Xiaoming Jia1, Einar Heiberg2, Maria Sejersten Ripa3, Henrik Engblom2, Marcus Carlsson2, Sigrun Halvorsen4, Håkan Arheden2, Dan Atar4, Peter Clemmensen5,6,7, Yochai Birnbaum1. 1. Department of Medicine, Section of Cardiology, Baylor College of Medicine, Houston, Texas, USA. 2. Department of Clinical Physiology, Clinical Sciences, Lund University and Skane University Hospital, Lund, Sweden. 3. Department of Cardiology, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 4. Department of Cardiology, Division of Medicine, Oslo University Hospital and Institute of Clinical Sciences, University of Oslo, Oslo, Norway. 5. Department of Medicine, Division of Cardiology, Nykøbing Falster Hospital, Nykøbing Falster, Denmark. 6. Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark. 7. Department of General and Interventional Cardiology, University Heart Center Hamburg, Hamburg-Eppendorf, Germany.
Abstract
The aim of our study was to examine the pathophysiology of ST depression (STD) in leads V1-V3 in the setting of inferior ST elevation myocardial infarction (iSTEMI) through the perspective of cardiac magnetic resonance (CMR). METHODS: Differences in myocardial area at risk (MaR), infarct size, ejection fraction and myocardial segment involvement by CMR were compared in MITOCARE trial patients with first iSTEMI with ST elevation (STE), STD or no ST changes (NST) in V1-V3. The frontal plane projection of the inferior wall MaR in relationship to the anterior/posterior chest wall was calculated and compared between groups. RESULTS: Fifty-six patients were included. Patients with STD (n = 38) and STE (n = 5) in V1-V3 had significantly larger mean MaR compared to NST (n = 13; 32 ± 7%LV, 36 ± 10%LV and 26 ± 6%LV, respectively; p = 0.01). STD in leads V1-V3 was associated with more apical inferior and mid inferoseptal involvement and had a larger mean frontal plane projection of MaR compared with NST (24 ± 6%LV vs. 20 ± 6%LV, p = 0.04). CONCLUSION: STD in V1-V3 in iSTEMI is associated with larger MaR, more extension into the inferoseptal segments and likely results from greater frontal plane projection of the MaR, leading to reciprocal changes on the electrocardiogram.
The aim of our study was to examine the pathophysiology of ST depression (STD) in leads V1-V3 in the setting of inferior ST elevation myocardial infarction (iSTEMI) through the perspective of cardiac magnetic resonance (CMR). METHODS: Differences in myocardial area at risk (MaR), infarct size, ejection fraction and myocardial segment involvement by CMR were compared in MITOCARE trial patients with first iSTEMI with ST elevation (STE), STD or no ST changes (NST) in V1-V3. The frontal plane projection of the inferior wall MaR in relationship to the anterior/posterior chest wall was calculated and compared between groups. RESULTS: Fifty-six patients were included. Patients with STD (n = 38) and STE (n = 5) in V1-V3 had significantly larger mean MaR compared to NST (n = 13; 32 ± 7%LV, 36 ± 10%LV and 26 ± 6%LV, respectively; p = 0.01). STD in leads V1-V3 was associated with more apical inferior and mid inferoseptal involvement and had a larger mean frontal plane projection of MaR compared with NST (24 ± 6%LV vs. 20 ± 6%LV, p = 0.04). CONCLUSION: STD in V1-V3 in iSTEMI is associated with larger MaR, more extension into the inferoseptal segments and likely results from greater frontal plane projection of the MaR, leading to reciprocal changes on the electrocardiogram.