Creative Commons Open Access Journal No author-side fee 
  • Users Online: 160
  • Print this page
  • Email this page
Submit article

 
Table of Contents
CASE REPORT
Year : 2022  |  Volume : 4  |  Issue : 1  |  Page : 33-36

A case of COVID-19 STEMI complicated by second: Degree heart block without pulmonary involvement


Department of Cardiology, Sabah Al Ahmed Cardiac Centre, Al Amiri Hospital, Kuwait City, Kuwait

Date of Submission01-Aug-2021
Date of Decision20-Oct-2021
Date of Acceptance25-Oct-2021
Date of Web Publication30-Jun-2022

Correspondence Address:
Dr. Ibrahim Mahmoud Ibrahim Elkholy
Department of Cardiology, Sabah Al Ahmed Cardiac Centre, Al Amiri Hospital, Kuwait City 15003
Kuwait
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ACCJ.ACCJ_17_21

Rights and Permissions
  Abstract 


We present a case of a coronavirus disease 2019 (COVID-19) patient who presented with acute myocardial infarction and was treated successfully with primary percutaneous intervention and stent implantation. During the hospital stay, the patient did not develop respiratory manifestations either clinically or radiologically. This report highlights the effect of COVID-19 disease on the cardiovascular system and its effect beyond common respiratory complications.

Keywords: Coronavirus disease 2019, second-degree heart block, STEMI


How to cite this article:
Ibrahim Elkholy IM, Al-Jarallah M, Dashti R. A case of COVID-19 STEMI complicated by second: Degree heart block without pulmonary involvement. Ann Clin Cardiol 2022;4:33-6

How to cite this URL:
Ibrahim Elkholy IM, Al-Jarallah M, Dashti R. A case of COVID-19 STEMI complicated by second: Degree heart block without pulmonary involvement. Ann Clin Cardiol [serial online] 2022 [cited 2022 Sep 29];4:33-6. Available from: http://www.onlineacc.org/text.asp?2022/4/1/33/349335




  Introduction Top


A novel infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2)[1] was detected in Wuhan, China, in December 2019. Patients with coronavirus disease 2019 (COVID-19) often present with pulmonary manifestations as SARS-CoV-2 gains entry to host cells via angiotensin-converting enzyme 2 (ACE2).[2] The virus mainly invades alveolar epithelial cells, resulting in respiratory symptoms. These symptoms are more severe in patients with cardiovascular disease (CVD), which might be associated with increased secretion of ACE2 in these patients compared with healthy individuals.[3],[4] The cardiovascular manifestations of COVID-19 disease have generated considerable concern. Moreover, acute myocardial injury has been seen in patients with COVID-19 and has been associated with worse outcomes.[5],[6]


  Case Report Top


A 47-year-old male patient presented to the emergency department with substernal chest pain for the past 5 days, with increased intensity 1 h before presentation. The patient reported fatigue and intense body ache for 7 days. His past medical history was notable for type two diabetes mellitus, which was controlled with gliclazide-modified release. The patient was not aware of any other cardiovascular risk factors. His vital signs upon admission showed a blood pressure of 120/70 mmHg, pulse rate of 55 beats/minute, temperature of 37.2°C, respiration of 20 breaths/minute, and peripheral capillary oxygen saturation of 99% on 2 L oxygen. His physical examination was unremarkable.

Electrocardiography (ECG) was performed on arrival, which revealed ST segment elevation, pathological Q waves in inferior leads, and reciprocal changes in leads 1, AVL, and V1-V4 consistent with inferior infarction associated with a 2:1 narrow complex heart block [Figure 1]. Labs were significant for white blood count of 11.9 cells/mcl, lymphocytes 17%, elevated cardiac enzymes, Troponin I of 23.7 ng/ml, CK 384 u/l, alanine aminotransferase of 80 u/l, aspartate aminotransferase 70 u/l, and elevated inflammatory markers (C-reactive protein 91.4 MG/DL, erythrocyte sedimentation rate 42 mm/h).
Figure 1: Electrogardiogram showing ST-segment elevation in inferior leads and ST segment depression in anterolateral leads with 2:1 heart block

Click here to view


The patient received aspirin, clopidogrel, and heparin and was then taken to the catheterization laboratory for primary percutaneous intervention. Coronary angiography was performed, which showed extensive thrombotic occlusion of the right coronary artery (RCA) from the proximal segment, with thrombolysis in myocardial infarction (TIMI) 0 flow distally. The left anterior descending coronary artery was diffusely diseased, and the left circumflex coronary artery showed atherosclerotic changes with multiple borderline stenoses. The heart team was activated, and the decision to treat the culprit lesion was made. After discussion with the patient, the RCA obstruction was recanalized with balloon angioplasty followed by thrombus aspiration and deployment of one drug-eluting stent. The stents were postdilated using a noncompliant balloon, with the achievement of good final angiographic results (TIMI 3 flow) [Figure 2],[Figure 3],[Figure 4].
Figure 2: Coronary angiogram showing thrombotic total occlusion of the right coronary artery from its proximal segment

Click here to view
Figure 3: Cornary angiogram showing diffusely diseased left anterior descending coronary artey and multiple border line left circumflex stenosis

Click here to view
Figure 4: Coronary angiogram showing the right coronary artery after recanalization and stent implantation

Click here to view


After intervention, the patient was transferred to the coronary care unit and continued to improve without reporting chest pain, and the ECG showed significant resolution of the ST-segment elevation, along with the resolution of the second degree heart block [Figure 5]. Echocardiography was obtained and showed impaired ejection fraction of 30%–35%, an akinetic apex, and hypokinesia of the inferoseptal and inferior walls. Later, at night, the patient developed a fever of 38.5° and was confirmed to be COVID-19 positive by the reverse transcription polymerase chain reaction assay (RT-PCR) through nasopharyngeal swab and was therefore transferred to a COVID-19-designated unit. However, the patient did not report any respiratory symptoms, and he maintained oxygen saturation on 2 L of oxygen. Chest X-ray and high-resolution computed tomography were requested, which showed mild bilateral pleural effusion without classic pulmonary findings for COVID-19 [Figure 6].
Figure 5: Electrocardiogram showing ST segment and heart block resolution after right cornary artery recanalization

Click here to view
Figure 6: Chest X-ray and high-resolution computed tomography of the lungs showing bilateral minimal pleural effusion

Click here to view


After 3 days, the fever subsided while receiving paracetamol; moreover, the patient remained stable without showing any respiratory symptoms, as oxygen saturation was maintained on ambient air. Chest X-ray was repeated at day 6 and day 14 and showed no evidence of air space opacification or consolidation, which was consistent with the clinical findings. The patient medications during hospitalization were aspirin, clopidogrel, angiotensin-converting enzyme inhibitor, omeprazole, nitrates, glycalazide-modified release, short-acting insulin, Vitamin C, zinc, and low dose selective beta blocker, which were initiated after the resolution of the heart block and careful observation. Later during the hospital course, guideline-directed medical therapy was titrated to the maximum tolerated dose. The hospital stay was unremarkable, as the patient stayed asymptomatic during the cardiac rehabilitation period and was discharged home after two negative RT-PCR results, with a total of 15 days of hospitalization.


  Discussion Top


Our case is important because it highlights the cardiac implications of COVID-19 disease and emphasizes that health-care workers should be alert to the cardiovascular manifestations to diagnose them early and treat them in a timely manner. As a general rule, initial therapy for acute MI is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or interventional means. Rapid reperfusion holds special importance in COVID-19 STEMI due to the loss of the protective ability of ACE 2 to improve responses to injury and limit infarct expansion.

The prevalence of CVDs in COVID-19 patients is unclear, but preexisting CVD may be associated with a more severe COVID-19 infection.[5],[6],[7],[8] The definite mechanism of cardiac injury caused by COVID-19 disease is unknown, and no study has described the incidence of ST-segment elevation myocardial infarction in COVID-19 disease; however, there are several hypotheses explaining the underlying pathogenies.

First, entry of SARS-CoV-2 into cells is facilitated by the interaction between viral S-protein and extracellular domains of the transmembrane ACE2 proteins, followed by subsequent downregulation of surface ACE2 expression.[9],[10],[11],[12] Impaired ACE2 activity in the heart leads to reduced production of Ang1-7, a bioactive metabolite of angiotensin II by ACE2. Ang1-7 binding to its receptor, Mas1R, initiates biological responses to counteract angiotensin II-mediated processes such as apoptosis, angiogenesis, vasoconstriction, and inflammation.[12],[13],[14],[15],[16] Second, ACE2 is highly expressed in pericytes, which act as the target cardiac cell of SARS-CoV-2. Pericyte injury due to virus infection may result in capillary endothelial cell dysfunction, inducing microvascular dysfunction. Furthermore, these patients may be at a higher risk of heart attack.[17] Moreover, plaque rupture and coronary thrombosis due to systemic inflammation can precipitate acute myocardial infarction in patients with COVID-19 disease.[17]

The impact of COVID-19 on STEMI outcomes is not known and remains to be determined. However, several experimental studies demonstrated that in ACE2-deficient hearts (mechanistically reflecting the effect of COVID-19 disease), myocardial infarction leads to enhanced activation of the renin-angiotensin system, resulting in increased mortality. This is driven in part by increased free LV wall rupture and adverse ventricular remodelling characterized by infarct expansion, greater ventricular dilation, and reduced systolic performance. Moreover, these studies attributed the changes to increased angiotensin II levels in the setting of reduced Ang1-7 levels, enhanced activation of NADPH oxidase, increased matrix metalloproteinase activities, and myocardial inflammation. Furthermore, they confirmed the ability of Angiotensin II to mediate adverse ventricular remodelling in ACE2-deficient hearts, which is likely facilitated by reduced Ang1-7 levels because Ang1-7 is a physiological antagonist of angiotensin II signalling and has been shown to mediate important cardio-protective effects.[12],[13],[14],[15]


  Conclusions Top


Patients with COVID-19 and risk factors are at an increased risk of adverse cardiac events. Patients with COVID-19 may present with ST-segment elevation myocardial infarction without pulmonary involvement, and primary coronary angiography should be considered per the guidelines. Rapid reperfusion holds special importance in COVID-19 STEMI due to the loss of the protective ability of ACE 2 to improve responses to injury and limit infarct expansion.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Coronaviridae Study Group of the International Committee on Taxonomy of Viruses. The species severe acute respiratory syndrome-related coronavirus: Classifying 2019-nCoV and naming it SARS-CoV-2. Nat Microbiol 2020;5:536-44.  Back to cited text no. 1
    
2.
Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: Molecular mechanisms and potential therapeutic target. Intensive Care Med 2020;46:586-90.  Back to cited text no. 2
    
3.
Xiong TY, Redwood S, Prendergast B, Chen M. Coronaviruses and the cardiovascular system: Acute and long-term implications. Eur Heart J 2020;41:1798-800.  Back to cited text no. 3
    
4.
Li B, Yang J, Zhao F, Zhi L, Wang X, Liu L, et al. Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China. Clin Res Cardiol 2020;109:531-8.  Back to cited text no. 4
    
5.
Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G, et al. Cardiovascular considerations for patients, health care workers, and health systems during the COVID-19 pandemic. J Am Coll Cardiol 2020;75:2352-71.  Back to cited text no. 5
    
6.
Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med 2020;46:846-8.  Back to cited text no. 6
    
7.
Murthy S, Gomersall CD, Fowler RA. Care for critically ill patients with COVID-19. JAMA 2020;323:1499-500.  Back to cited text no. 7
    
8.
Li W, Moore MJ, Vasilieva N, Sui J, Wong SK, Berne MA, et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 2003;426:450-4.  Back to cited text no. 8
    
9.
Wang K, Gheblawi M, Oudit GY. Angiotensin converting enzyme 2: A double-edged sword. Circulation 2020;142:426-8.  Back to cited text no. 9
    
10.
Walls AC, Park YJ, Tortorici MA, Wall A, McGuire AT, Veesler D. Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein. Cell 2020;181:281-92.e6.  Back to cited text no. 10
    
11.
Yan R, Zhang Y, Li Y, Xia L, Guo Y, Zhou Q. Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2. Science 2020;367:1444-8.  Back to cited text no. 11
    
12.
Crackower MA, Sarao R, Oudit GY, Yagil C, Kozieradzki I, Scanga SE, et al. Angiotensin-converting enzyme 2 is an essential regulator of heart function. Nature 2002;417:822-8.  Back to cited text no. 12
    
13.
Kassiri Z, Zhong J, Guo D, Basu R, Wang X, Liu PP, et al. Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction. Circ Heart Fail 2009;2:446-55.  Back to cited text no. 13
    
14.
Kim MA, Yang D, Kida K, Molotkova N, Yeo SJ, Varki N, et al. Effects of ACE2 inhibition in the post-myocardial infarction heart. J Card Fail 2010;16:777-85.  Back to cited text no. 14
    
15.
Der Sarkissian S, Grobe JL, Yuan L, Narielwala DR, Walter GA, Katovich MJ, et al. Cardiac overexpression of angiotensin converting enzyme 2 protects the heart from ischemia-induced pathophysiology. Hypertension 2008;51:712-8.  Back to cited text no. 15
    
16.
Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res 2020;116:1097-100.  Back to cited text no. 16
    
17.
Welt FG, Shah PB, Aronow HD, Bortnick AE, Henry TD, Sherwood MW, et al. Catheterization laboratory considerations during the coronavirus (COVID-19) pandemic: From the ACC's interventional council and SCAI. J Am Coll Cardiol 2020;75:2372-5.  Back to cited text no. 17
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Case Report
Discussion
Conclusions
References
Article Figures

 Article Access Statistics
    Viewed269    
    Printed16    
    Emailed0    
    PDF Downloaded45    
    Comments [Add]    

Recommend this journal