Mass General Hospital
May 2008

Young Man with Chest Pain and Positive Cardiac Enzymes
Leon Shturman, MD, Amar Shah, MD, Erick Avelar, MD, Kathlyn Lam, MD, Ricardo C. Cury, MD
  Clinical History
An 18 year-old previously healthy man presented to an outside hospital emergency room with non-exertional, constant aching sensation in the center of his chest that was preceded by a 1 week history of "flu-like" symptoms. His presenting EKG demonstrated a concave ST segment elevation (Fig. 1) and his presenting cardiac enzymes were elevated (troponin 1.78 and CK-MB 65). A cardiac ultrasound (ECHO) demonstrated a structurally normal heart with a low-normal left ventricular ejection fraction (LVEF) of 50%; without obvious regional wall motion abnormalities. He was given a provisional diagnosis of myocarditis, and subsequently transferred to MGH for further evaluation and management.

Cardiac magnetic resonance (CMR) revealed increased T2 signal of the sub-epicardial myocardium, predominantly affecting the inferior-lateral wall (Fig. 2). Post-gadolinium delayed enhancement images showed sub-epicardial hyper-enhancement of ~50% (pathognomonic for non-ischemic injury) in the same region of the left ventricular myocardial wall (Fig. 3 and 4). Mild inferio-lateral hypokinesis was noted with calculated LVEF of 49% (End-diastolic volume 153 cc, End-systolic volume 78 cc, and Stroke volume 75 cc)

Figure 1. Initial EKG
Figure 1. Initial EKG
Figure 2. T2-weighted short axis
Figure 2. T2-weighted short axis

Figure 3. Delayed enhancement: short axis of the left ventricle
Figure 3. Delayed enhancement:
short axis of the left ventricle
Figure 4. Delayed enhancement: 4 Chamber view
Figure 4. Delayed enhancement: 4 Chamber view

(Click on images to enlarge)

Acute myocarditis is an inflammatory reaction with myocyte injury, commonly due to a viral infection or autoimmune etiology. Clinical outcomes range from spontaneous recovery to dilated cardiomyopathies and life-threatening arrhythmias. Myocarditis is commonly under-diagnosed clinically, serving as a diagnosis of exclusion for patients presenting with chest pain or heart failure despite a normal coronary angiogram.

Both acute inflammation and necrosis result in edema, which can be detected by T2-weighted CMR imaging. Myocardial necrosis also contributes to sub-epicardial post-gadolinium delayed hyper-enhancement. Acute myocardial infarction, in contrast to myocarditis, is characterized by sub-endocardial or transmural enhancement on delayed post-gadolinium images. Our case illustrates that CMR is an attractive clinical imaging modality for the non-invasive diagnosis of myocarditis.

1. Aretz HT, Billingham ME, Edwards WD, et al. Myocarditis. A histopathologic definition and classification. Am J Cardiovasc Pathol 1987;1:3–14.
2. Abdel-Aty H, Boyé P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol 2005;45:1815–22.
3. Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation 2004;109:2411– 6.

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Suhny Abbara, MD
MGH Department of Radiology
Wilfred Mamuya, MD, PhD
MGH Division of Cardiology

Phone: 617-726-5954