Myocardial Infarction Due to Left Circumflex Artery Occlusion: A Subtle Trojan Horse

Abstract A 47–year–old man presented to the emergency department complaining of recurrent chest pain (CP) since the previous day. His medical history included active smoking and dyslipidemia. The ECG revealed sinus bradycardia (56 bpm) with widespread ST elevation, consistent with benign early repolarization, and hyperacute and broad–based T waves in V2–V3 (Fig. A). The echocardiography showed normal left and right ventricular systolic function and no valvular abnormalities. A low but abnormal initial high–sensitivity cardiac troponin I value (40 pg/mL, normal range: 1.7– 34,2 pg/mL) and a slightly and early increase after two hours (52 pg/ml) were seen. Therefore, the patient was admitted to our intensive cardiac care unit (ICCU) with a working diagnosis of non–ST–segment elevation myocardial infarction (NSTEMI). No sign or symptoms of heart failure on physical examination were recorded. GraceScore 2.0 was calculated as 68 points and coronary angiography was organized within 24h. Two hours after admission to the ICCU, the patient experienced a new episode of CP. Consequently, ECG and echo were repeated. Compared to the previous results, ECG showed dynamic changes in V2–V3, with the resolution of hyperacute T waves (Fig B); bedside echo remained unchanged. Considering the unresponsiveness to nitrate therapy, the cath lab was activated for a time–dependent coronary angiography. The exam showed an acute total thrombotic occlusion of the mid–segment of the circumflex branch (LCx) in the setting left–sided dominant circulation. A drug eluting stent was deployed into the culprit lesion (Fig. C), and the coronary flow was restored completely (TIMI Flow 3). The subsequent hospital stay proceeded without complications. The peak troponin level was 60’000 pg/ml. The patient was discharged on the fifth day, asymptomatic and hemodynamically stable, with instructions to continue dual antiplatelet therapy. The case report focuses on the electrocardiographic and angiographic expression of LCx total occlusion. Despite acute myocardial infarction (AMI) size was large, as confirmed by the abnormal troponin I values and the angiographic total occlusion, the first and the repeated ECGs showed only vague repolarization changes without clear ST–segment modifications. LCx occlusion is often characterized by the absence of significant ST–elevation, therefore categorized as NSTEMI. Greater awareness of the presentation of LCx–related AMI can be crucial to avoid delays in reperfusion.