Abstract 1922: Cardiac Magnetic Resonance Identifies Infrequent Remote Areas of Myocardial Necrosis in First Acute Myocardial Infarction
Background: Atherosclerosis biology, rather than plaque size, determines propensity for acute coronary events. IVUS and angioscopy studies have suggested the presence of multiple ruptured plaques in ACS. Yet it remains unknown whether this results in multiple simultaneous areas of myocardial necrosis. Cardiac magnetic resonance (CMR) identifies micro-infarcts of as little as 1–2% of the myocardial mass. We studied by CMR whether micro-infarcts occur in non infarct-related territories in subjects presenting with a first acute myocardial infarction.
Methods: We prospectively studied 50 subjects by CMR within 12h after primary angioplasty and stenting for STEMI. Cardiac function was assessed on a 1.5T scanner with dedicated cardiac coil by standard b-SSFP technique; myocardial necrosis was identified by delayed-enhancement imaging 10–12 minutes after 0.2 mmol/kg gadolinium-DTPA IV and adjustment of inversion time to null normal myocardium. Necrosis was defined by automated software set to identify greater than 2.5 SD increased gray value compared to remote non-infarcted myocardium. Acute necrosis was confirmed by T2 edema-weighted imaging to differentiate from chronic events.
Results: No complications occurred as a result of very early CMR. 3 subjects required gentle sedation for anxiety related to mild claustrophobia. Subjects were similar to typical cohorts (Age: 55 ± 13 y, male gender: 70%, diabetes: 25%). Mean door-to-balloon was inferior to 60 min. Infarct-related territory was anterior in 43%, inferior in 50%, and lateral in 7%. 70% were Killip I–II and LVEF was 58 ± 13%. Necrotic myocardium represented 19% of total myocardium. An area of necrosis remote from the infarct-related territory was identified in 18% of subjects. Acuteness of the necrosis was confirmed by T2 imaging in all segments. No subject presented greater than 2 necrotic territories.
Conclusion: Despite suggestions that multiple plaque ruptures occur during ACS, micro-infarctions remote from the infarct-related territory are identified infrequently. It remains to be determined whether this reflects the difficulty in identifying ruptured plaque or whether these only rarely result in a thrombus burden large enough to incur necrosis.