ABSTRACT
PURPOSE: To demonstrate the feasibility of sodium 23 ((23)Na) 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 (23)Na 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 (23)Na 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 (23)Na signal intensity. Only 10 patients in the subacute and nine in the chronic group revealed late enhancement; significant correlation with (23)Na 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 (23)Na signal intensity but was extensively larger. CONCLUSION: (23)Na MR imaging demonstrates dysfunctional myocardium caused by subacute and chronic myocardial infarction.
Subject(s)
Magnetic Resonance Imaging/methods , Myocardial Infarction/pathology , Sodium , Adult , Aged , Aged, 80 and over , Chronic Disease , Feasibility Studies , Female , Humans , Image Enhancement , Male , Middle Aged , Time FactorsABSTRACT
PURPOSE: Sodium is elevated in acute/subacute myocardial infarction due to three distinct mechanisms: Breakdown of ion homeostasis with accumulation of intracellular sodium, extracellular edema formation and, during scar formation, increase of extracellular vs. intracellular space as cardiomyocytes are replaced by connective tissue. 23Na MRI has previously been shown to have the potential to demonstrate myocardial infarction in an animal model. Aim of this study was, therefore, to demonstrate myocardial infarction with the use of 23Na-MRI in patients. MATERIAL AND METHODS: 10 patients were examined 14 +/- 7 days after first myocardial infarction using a 23Na surface coil at 1.5 T. Double angulated short axis images of the entire heart were imaged using an ECG-triggered 3d-FLASH-sequence (FOV, 450 mm; matrix, 64 x 128; spatial resolution, 3.5 x 7 mm2; slice thickness, 16 mm; 32 acquisitions). Areas of elevated sodium signal intensity were correlated with infarct-related wall motion abnormalities imaged by Cine MRI in breathhold-technique. RESULTS: 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 Cine MRI. CONCLUSIONS: Elevated 23Na MR image signal intensity demonstrates subacute myocardial infarction in patients.
