Preclinical Study Evaluates Primary Lesion Treatment With CSI's Orbital Atherectomy System Before Drug Delivery in Calcified PAD

May 20, 2015—CBSET, a preclinical biomedical research institute, announced findings from a cadaver study suggesting that modification of atherosclerotic plaque with the Diamondback 360 orbital atherectomy system (Cardiovascular Systems, Inc. [CSI]) improved drug uptake in calcified peripheral lesions. Gunnar Tepe, MD, from RoMed Hospital in Rosenheim, Germany, stated in CBSET's announcement, “This preclinical study could have a significant clinical impact by demonstrating improved drug delivery after modification of calcified lesions.”

The study results were presented by CBSET Chairman Elazer Edelman, MD, in a dedicated session on peripheral interventions at the EuroPCR 2015 conference being held May 19–22 in Paris, France.

In a separate press release, CSI specified the findings showed that primary treatment with CSI’s Diamondback 360 improved paclitaxel absorption by 50% in the calcified cadaveric peripheral arteries. Historically, noted the company, calcified plaque barriers in arteries have been reported to make drug diffusion and retention more difficult.
 
In CBSET’s press release, Dr. Edelman stated, “The data are exciting in that they suggest that subtle modification to the plaque surface can have profound effects on drug penetration. Massive debulking may be a relic of the past, and a more muted approach may extend endovascular intervention for peripheral artery disease (PAD) treatment into vessels even below the knee.”

Peter Markham, Chief Executive Officer of CBSET, added, “A more sophisticated understanding of drug transfer after plaque modification is critically important to optimizing PAD therapies for improved clinical outcomes.”

Also in the announcement, Rami Tzafriri, PhD, Principal Scientist at CBSET, explained, “This study is part of a larger effort by CBSET, Massachusetts Institute of Technology, and collaborating companies to leverage benchtop, animal, and computational studies in order to define the barriers to drug distribution in healthy and diseased arteries. While these initial findings illustrate, for the first time, the barrier effects of calcified plaque on arterial drug diffusion, they provide a path for improved therapy, as even relatively benign modification of this plaque barrier can profoundly improve drug delivery into diseased peripheral arteries.”