PURPOSE: To demonstrate the feasibility of sodium 23 (²³Na) magnetic resonance (MR) imaging for assessment of subacute and chronic myocardial infarction and compare with cine, late enhancement, and T2-weighted imaging.

MATERIALS AND METHODS: Thirty patients underwent MR imaging 8 days ± 4 (subacute, n = 15) or more than 6 months (chronic, n = 15) after myocardial infarction by using a ²³Na surface coil with a double angulated electrocardiogram-triggered three-dimensional gradient-echo sequence at 1.5 T. In addition, cine, inversion-recovery gradient-echo, and, in the subacute group, T2-weighted images (n = 9) were obtained. Myocardial infarction mass was depicted as elevated signal intensity or wall motion abnormalities and expressed as a percentage of total left ventricular mass for all modalities. Correlations were tested with correlation coefficients.

RESULTS: All patients after subacute infarction and 12 of 15 patients with chronic infarction had an area of elevated ²³Na signal intensity that significantly correlated with wall motion abnormalities (subacute; r = 0.96, P < .001, and chronic; r = 0.9, P < .001); three patients had no wall motion abnormalities or elevated ²³Na signal intensity. Only 10 patients in the subacute and nine in the chronic group revealed late enhancement; significant correlation with ²³Na MR imaging occurred only in subacute group (r = 0.68, P < .05). Myocardial edema in subacute infarction correlated (r = 0.71, P < .05) with areas of elevated ²³Na signal intensity but was extensively larger.

CONCLUSION:²³Na MR imaging demonstrates dysfunctional myocardium caused by subacute and chronic myocardial infarction.