1. The Clinical Challenge of Myocarditis: A Case of Myocarditis with wall
motion abnormality mimicking AMI and EKG normalization after Thrombolysis
Introduction
Myocarditis has been referred to as displaying polymorphism in its presentation. 1
Patients with this pathology may vary in clinical presentation including describing a viral
syndrome, relating substernal chest pain, arrythmias, and finally congestive heart
failure. Myocarditis has been associated with viral etiologies, including HIV as well as
chronic inflammatory states such as Lupus and Sarcoidosis. One retrospective study
evaluated sixty patients with either pericarditis or myocarditis that excluded the
diagnosis 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 pain
with posture or respiration, while a smaller percentage of less than one-third described
classic pleuritic pain.2 The non-specific pattern of the clinical presentation of myocarditis
has made establishing any diagnostic criteria extremely difficult. Often the term
myopericarditis is used to describe the inflammatory process that tends to encompass
both layers of the heart. The Dallas Criteria in 1986 only provided a histopathological
basis of diagnosis that requires an inflammatory infiltrate and associated myocyte
necrosis only to be found by biopsy.3 Further histochemical categories of viral disease
include fulminant, chronic active, eosinophilic and giant cell. 4
Much more complicated is the task in evaluation of the initial presentation of this
entity where the combination of the history, exam findings and electrocardiogram
findings may not lend itself to favor one diagnosis over the other. Further challenge is
imposed when catheterization is not a timely option, and a decision to initiate a
potentially lethal thrombolytic if the diagnosis is not correct versus withholding a
medication that could salvage ischemic myocardium. There are studies that have
attempted to distinguish electrocardiogram characteristics of myocarditis. In one
analysis that retrospectively evaluated eleven patients with myocarditis, 100% had ST
elevations and 64% had Q waves on initial electrocardiogram. 5 One case report
discusses an 18 year old patient with a clinical presentation more suggestive of a viral
etiology than myocardial infarction but an ECG that pointed towards an infarct pattern. 6
The decision to withhold thrombolysis was made on the basis of a stat echocardiogram
which did not demonstrate any wall motion abnormalities. 7 Our report represents a
unique case in that our patient, who was later confirmed to have myocarditis, exhibited
not only initial segmental wall motion abnormality on Echo but also demonstrated an
immediate normalization of his ECG after thrombolytics were given as an acute
myocardial infarction would be expected to do.
Case Report
This is a case of at 19 year old male, with no previous medical history, who
presented with complaint that he awoke from sleep that morning with severe, sharp and
retrosternal chest pain that non radiating, was constant in duration and associated with
diaphoresis. Social history was remarkable for cannabis use and past medical and
family cardiac history was non-contributory. His initial electrocardiogram at time of
arrival showed ST elevations in the inferior leads, ST depressions in VI and AVL, and
mild ST elevations in V4-V6 without reciprical changes or PR interval depressions. A
bedside trans-thoracic echo demonstrated hypo-kinetic walls in the inferior aspect of the
heart and the patient subsequently received thrombolytics in addition to aspirin and
plavix. Initial troponin was 38. The patient’s immediate ECG after the completion of
thrombolytic therapy returned to normal. The patient still reported chest pain after
therapy but not as severe as initial presentation. The patient was then transferred to a
cardiac center where he underwent catheterization which demonstrated patent coronary

2. arteries. A venogram was subsequently performed that showed hypokinetic, mid-
apical, anterior and inferior wall motion with an ejection fraction of 35%. Troponins rose
to > 50. Repeat ECG remained normal a Cardiac MRI was performed which reported
areas of myocardial fibrosis and inflammation consistent with myocarditis rather than
myocardial infarction. The patient started having fevers (101F) which resolved. The
patient remained in the hospital for a total of three days and during that time, he had
multiple runs of non-sustained ventricular tachycardia. As a result, he was discharged
with 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 present
to the emergency department two months later for case of mild chest pain, with no ECG
changes. Troponin was noted to be 0.10. The patient was observed overnight and
discharged 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 the
subject of myocarditis mimicking myocardial infarction; however, there were no case
reports that described ECG normalization after TPA given in a case of myocarditis.
There were cases reported of thrombolytics being given to patients where the initial
diagnosis was assumed to be myocardial infarction that was in fact myocarditis. One
paper reports two cases in which thrombolytics were given to two patients where the
diagnosis was later determined to be myocarditis and later were seen to have clear
coronary arteries on catheterization and there was no adverse outcomes reported with
those two patients.8 In another case, a 30 year old man was reported to have ST
elevations in leads V1-V4, and in leads II,III and AVF and thrombolytic therapy was
given.9 During thrombolytic therapy, the patient developed ventricular tachycardia which
degenerated into ventricular fibrillation and the patient expired. 10 The diagnosis of acute
lymphocytic myocarditis was established on post-mortum immunohistochemical study. 11
While there were no individual case reports mentioning normalization of ECG to
baseline in myocarditis after thrombolytic administration there was a retrospective study
conducted and published in the European Heart Journal which discussed nine patients
with myocarditis that were thrombolyzed after an initial mis-diagnosis of acute
myocardial infraction was made.12 It was mentioned that in each of the cases, the ECG
ultimately normalized; however, no interval was mentioned in relation to hours or days
after thrombolytic therapy.13 Interestingly, three of the nine patients in this retrospective
study received echos that had significant wall motion abnormalities prior to thrombolysis
who also had a normal catheterization. All nine patients had uneventful courses after
the thrombolytic therapy. Segmental wall motion abnormality seems to only be a
finding in a minority of the cases. Nakashima’s retrospective study that evaluated 11
patients with myocarditis described that three of eleven patients with myocarditis
diagnosed on biopsy had ventricular wall motion abnormalities. 14 Our patient did
receive thrombolytics and an immediate post-lytic ECG did reveal a return to baseline
which at the time suggested that the underlying diagnosis was an acute myocardial
infaraction; however, the evidence gathered from the normal catherization and the
interpretation of the cardiac MRI indicates that the diagnosis remains Myocarditis.
Conclusion
Distinguishing between an acute myocardial infarction and peri-myocarditis can be
confounding for the Emergency Physician. Given not only the similarities in clinical
presentation and ECG findings but the striking copying of echo wall motion
abnormalities that myocarditis can have, myocarditis clearly represents an entity that is
indistinguishable from an AMI, especially in a young person. Moreover, our case

3. demonstrates that a resolution of EKG abnormality after thrombolytic administration
does not bear any confirmation as to the underlying diagnosis.

4. 1 Sinagra G, Maras P, D'Ambrosio A, et al. Clinical polymorphic presentation and natural history of active
myocarditis: 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): 433-442
3 Sinagra G, Maras P, D'Ambrosio A, et al.
4 Baughman K. Diagnosis of Myocarditis, Death of Dallas Criteria, Circulation 2006: 113: 593-595
5 Nakashima H, Honda Y, Katayama T. Serial electrocardiographic findings in
acute myocarditis. Intern Med. 1994 Nov;33(11):659-66
6 Hesham O, Ahmed F, Rania R, Mohamed E. Acute Perimyocarditis mimicking transmural myocardial
infarction, 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 coronary
thrombosis. Clinical Cardiology, Michigan Heart and Vascular Institute, St.Joseph Mercy Hospital, Ann
Arbor, Jan 1993, 67-71
9 Pomara C, Villani A, D’Errico S, et al, Acute Myocarditis mimicking acute myocardial infarction: a clinical
nightmare with forensic implications, International Journal of Cardiology, Sept, 2006, 10; 112(1): 119-21
10 Pomara C, Villani A, D’Errico S, et al
11 Pomara C, Villani A, D’Errico S, et al
12 Millaire A, De Groote P, Decoulx E, et al, Outcome after thrombolytic therapy of nine cases of
myopericarditis misdiagnosed as myocardial infarction, European Heart Journal (1995) 16, 333-338.
13 Millaire A, De Groote P, Decoulx E, et al
14 Nakashima H, Honda Y, Katayama, 665.