This 50-year-old man came to the Emergency Department complaining of having substernal chest pain for more than 10 hours. The pain was sharp and not exertion-related. It could radiate to the left shoulder, back, and scapula. It seemed positional, as inspiration could worsen it, and leaning forward could somewhat mitigate the pain. At times, he also experienced nausea, dyspnea, and cold sweats. Reportedly, he had flu-like symptoms with a runny nose and sore throat but didn’t visit any clinic seeking help. Past medical history was significant for thalassemia, mild GERD, and gallbladder stone diagnosed ten years ago. He looked apprehensive due to chest pain, but he was alert. BT/PR/RR measured 37 ℃ /86 /min/14/min, and blood pressure was 123/66 mmHg. There was no JVD or leg edema. PMI was in the mid-clavicular line at the left 4th/5th intercostal space. There were no murmurs, but both systolic and diastolic friction rubs and bilateral basilar crackles were audible. The rest of the physical findings were unremarkable. ECG showed sinus rhythm at 72/min. Notably, there was diffuse ST segment elevation in all leads except for aVR with P-R segment depression in inferior and anterior chest leads; also, there was a QS pattern in leads V1 and V2 suggestive of old antero-septal MI. The chest X-ray revealed slight cardiomegaly, torturous aorta, increased lung infiltrates at the right lower and left middle lung field, and prominent hilum on the right side, suggesting an infectious process. Pertinent laboratory data include Hb 12.5 g/dl, Hct 39.1 %, WBC 8.89 x10^3/ul (baso 0.1 %, eos 1.1 %, lym 9.1 %, mono 7.2 %, neut 82.5 %), Plt 215 x10^3/ul, BUN 9 mg/dl, Cr 0.72 mg/dl, glucose 132 mg/dl, Na 138 mmol/l, K 4.0 mmol/l, GOT 22 U/l, CK 59 U/l, CK-MB 1.4 ng/ml, troponin I 0.01 ng/ml. Two hours later, his symptoms persisted, and cardiac enzymes showed a slight increase in troponin I 0.05 ng/ml. ECG showed diminished voltage in precordial leads and Q waves in V1-V3. To rule out coronary syndrome (ACS), the care team did an emergency cardiac catheterization with coronary angiography, which revealed all arteries were patent. A subsequent chest CT scan also excluded aortic dissection. Still, it disclosed mild calcification over coronary arteries and aorta, pericardial thickening with mild pericardial effusion, and a small amount of bilateral pleural effusion. He then developed a low-grade fever (37.6-38.2℃). The corresponding CRP measured 23.1, ESR 16, and WBC 11.17. The echocardiography revealed slight concentric LV hypertrophy with an EF of 71% and a small pericardial effusion. The care team empirically started levofloxacin to combat possible bacterial infection. RA factor was normal, and so were Weil-Felis (rickettsia infection) and Widal (typhoid and paratyphoid) tests. With supportive therapy, the rest of the clinical course went uneventfully, and he could return home in two weeks. Before discharge, the care team had given him a schedule of follow-up plans.