Ultrasonic cavitation-enabled treatment for therapy of hypertrophic cardiomyopathy: Proof-of-principle

Ultrasound myocardial cavitation enabled treatment (MCET) creates scattered microlesions in the myocardium, which can be accumulated to produce a desired macrolesion. MCET was applied to the SS-16BN rat model of hypertrophic cardiomyopathy (HCM) for proof-of-principle as a means for myocardial reduction. A focused ultrasound transducer was targeted using 10 MHz imaging (10S, GE Vivid 7) to the left ventricular wall of anesthetized rats in a warmed water bath. Pulse bursts of 4 MPa peak rarefactional pressure amplitude were intermittently triggered 1:8 heartbeats during 10 min infusion of a microbubble suspension. Methylprednisolone was given to reduce initial inflammation and Losartan was given to improve healing. MCET significantly reduced the targeted wall thickness (n = 11) at 28 d post treatment by 16.2% (P<0.01) relative to shams (n = 8), with myocardial strain rate and endocardial border displacement reduced by 34% and 29%, respectively. This demonstrates sufficient effect for a therapeutic outcome similar to surgical myectomy or alcohol ablation. Premature ECG complexes and plasma troponin measurements at the time of treatment were found to be useful to gauge optimal and suboptimal treatments, and thus aid in achieving a desired impact. With clinical translation, MCET therapy should fill the need for a new non-invasive HCM therapy option.