International Journal of Cardiology 121 (2007) e7 – e8 www.elsevier.com/locate/ijcard
Letter to the Editor
Acute myocarditis due to Chikungunya virus assessed by contrast-enhanced MRI Mariana Mirabel a , Olivier Vignaux b , Pierre Lebon c , Paul Legmann b , Simon Weber a , Christophe Meune a,⁎ a
Department of Cardiology, Cochin Hospital, Paris V René Descartes University, Paris, France Department of Radiology A, Cochin Hospital, Paris V René Descartes University, Paris, France Department of Virology, Saint-Vincent de Paul Hospital, Paris V René Descartes University, Paris, France b
c
Received 8 February 2007; accepted 25 April 2007 Available online 13 August 2007
Keywords: Myocarditis; Magnetic resonance imaging; Chikungunya
Myocarditis is defined as an inflammatory infiltrate of the myocardium with necrosis and/or degenerative changes but with no typical sign of infarction [1]. Among the various mechanisms reported, viral origin seems the most common [2]. Chikungunya, a Togaviridae virus vectored by mosquito, is one of the emerging arboviral diseases. Actually considered a major health problem in the Indian Ocean, it has affected more than 200,000 people since 2005 and was responsible of 73 deaths in Reunion Island [3]. Human infection is considered as benign in most cases; it associates fever, arthralgia, myalgia, oedema and maculopapular rash. However, it may be lethal in case of encephalitis and sudden death have been reported. We report a case of established acute myocarditis following Chikugunya infection. M. K., a previously healthy 19 years old man, was admitted to the ICU for fever, myalgia and chest pain. Chikungunya infection was diagnosed on the basis of clinical features several weeks ago while living in Reunion Island. He presented to the Emergency department 4 days after the onset of symptoms which appeared less than 1 week after his arrival to Europe. At clinical examination temperature was of 38.2 °C, heart sounds were found normal besides some premature beats. ECG was abnormal showing diffuse ST changes. Serum tropinin Ic and NT-pro Brain ⁎ Corresponding author. 27 rue du Fg St-Jacques, 75014 Paris, France. Tel.: +33 1 58 41 22 80; fax: +33 1 58 41 16 05. E-mail address:
[email protected] (C. Meune). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.04.153
Natriuretic Peptide were markedly increased (11.4 ng/ml and 618 pg/ml respectively). Inflammation was assessed by leucocytosis (10,800/mm3) and high levels of C-reactive protein (24 mg/l). At admission to ICU, he presented frequent ventricular premature beats. Echocardiography showed isolated moderate apical hypokinesis; global left ventricular ejection fraction was preserved. Myocarditis was confirmed by contrast-enhanced Magnetic Resonance Imaging (ceMRI) which exhibited multiple supepicardial and midwall intramyocardial foci with increased signal intensities on both early and delayed gadolinium-DOTA-enhanced images, which did not correspond to any particular epicardial coronary artery distribution (Fig. 1). This specific feature of enhancement was highly suggestive of acute myocarditis [4]. Antibodies towards Chikungunya appeared to be positive at 1/512 (determination by neutralization of the cytopathogenic effect of fibroblastic cells in the presence of 100 infectious doses 50/ml. Microbial strain isolated from cerebrospinal fluid of an infected patient). Other possible viral origins, including HIV, hepatitis, enterovirus, parvovirus and dengue were ruled out; non-infectious origins were also ruled out after careful investigations. Patient was discharged on Day 3 on acebutolol 200 mg and ramipril 2.5 mg daily. Follow-up was uneventful at 12 months, premature beats disappeared. Besides the suspected origin of infection, our observation is singular because of the unusual ceMRI pattern. Usual
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observation, abnormalities were widespread, including septal involvement. This observation lacks of direct evidence of infected myocardium by Chikungunya. However, we did not find any other cause after careful evaluation and considered unethical to perform myocardial biopsies in this patient with already proven myocarditis [4]. Our observation may have meaningful clinical implications. Clinicians should be aware of a possible myocardial involvement in Chikungunya infection, and patients should be referred for cardiac evaluation while having symptoms possibly suggestive of such a complication. This is particularly relevant since myocarditis may have lethal complication, and few sudden death have been reported in patients presenting with Chikungunya infection, but without any sign of neurological infection. In the actual worldwide resurgence of arboviral infections new clinical patterns may appear [3]. Attention should be paid to this potential lethal complication in the outbreak of viral diseases. References [1] Aretz HT, Billingham ME, Edwards WE, et al. Myocarditis: a histopathologic definition and classification. Am J Cardiol Pathol 1985;1:1–10. [2] Kawai C. From myocarditis to cardiomyopathy: mechanisms of inflammation and cell death. Learning from the past to the future. Circulation 1999;99:1091–100. [3] Gubler DJ. The global emergence /resurgence of arboviral diseases as public ealth problems. Arch Med Res 2002;33:330–42. [4] Mahroldt H, Goedecke C, Wagner A, et al. Cardiovascular magnetic resonance assessment of human myocarditis. A comparison to histology and molecular pathology. Circulation 2004;109:1250–8. [5] Laissy JP, Messin B, Varenne O, et al. MRI of acute myocarditis: a comprehensive approach based on various imaging sequences. Chest 2002;122:1638–48.
Fig. 1. CeMRI, short-axis inversion prepared gadolinium-enhancement gradient echo sequence (A) early phase 2 min after gadolinium injection showing mid-wall septal and subepicardial inferior increased signal intensities (arrows). (B) delayed phase 10 min after gadolinium injection showing less obvious increased signal intensities probably reflecting myocardial necrosis associated with inflammation.
presentation of myocarditis by MRI examination is characterized by some area of hyper-enhancement sparing the subendocardium without matching a coronary artery territory as in our observation, but most abnormalities are confined to the lateral and apical myocardium [4,5]. In our
