Fulminant myocarditis presenting with wide complex tachycardia.

Abstract: Fulminant myocarditis is an uncommon diagnosis characterized by cardiac failure preceded by symptoms of a viral illness. Presentation can frequently mimic acute myocardial infarction. The electrocardiographic changes are frequently nonspecific, but include ST segment elevation and T wave changes, as well as conduction abnormalities. We report the case of a patient with fulminant myocarditis that presented with sinus rhythm, a conduction system abnormality, and severe ST segment elevation mimicking ventricular tachycardia. Myocarditis should be considered in young persons with unexplained heart failure and similar electrocardiographic abnormalities.

Key Words: electrocardiography, fulminant myocarditis, ventricular tachycardia

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Myocarditis is characterized by inflammation of the heart muscle, frequently caused by infectious processes. (1) The clinical syndrome is variable and can include chest pain, arrhythmias, signs of right or left heart failure, or a progressive course with cardiogenic shock. Electrocardiographic abnormalities are common and often consist of conduction system abnormalities, bundle branch blocks, and ST and T wave changes. (2) In this report, we describe a patient in whom fulminant myocarditis was identified and associated with a wide complex tachycardia.

Case Report

A 56-year-old female with a history of breast cancer and left mastectomy presented to her local family practice physician for preoperative evaluation before breast biopsy, and had nonspecific complaints of a cold-like syndrome. She stated that she had one day of cough, diaphoresis, nausea, "stuffiness" in her chest, and dizziness. Routine electrocardiogram (EKG) revealed what appeared to be a wide complex tachycardia (Fig. 1). She was sent to the emergency room where she was thought to be in ventricular tachycardia, and received a precordial cardioversion without any change in her EKG. Intravenous amiodarone was given along with aspirin, heparin, and tirofiban. She was referred to Emory University Hospital with suspected acute myocardial infarction.

Her past history was remarkable for breast cancer and a right mastectomy in 1994. She also had a history of hypertension, esophageal reflux, lumbar disk disease, and obstructive pulmonary disease. She had a history of three miscarriages and was amenorrheic since her last miscarriage in 1991. She had no drug allergies and took only amitriptyline 25 mg nightly. She smoked 1.5 packs of cigarettes daily, and had a history of alcohol use including about six beers per week. There was no family history of coronary artery disease or sudden death.

On examination, her temperature was 37.5[degrees]C, blood pressure was 109/57, and pulse was 120. She had a normal head and neck examination. There was no jugular venous distension and no carotid bruits. She had a regular rhythm, normal [S.sub.1] and [S.sub.2] without [S.sub.3] or [S.sub.4]. A II/VI holosystolic murmur was present at the left lower sternal border. Her lung fields were clear and abdomen was not remarkable.

Laboratory data at arrival included a white blood cell count of 7.4k/cmm, hematocrit of 41.7% and platelet count of 328 k/cmm. Differential consisted of 50% granulocytes, 33% lymphocytes, 13% monocytes, 2% eosinophils and 1% basophils. Sodium was 134 mEq/L, potassium 3.9 mEq/L, chloride 98 mEq/L, blood urea nitrogen 11 mg/dL, creatinine 0.6 mg/dL. Creatinine kinase was 945 U/L, MB fraction was 167 ng/mL and troponin I was 27.5 ng/mL.

Electrocardiogram was obtained and revealed a supraventricular tachycardia without visible P waves, wide QRS complexes with impressive ST segment elevation that fused with the QRS complexes producing a monophasic complex. Chest radiograph revealed multiple healed rib fractures, absent right breast, and no evidence of focal pulmonary disease.

Cardiac catheterization was performed on the evening of admission and revealed normal right and left coronary arteries and an ejection fraction of 30% with global hypokinesis. She continued to be hemodynamically unstable, and an intra-aortic balloon pump was placed in the catheterization laboratory.

Her clinical status continued to deteriorate, and the next day an echocardiogram showed that her left ventricular ejection fraction had decreased further to 10 to 15% with severe global hypokinesis of both ventricles. A right heart biopsy (Fig. 2) was performed, revealing diffuse mononuclear cell infiltrates, scattered eosinophils, and extensive myocyte loss consistent with acute fulminant myocarditis. Intravenous methylprednisolone was given; however, her clinical status continued to deteriorate with hypotension, tachycardia, and respiratory failure. She died shortly thereafter with hypotension.

Discussion

The spectrum of disease associated with myocarditis is wide, and presentation can vary from a subclinical course to fulminant cardiac failure and death. The etiology is commonly thought to be infectious, but can include systemic diseases, immune processes, drugs, and toxins. (1)

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The clinical features of myocarditis vary. It may present asymptomatically with EKG abnormalities. It may also present as fulminant cardiac failure with ventricular dilation and left ventricular dysfunction. (2) Patients often have a history of recent flu-like illness accompanied by fever, arthralgia, and malaise. (1) Creatinine kinase and cardiac troponins are frequently elevated. (1) Other laboratory markers may suggest infection, autoimmune disease, or poor peripheral perfusion. (3)

Because it can sometimes present with angina-like chest pain, EKG changes and elevation of cardiac enzymes, myocarditis must be considered in the differential diagnosis of myocardial infarction. (4) However, because these processes differ importantly in their management and prognosis, differentiation is important. (5) Differentiation may be aided by endomyocardial biopsy in patients with clinical, EKG, and laboratory evidence of myocardial infarction with normal coronaries. (4)

The most common electrocardiographic abnormality associated with myocarditis is T wave changes without ST segment abnormalities. (6) Myocarditis and pericarditis can coexist, and so the EKG abnormalities associated with pericarditis are sometimes present. (6) In addition, atrial and ventricular arrhythmias, conduction system defects, and, rarely, abnormal Q waves may be seen. (3) Our patient's high ST segment elevations fused with the prolonged QRS gave the appearance of a ventricular arrhythmia. This EKG pattern persisted until her death.

Conclusion

The case presented here demonstrates a patient with flu-like symptoms followed by fulminant cardiac failure who was treated for acute myocardial infarction and ventricular tachycardia. Retrospectively, the EKG likely represents an undetermined supraventricular rhythm with a nonspecific intraventricular conduction abnormality fused with dramatic ST segment changes. Cardioversion, retrospectively, could not have been expected to help. Similarly, lidocaine and amiodarone were ineffective. She deteriorated rapidly despite aggressive intervention. Acute fulminant myocarditis was confirmed by endomyocardial biopsy (Fig. 2). This case demonstrates the importance of considering fulminant myocarditis in the differential diagnosis of a wide complex tachycardia.

Blessed is the man, who having nothing to say, abstains from giving
wordy evidence of the fact.
--George Eliot

Acknowledgment

We would like to acknowledge Robert Santoianni of the Department of Pathology for assistance with photomicrograph reproduction.

Accepted April 5, 2004.

References

1. Feldman AM, McNamara D. Myocarditis. N Engl J Med 2000;343:1388-1398.

2. Fuster V, Alexander RW, O'Rourke RA, et al. Hurst's The Heart, New York, McGraw-Hill, 2001, ed 10, pp 2003-2013.

3. Liu PP, Mason JW. Advances in the understanding of myocarditis. Circulation 2001;104:1076-1082.

4. Costanzo-Nordin MR, O'Connell JB, Subrahamian R, et al. Myocarditis confirmed by biopsy presenting as an acute myocardial infarction. Br Heart J 1985;53:25-29.

5. Stratmann HG. Acute myocarditis versus myocardial infarction: evaluation and management of the young patient with prolonged chest pain--case reports. Angiology 1988;39:258-268.

6. Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice. Philadelphia, W.B. Saunders, 2001, ed 5, pp 245-247.

RELATED ARTICLE: Key Points

* Myocarditis can have a rapidly progressive course causing cardiac failure and death.

* Differentiation between acute myocardial infarction and myocarditis is not always straightforward, but is important because of different treatments and prognoses.

* Fulminant myocarditis should be considered in the differential diagnosis of wide complex tachycardia.

Mark A. Stankewicz, MD, and Stephen D. Clements Jr, MD

From the Department of Medicine, Division of Cardiology, Emory University Hospital, Atlanta, GA.

Reprint requests to Stephen D. Clements Jr, MD, The Emory Clinic, 1365 Clifton Road, Atlanta, GA, 30322.