Relationship of elevated 23Na magnetic resonance image intensity to infarct size after acute reperfused myocardial infarction

Background-Elevated Na-23 MR image intensity after acute myocardial infarction has previously been shown to correspond to high tissue [Na+] and loss of myocardial viability. In this study, we explored the potential of in vivo Na-23 MRI to assess infarct size and investigated possible mechanisms for elevated Na-23 image intensity. Methods and Results-Thirteen dogs and 8 rabbits underwent in situ coronary artery occlusion and reperfusion and were imaged by Na-23 MRI. For anatomically matched left ventricular short-axis cross sections (n=46), infarct size measured by in vivo Na-23 MRI correlated well with triphenyltetrazolium chloride staining (r=0.87, y=0.92x+3.37, P<0.001). Elevated Na-23 image intensity was observed in infarcted myocardium (206+/-37% of remote in dogs, P<0.001; 215+/-58% in rabbits, P<0.002) but was not observed after severe but reversible ischemic injury (101+/-11% of baseline, P=NS). High-resolution ex vivo imaging revealed that regions of elevated Na-23 image intensity appeared to be identical to those of infarcted regions (r=0.97, y=0.92x+1.52, P<0.001). In infarcted regions, total tissue [Na+] was elevated (89+/-12 versus 37+/-9 mmol/L in control tissue, 156+/-60% increase, P<0.001) and was associated with increased intracellular sodium (254+/-68% of control, P<0.005) and an increased intracellular sodium/potassium ratio (868+/-512% of control, P<0.002). Morphometric analysis demonstrated only a minor increase in extracellular volume (17+/-8% versus 14+/-5%, P<0.05) in the infarcted territory. Conclusions-Elevated Na-23 MR image intensity in vivo measures infarct size after reperfused infarction in both a large and a small animal model. The mechanism of elevated Na-23 image intensity is probably intracellular sodium accumulation secondary to loss of myocyte ionic homeostasis.