American Journal of Emergency Medicine xxx (2014) xxx–xxx

Contents lists available at ScienceDirect

American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem

Case Report

Myocarditis with normal left ventricular function and troponin of 266 Abstract We are reporting a case, which may represent a new entity within the diagnosis of acute myocarditis. The patient was admitted with new onset atrioventricular block, very high troponin I, peaking at 266 ng/mL, and normal left ventricular function. We also used a novel computer tomography technique with delayed enhancement to diagnose myocarditis, as the patient with a permanent pacemaker could not have magnetic resonance imaging. Since the advent of the troponin I (TnI) assay, markedly elevated levels of this enzyme were largely associated with acute coronary syndromes, with modestly elevated levels seen in myocardial disease and mild abnormalities present with almost every supply/demand mismatch. In myocarditis, TnI is elevated only in 34% of cases [1]. Most patients with acute myocarditis present with new onset heart failure associated with compromised left ventricular ejection fraction (LVEF). We are presenting a case of myocarditis without heart failure or left ventricular (LV) dysfunction but with unusually high TnI. A 52-year-old man with no medical history presented to emergency department with 4 days of night sweats and progressively debilitating fatigue of new onset, culminating in feelings of impending doom. He could not recall any recent infections. On examination, he had heart rate of 38 beats per minute, regular, with distal sounds. There were occasional cannon waves on jugular veins. His blood pressure was 102/82 mm Hg. Lungs were clear; there was no abdominal distension or peripheral edema. He had third-degree heart block on the electrocardiogram. Troponin I was elevated to 25 ng/mL. Emergent coronary angiography showed normal arteries. A temporary pacing wire was placed with immediate improvement of symptoms. A permanent dual chamber pacemaker was implanted on the same day. Bedside echocardiogram revealed normal heart with septal motion abnormalities consistent with right ventricular pacing. The next morning, TnI was elevated to 170 ng/mL. The patient was feeling well but developed paroxysmal atrial flutter and transient paresthesias in the toes and fingers. He spiked a fever of 101°F. Cultures were taken; no growth was noted. Troponin I peaked at 266 ng/mL, then trended down (Fig. 1). Lyme titers, human immunodeficiency virus testing, and rheumatologic work-up was unremarkable. On the third day, paresthesias resolved, and temperature normalized. Cardiac magnetic resonance imaging (MRI) was contraindicated in this patient due to the presence of a cardiac pacer. Delayed enhancement cardiac computed tomography (CT) was thus performed. Retrospectively gated, delayed images of the heart were obtained after 85 cm3 intravenous contrast was administered (Isoview 370; Bracco Diagnostics Inc, Princeton, NJ). Delayed enhancement cardiac CT images demonstrated abnormal contrast accumulation with a subepicardial distribution predominantly involving the mid and apical LV segments, compatible with myocardial injury/ inflammation (Fig. 2 A and B). The distribution of contrast accumulation was suggestive of myocarditis with sarcoid unlikely given the clinical

setting. We considered empiric steroids but decided against it. Endomyocardial biopsy was performed, with evidence of interstitial edema, perivascular, and interstitial lymphocytic infiltration and evolving myocardial fiber necrosis consistent with lymphocytic myocarditis. The patient remained afebrile and asymptomatic. Repeat transthoracic echocardiogram showed LVEF of 54%. No regional wall motion abnormalities were detected.. The patient was discharged to home. We are presenting a very unusual case of acute myocarditis with normal LVEF and extremely high (peak, 266 ng/mL) TnI. This may represent a distinct clinical entity. Typically, patients with myocarditis present with new onset LV systolic dysfunction and very modest—in single digits—elevation of TnI [2]. Troponin I reaches double digits and rarely triple digits in fulminant myocarditis with severe hemodynamic compromise and LVEF 5% to 10% [3]. Interestingly, some studies report better outcomes in myocarditis with higher TnI levels [4], although this observation was also made in the setting of severely compromised LVEF. Complete atrioventricular block is not very common in acute lymphocytic myocarditis and occurs in 8.3% of cases [5]. Another highlight of the case is the modification of cardiac CT with delayed enhancement, which allowed visualization of typical subepicardial accumulation of contrast indicating inflammation and guided the diagnostic biopsy to be sampled from the region with marked inflammatory changes. Classically, the standard of care for the diagnosis of myocarditis has been MRI, which was contraindicated in the presence of permanent pacemaker. We demonstrated that retrospectively gated delayed-enhancement cardiac CT with intravenous contrast can be successfully used in this setting. In summary, we are reporting a case of myocarditis with preserved LVEF and massively elevated troponin, which may represent a new entity

Fig. 1. Troponin I trend from admission to discharge.

0735-6757/© 2014 Elsevier Inc. All rights reserved.

Please cite this article as: Ramos-Matos C, et al, Myocarditis with normal left ventricular function and troponin of 266, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.034

2

C. Ramos-Matos et al. / American Journal of Emergency Medicine xxx (2014) xxx–xxx

Fig. 2. Four-chamber view(A) and short-axis view (B). Delayed enhancement cardiac CT images in the 2-chamber, 4-chamber, and short axis of the heart demonstrate abnormal accumulation of contrast with subepicardial distribution involving the basal, mid, and apical segments (with relative sparing of the basal septum) suggestive of myocarditis.

Maya Guglin MD, PhD Department of Cardiology University of South Florida Tampa, FL E-mail address: [email protected]

within acute myocarditis and describing a novel use of cardiac CT for the diagnosis of myocardial inflammation when MRI is contraindicated. Carlos Ramos-Matos MD Department of Internal Medicine University of South Florida Tampa, FL

http://dx.doi.org/10.1016/j.ajem.2014.04.034 Michael Scholfield MD Department of Cardiology University of South Florida Tampa, FL Joao Fontuoro MD Department of Internal Medicine/Pediatrics University of South Florida Tampa, FL Carlos A. Rojas MD Department of Radiology University of South Florida Tampa, FL

References [1] Smith SC, Ladenson JH, Mason JW, Jaffe AS. Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. Circulation 1997;95:163–8. [2] Ammann P, Naegeli B, Schuiki E, et al. Long-term outcome of acute myocarditis is independent of cardiac enzyme release. Int J Cardiol 2003;89:217–22. [3] Stankewicz MA, Clements Jr SD. Fulminant myocarditis presenting with wide complex tachycardia. South Med J 2004;97:1007–9. [4] Freixa X, Sionis A, Castel A, et al. Low troponin-I levels on admission are associated with worse prognosis in patients with fulminant myocarditis. Transplant Proc 2009;41:2234–6. [5] Davidoff R, Palacios I, Southern J, Fallon JT, Newell J, Dec GW. Giant cell versus lymphocytic myocarditis. A comparison of their clinical features and long-term outcomes. Circulation 1991;83:953–61.

Please cite this article as: Ramos-Matos C, et al, Myocarditis with normal left ventricular function and troponin of 266, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.04.034

Myocarditis with normal left ventricular function and troponin of 266.

We are reporting a case, which may represent a new entity within the diagnosis of acute myocarditis. The patient was admitted with new onset atriovent...
507KB Sizes 2 Downloads 4 Views