Tissue sodium concentration in myocardial infarction in humans: a quantitative 23Na MR imaging study

Abstract

Purpose: To prospectively determine whether the absolute tissue sodium concentration (TSC) increases in myocardial infarctions (MIs) in humans and whether TSC is related to infarct size, infarct age, ventricular dysfunction, and/or electrophysiologic inducibility of ventricular arrhythmias.

Materials and methods: Delayed contrast material-enhanced 1.5-T hydrogen 1 ((1)H) magnetic resonance (MR) imaging was used to measure the size and location of nonacute MIs in 20 patients (18 men, two women; mean age, 63 years +/- 9 [standard deviation]; age range, 48-82 years) examined at least 90 days after MI. End-systolic and end-diastolic volumes, ejection fraction, and left ventricle (LV) mass were measured with cine MR imaging. The TSC in normal, infarcted, and adjacent myocardial tissue was measured on sodium 23 ((23)Na) MR images coregistered with delayed contrast-enhanced (1)H MR images. Programmed electric stimulation to induce monomorphic ventricular tachycardia (MVT) was used to assess arrhythmic potential, and myocardial TSC was compared between the inducible MVT and noninducible MVT patient groups.

Results: The mean TSC for MIs (59 micromol/g wet weight +/- 10) was 30% higher than that for noninfarcted (remote) LV regions (45 micromol/g wet weight +/- 5, P < .001) and that for healthy control subjects, and TSC did not correlate with infarct age or functional and morphologic indices. The mean TSC for tissue adjacent to the MI (50 micromol/g wet weight +/- 6) was intermediate between that for the MI and that for remote regions. The elevated TSC measured in the MI at (23)Na MR imaging lacked sufficient contrast and spatial resolution for routine visualization of MI. Cardiac TSC did not enable differentiation between patients in whom MVT was inducible and those in whom it was not.

Conclusion: Absolute TSC is measurable with (23)Na MR imaging and is significantly elevated in human MI; however, TSC increase is not related to infarct age, infarct size, or global ventricular function. In regions adjacent to the MI, TSC is slightly increased but not to levels in the MI.

(c) RSNA, 2008.

Figures

Figure 1:

A, Short-axis delayed contrast-enhanced MR image (5.4/1.3/175, 20° flip angle, 40-cm field of view, 256 × 160 matrix, 8-mm section thickness with 10-mm spacing) in 58-year-old man with extensive MI (arrows). B, Image in A overlapping 1H fast spin-echo MR image, with cut planes positioned to reveal the intersection of the two data sets on a line through the LV. Landmarks such as the epicardial and endocardial boundaries, aorta, apex, and base are used to guide manual registration of the partially transparent images, which are rendered stereoscopically. Arrow shows position of MI. Fast spin-echo image depicts signals from the three reference phantoms embedded in 23Na coil.

Figure 2:

Sagittal MR images in 53-year-old man with posterior MI show placements of ROIs for quantification of TSC. A, Fast gradient-echo 1H image (100/4.2, 90° flip angle, 36-cm field of view, 256 × 192 matrix, 5-mm section thickness) shows signal intensity level contours. The signal intensity level contours outlined in yellow are copied onto corresponding 23Na image (B) (85/0.4, 90° flip angle, 22-cm field of view, three-dimensional twisted spiral acquisition, 6-mm isotropic spatial resolution), where they are outlined in gray. In B, ROI 1 is MI used to calculate MI TSC (48 μmol/g wet weight in this patient); ROIs 2 and 3, adjacent posterior LV wall (TSC, 44 μmol/g wet weight); ROI 4, noninvolved (remote) LV wall (TSC, 39 μmol/g wet weight); and ROI 5, LV blood (TSC, 72 μmol/g wet weight). For display purposes, the color scale was designed to be approximately proportional to the sodium concentrations by using a calculated B1 map of the coil to correct for receiver coil sensitivity. C, Short-axis delayed contrast-enhanced image.

Figure 3:

Axial 1H fast spin-echo MR image (gated to 1 R-R interval, 845/17, echo train length of four, 90° flip angle, 40-cm field of view, 256 × 192 matrix, 7.5-mm section thickness, 2.5-mm intersection gap) merged with corresponding 23Na twisted projection MR image (85/0.4, 90° flip angle, 22-cm field of view, three-dimensional twisted spiral acquisition, isotropic spatial resolution of 6 mm) in 61-year-old man with remote septal MI (arrows). Left: Fast spin-echo 1H MR image. Middle: Receive coil sensitivity–corrected twisted projection 23N MR image only, with color scale proportional to TSC and including calculated B1 correction. Right: Twisted projection 23Na MR image as a color map overlaid on 1H MR image, with saturation of 23Na color map modulated by the 1H MR signal intensity such that 23Na map colors are suppressed in areas where 1H image is dark. Note the increase in sodium signal intensity in the distal part of the septum (arrow), which corresponds to infarcted region determined by delayed contrast-enhanced MR imaging, to nearly the signal intensity of the sodium in the LV blood.

Figure 4:

Graph shows TSC values in MI in 20 patients, in adjacent LV tissue in 11 patients, and in remote LV tissue in 20 patients, with mean values ± 1 standard deviation. MI TSC is significantly increased compared with remote LV TSC, with Bonferroni correction (κ = 3, α = .017). Adjacent LV TSC does not differ significantly from remote region or MI values at similar analysis. N.S. = nonsignificant difference.

Figure 5:

Graph shows TSC values in MI, adjacent LV tissue, and remote LV tissue as a function of infarct age (in days) in the 17 patients in whom infarct age was known. Mean TSC values measured in infarcted myocardium in each of 20 patients, in remote noninvolved myocardium in 17 patients, and in adjacent myocardial regions in the eight subjects who had quantifiable adjacent regions and known infarct age are shown. Some of the older MIs still showed a large increase in TSC relative to the remote LV, and some younger MIs did not show a substantial elevation in TSC. Consequently, the correlation between MI TSC and infarct age was poor (Pearson product moment r= 0.09).

Figure 6:

Graphs show TSC values in MI, adjacent LV, and remote LV, which did not correlate with, A, end-diastolic volume (EDV) (r= −0.002, P > .05), B, ejection fraction (EF) (r= −0.095, P > .05), C, absolute infarct size (r= −0.16, P> .05), or, D, LV mass (r= 0.005, P> .05). Mean TSC values in MI (20 patients), remote noninvolved myocardium (20 patients), and adjacent myocardial regions (11 patients) are shown. Although one might expect the larger infarcts to lead to stress and possibly increased TSC in remote LV tissue or to larger LV mass, or the higher TSC in MI or adjacent tissue to possibly impair cardiac function (as expressed by ejection fraction), no such correlations were apparent from our data.

Figure 7:

Bar graph shows cardiac TSC in MI, adjacent LV tissue, and remote LV regions in nine patients in whom MVT was inducible at electrophysiologic testing and in seven patients in whom MVT was not inducible. For this analysis, adjacent LV tissue was assessed in five patients. Mean TSC in MI was 57 μmol/g wet weight ± 13 for nine patients in inducible group and 61 μmol/g wet weight ± 10 for seven patients in noninducible group (P> .05). Mean TSC in adjacent zones assessed in five patients was 54 μmol/g wet weight ± 14 for inducible group and 52 μmol/g wet weight ± 7 for noninducible group (P> .05). Mean TSC in remote myocardial tissue was 46 μmol/g wet weight ± 7 for nine patients in inducible group and 45 μmol/g wet weight ± 4 for seven patients in noninducible group (P> .05).