Acute Myocardial Infarction: The Relationship between Duration of Ischaemia and Infarct Size in Humans - Assessment by MRI and SPECT

Abstract: The effect of duration of ischaemia on final infarct size is well established in animal studies, but not fully evaluated in humans. Delayed contrast-enhanced magnetic resonance imaging (DE-MRI) can be used to distinguish between viable and non-viable myocardium and thus to quantify infarct size. We therefore used DE-MRI to investigate how duration of ischaemia affects final infarct size normalized to myocardium at risk in humans (Paper IV). The results showed that 20-40 % of myocardium at risk was infarcted after 2-3 hours of occlusion, indicating that a major part of myocardium at risk may be salvaged if reperfusion is performed within the first few hours of occlusion. In order to study infarct evolution in humans, we first investigated the correlation between perfusion defect size assessed by myocardial single photon emission computed tomography (SPECT) perfusion imaging with final infarct size by DE-MRI (Paper I), showing that measurements by the two methods do not differ much for revascularized myocardial infarction. Biochemical markers of cardiac injury are used to estimate myocardial infarct size. The agreement between cumulative as well as peak values of biochemical markers and DE-MRI in patients with an occluded coronary artery was studied for Paper II.We showed that in order to estimate infarct size, serial measurements may be substituted by acquisitions at 3, 6, and 12 hours after reperfusion, saving both cost and time in the clinical setting. Finally, experimental infarction in pig was studied in collaboration with Uppsala University in order to provide a basis for further investigations on how MR contrast agents distribute in perfused and non-perfused myocardium in humans (Paper III). This study showed that perfusion is needed for delivery of contrast agent, and that the non-perfused myocardium, despite absence of contrast agent in this region, appears bright when nulling the signal from viable perfused myocardium using inversion-recovery DE-MRI.