Abstract
BackgroundMyocardial cavitation-enabled therapy (MCET) has been proposed as a means to achieve minimally invasive myocardial reduction using ultrasound to produce scattered microlesions by cavitating contrast agent microbubbles.MethodsRats were treated using burst mode focused ultrasound at 1.5 MHz center frequency and varying envelope and pressure amplitudes. Evans blue staining indicated lethal cardiomyocytic injury. A previously developed quantitative scheme, evaluating the histologic treatment results, provides an insightful analysis for MCET treatment parameters. Such include ultrasound exposure amplitude and pulse modulation, contrast agent dose, and infusion rate.ResultsThe quantitative method overcomes the limitation of visual scoring and works for a large dynamic range of treatment impact. Macrolesions are generated as an accumulation of probability driven microlesion formations. Macrolesions grow radially with radii from 0.1 to 1.6 mm as the ultrasound exposure amplitude (peak negative) increases from 2 to 4 MPa. To shorten treatment time, a swept beam was investigated and found to generate an acceptable macrolesion volume of about 40 μL for a single beam position.ConclusionsUltrasound parameters and administration of microbubbles directly influence lesion characteristics such as microlesion density and macrolesion dimension. For lesion generation planning, control of MCET is crucial, especially when targeting larger pre-clinical models.
Highlights
Hypertrophic cardiomyopathy (HCM) is a common genetic cardiovascular disease, which is usually clinically recognized by a maximal left ventricular wall thickness greater than 15 mm [1]
(MCET), has been proposed as a means to achieve minimally invasive myocardial reduction by cavitating contrast agent microbubbles with ultrasound to produce a fractional macrolesion containing sparse and histologically definable microlesions [4]
Cavitation is enabled by the injection of ultrasound contrast agents
Summary
Hypertrophic cardiomyopathy (HCM) is a common genetic cardiovascular disease, which is usually clinically recognized by a maximal left ventricular wall thickness greater than 15 mm [1]. An innovative therapeutic scheme, named myocardial cavitation-enabled therapy (MCET), has been proposed as a means to achieve minimally invasive myocardial reduction by cavitating contrast agent microbubbles with ultrasound to produce a fractional macrolesion containing sparse and histologically definable microlesions [4]. In vivo experiments reveal that cavitation-induced lesions take place at peak rarefactional pressures larger than 2 MPa as obtained under free field conditions. In this case, ECG is monitored for premature complexes. Myocardial cavitation-enabled therapy (MCET) has been proposed as a means to achieve minimally invasive myocardial reduction using ultrasound to produce scattered microlesions by cavitating contrast agent microbubbles
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