Abstract
BackgroundMyocardial fibrosis is a common hallmark of many diseases of the heart. Late gadolinium enhanced MRI is a powerful tool to image replacement fibrosis after myocardial infarction (MI). Interstitial fibrosis can be assessed indirectly from an extracellular volume fraction measurement using contrast-enhanced T1 mapping. Detection of short T2* species resulting from fibrotic tissue may provide an attractive non-contrast-enhanced alternative to directly visualize the presence of both replacement and interstitial fibrosis.ObjectiveTo goal of this paper was to explore the use of a T2*-weighted radial sequence for the visualization of fibrosis in mouse heart.MethodsC57BL/6 mice were studied with MI (n = 20, replacement fibrosis), transverse aortic constriction (TAC) (n = 18, diffuse fibrosis), and as control (n = 10). 3D center-out radial T2*-weighted images with varying TE were acquired in vivo and ex vivo (TE = 21 μs-4 ms). Ex vivo T2*-weighted signal decay with TE was analyzed using a 3-component model. Subtraction of short- and long-TE images was used to highlight fibrotic tissue with short T2*. The presence of fibrosis was validated using histology and correlated to MRI findings.ResultsDetailed ex vivo T2*-weighted signal analysis revealed a fast (T2*fast), slow (T2*slow) and lipid (T2*lipid) pool. T2*fast remained essentially constant. Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts. T2*slow correlated with the presence of diffuse fibrosis in TAC hearts (r = 0.82, P = 0.01). Ex vivo and in vivo subtraction images depicted a positive contrast in the infarct co-localizing with the scar. Infarct volumes from histology and subtraction images linearly correlated (r = 0.94, P<0.001). Region-of-interest analysis in the in vivo post-MI and TAC hearts revealed significant T2* shortening due to fibrosis, in agreement with the ex vivo results. However, in vivo contrast on subtraction images was rather poor, hampering a straightforward visual assessment of the spatial distribution of the fibrotic tissue.
Highlights
Myocardial fibrosis is the formation of excessive collagen and other extracellular matrix (ECM) components in the interstitium and perivascular regions of the myocardium
C57BL/6 mice were studied with myocardial infarction (MI) (n = 20, replacement fibrosis), transverse aortic constriction (TAC) (n = 18, diffuse fibrosis), and as control (n = 10). 3D center-out radial T2*weighted images with varying TE were acquired in vivo and ex vivo (TE = 21 μs-4 ms)
Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts
Summary
Myocardial fibrosis is the formation of excessive collagen and other extracellular matrix (ECM) components in the interstitium and perivascular regions of the myocardium. This accumulation is a consequence of the disruption of the equilibrium between synthesis and degradation of ECM components [1]. Functional consequences of fibrosis are increased myocardial stiffness, decreased myocardial perfusion and perfusion reserve, and mechano-electrical uncoupling. Together these form a substrate for impaired ventricular relaxation leading to diastolic dysfunction, inappropriate pressure development for systemic perfusion resulting in impaired systolic function, ischemia, and arrhythmia [1,3].
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