiovascular Disease. Circulation 2020.
In article      View Article  PubMed
 
[2]  Guo T, Fan Y, Chen M, et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol 2020.
In article      View Article  PubMed
 
[3]  Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol 2020.
In article      View Article  PubMed
 
[4]  Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell 2020.
In article      View Article  PubMed
 
[5]  Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa. International Journal of Oral Science 2020; 12(1): 8.
In article      View Article  PubMed
 
[6]  Tikellis C, Bernardi S, Burns WC. Angiotensin-converting enzyme 2 is a key modulator of the renin-angiotensin system in cardiovascular and renal disease. Curr Opin Nephrol Hypertens 2011; 20(1): 62-8.
In article      View Article  PubMed
 
[7]  Zheng Y-Y, Ma Y-T, Zhang J-Y, Xie X. COVID-19 and the cardiovascular system. Nature Reviews Cardiology 2020.
In article      View Article  PubMed
 
[8]  Kwong JC, Schwartz KL, Campitelli MA, et al. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med 2018; 378(4): 345-53.
In article      View Article  PubMed
 
[9]  Madjid M, Connolly AT, Nabutovsky Y, Safavi-Naeini P, Razavi M, Miller CC. Effect of High Influenza Activity on Risk of Ventricular Arrhythmias Requiring Therapy in Patients With Implantable Cardiac Defibrillators and Cardiac Resynchronization Therapy Defibrillators. Am J Cardiol 2019; 124(1): 44-50.
In article      View Article  PubMed
 
[10]  Kytomaa S, Hegde S, Claggett B, et al. Association of Influenza-like Illness Activity With Hospitalizations for Heart Failure: The Atherosclerosis Risk in Communities Study. JAMA Cardiol 2019; 4(4): 363-69.
In article      View Article  PubMed
 
[11]  Wang YD, Zhang SP, Wei QZ, et al. [COVID-19 complicated with DIC: 2 cases report and literatures review]. Zhonghua Xue Ye Xue Za Zhi 2020; 41(0): E001.
In article      
 
[12]  Chang C-T, Lu Y-H, Chu C-Y, Sheu S-H, Hsu P-C. Two Consecutive Episodes of Acute Myocardial Infarction Occurring in Different Coronary Arteries of a Single Patient with Sepsis. Acta Cardiol Sin 2014; 30(6): 578-81.
In article      
 
[13]  Shibusawa M, Matsumura T, Tsutsumi H, Itou Y, Shibata Y. Unexpected Acute Myocardial Infarction Due to Disseminated Intravascular Coagulation. American Journal of Medical Case Reports 2015; 3(2): 42-45.
In article      View Article
 
[14]  Shi C, Wang C, Wang H, et al. Clinical observations of low molecular weight heparin in relieving inflammation in COVID-19 patients: A retrospective cohort study. medRxiv 2020:2020.03.28. 20046144.
In article      
 
[15]  Thachil J. The versatile heparin in COVID-19. J Thromb Haemost 2020.
In article      View Article
 
[16]  Jing, ZC, Zhu HD, Yan XW et al. Recommendations From The Peking Unioun Medical College Hospital for the Management of Acute Myocardial Infarction During the COVID-19 Outbreak. European Heart Journal.
In article      
 

Published with license by Science and Education Publishing, Copyright © 2020 Pramod Theetha Kariyanna, Naseem A. Hossain, Apoorva Jayarangaiah, Nimrah.A. Hossain, Jonathan Christopher Francois, Jonathan D. Marmur, Moro O. Salifu and Samy. I. McFarlane

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Cite this article:

Normal Style
Pramod Theetha Kariyanna, Naseem A. Hossain, Apoorva Jayarangaiah, Nimrah.A. Hossain, Jonathan Christopher Francois, Jonathan D. Marmur, Moro O. Salifu, Samy. I. McFarlane. Pharmaco-invasive Therapy for STEMI in a Patient with COVID-19: A Case Report. American Journal of Medical Case Reports. Vol. 8, No. 7, 2020, pp 192-196. http://pubs.sciepub.com/ajmcr/8/7/9
MLA Style
Kariyanna, Pramod Theetha, et al. "Pharmaco-invasive Therapy for STEMI in a Patient with COVID-19: A Case Report." American Journal of Medical Case Reports 8.7 (2020): 192-196.
APA Style
Kariyanna, P. T. , Hossain, N. A. , Jayarangaiah, A. , Hossain, N. , Francois, J. C. , Marmur, J. D. , Salifu, M. O. , & McFarlane, S. I. (2020). Pharmaco-invasive Therapy for STEMI in a Patient with COVID-19: A Case Report. American Journal of Medical Case Reports, 8(7), 192-196.
Chicago Style
Kariyanna, Pramod Theetha, Naseem A. Hossain, Apoorva Jayarangaiah, Nimrah.A. Hossain, Jonathan Christopher Francois, Jonathan D. Marmur, Moro O. Salifu, and Samy. I. McFarlane. "Pharmaco-invasive Therapy for STEMI in a Patient with COVID-19: A Case Report." American Journal of Medical Case Reports 8, no. 7 (2020): 192-196.
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  • Figure 2. 12-lead ECG showing sinus tachycardia, Q waves with ST-elevation in leads III and aVF, ST segment elevation in leads II, V4, V5, V6 and ST segment depression in lead I and aVL
[1]  Clerkin KJ, Fried JA, Raikhelkar J, et al. Coronavirus Disease 2019 (COVID-19) and Cardiovascular Disease. Circulation 2020.
In article      View Article  PubMed
 
[2]  Guo T, Fan Y, Chen M, et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol 2020.
In article      View Article  PubMed
 
[3]  Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol 2020.
In article      View Article  PubMed
 
[4]  Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell 2020.
In article      View Article  PubMed
 
[5]  Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa. International Journal of Oral Science 2020; 12(1): 8.
In article      View Article  PubMed
 
[6]  Tikellis C, Bernardi S, Burns WC. Angiotensin-converting enzyme 2 is a key modulator of the renin-angiotensin system in cardiovascular and renal disease. Curr Opin Nephrol Hypertens 2011; 20(1): 62-8.
In article      View Article  PubMed
 
[7]  Zheng Y-Y, Ma Y-T, Zhang J-Y, Xie X. COVID-19 and the cardiovascular system. Nature Reviews Cardiology 2020.
In article      View Article  PubMed
 
[8]  Kwong JC, Schwartz KL, Campitelli MA, et al. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med 2018; 378(4): 345-53.
In article      View Article  PubMed
 
[9]  Madjid M, Connolly AT, Nabutovsky Y, Safavi-Naeini P, Razavi M, Miller CC. Effect of High Influenza Activity on Risk of Ventricular Arrhythmias Requiring Therapy in Patients With Implantable Cardiac Defibrillators and Cardiac Resynchronization Therapy Defibrillators. Am J Cardiol 2019; 124(1): 44-50.
In article      View Article  PubMed
 
[10]  Kytomaa S, Hegde S, Claggett B, et al. Association of Influenza-like Illness Activity With Hospitalizations for Heart Failure: The Atherosclerosis Risk in Communities Study. JAMA Cardiol 2019; 4(4): 363-69.
In article      View Article  PubMed
 
[11]  Wang YD, Zhang SP, Wei QZ, et al. [COVID-19 complicated with DIC: 2 cases report and literatures review]. Zhonghua Xue Ye Xue Za Zhi 2020; 41(0): E001.
In article      
 
[12]  Chang C-T, Lu Y-H, Chu C-Y, Sheu S-H, Hsu P-C. Two Consecutive Episodes of Acute Myocardial Infarction Occurring in Different Coronary Arteries of a Single Patient with Sepsis. Acta Cardiol Sin 2014; 30(6): 578-81.
In article      
 
[13]  Shibusawa M, Matsumura T, Tsutsumi H, Itou Y, Shibata Y. Unexpected Acute Myocardial Infarction Due to Disseminated Intravascular Coagulation. American Journal of Medical Case Reports 2015; 3(2): 42-45.
In article      View Article
 
[14]  Shi C, Wang C, Wang H, et al. Clinical observations of low molecular weight heparin in relieving inflammation in COVID-19 patients: A retrospective cohort study. medRxiv 2020:2020.03.28. 20046144.
In article      
 
[15]  Thachil J. The versatile heparin in COVID-19. J Thromb Haemost 2020.
In article      View Article
 
[16]  Jing, ZC, Zhu HD, Yan XW et al. Recommendations From The Peking Unioun Medical College Hospital for the Management of Acute Myocardial Infarction During the COVID-19 Outbreak. European Heart Journal.
In article