Sodium is elevated in acute/subacute myocardial infarction due to three dis
tinct mechanisms: Breakdown of ion homeostasis with accumulation of intrace
llular sodium, extracellular edema formation and, during scar formation, in
crease of extracellular vs, intracellular space as cardiomyocytes are repla
ced by connective tissue. Na-23 MRI has previously been shown to have the p
otential to demonstrate myocardial infarction in an animal model. Aim of th
is study was, therefore, to demonstrate myocardial infarction with the use
of Na-23-MRI in patients. Material and Methods: 10 patients were examined 1
4+/-7 days after first myocardial infarction using a Na-23 surface coil at
1.5 T. Double angulated short axis images of the entire heart were imaged u
sing an EGG-triggered 3d-FLASH-sequence (FOV, 450 mm; matrix, 64 x 128; spa
tial resolution, 3.5 x 7 mm(2); slice thickness, 16 mm; 32 acquisitions). A
reas of elevated sodium signal intensity were correlated with infarct-relat
ed wall motion abnormalities imaged by Cine MRI in breathhold-technique. Re
sults: All patients showed an area of elevated sodium signal intensity that
correlated well with the clinically determined localization of myocardial
infarction as well as with regional wall motion abnormalities detected by C
ine MRI. Conclusions: Elevated Na-23 MR image signal intensity demonstrates
subacute myocardial infarction in patients.