Mass General Hospital
May 2008
ISSUE 8

 
 
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.

Findings
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)

Discussion
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.


 
 
REFERENCES
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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Editors:
Suhny Abbara, M.D.
MGH Department of Radiology
Wilfred Mamuya, M.D., Ph.D.
MGH Division of Cardiology

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