Authors:

Alyssa Richards

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About Paper:

Cardiomyopathy is a result of the cardiovascular phenotype of Duchenne muscular dystrophy (DMD), which leads to congestive heart failure and early mortality. Cardiomyopathy remains the number one cause of death in DMD. Our objective was to characterize the progression of cardiomyopathy in a murine model of DMD. We hypothesized that a genetic mouse model of DMD will exhibit significantly lower function over time as measured by ejection fraction when given an isoproterenol challenge. The murine model of DMD C57BL/10ScSn-Dmdmdx/J (B10.mdx; n=6 female) was examined in comparison to the wild-type control strain C57BL/10ScSnJ (B10; n=6 female). Intraperitoneal isoproterenol administered via daily injections at 3 mg/kg were given for five consecutive days. Cardiac function was assessed by 2D cine ultrasound using a Vevo3100 imaging system (FUJIFILM, VisualSonics) and 4D ultrasound using a MATLAB graphical user interface. Decreases in ejection fraction between baseline and day 7 occurred in both groups following the isoproterenol injections. The changes in B10.mdx ejection fraction decreased significantly from 66% to 45%. Significant decreases in strain in the B10.mdx group between baseline and day 7 were observed in the basal circumferential strain, mid-LV circumferential strain, mid-LV surface area strain, apical surface area strain, and anterior longitudinal strain (p<0.05). Murine B10.mdx models exhibit DMD-associated cardiomyopathy comparable to humans. A series of low-dose isoproterenol injections has the potential to unmask changes such as ejection fraction and strain within 7 days.

Source:

Purdue University / 2023

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Co-authors:

Alyssa Richards