A 46-year-old woman had suffered from left anterior chest pain lasting 2 days visited our hospital. She had been undergoing chemotherapy for 3 years due to myelodysplastic syndrome. She did not ever smoke and does not have medical history of diabetes or hypertension. Her blood pressure on admission was 120/80 mmHg and body temperature was 36.5 ℃.

Her electrocardiogram (ECG) at admission showed ST segment elevation in V2-V4 with T wave inversion in V2-V5 (Fig. 1). In initial laboratory examination, bicytopenia was detected (WBC count = 1,300 /mm3, platelet count = 5,000 /mm3). Her cardiac markers were within normal limit (Troponin I = 0.001 ng/mL, CK-MB = 5.1 U/L, AST = 14 U/L) and C-reactive protein was elevated up to 21.5 mg/dL (reference level= 0~0.3 mg/dL). Transthoracic echocardiogram performed with suspicion of acute coronary syndrome revealed hypokinesia in apical septal and apical anterior wall of left ventricle (LV). In apical pericardial area just adjacent hypokinetic lesion, hypoechoic lesion was found, it suggested abscess (TTE, Fig. 2). The size of lesion was 27.2 x 11.9 mm in the 2D echocardiogram. Cardiac computed tomography demonstrated mild diffuse thickening with contrast enhancement of pericardium and loculated fluid collection in anterior myocardium and pericardium without definite luminal narrowing in coronary arteries (Fig. 3).

We consulted to thoracic surgeon and interventional radiologist for tissue diagnosis. But her extremely lower platelet count and small size of the lesion made them to hesitate to do invasive diagnostic procedure. We had to give her conservative treatment with antibiotics (third generation cephalosporin plus aminoglycoside). Follow-up TTE had done in 2 weeks later since the first exam showed no significant interval changes (Fig. 4-A and B). Follow-up chest CT conducted 3 weeks later since antibiotics treatment revealed marked improvement of previous seen loculated fluid collection in anterior myocardiaum and pericardium, but still remained focal wall thickening and enhancement (Fig. 5). Follow-up 2D echocardiogram done in 7 weeks later demonstrated complete resolution of the lesion (Fig. 4-C and D).

Myocardial abscess, a suppurative infection of the myocardium, endocardium, valves, perivalvular structures, or the cardiac conduction system, have been described very rarely.1 Generally, this disease occurs as a complication of infective endocarditis, acute myocardial infarction, or other infections in the setting of debilitating condition. In our case, interestingly, there was no definite infection focus or coronary obstruction in cardiac CT. To the best of our knowledge, this is the first report concerning the possibility of occurrence of myocardial abscess presented as AMI, not a following consequence of AMI.