(Circulation. 1996;94:775-778.)
© 1996 American Heart Association, Inc.
Articles |
the Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, Calif.
Correspondence to Robert J. Siegel, MD, Division of Cardiology, Rm 5335, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048.
Background External ultrasound has a synergistic effect on thrombus disruption with thrombolytic agents in vitro. We hypothesized that transcutaneous ultrasound could augment thrombolysis in vivo.
Method and Results Thrombus formation was induced electrically in 48 pairs of iliofemoral arteries of 24 rabbits; arterial occlusions were documented angiographically. In 17 of 24 rabbits, 25 000 units/kg streptokinase was then administered intravenously. The pairs of iliofemoral arteries were randomized to receive ultrasound treatment or no ultrasound treatment. Low-frequency (26 kHz) ultrasound (continuous wave, 18 W/cm2) was applied transcutaneously over the area of occlusion. In 7 of 24 rabbits, 14 thrombotically occluded iliofemoral arteries were exposed to ultrasound alone without streptokinase. The results were evaluated through the use of angiography (TIMI grade flow) and histopathology. After 30±10 minutes of activated sonication combined with intravenous streptokinase, 10 of 17 iliofemoral arteries (59%) treated with transcutaneous ultrasound were widely patent angiographically, with TIMI grade 3 flow. Histologically, the patent arteries had only minimal focal mural thrombus. The angiographic patency rate was significantly lower in the control groups: 1 of 17 arteries (6%) treated with streptokinase alone (P=.0012) and 1 of 14 arteries (7%) treated with ultrasound alone (P=.0036).
Conclusions In vivo transcutaneous ultrasound significantly augments lysis of thrombi with streptokinase in rabbit iliofemoral arteries.
Key Words: ultrasound thrombolysis streptokinase
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