The Association between Diffuse Myocardial Fibrosis on Cardiac Magnetic Resonance T1 Mapping and Myocardial Dysfunction in Diabetic Rabbits

Abstract

The objective of this study was to assess the relationship between imaging surrogates for diffuse fibrosis and myocardial dysfunction. Thirty-six New Zealand white rabbits were classified into two groups: a control group (n = 18) and an alloxan-induced diabetes mellitus (DM) group (n = 18). For all rabbits, conventional ultrasonography, two-dimensional speckle tracking, and cardiac magnetic resonance (CMR) T1 mapping were performed; all of the rabbits were then sacrificed for Masson’s staining. The extracellular volume (ECV) was calculated from pre- and post-contrast T1 values and compared with myocardial function measured by echocardiography using Pearson’s correlation. In the DM group, ECV increased as the duration of diabetes increased, consistent with the changes in myocardial fibrosis verified by pathology. Moreover, ECV was strongly correlated with the early diastolic strain rate (r = −0.782, p < 0.001) and moderately correlated with the radial systolic peak strain (r = 0.478, p = 0.045). Thus, ECV is an effective surrogate for myocardial diffuse fibrosis on CMR imaging, and higher ECV values are associated with an increased impairment of myocardial diastolic function.

Quantification of Early Diffuse Myocardial Fibrosis Through 7.0 T Cardiovascular Magnetic Resonance T1 Mapping in a Type 1 Diabetic Mellitus Mouse Model

“…FS and EF progressively decreased in the T1DM group from 4 to 24 weeks, whereas EF was preserved; FS and EF values signi cantly differed at 16 weeks, whereas the E/A ratio signi cantly differed at 12 weeks between the T1DM and control groups. Diastolic dysfunction occurred earlier than systolic dysfunction, and the diastolic function gradually deteriorated in the T1DM group; this nding is consistent with that of previous studies [14,23] .…”

“…Our study showed that the ECV value was strongly correlated with CVF, and the postcontrast T1 value was moderately associated with the CVF value. The main reason is likely that the gadolinium agent (as an extracellular contrast agent) could not pass through the cell membrane and enter the cell; therefore, the postcontrast T1 value was mainly associated with the contrast agent concentration in the extracellular matrix, which is consistent with the ndings of our previous studies [23,29] and another study [28] . In addition, our study showed that the ECV value was higher than CVF, possibly because the CVF value re ects only the extracellular collagen ber content, whereas the ECV value can also indicate mucus matrix, lipid, and necrosis components outside cells.…”

Association of Elevated NT-proBNP With Myocardial Fibrosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

“…Understanding the pathogenesis of interstitial fibrosis in the stressed heart and dissecting the mechanisms responsible for adverse cardiac outcomes are crucial to design new strategies for prevention of cardiac failure and myopathy. In an animal model, the change of ECV occurred earlier than myocardial dysfunction in diabetic rabbits (28). It is generally accepted that in the process of the pathological remodeling of cardiomyopathy, progressive accumulation of extracellular matrix components increases cardiac stiffness (29,30).…”

Myocardial fibrosis evaluated by diffusion‐weighted imaging and its relationship to 3D contractile function in patients with hypertrophic cardiomyopathy

“…13 Myocardial extracellular volume (ECV), which is acquired noninvasively with T 1 mapping before and after gadolinium administration, can be robustly quantified by comparing changes in relaxation rate between the pre-and postcontrast state in myocardium to blood. [14][15][16] ECV has been histologically validated for quantification of diffuse myocardial fibrosis [17][18][19] and has been shown to correspond to the histologically measured extent of fibrosis in surgical samples in HCM. 15,20 Contrast-free quantitative cardiac MR techniques have been demonstrated to be promising for evaluating replacement myocardial fibrosis in chronic myocardial infarction.…”