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Table of Contents
Year : 2020  |  Volume : 21  |  Issue : 4  |  Page : 284-288  

Myopericarditis presenting as acute ST-elevation myocardial infarction with atrioventricular dissociation

1 Department of Internal Medicine, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar
2 Department of Radiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
3 Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar

Date of Submission12-May-2020
Date of Acceptance03-Nov-2020
Date of Web Publication14-Jan-2021

Correspondence Address:
Dr. Fateen Ata
Hamad Medical Corporation, Doha
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Source of Support: None, Conflict of Interest: None


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Myopericarditis, which is an inflammatory process involving the myocardium and pericardium, is not a rare condition encountered in cardiac emergencies. Rarely though, it can give an acute myocardial infarction picture on electrocardiogram (ECG), leading to urgent angiography. More rarely, it can be associated with atrioventricular (AV) dissociation, which is a condition of dyssynchrony of electrical activity between atria and ventricles. We present the case of a young female, who presented with severe chest pain, associated with ST elevation in anterior leads of ECG and raised troponins, necessitating urgent coronary angiography. Normal coronaries led to further evaluation, including cardiac magnetic resonance imaging, which established the diagnosis of myopericarditis. The patient had AV dissociation secondary to myopericarditis. With the treatment of myopericarditis and transvenous pacing, the patient stabilized and was subsequently discharged asymptomatic.

Keywords: Atrioventricular dissociation, myocardial infarction, myopericarditis

How to cite this article:
Ata F, Chaudhry HS, Bilal AB, Lopez Md. Myopericarditis presenting as acute ST-elevation myocardial infarction with atrioventricular dissociation. Heart Views 2020;21:284-8

How to cite this URL:
Ata F, Chaudhry HS, Bilal AB, Lopez Md. Myopericarditis presenting as acute ST-elevation myocardial infarction with atrioventricular dissociation. Heart Views [serial online] 2020 [cited 2023 Mar 22];21:284-8. Available from: https://www.heartviews.org/text.asp?2020/21/4/284/307041

   Introduction Top

Myopericarditis is one of the differential diagnoses of acute coronary syndrome. It becomes more critical as a possibility when a patient presents with a clinical, electrocardiographical, and biochemical picture consistent with acute myocardial infarction but a normal coronary angiography. Our patient presented with a similar initial picture of an acute ST-elevation myocardial infarct. She had normal coronaries. Cardiac magnetic resonance imaging (MRI) established the diagnosis of myopericarditis, with resolution of symptoms via medical treatment. During the hospital stay, the patient had atrioventricular (AV) dissociation evident on electrocardiogram (ECG), possibly secondary to myopericarditis.

   Case Presentation Top

A 22-year-old female with no past medical history was brought to the hospital with a dry cough and progressively severe central chest pain for 2 days. She was also febrile for 1 day. The pain was sharp, pressure like, and radiating to the left shoulder.

ECG revealed sinus tachycardia at 140 beats/min with advanced-degree AV block and ST-segment elevation in the anteroseptal leads [Figure 1]. She was loaded with aspirin and clopidogrel 300 mg each and received sublingual nitroglycerine. The patient became hypotensive (blood pressure: 99/46 mmHg) with the sublingual nitroglycerine and was subsequently started on norepinephrine by the paramedics.
Figure 1: Initial electrocardiogram showing ST elevation in anteroseptal leads and atrioventricular dissociation

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On arrival to the emergency, the cardiac cath lab was activated for primary percutaneous coronary intervention. Troponin had a rising trend [Graph 1] with a high brain natriuretic peptide level [Table 1]. The initial biochemistry panel was within the normal range [Table 1]. Coronary angiogram, which was performed within the 1st h of hospital admission, revealed healthy coronary arteries.

Table 1: Complete blood profile and biochemistry

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Due to her young age with no risk factors, normal coronary angiogram, and chest pain resistant to nitrates, the patient was suspected of having myopericarditis. A transthoracic echocardiogram showed global hypokinesia with apical sparing and mildly reduced ejection fraction (47%).

The patient was transferred to the coronary intensive care unit and was continued on aspirin (600 mg, 3×/day) and clopidogrel (75 mg once daily) with enoxaparin (40 mg twice daily, which was later reduced to once daily) for thromboprophylaxis. The possibility of myocardial infarction with microvascular disease was entertained. Colchicine (0.5 mg once daily) was added as the suspicion of myopericarditis was high.

The patient's chest pain improved significantly in the second postadmission day and was effectively gone by day 3. The noradrenaline was stopped, and she was started on dobutamine. At this point, she was noted to have AV dissociation but was maintaining a heart rate of 70/min. Basic labs showed a significant elevation of her cardiac enzymes [Graph 1].

On day 4, the patient became hypotensive and bradycardic once her dobutamine was tapered down. ECG showed a complete heart block [Figure 2], necessitating a temporary transvenous pacemaker. Repeated laboratory examination showed significantly raised liver enzymes [Table 1] secondary to colchicine, which was proven by marked improvement after discontinuation of the drug.
Figure 2: Third-degree heart block, blue arrows: P-P red arrows: R-R

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After stabilization over the next few days, a cardiac MRI scan was performed, which revealed normal biventricular volumes and function, myocardial edema in the lateral wall, and subepicardial fibrosis involving the basal to the apical lateral wall extending to the anterolateral, inferolateral, and inferior walls. There was also enhancement of the adjacent pericardium. Based on the findings and clinical improvement with treatment, the diagnosis of myopericarditis was confirmed.

On the 5th hospital day, the patient stopped requiring pacing, and the pacemaker was removed. The patient was shifted to the general cardiology ward, from where she was discharged with normal sinus rhythm on ECG [Figure 3].
Figure 3: Discharge electrocardiogram showing normal sinus rhythm

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The patient, on phone follow-up, reported no symptoms (because of the corona pandemic, the HMC outpatient clinic was closed and only emergencies were seen).

   Discussion Top

Myopericarditis is a clinical syndrome in cardiology, which includes pericardial inflammation associated with biochemically proven myocardial injury.[1] The most common cause of this inflammatory entity is attributed to viral infections such as coxsackieviruses, adenoviruses, herpes viruses, echovirus, influenza virus, hepatitis C virus, and parvovirus B19.[2] Other uncommon causes include bacterial infections, including tuberculous pericarditis.[3]

The classic clinical picture is of a patient with pleuritic chest pain, which increases with inspiration, preceded by a febrile illness, associated with diffuse ST-segment elevations and PR-segment depression on ECG and raised troponin. However, there are many variations in which a patient with myopericarditis may present depending on the extent of myocardial and pericardial involvement as well as the predominant involvement of one on the other.[2] It is not very rare, but clinically very important, that sometimes focal myopericarditis can mimic acute ST-elevation myocardial infarction with respect to clinical and biochemical presentation. Although considered highly sensitive, approximately 3% of patients presenting with focal ST elevation have normal coronary vasculature.[4] Some of the essential differentials in such patients include myopericarditis, myocardial infarction due to microvascular stenosis, vasospasm, and Takotsubo cardiomyopathy.[5]

A very high clinical suspicion is necessary in promptly diagnosing myopericarditis. The results of investigations such as ECG, cardiac enzymes, evidence of current or prior viral infection with viral panels and inflammatory markers, echocardiographic findings, and cardiac MRI can aid in making a diagnosis of myopericarditis. Definite diagnosis needs histopathological evidence by endomyocardial biopsy. However, it may be inconclusive in focal involvements. It may be indicated with specific conditions, i.e., previously undiagnosed heart failure, which is either associated with hemodynamic instability, dilated left ventricle, or resistant to traditional heart failure management. Other clues include conduction blocks, including Mobitz type 2 and complete heart block.[6]

An echocardiogram can show evidence of pericardial involvement with features such as pericardial effusion. Still, in most of the cases, it is normal,[7] which in itself is an important finding, as it diminishes the possibility of myocardial infarction.

In most of the cases, diagnosis is expertly made by certain features seen on cardiac MRI scan, which can differentiate myopericarditis from myocardial infarction. These findings include myocardial edema, increased myocardial early gadolinium enhancement (indicating capillary leakage), and late transmural gadolinium enhancement (indicating tissue injury) with normal ventricular volumes and functions.[8]

High-degree AV block caused by conduction defects in myocarditis is rare (1.1%), as illustrated by Ogunbayo et al.[9] Data regarding heart blocks in myopericarditis are limited to a few case reports.[10],[11],[12]

Our case highlights the possibility of AV dissociation secondary to myopericarditis, necessitating the need for a temporary pacemaker. As was seen in our case, high-degree heart blocks can be reversible if the cause is timely diagnosed or empiric management is initiated.

The management of myopericarditis is not well studied. In general, the treatment of myopericarditis consists of nonsteroidal anti-inflammatory agents (NSAIDs), aspirin, and colchicine. The use of NSAIDs should be judicious, as animal studies showed progression of the disease with the use of NSAID doses similar to pericarditis.[13] It is also essential to treat any underlying cause if identified. In addition, until the diagnosis is confirmed, the patients are usually kept on anti-ischemic therapy, given the similarity of presentation to myocardial infarction.

   Conclusions Top

Myopericarditis is a rare but important mimic of acute ST-elevation myocardial infarction. It requires a high level of clinical suspicion with relevant biochemical investigations and imaging studies, particularly MRI, as in our patient. Rarely does it present with AV dissociation as in our patient. More research is required in the rapid diagnostic and treatment modalities of myopericarditis to avoid permanent morbidities.

Statement of consent

Written informed consent was taken from the patient by Fateen Ata, the first author. The consent form was explained to the patient in her language.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name 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


Conflicts of interest

There are no conflicts of interest.

   References Top

Imazio M, Cooper LT. Management of myopericarditis. Expert Rev Cardiovasc Ther 2013;11:193-201.  Back to cited text no. 1
Imazio M, Trinchero R. Myopericarditis: Etiology, management, and prognosis. Int J Cardiol 2008;127:17-26.  Back to cited text no. 2
Syed FF, Ntsekhe M, Gumedze F, Badri M, Mayosi BM, Myopericarditis in tuberculous pericardial effusion: Prevalence, predictors and outcome. Heart 2014;100:135-9.10.1136/heartjnl-2013-304786.  Back to cited text no. 3
Hochman JS, Tamis JE, Thompson TD, Weaver WD, White HD, Van de Werf F, et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes IIb Investigators. N Engl J Med 1999;341:226-32.  Back to cited text no. 4
Da Costa A, Isaaz K, Faure E, Mourot S, Cerisier A, Lamaud M, Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients. Eur Heart J 2001;22:1459-65.10.1053/euhj.2000.2553.  Back to cited text no. 5
Caforio AL, Pankuweit S, Arbustini E, Basso C, Gimeno-Blanes J, Felix SB, et al. European Society of Cardiology Working Group on M, and Pericardial D, Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013;34: 2636-48, 2648a-2648d.10.1093/eurheartj/eht210.  Back to cited text no. 6
Imazio M, Brucato A, Cemin R, Ferrua S, Maggiolini S, Beqaraj F, et al. Investigators I, A randomized trial of colchicine for acute pericarditis. N Engl J Med 2013;369:1522-8.10.1056/NEJMoa1208536.  Back to cited text no. 7
Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT, et al. Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol 2009;53:1475-87.  Back to cited text no. 8
Ogunbayo GO, Elayi SC, Ha LD, Olorunfemi O, Elbadawi A, Saheed D, et al. Outcomes of heart block in myocarditis: A review of 31,760 patients. Heart Lung Circ 2019;28:272-6.  Back to cited text no. 9
Hyttinen L, Kaipiainen-Seppänen O, Halinen M. Recurrent myopericarditis in association with Crohn's disease. J Intern Med 2003;253:386-8.  Back to cited text no. 10
Maeder HU. The complete heart-block-an extraintestinal manifestation of ulcerative colitis. Z Gastroenterol 1996;34:27-9.  Back to cited text no. 11
Ballinger A, Farthing MJ. Ulcerative colitis complicated by Wenckebach atrioventricular block. Gut 1992;33:1427-9.  Back to cited text no. 12
Khatib R, Reyes MP, Smith FE. Enhancement of coxsackievirus B3 replication in Vero cells by indomethacin. J Infect Dis 1990;162:997-8.  Back to cited text no. 13


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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