PB0012 - Destruction of advanced atherosclerotic intraplaque neovessels, using Super- Paramagnetic Iron Oxide Nanoparticles (SPION)- mediated alternating magnetic field- based hyperthermic therapy

Background: Atherosclerosis is the leading cause of cerebrovascular and cardiovascular diseases. Atherosclerosis result in plaque formation and plaque rupture leads to arterial thromboembolism. Plaque neovascularization is the main feature of vulnerable plaques.

Aims: In this study, we developed an experimental alternating magnetic field- based Super- Paramagnetic Iron Oxide Nanoparticles (SPION)- mediated hyperthermic therapy system and investigated its effectiveness on advanced neovessel- rich atherosclerotic plaque regression, wherein diagnostic B- mode ultrasound is combined with therapeutic system, with a goal of increased safety.

Methods: Briefly, New Zealand white rabbits underwent primary ballooning injury at the right common carotid artery followed by a 1.5 % cholesterol- rich diet injury for 14 weeks. Histopathology and ultrasonography results showed the formation of advanced atherosclerosis with neovessels– rich plaque and severe stenosis (> 70%) in all of the rabbits’ arteries. The animals treated by Helmholtz coil- based alternating magnetic field system accompanied by intravenous Super- Paramagnetic Iron Oxide Nanoparticles (SPION) (10 ml/kg) administration.

Results: Results from histology, B-mode and color Doppler ultrasonography at the atherosclerotic region showed a significant reduction in the mean value for blood mean velocity, intraplaque neovessels density, wall mean thickness and percentage of luminal cross- sectional area of stenosis and significant increase in the mean value for blood volume flow in the treatment group compared with the other groups (p < 0.05).

Conclusion(s): Magneto- hyperthermal and magneto- hypervibrational effects of Super- Paramagnetic Iron Oxide Nanoparticles, induced by Helmholtz coil- based alternating magnetic field, can cause to destroy the intraplaque neovessels, resulting in the intraplaque lipid and immune cells content reduction and significant dilate the luminal cross- sectional area of stenosis.