Joseph Allencherril1, Yama Fakhri2, Henrik Engblom3, Einar Heiberg3, Marcus Carlsson3, Jean-Luc Dubois-Rande4, Sigrun Halvorsen5, Trygve S Hall5, Alf-Inge Larsen6, Svend Eggert Jensen7, Hakan Arheden3, Dan Atar5, Peter Clemmensen8, Maria Sejersten Ripa9, Yochai Birnbaum10. 1. Section of Cardiology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA. Electronic address: allenche@bcm.edu. 2. Department of Cardiology, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Department of Medicine, Nykøbing F Hospital, Nykøbing F, Denmark. 3. Department of Clinical Physiology, Lund University, Skåne University Hospital, Lund, Sweden. 4. Assistance Publique Hôpitaux de Paris, Hôpital Henri Mondor, Créteil, France. 5. Department of Cardiology B, Oslo University Hospital Ullevål, and Faculty of Medicine, Al, Oslo, Norway. 6. Department of Cardiology, Stavanger University Hospital, Stavanger, Norway; Department of Clinical Science, University of Bergen, Bergen, Norway. 7. Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark; Department of Clinical Medicine, Aalborg University Hospital, Aalborg, Denmark. 8. Department of Medicine, Nykøbing F Hospital, Nykøbing F, Denmark; Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark; Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany. 9. Department of Cardiology, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 10. Section of Cardiology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA.
Abstract
BACKGROUND: Anteroseptal ST elevation myocardial infarction (STEMI) is traditionally defined on the electrocardiogram (ECG) by ST elevation (STE) in leads V1-V3, with or without involvement of lead V4. It is commonly taught that such infarcts affect the basal anteroseptal myocardial segment. While there are suggestions in the literature that Q waves limited to V1-V4 represent predominantly apical infarction, none have evaluated anteroseptal ST elevation territories. We compared the distribution of the myocardium at risk (MaR) in STEMI patients presenting with STE limited to V1-V4 and those with more extensive STE (V1-V6). METHODS: We identified patients in the MITOCARE study presenting with a first acute STEMI and new STE in at least two contiguous anterior leads from V1 to V6. Patients underwent cardiac magnetic resonance (CMR) imaging three to five days after acute infarction. RESULTS: Thirty-two patients met inclusion criteria. In patients with STE in V1-V4 (n = 20), myocardium at risk (MaR) > 50% was seen in 0%, 85%, 75%, 100%, and 90% in the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. The group with STE in V1-V6 (n = 12), MaR > 50% was seen in 8%, 83%, 83%, 92%, and 83% of the same segments. CONCLUSIONS: Patients with acute STEMI and STE in leads V1-V4, exhibit MaR in predominantly apical territories and rarely in the basal anteroseptum. We found no evidence to support existence of isolated basal anteroseptal or septal STEMI. "Anteroapical" infarction is a more precise description than "anteroseptal" infarction for acute STEMI patients exhibiting STE in V1-V4.
RCT Entities:
BACKGROUND: Anteroseptal ST elevation myocardial infarction (STEMI) is traditionally defined on the electrocardiogram (ECG) by ST elevation (STE) in leads V1-V3, with or without involvement of lead V4. It is commonly taught that such infarcts affect the basal anteroseptal myocardial segment. While there are suggestions in the literature that Q waves limited to V1-V4 represent predominantly apical infarction, none have evaluated anteroseptal ST elevation territories. We compared the distribution of the myocardium at risk (MaR) in STEMI patients presenting with STE limited to V1-V4 and those with more extensive STE (V1-V6). METHODS: We identified patients in the MITOCARE study presenting with a first acute STEMI and new STE in at least two contiguous anterior leads from V1 to V6. Patients underwent cardiac magnetic resonance (CMR) imaging three to five days after acute infarction. RESULTS: Thirty-two patients met inclusion criteria. In patients with STE in V1-V4 (n = 20), myocardium at risk (MaR) > 50% was seen in 0%, 85%, 75%, 100%, and 90% in the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. The group with STE in V1-V6 (n = 12), MaR > 50% was seen in 8%, 83%, 83%, 92%, and 83% of the same segments. CONCLUSIONS:Patients with acute STEMI and STE in leads V1-V4, exhibit MaR in predominantly apical territories and rarely in the basal anteroseptum. We found no evidence to support existence of isolated basal anteroseptal or septal STEMI. "Anteroapical" infarction is a more precise description than "anteroseptal" infarction for acute STEMI patients exhibiting STE in V1-V4.