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  1. 1. The Clinical Challenge of Myocarditis: A Case of Myocarditis with wallmotion abnormality mimicking AMI and EKG normalization after ThrombolysisIntroduction Myocarditis has been referred to as displaying polymorphism in its presentation. 1Patients with this pathology may vary in clinical presentation including describing a viralsyndrome, relating substernal chest pain, arrythmias, and finally congestive heartfailure. Myocarditis has been associated with viral etiologies, including HIV as well aschronic inflammatory states such as Lupus and Sarcoidosis. One retrospective studyevaluated sixty patients with either pericarditis or myocarditis that excluded thediagnosis of endocarditis and found that close to half of the patients presented with sub-sternal chest pain without a pleuritic component, as being reflected by change in painwith posture or respiration, while a smaller percentage of less than one-third describedclassic pleuritic pain.2 The non-specific pattern of the clinical presentation of myocarditishas made establishing any diagnostic criteria extremely difficult. Often the termmyopericarditis is used to describe the inflammatory process that tends to encompassboth layers of the heart. The Dallas Criteria in 1986 only provided a histopathologicalbasis of diagnosis that requires an inflammatory infiltrate and associated myocytenecrosis only to be found by biopsy.3 Further histochemical categories of viral diseaseinclude fulminant, chronic active, eosinophilic and giant cell. 4 Much more complicated is the task in evaluation of the initial presentation of thisentity where the combination of the history, exam findings and electrocardiogramfindings may not lend itself to favor one diagnosis over the other. Further challenge isimposed when catheterization is not a timely option, and a decision to initiate apotentially lethal thrombolytic if the diagnosis is not correct versus withholding amedication that could salvage ischemic myocardium. There are studies that haveattempted to distinguish electrocardiogram characteristics of myocarditis. In oneanalysis that retrospectively evaluated eleven patients with myocarditis, 100% had STelevations and 64% had Q waves on initial electrocardiogram. 5 One case reportdiscusses an 18 year old patient with a clinical presentation more suggestive of a viraletiology than myocardial infarction but an ECG that pointed towards an infarct pattern. 6The decision to withhold thrombolysis was made on the basis of a stat echocardiogramwhich did not demonstrate any wall motion abnormalities. 7 Our report represents aunique case in that our patient, who was later confirmed to have myocarditis, exhibitednot only initial segmental wall motion abnormality on Echo but also demonstrated animmediate normalization of his ECG after thrombolytics were given as an acutemyocardial infarction would be expected to do.Case Report This is a case of at 19 year old male, with no previous medical history, whopresented with complaint that he awoke from sleep that morning with severe, sharp andretrosternal chest pain that non radiating, was constant in duration and associated withdiaphoresis. Social history was remarkable for cannabis use and past medical andfamily cardiac history was non-contributory. His initial electrocardiogram at time ofarrival showed ST elevations in the inferior leads, ST depressions in VI and AVL, andmild ST elevations in V4-V6 without reciprical changes or PR interval depressions. Abedside trans-thoracic echo demonstrated hypo-kinetic walls in the inferior aspect of theheart and the patient subsequently received thrombolytics in addition to aspirin andplavix. Initial troponin was 38. The patient’s immediate ECG after the completion ofthrombolytic therapy returned to normal. The patient still reported chest pain aftertherapy but not as severe as initial presentation. The patient was then transferred to acardiac center where he underwent catheterization which demonstrated patent coronary
  2. 2. arteries. A venogram was subsequently performed that showed hypokinetic, mid-apical, anterior and inferior wall motion with an ejection fraction of 35%. Troponins roseto > 50. Repeat ECG remained normal a Cardiac MRI was performed which reportedareas of myocardial fibrosis and inflammation consistent with myocarditis rather thanmyocardial infarction. The patient started having fevers (101F) which resolved. Thepatient remained in the hospital for a total of three days and during that time, he hadmultiple runs of non-sustained ventricular tachycardia. As a result, he was dischargedwith a life-vest and started on a low dose beta-blocker and ace-inhibitor. The patient did not return for his scheduled follow-up appointment but did presentto the emergency department two months later for case of mild chest pain, with no ECGchanges. Troponin was noted to be 0.10. The patient was observed overnight anddischarged the following day with an uneventful hospital stay.Discussion A literature search was conducted on PubMed using search words: myocarditis,pericarditis, thrombolytics, tpa, ekg. There were several case reports written on thesubject of myocarditis mimicking myocardial infarction; however, there were no casereports that described ECG normalization after TPA given in a case of myocarditis.There were cases reported of thrombolytics being given to patients where the initialdiagnosis was assumed to be myocardial infarction that was in fact myocarditis. Onepaper reports two cases in which thrombolytics were given to two patients where thediagnosis was later determined to be myocarditis and later were seen to have clearcoronary arteries on catheterization and there was no adverse outcomes reported withthose two patients.8 In another case, a 30 year old man was reported to have STelevations in leads V1-V4, and in leads II,III and AVF and thrombolytic therapy wasgiven.9 During thrombolytic therapy, the patient developed ventricular tachycardia whichdegenerated into ventricular fibrillation and the patient expired. 10 The diagnosis of acutelymphocytic myocarditis was established on post-mortum immunohistochemical study. 11 While there were no individual case reports mentioning normalization of ECG tobaseline in myocarditis after thrombolytic administration there was a retrospective studyconducted and published in the European Heart Journal which discussed nine patientswith myocarditis that were thrombolyzed after an initial mis-diagnosis of acutemyocardial infraction was made.12 It was mentioned that in each of the cases, the ECGultimately normalized; however, no interval was mentioned in relation to hours or daysafter thrombolytic therapy.13 Interestingly, three of the nine patients in this retrospectivestudy received echos that had significant wall motion abnormalities prior to thrombolysiswho also had a normal catheterization. All nine patients had uneventful courses afterthe thrombolytic therapy. Segmental wall motion abnormality seems to only be afinding in a minority of the cases. Nakashima’s retrospective study that evaluated 11patients with myocarditis described that three of eleven patients with myocarditisdiagnosed on biopsy had ventricular wall motion abnormalities. 14 Our patient didreceive thrombolytics and an immediate post-lytic ECG did reveal a return to baselinewhich at the time suggested that the underlying diagnosis was an acute myocardialinfaraction; however, the evidence gathered from the normal catherization and theinterpretation of the cardiac MRI indicates that the diagnosis remains Myocarditis.ConclusionDistinguishing between an acute myocardial infarction and peri-myocarditis can beconfounding for the Emergency Physician. Given not only the similarities in clinicalpresentation and ECG findings but the striking copying of echo wall motionabnormalities that myocarditis can have, myocarditis clearly represents an entity that isindistinguishable from an AMI, especially in a young person. Moreover, our case
  3. 3. demonstrates that a resolution of EKG abnormality after thrombolytic administrationdoes not bear any confirmation as to the underlying diagnosis.
  4. 4. 1 Sinagra G, Maras P, DAmbrosio A, et al. Clinical polymorphic presentation and natural history of activemyocarditis: experience in 60 cases. G Ital Cardiol. 1997 Aug;27(8):758-74.2 Gardiner AJ, Short D, Four faces of Acute Myopericarditis, British Heart Journal, 1973, April 35(4): 433-4423 Sinagra G, Maras P, DAmbrosio A, et al.4 Baughman K. Diagnosis of Myocarditis, Death of Dallas Criteria, Circulation 2006: 113: 593-5955 Nakashima H, Honda Y, Katayama T. Serial electrocardiographic findings inacute myocarditis. Intern Med. 1994 Nov;33(11):659-666 Hesham O, Ahmed F, Rania R, Mohamed E. Acute Perimyocarditis mimicking transmural myocardialinfarction, International Archives of Medicine 2009, 2:37,7 Hesham O, Ahmed F, Rania R, Mohamed E.8 Kahn, JK. Inadvertent thrombolytic therapy for cardiovascular diseases masquerading as acute coronarythrombosis. Clinical Cardiology, Michigan Heart and Vascular Institute, St.Joseph Mercy Hospital, AnnArbor, Jan 1993, 67-719 Pomara C, Villani A, D’Errico S, et al, Acute Myocarditis mimicking acute myocardial infarction: a clinicalnightmare with forensic implications, International Journal of Cardiology, Sept, 2006, 10; 112(1): 119-2110 Pomara C, Villani A, D’Errico S, et al11 Pomara C, Villani A, D’Errico S, et al12 Millaire A, De Groote P, Decoulx E, et al, Outcome after thrombolytic therapy of nine cases ofmyopericarditis misdiagnosed as myocardial infarction, European Heart Journal (1995) 16, 333-338.13 Millaire A, De Groote P, Decoulx E, et al14 Nakashima H, Honda Y, Katayama, 665.