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Open Access Research

Modelling ultrasound-induced mild hyperthermia of hyperplasia in vascular grafts

Mark R Brinton15, Russell J Stewart2, Alfred K Cheung34, Douglas A Christensen12 and Yan-Ting E Shiu23*

Author Affiliations

1 Department of Electrical and Computer Engineering, University of Utah, Salt Lake City, UT, USA

2 Department of Bioengineering, University of Utah, Salt Lake City, UT, USA

3 Department of Medicine, Division of Nephrology & Hypertension, University of Utah, Salt Lake City, UT, USA

4 Medical Service, Veterans Affairs Salt Lake City Healthcare System, UT, USA

5 Department of Electrical Engineering, Stanford University, 350 Serra Mall (Mail Code: 9505), Stanford, CA 94305-9505, USA

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Theoretical Biology and Medical Modelling 2011, 8:42  doi:10.1186/1742-4682-8-42

Published: 3 November 2011

Abstract

Background

Expanded polytetrafluoroethylene (ePTFE) vascular grafts frequently develop occlusive neointimal hyperplasia as a result of myofibroblast over-growth, leading to graft failure. ePTFE exhibits higher ultrasound attenuation than native soft tissues. We modelled the selective absorption of ultrasound by ePTFE, and explored the feasibility of preventing hyperplasia in ePTFE grafts by ultrasound heating. Specifically, we simulated the temperature profiles of implanted grafts and nearby soft tissues and blood under ultrasound exposure. The goal was to determine whether ultrasound exposure of an ePTFE graft can generate temperatures sufficient to prevent cell growth on the graft without damaging nearby soft tissues and blood.

Methods

Ultrasound beams from two transducers (1.5 and 3.2 MHz) were simulated in two graft/tissue models, with and without an intra-graft cellular layer mimicking hyperplasia, using the finite-difference time-domain (FDTD) method. The resulting power deposition patterns were used as a heat source for the Pennes bioheat equation in a COMSOL® Multiphysics heat transfer model. 50°C is known to cause cell death and therefore the transducer powers were adjusted to produce a 13°C temperature rise from 37°C in the ePTFE.

Results

Simulations showed that both the frequency of the transducers and the presence of hyperplasia significantly affect the power deposition patterns and subsequent temperature profiles on the grafts and nearby tissues. While neither transducer significantly raised the temperature of the blood, the 1.5-MHz transducer was less focused and heated larger volumes of the graft and nearby soft tissues than the 3.2-MHz transducer. The presence of hyperplasia had little effect on the blood's temperature, but further increased the temperature of the graft and nearby soft tissues in response to either transducer. Skin cooling and blood flow play a significant role in preventing overheating of the native tissues.

Conclusions

Modelling shows that ultrasound can selectively heat ePTFE grafts and produce temperatures that cause cell death on the graft. The temperature increase in blood is negligible and that in the adjacent soft tissues may be minimized by skin cooling and using appropriate transducers. Therefore, ultrasound heating may have the potential to reduce neointimal hyperplasia and failure of ePTFE vascular grafts.