International Journal of Case Reports and Images - IJCRI - Case Reports, Case Series, Case in Images, Clinical Images

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Case Report
 
Coxsackie myocarditis and temporary pacing: A case report
Moushumi Lodh1, Ashok Kumar Parida2, Joy Sanyal3, Arunangshu Ganguly4
1Senior Consultant and Head, Department of Biochemistry, The Mission Hospital, Durgapur, West Bengal, India.
2Head, Department of Cardiology, The Mission Hospital, Durgapur, West Bengal, India.
3Consultant, Department of Cardiology, The Mission Hospital, Durgapur, West Bengal, India.
4Senior Consultant Cardiologist and V.C, Mission Hospital, Durgapur, West Bengal, India.

doi:10.5348/ijcri-2012-05-125-CR-10

Address correspondence to:
Dr Moushumi Lodh,
Senior Consultant and Head of Biochemistry, The Mission Hospital
Immon Kalyan Sarani, Sector 2C
Bidhannagar, Durgapur, West Bengal
India - 713212
Phone: +91-9800881640
Fax: 0343-2532550
Email: drmoushumilodh@gmail.com

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How to cite this article:
Lodh M, Parida AK, Sanyal J, Ganguly A. Coxsackie myocarditis and temporary pacing: A case report. International Journal of Case Reports and Images 2012;3(5):45–49.


Abstract
Introduction: We report here a case of complete heart block from coxsackie myocarditis in a 15- year-old, treated by temporary pacing.
Case Report: The patient presented with history of fever five days prior to admission. This lasted for three days, followed by history of chest pain and fatiguability. ECG on admission revealed complete heart block, wide QRS escape. Blood examination revealed IgG antibody to Coxsackie virus. The patient was put on backup temporary pacing. Spontaneous recovery was seen with reversion to sinus rhythm.
Conclusion: Viral myocarditis with complete heart block can be treated conservatively and observed for recovery of conduction abnormality as in our case.

Key Words: Complete heart block, Myocarditis, Coxsackie virus, Temporary pacing


Introduction

Coxsackie B is a frequent cause of viral myocarditis. Most of them are benign and self limited. They can be virulent in children. With loss of cardiac cells increasing progressively, infected individual experience abnormalities in left ventricular systolic and diastolic function as well as electrical conduction defects manifesting as cardiac dysarrythmias. As a result, ejection fraction decreases substantially. Complete heart block may occur and can present after several years with dilated cardiomyopathy. We present the case of a young female with Coxsackie virus infection, who developed complete heart block. Quick diagnosis and conservative management with temporary pacing prevented any possible complications in later life.


Case Report

A 15-year-old, normotensive, non-diabetic, female child presented with febrile episode five days prior to admission. She developed chest pain and fatiguability, followed by one episode of convulsion in the morning on the day of admission. ECG (on admission) showed complete heart block and she was shifted to our tertiary care hospital for evaluation and management.

On examination, patient was conscious, heart rate was 36/min and blood pressure was 100/70 mm Hg. Chest examination revealed bilateral normal vesicular breath sound. Cardiovascular examination revealed S1+, S2+ S30, no murmur. Electrocardiogram (ECG) revealed complete heart block, wide QRS complex. Echocardiography (ECHO) revealed minimal dilatation of left ventricle with global hypokinesia, left ventricular ejection fraction (LVEF) was 40% and mild mitral regurgitation was present.


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Figure 1: ECG of patient at presentation showing complete heart block.


The patient on admission had complete heart block and was put on backup temporary pacing. Laboratory test results were as follows: WBC 15600/mm3 (4000–7000/mm3), troponin I 25 µg/L (<0.01 mm3), CPK-MB 92.5 ng/ml (<5 mm3), AST 1289 IU/L (0–35 IU/L), ALT 796 IU/L (0–35 IU/L), lactate dehydrogenase 1509 U/L (400–800 U/L), CRP 10.76 mg/L (<5 Mg/L). Serological studies for HIV, HBV, HCV, Dengue, malaria, echinococcus, Leptospira, adenovirus were negative. IgG antibody to Coxsackie virus was positive. The patient remained in complete heart block for 10 days. As per the temporal profile of the patient, myocarditis leading to complete heart block was considered as the diagnosis. She was treated with cefoperazone and sulbactam (1.5 gm) IV twice a day and amikacin 500 mg IV twice a day for 10 days. After the first week, the patient progressed to 2:1 AV block followed by Wenkebach rhythm and then reverted to sinus rhythm. On discharge, patient was in sinus rhythm. ECHO doppler studies revealed ejection fraction 40%, mild mitral regurgitation and global hypokinesia. Her functional class was NYHA II. At discharge, she was prescribed diuretics (furosemide 20 mg twice a day and spironolactone 25 mg once a day for three months). At three months follow up, patient was asymptomatic, had residual right bundle branch block (RBBB) on ECG and LVEF of 60 %.


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Figure 2: Complete paced beat.



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Figure 3: Normal sinus rhythm at discharge.



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Table 1: Hematological investigations of the patient from admission to discharge.



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Table 2: Biochemical test results of the patient from admission to discharge.




Discussion

Persistent complete AV heart block is rarely seen in young people, and when it does occur it is almost always congenital. Cardiac irregularities, with varying degrees of defective conduction between atria and ventricles are not uncommon during the course of diphtheria, acute rheumatic fever and occasionally other infections. If complete heart block develops, however, the usual outcome is either recovery, with restoration of normal rhythm, or death. Towers and Bremer in 1947 provided a review of complete heart block in young people.[1]

The six serotypes of the group B coxsackie viruses (CVB) are common human enteroviruses linked etiologically to inflammatory cardiomyopathies. This has been demonstrated by molecular detection of enteroviral RNA in human heart tissue, serologic associations with disease and virus isolation from cases of fulminant myocarditis. Human CVB3 isolates demonstrate varying degrees of cardiovirulence in the murine model; one site of virulence determination has been mapped to domain II of the 5 non-translated region. The interplay of CVB replication and the immune response to that replication in the heart is a complex interaction determining the extent to which the virus replication is limited and the degree to which a pathogenic inflammation of cardiac muscle occurs. While CVB are associated with 20–25% of cases of myocarditis or cardiomyopathy, the severity of the disease and the existence of attenuated strains shown to generate protective immunity in animal models indicates that vaccination against the CVBs would be valuable. [2]

It has also been shown that the initial antibody response to group B coxsackie viruses infections consists of the production of IgM antibody, which is gradually replaced in four to six weeks by IgG. [3] It has been speculated that pericarditis, myocarditis or pleurodynia may occur relatively late in the course of coxsackieviruses infections, at a time when antibody levels are already elevated and virus is no longer being shed or is combined with antibody. [4]

Insertion of a pacemaker in children and adolescents who are severely ill with myocarditis is a difficult and potentially life threatening procedure. The damaged myocardium may be irritable, and tacchyarhythmias may be provoked. [5] In one study, Vietnamese children and adolescents with diphtheritic myocarditis and severe conduction abnormalities were treated prospectively with temporary insertion of a cardiac pacemaker. Five of 32 patients died before the procedure could be performed; the remaining 27 patients underwent successful pacemaker insertion. [6]

A clinical diagnosis of myocarditis mimicking myocardial infarction required ECG signs (ST-segment elevation followed by T-wave inversion) and a simultaneous detection of serum markers of acute myocardial injury (CK-MB and/or troponin T) in an infectious patient with chest pain. This form of myocarditis was diagnosed in 98 men, the incidence being 0.17 (95% CI 0.14–0.21, 1000 man-years). [1] Causative microbes were those commonly infecting the conscripts, but coxsackievirus etiology could be confirmed in only 4% of the cases. Nine patients presented with dilated cardiomyopathy of recent origin (incidence 0.02/1000 man-years). None had histopathological evidence of myocarditis. Myocarditis caused one of the 10 sudden unexpected deaths. [7]


Conclusion

In countries where resources are limited, it is important to identify patients who are most likely to benefit from use of a pacemaker and ensure that those for whom there is no hope of survival are not subjected to this procedure. In this study, the adolescent survived after a cardiac pacemaker was temporarily inserted for the treatment of severe conduction disturbances in association with coxsackie myocarditis. Complete heart block should no longer always be considered fatal in patients who have viral myocarditis – temporary insertion of a cardiac pacemaker may improve the outcome.


References
  1. Towers JR H, Bremer C. Complete heart block in young people. British Medical Journal 1947 Dec;6:906-8.   [CrossRef]   [Pubmed]    Back to citation no. 1
  2. Kim KS, Hufnagel G, Chapman NM, Tracy S. The group B Coxsackieviruses and myocarditis. Reviews in Medical Virology 2001;11:355–68.   [CrossRef]   [Pubmed]    Back to citation no. 2
  3. Schmidt NJ, Lennette EH, Dennis J. Characterization of antibodies produced in natural and experimental coxsackievirus infections. J Immunol 1968;100:99–106.   [Pubmed]    Back to citation no. 3
  4. Schmidt NJ, Magoffin RL, Lennette EH. Association of group B coxsackie viruses with cases of pericarditis, myocarditis, or pleurodynia by demonstration of immunoglobulin M antibody. Infect Immun 1973 Sep;8(3):341–8.   [Pubmed]    Back to citation no. 4
  5. Bethell DB, Nguyen Minh Dung, Ha Thi Loan, et al. Prognostic value of electrocardio-graphic monitoring in severe diphtheria. Clin Infect Dis 1995;20:1259–65.   [CrossRef]   [Pubmed]    Back to citation no. 5
  6. Dung NM, Kneen R, Kiem N, et al. Treatment of Severe Diphtheritic Myocarditis by Temporary Insertion of a Cardiac Pacemaker. Clinical Infectious Diseases 2002;35:1425–9.   [CrossRef]   [Pubmed]    Back to citation no. 6
  7. Karjalainen J, Heikkila J. Incidence of three presentations of acute Myocarditis in young men in military service:A 20-year experience. European Heart Journal 1999;20:1120–5.   [CrossRef]   [Pubmed]    Back to citation no. 7
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Author Contributions:
Moushumi Lodh - Substantial contributions to conception and design, Acquisition of data, Drafting the article, Final approval of the version to be published
Ashok Kumar Parida - Substantial contributions to conception and design, Revising it critically for important intellectual content, Final approval of the version to be published
Joy Sanyal - Substantial contributions to conception and design, acquisition of data, Revising it critically for important intellectual content, Final approval of the version to be published
Arunangshu Ganguly - Substantial contributions to conception and design, Acquisition of data, Drafting the article, Final approval of the version to be published
Guarantor of submission:
The corresponding author is the guarantor of submission.
Source of support:
None
Conflict of interest:
Authors declare no conflict of interest.
Copyright:
© Moushumi Lodh et al. 2012; This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any means provided the original authors and original publisher are properly credited. (Please see Copyright Policy for more information.)



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