Ultrasonic Angioplasty: Assessing the Risk of Arterial Perforation

Atherosclerosis is a cardiovascular disease that effects large and medium muscular arteries (such as coronary and iliac) and also large elastic arteries (such as aorta) [1]. It causes thickening of the arterial wall and over time can result in a completely blocked artery or chronic total occlusion (CTO). While the majority of atherosclerotic lesions can be attempted by typical Percutaneous Transluminal Coronary Angioplasty (PTCA) such as balloon and stent implantation, calcified CTOs are often problematic as they do not lend themselves to be accessed by the guidewire which is required to implant the balloon and stent. Excessive guidewire pushing force may result in arterial perforation with CTOs often requiring invasive by-pass surgery. An alternative method proposes the use of low frequency high power ultrasound transmitted through wire waveguides for the removal of the calcified material from advanced atherosclerotic lesions. This type of energy manifests itself as a mechanical vibration at the distal tip of the wave guide with amplitudes of up to 100 microns and frequencies ranging between 20-45 kHz commonly reported. The ultrasound acts to disrupt calcified diseased tissue by means of direct contact ablation, cavitation, acoustic steaming and other pressure wave components while the elastic tissue remains largely unaffected [2]. In this study the effects of this form of ultrasound on healthy arterial tissue (porcine aorta) is examined. Experiments were carried out to determine the force required to perforate healthy porcine arterial tissue both with and without ultrasound at various distal tip displacements