014) 465.e11e465.e12 www.onlinecjc.caCanadian Journal of Cardiology 30 (2Letters to the EditorErysipelas and Myocarditis

Recently, Dominguez et al. reported in the Canadian Journalof Cardiology an association between erysipelas, or presumedstreptococcal-associated cellulitis, with acute myocarditis.1 Weencountered a similar case, which might support the notion ofa relationship.

A 41-year-old man presented with 3 days of left lowerextremity pain and erythema. History included previous leftankle surgeries with hardware retention, and a malleolarosteotomy in 2008. There were no other complaints includingan absence of pharyngitis and arthralgias. He was afebrile. Theskin lesion consisted of nonblanching, dark erythematousmacules surrounded by a lighter, blanching erythema withincreased warmth and tenderness to palpation. There were noidentifiable portals of entry, although the erythema did overlayformer surgical incision scars (Fig. 1A). Lower extremityvascular ultrasound did not demonstrate thromboembolism.His cellulitis improved with vancomycin.

On hospital day 2 he noted sudden onset of dull, aching,substernal chest pain. Electrocardiogram showed sinus rhythmwith a rate of 63 beats per minute and T wave inversions in IIIand V2. Initial troponin was 10.41 ng/mL and CK-MB of62.1 ng/mL (normal, < 0.04 ng/mL and < 9ng/mL,respectively). A transthoracic echocardiogram identified anejection fraction of 60% and mild concentric left ventricularhypertrophy. Left heart catheterization showed no stenoses.Cardiac magnetic resonance imaging demonstrated sub-epicardial delayed enhancement within the lateral andinferolateral walls with corresponding myocardial edema(Fig. 1B and C), consistent with acute myocarditis. Anendomyocardial biopsy was deferred.

Blood and skin biopsy cultures were negative. Histopa-thology demonstrated an unremarkable epidermis, withdermal edema and a predominantly mononuclear, rarelyneutrophilic infiltrate. Stains were negative for microorgan-isms. Further analyses included negative HIV testing, nonre-active rapid plasma reagin, normal complement levels, and anantinuclear antibody titer of 1:40. Antistreptolysin O anti-body titer was 138 IU/mL (normal, < 200 IU/mL).0828-282X/$ - see front matter 2014 Canadian Cardiovascular Society. Publishehttp://dx.doi.org/10.1016/j.cjca.2013.11.029As in the report by Dominguez et al.,1 Jones criteria foracute rheumatic fever were not met. A toxin-mediatedmechanism is proposed on the following assumptions: (1)skin findings were representative of cellulitis; (2) Strepto-coccus might have been involved; and (3) an association withthe myocarditis event. The acuity forms the basis for linkageto a toxin-based process, as opposed to an antibody-mediatedone. Nonetheless, an autoimmune process might be respon-sible, including a vasculitis or an underrecognized response toa pathogen, which might or might not be Streptococcus.Considering the infrequently reported associations withstreptococcal pharyngotonsillitis,2,3 presumed cutaneousstreptococcal-associated myocarditis might require a specificinterplay between immunology and variable microorganismvirulence factors.4Julie Lynn Friedman, MDjulie.friedman1@northwestern.edu

Caitlin Toomey, MDIgnacio A. Echenique, MD

Egon Ozer, MD, PhDDisclosuresThe authors have no conflicts of interest to disclose.

References

1. Dominguez F, Cobo-Marcos M, Guzzo G, et al. Erysipelas and acutemyocarditis: an unusual combination. Can J Cardiol 2013;29:1138.e3-5.

2. Karjalainen J. Streptococcal tonsillitis and acute nonrheumatic myoper-icarditis. Chest 1989;95:359-63.

3. Upadhyay GA, Gainor JF, Stamm LM, et al. Acute nonrheumatic strep-tococcal myocarditis: STEMI mimic in young adults. Am J Med2012;125:1230-3.

4. Ellis NM, Kurahara DK, Vohra H, et al. Priming the immune system forheart disease: a perspective on group A streptococci. J Infect Dis 2010;202:1059-67.d by Elsevier Inc. All rights reserved.

mailto:julie.friedman1@northwestern.eduhttp://refhub.elsevier.com/S0828-282X(13)00011-1/sref1http://refhub.elsevier.com/S0828-282X(13)00011-1/sref1http://refhub.elsevier.com/S0828-282X(13)00011-1/sref2http://refhub.elsevier.com/S0828-282X(13)00011-1/sref2http://refhub.elsevier.com/S0828-282X(13)00011-1/sref3http://refhub.elsevier.com/S0828-282X(13)00011-1/sref3http://refhub.elsevier.com/S0828-282X(13)00011-1/sref3http://refhub.elsevier.com/S0828-282X(13)00011-1/sref4http://refhub.elsevier.com/S0828-282X(13)00011-1/sref4http://refhub.elsevier.com/S0828-282X(13)00011-1/sref4http://dx.doi.org/10.1016/j.cjca.2013.11.029http://dx.doi.org/10.1016/j.cjca.2013.11.029http://dx.doi.org/10.1016/j.cjca.2013.11.029http://www.onlinecjc.ca

Figure 1. (A) Left lower extremity, medial aspect, on initial presentation. The area of pain corresponded to the regions of erythema. The superioraspect is demarcated by marker. Inferiorly, remote surgical scars are appreciated from earlier orthopaedic interventions. No clear portal of entry wasappreciated. (B, C) Cardiac magnetic resonance imaging: long-axis view (B) and short-axis view (C) demonstrate subepicardial delayed enhance-ment within the lateral and inferolateral walls with corresponding myocardial edema in this region.

465.e12 Canadian Journal of CardiologyVolume 30 2014

Erysipelas and MyocarditisDisclosuresReferences