Background—Elevated ²³Na 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 ²³Na MRI to assess infarct size and investigated possible mechanisms for elevated ²³Na image intensity.

Methods and Results—Thirteen dogs and 8 rabbits underwent in situ coronary artery occlusion and reperfusion and were imaged by ²³Na MRI. For anatomically matched left ventricular short-axis cross sections (n=46), infarct size measured by in vivo ²³Na MRI correlated well with triphenyltetrazolium chloride staining (r=0.87, y=0.92x+3.37, P<0.001). Elevated ²³Na 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 ²³Na 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 ²³Na MR image intensity in vivo measures infarct size after reperfused infarction in both a large and a small animal model. The mechanism of elevated ²³Na image intensity is probably intracellular sodium accumulation secondary to loss of myocyte ionic homeostasis.