Diffusion Tensor Magnetic Resonance Imaging Mapping the Fiber Architecture Remodeling in Human Myocardium After Infarction

Abstract

BACKGROUND: Diffusion tensor magnetic resonance imaging (DT-MRI) provides a means for nondestructive characterization of myocardial architecture. We used DT-MRI to investigate changes in direction-dependent water diffusivity to reflect alterations in tissue integrity (trace apparent diffusion coefficients [ADCs] and fractional anisotropy [FA]), as well as indicators of remodeling of fiber helix angles, in patients after myocardial infarction. METHODS AND RESULTS: Thirty-seven patients (35 men, 2 women; median age, 59) after acute myocardial infarction (median interval from onset, 26 days) were enrolled. DT-MRI was performed at the midventricular level to measure trace ADC, FA, and helix angles of myofibers. Helix angles were grouped into left-handed helical fibers, circumferential fibers, and right-handed helical fibers. Measurements were correlated with viability and regional wall motion assessed by contrast-delay-enhancement and cine MRI, respectively. The infarct zone showed significantly increased trace ADC and decreased FA than the remote zone. The percentage of left-handed helical fibers increased from the remote zone (mean +/- SD, 13.3 +/- 5.8%) to the adjacent zone (19.2 +/- 9.7%) and infarct zone (25.8 +/- 18.4%) (MANOVA, P = 0.004). The percentage of right-handed helical fibers decreased from the remote zone (35.0 +/- 9.0%) to the adjacent zone (25.5 +/- 11.5%) and infarct zone (15.9 +/- 9.2%) (P < 0.001). Multiple linear regression showed that the percentage of left-handed helical fibers of the infarct zone was the strongest correlate of infarct size and predictor of ejection fraction. CONCLUSIONS: In vivo DT-MRI of postinfarct myocardium revealed a significant increase in trace ADC and a decrease in FA, indicating altered tissue integrity. The redistribution of fiber architecture correlated with infarct size and left ventricular function. This technique may help us understand structural correlates of functional remodeling after infarction.