This case was submitted by Dr Cameron Bridgman and Dr Joseph Selvanayagam

Flinders Medical Centre, Adelaide, SA. 


A 62 year old male presented to hospital with 60 minutes of central chest pain. There were no associated symptoms or prodrome. His cardiovascular risk was low as calculated by the Australian Absolute CV risk calculator.

The electrocardiogram was normal however his hs-troponin T was positive at 382ng/l. Creatine kinase and CRP were normal. LV function was normal at echocardiography. Coronary angiography showed minor non-occlusive coronary disease with sluggish flow in the left anterior descending artery.

Cardiac MRI was performed to clarify the aetiology of the presentation. Left ventricular function was normal. STIR T2 (oedema) imaging demonstrated increased signal intensity from the midwall and epicardial aspect of the basal septum consistent with inflammation (Figure 1&2: A). The late gadolinium acquisitions showed hyperenhancement in the same area (Figure 1&2: B, Figure 3). This pattern of hyperenhancement is suggestive of myocarditis (probably as a result of Human Herpes Virus 6) as opposed to myocardial infarction which begins at the subendocardium(1) .


Figure 1 - Horizontal Long axis view showing matched increased signal within the septum on: A) STIR T2 weighted images; and B) Late gadolinium acquistions

Figure 2 - Short axis view showing matched increased signal within the midwall of the septum on: A) STIR T2 weighted; and B) Late gadolinium enhancement imaging.

Figure 3 - Cross cut of short axis showing midwall basal septal hyperenhancement. 


The most common location of myocardial damage and subsequent hyperenhancement on CMR in viral myocarditis is the subepicardium of the inferolateral left ventricle. This pattern seems to occur with parvovirus B19 (PVB19) infection as demonstrated by Marholdt et al(2) rather than  HHV6 which has a predilection for the anteroseptum. In this study, patients with PVB19 more commonly presented with chest pain and ECG changes whereas those with HHV6 may have a less acute presentation with heart failure, chest pain and bundle branch block.



This case demonstrates how CMR can easily clarify the aetiology of troponin positive chest pain and change the diagnosis completely. Converse to this case, we quite often demonstrate myocardial infarction in patients with angiographically smooth coronary arteries.


1. Reimer KA, Jennings RB. The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest 1979;40(6):633-44.

2. Mahrholdt H, Wagner A, Deluigi CC, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation. 2006;114(15):1581–1590.