LAUSR

In acute myocardial infarction, 12-lead electrocardiogram (ECG) usually allows attribution of the infarct territory to the ‘culprit’ coronary vessel. In some cases, an altered cardiac anatomy in the left hemithorax or of coronary arteries can hinder this correlation and be misleading to clinicians [1, 2]. We present a case of inferior ST-elevation myocardial infarction with newly diagnosed ST-elevation in anterior leads after PCI of the right coronary artery (RCA). A 62-year-old man was admitted to our hospital for acute coronary syndrome with persistent angina pectoris for approximately 9 h and possible signs of Q-wave infarction and borderline-significant ST-elevation in preclinical ECGleads III and aVF (Fig. 1, 1st column). Preclinical blood pressure was 115/76 mmHg and heart rate was at 78/min. The patient was free from dyspnea, rales or other clinical signs of congestion were not present. As angina was persistent, suggesting ongoing ischemia, and the ECG was borderline-significant, the patient was diagnosed as ST-elevation myocardial infarction and transferred directly to the catheterization laboratory for immediate coronary angiography. Thrombotic proximal RCA occlusion was diagnosed and successfully treated by percutaneous coronary intervention (PCI) and drug-eluting stent implantation (Fig. 2, left panel, a–d). Final thrombolysis in myocardial infarction (TIMI) flow grade was III. Diagnosis to device and door to device times were within current recommendations (34 and 18 min, respectively). In the ECG post-PCI, new ST-elevations in leads V1–V3 were detected and no relevant ST-resolution in leads III and aVF (Fig. 1, 2nd column) despite full resolution of symptoms. Revisiting the angiogram showed no compromise of the left anterior descending coronary artery, but a compromised right ventricular branch suggesting severe right ventricular involvement (TIMI grade I flow, blue arrow, Fig. 2b). The ST-segment elevations were regressing in a follow-up ECG 4 h later (Fig. 1, 3rd column). Total and MB-creatine kinase peaked 6 h after PCI at 26.1 μmol/l and 3.21 μmol/l (reference values < 3.17 μmol/l and 0.41 μmol/l) indicating overall moderate infarction and were declining thereafter. Additional contrast enhanced cardiac magnetic resonance imaging (CMR) revealed large inferior infarction with microvascular obstruction (red arrow, Fig. 2, right panel, a) and relevant right ventricular involvement (white arrow, Fig. 2, right panel, a) with only minor myocardial salvage. Left ventricular ejection fraction was mildly reduced (49%). An unusually far left position of the heart’s sagittal axis towards the left hemithorax with left anterior right ventricle position was found on four-chamber view (green arrow, Fig. 2, right panel, c).