Influenza myocarditis complicated with atrioventricular block in a pregnant woman

Chee Yik Chang; Joshua Bui Khiong Chung; David Perera

doi:10.4103/njc.njc_2_20

CASE REPORT

Year : 2020 | Volume : 17 | Issue : 1 | Page : 79-81

Influenza myocarditis complicated with atrioventricular block in a pregnant woman

Chee Yik Chang¹, Joshua Bui Khiong Chung¹, David Perera²
¹ Department of Medical, Sarawak General Hospital, Ministry of Health, Kuching, Malaysia
² Institute of Health and Community Medicine, University Malaysia Sarawak, Sarawak, Malaysia

Date of Submission	11-Jan-2020
Date of Acceptance	18-Mar-2020
Date of Web Publication	30-Jun-2020

Correspondence Address:
Dr. Chee Yik Chang
Department of Medical, Sarawak General Hospital, Ministry of Health, Kuching
Malaysia

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/njc.njc_2_20

Abstract

Acute myocarditis is a well-recognized complication of influenza infection. The incidence of myocardial involvement in influenza infection is variable, and the clinical severity can range from asymptomatic to fulminant forms. Influenza infection can rarely be complicated by acute myocarditis leading to high-degree atrioventricular block and cardiogenic shock. We report a previously healthy pregnant woman, who initially presented with symptoms of influenza-like illness, later confirmed as influenza A infection. She developed hypotension shortly after admission that did not respond to fluid bolus and required inotropic support. On day 5, the electrocardiogram showed Mobitz I second-degree heart block, which later progressed to the third-degree heart block. Echocardiogram showed good cardiac contractility and minimal pericardial effusion while cardiac biomarkers were normal. A diagnosis of influenza myocarditis was made. She completed a course of oral oseltamivir and had temporary cardiac pacing performed, and subsequently recovered well.

Keywords: Heart block, influenza, myocarditis, pregnant

How to cite this article:
Chang CY, Khiong Chung JB, Perera D. Influenza myocarditis complicated with atrioventricular block in a pregnant woman. Nig J Cardiol 2020;17:79-81

How to cite this URL:
Chang CY, Khiong Chung JB, Perera D. Influenza myocarditis complicated with atrioventricular block in a pregnant woman. Nig J Cardiol [serial online] 2020 [cited 2023 Jun 8];17:79-81. Available from: https://www.nigjcardiol.org/text.asp?2020/17/1/79/288643

Introduction

Myocarditis is defined as an inflammatory disease of the heart muscle and can potentially lead to acute heart failure, dilated cardiomyopathy, and sudden death. Viruses are the most frequent cause of myocarditis, which could induce an immune response causing inflammation even when the pathogen has been cleared.^[1] Other etiologies of myocarditis include bacterial and protozoal infections, toxins, drug reactions, autoimmune diseases, giant cell myocarditis, and sarcoidosis.^[1],[2]

Acute myocarditis is a well-known complication of influenza infection, occurring with a prevalence rate of up to 10%.^[3],[4] The disease spectrum varies from asymptomatic to fulminant myocarditis, which can result in severe hemodynamic dysfunction, requiring high-dose vasopressors and mechanical circulatory support.^[5]

We present a case of a pregnant woman with myocarditis due to confirmed influenza A infection complicated with complete heart block which required temporary cardiac pacing, and recovered well after that.

Case Report

A 32-year-old female, gravida 2 para 1, at 29 weeks' pregnancy presented to Sarawak General Hospital, Sarawak, Malaysian Borneo, with a 2-day history of fever associated with cough, rhinorrhea, and sore throat. She reported no chest pain or any symptoms of heart failure. There was no recent history of traveling before this febrile illness. One week before that her 10-year-old son also had similar symptoms but had subsequently recovered.

Upon arrival at the hospital, she was alert and not toxic looking. Physical examination revealed a blood pressure of 110/70 mmHg, pulse rate of 100 beats/minute, and temperature of 37.9°C. She was mildly tachypniec with respiratory rate of 20 breaths/minute and oxygen saturation on room air as measured by the pulse oximetry was 100%. The peripheral perfusion was good. Examination of the cardiovascular and respiratory system was normal. Her throat was injected with mild tonsillar enlargement. The remainder of systemic examination was otherwise unremarkable. Bedside echocardiogram was normal, and antenatal scan showed a healthy, developing fetus.

Hematological analysis showed hemoglobin of 11.1 g/dL, white blood cell count of 10.1 × 10³/μL (lymphocyte = 0.6 × 10³/μL; monocyte = 0.9 × 10³/μL; and lymphocyte: monocyte ratio = 0.67), and platelet count of 256 × 10³/μL. The renal and liver function tests were within the normal range. The blood gas analysis revealed good arterial oxygenation without metabolic disturbance. The chest radiograph and electrocardiogram on admission were normal. The patient was immediately isolated in view of suspected influenza-like illness, and started on oral oseltamivir 75 mg every 12 h after the sampling of nasopharyngeal swab for influenza polymerase chain reaction (PCR).

In the ward, she developed hypotension associated with a drop of blood pressure to 80/50 mmHg. She was resuscitated with three pints of crystalloid and subsequently started on intravenous noradrenaline infusion at a rate of 0.1 mcg/kg/min in view of persistent hypotension. Intravenous ceftriaxone 2 g once-daily and oral azithromycin 500 mg once-daily were also added to treat for possible superimposed bacterial pneumonia. Over the next few days, she had worsening hypotension that failed to respond to fluid challenge, and gradually required higher dosage of noradrenaline infusion up to 0.4 mcg/kg/min. There was no desaturation episode throughout the hospital admission. The serum lactate was never increased.

The nasopharyngeal swab for influenza PCR was positive for influenza A, and so oral oseltamivir was continued for 5 days. Her symptoms improved with treatment but she was unable to wean off the inotrope. On day 5 of hospitalization, she complained of dizziness during a few episodes of bradycardia (heart rate: 50–60 beats/min). Continuous intravenous infusion of milrinone was started and maintained at 0.5 mcg/kg/min. An electrocardiogram showed Mobitz I second-degree heart block [Figure 1]. A diagnosis of myocarditis due to influenza A was made. She was admitted to the intensive care unit for close monitoring. An urgent echocardiogram revealed a normal left ventricular contractility (ejection fraction ≥55%) with no regional wall motion or valvular abnormality, and the presence of minimal pericardial effusion. The cardiac biomarkers were not increased as the creatine kinase (CK) and CK-MB levels were 56 and 7 U/L, respectively.

Figure 1: Electrocardiogram shows Mobitz I second-degree atrioventricular block

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Over the next few hours, the cardiac rhythm progressed to the third-degree (complete) heart block [Figure 2]. However, she reported no giddiness, palpitation, and chest pain, while her blood pressure remained stable on inotropes. The cardiology team was consulted and temporary transvenous cardiac pacing was done for this patient. During monitoring in the coronary care unit, she did not have any recurrence of heart block, hence pacing was stopped. She was able to taper off inotrope and made a full recovery.

Figure 2: Electrocardiogram shows third-degree atrioventricular block

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Discussion

Influenza is a potentially life-threatening respiratory illness which accounts for 3–5 million cases of severe illness and up to 300,000 deaths annually. Myocarditis is a rare complication of influenza infection which can result in significant impairment of cardiac function and associated with a high mortality. The frequency of myocardial involvement in influenza infection is variable with a reported rate of up to 10%, although this was dependent on the methods used to detect myocardial involvement.^[4]

Till date, there were limited studies done on human myocardial tissue in delineating the pathophysiology of viral myocarditis. Viral myocarditis has been studied in many experimental models, and it is known that the inflammatory reaction in viral myocarditis is due to the direct injury caused by the virus or the antiviral immune response and is related to the genetic susceptibility of the host.^[6] In myocarditis of viral etiology, the virus has been demonstrated to replicate in the heart and results in focal infiltration of inflammatory cells, usually mononuclear cells, accompanied by interstitial edema, and cardiac necrosis. In some cases, inflammation may also occur concomitantly in the pericardium.^[7]

Common cardiac symptoms of myocarditis include dyspnea, chest discomfort, hypotension, peripheral edema, and syncope.^[5] Echocardiography is an important diagnostic tool for myocardial dysfunction and is useful in excluding other causes of heart failure and identifying the fulminant course of the disease. Typical findings of myocarditis include global hypokinesia, with or without pericardial effusion, variable degree of myocardial dilation, and heart valve regurgitation.^[8]

In this present case, our patient presented initially with symptoms suggestive of influenza-like illness which was later confirmed to be influenza A infection. She then developed hypotension, necessitating up-titration of an inotropic agent. Myocarditis was diagnosed clinically on the basis of atrioventricular block causing cardiogenic shock and the presence of pericardial effusion. Endomyocardial biopsy is considered a gold standard for the diagnosis of myocarditis.^[9],[10] In this instance, the patient had a laboratory-confirmed result for influenza A infection, which was potentially associated with subsequent episode of myocarditis as observed after the hospital admission. The patient responded well to antiviral therapy and supportive intervention (temporary cardiac pacing), and therefore, endomyocardial biopsy was deemed unnecessary.

Atrioventricular block in acute myocarditis has been previously reported and described as transient and required the placement of a temporary pacemaker.^{[11],[12],[13]} High-grade atrioventricular block corresponds to greater myocardial injury, and severity of pathological changes may reflect the reversibility of atrioventricular block. In most cases, the cardiac rhythm abnormality is only transient whereby the implantation permanent pacemaker placement is not required.^[12]

Conclusion

Fulminant myocarditis associated with influenza virus infection may present in the form of atrioventricular block and cardiogenic shock, which were responsible for substantial morbidity and mortality. In view of the increasing incidence of influenza cases worldwide, clinicians should be more alert of this rare but potentially fatal complication since prompt diagnosis and supportive measures are essential for better clinical outcomes.

Acknowledgments

We would like to thank the Director General of Health Malaysia for his permission to publish this article. The authors thank the staff of Sarawak General Hospital involved in the management of this patient.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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