Quantification of murine cardiac hypertrophy using 4D ultrasound

Abstract

Cardiac hypertrophy is abnormal thickening, followed by dilation, of the heart which can lead to congestive heart failure. Herein, we use a mouse model of hypertrophy to explore the relationship between in vivo strain and the resultant hypertrophic state. To do so, osmotic pumps containing saline (n = 5) or angiotensin II (AngII; n = 10) were surgically implanted into the dorsal flank of C57BL/6J mice. AngII increased blood pressure and cardiac afterload, causing myocardial hypertrophy. Mice were imaged weekly using a VisualSonics Vevo2100 ultrasound system with a MS550D transducer (40 MHz center frequency) to collect ECG-gated Kilohertz Visualization data. In combination with a linear stepper motor, we also collected four dimensional (4D) cardiac data (3D + time). Two weeks post-surgery, pumps were removed from a subset of mice to assess the heart’s ability to repair itself post-insult (n = 5). All mice were euthanized at 4 weeks. Standard metrics of left ventricular mass measured via two-dimensional slices of the 4D data indicated significantly increased mass in the AngII mice by day 14. Removal of the pump enabled significant, but partial, recovery. Current work is being performed to calculate strain within the cardiac wall. Ultimately, we aim to determine if increases in in vivo strain precede increases in cardiac mass.