Imaging of Acute Myocardial Infarction and Reperf usion

Abstract

During the last 20 years there has been a large amount of investigation designed to determine what is the best way of imaging acute myocardial infarction (AMI) using radiopharmaceuticals. ^99mTc pyrophosphate is ideal for cases where the clinical diagnosis cannot be made but it is insensitive to detect subendocardial AMI and is taken up by reversibly-injured myocytes. Antimyosin antibody imaging is specific for AMI but it is flow-dependent at low myocardial flows and it distributes in a nonuniform way in reperfused infarcts requiring high nuclear imaging (SPECT or PET) spatial resolution for proper measurement. ¹⁸F fluorodeoxyglucose (FDG) is taken up by viable cells but likely by macrophages too, in the core of AMI. ^99mTc glucarate has not been investigated in detail but this sugar analog is more accurate than FDG in AMI. ^99mTc sestamibi has been extensively used for AMI measurement but SPECT quantitation of transmural infarcts has not been achieved. Unresolved issue is imaging of AMI during reperfusion where there is widespread microvascular injury and capillary plugging.

Non-invasive imaging of microvascular damage

“…It should be noted that 18 F-FDG uptake, an index of viability and predictor of recovery in chronic situations, 44 in the acute phase not necessarily represent surviving myocytes but rather leukocytes accumulating during reperfusion 45 (Figure 3), although the volume of these cell elements seems to be small compared to myocyte volume. 46 A validation study compared intra-coronary Doppler flow measurements against early (26 ± 9 hours after PCI) myocardial perfusion PET in patients successfully reperfused by primary PCI showing a significant correlation between coronary flow reserve and myocardial perfusion reserve in both infarct and non-infarct regions suggesting that either technique can be used to assess the early impact of successful primary PCI.…”