Author + information
- Received January 12, 1989
- Revision received February 6, 1989
- Accepted September 13, 1989
- Published online March 1, 1990.
- Uri Rosenschein, MD∗,
- Jonathan J. Bernstein, BSE§,
- Elio DiSegni, MD1,∗,
- Elieser Kaplinsky, MD∗,
- Joelle Bernheim, MD‡ and
- Leon A. Rozenzsajn, PhD†∥
- ↵1Address for reprints: Uri Rosenschein, MD, Division of Cardiology. Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032.
To investigate the use of high energy ultrasound as an alternative energy for angioplasty, an experimental ultrasonic angioplasty device was developed. The device was studied in two bioassay systems: an in vitro system for the disruption of atherosclerotic plaques and thrombi and an in vivo system for the recanalization of occluded canine femoral arteries.
In vitro, sonication efficiently reduced the size of the plaques. Atheromatous plaques (n = 11) disrupted at a rate of 21 ± 8 s/cm2; complicated plaques (n = 14) disrupted at a rate of 132 ± 45 s/CM2 (p < 0.001). Histologic examination revealed that the disruption of the plaques took place without concurrent damage to the media or adventitia. Ninety percent of the disrupted plaque debris had a diameter of <20 μm and was composed primarily of cholesterol monohydrate crystals. Solid thrombus (n = 5) weight was reduced from 1.6 ±0.2 to 0.4 ± 0.1 (p<0.0001) after 20 s of sonication.
In vivo, sonication resulted in recanalization in all seven arteries tested in seven dogs. The obstruction was reduced from 93 ± 11% to 18 ± 7% (p < 0.001). On histologic examination, the arterial wall injury index was found to be 1.56 ± 0.42 in the test arteries compared with 1.37 ± 0.47 in the control arteries (p = NS).
The disruption of atherosclerotic plaques and thrombi, together with the efficient recanalization of the occluded arteries, demonstrates the potential of ultrasound angioplasty as a catheter-based technique for angioplasty. The histologic findings suggest that the ultrasonic angioplasty device selectively disrupts the ultrasound-sensitive atherosclerotic plaques and thrombi, with minimal damage to the ultrasound-resistant arterial wall.
- Received January 12, 1989.
- Revision received February 6, 1989.
- Accepted September 13, 1989.