“…Härdig et al [45] measured a 31.2% enhancement of streptokinase thrombolysis in human whole blood clots exposed to 1.0-MHz pulsed ultrasound with a duty cycle of 10% and a spatial average, temporal average intensity of 0.5 W/cm 2 . These investigators also noted a decrease in ultrasound enhancement of streptokinase thrombolysis at higher exposure level (above 1 W/ cm 2 ).…”
Introduction-Thrombolytics such as recombinant tissue plasminogen activator (rt-PA) have advanced the treatment of ischemic stroke, myocardial infarction, deep vein thrombosis and pulmonary embolism.
“…Härdig et al [45] measured a 31.2% enhancement of streptokinase thrombolysis in human whole blood clots exposed to 1.0-MHz pulsed ultrasound with a duty cycle of 10% and a spatial average, temporal average intensity of 0.5 W/cm 2 . These investigators also noted a decrease in ultrasound enhancement of streptokinase thrombolysis at higher exposure level (above 1 W/ cm 2 ).…”
Introduction-Thrombolytics such as recombinant tissue plasminogen activator (rt-PA) have advanced the treatment of ischemic stroke, myocardial infarction, deep vein thrombosis and pulmonary embolism.
“…[25][26][27][28][29][30][31][32][33][34][35][36][37][38] According to Blinc et al, 25 the degree of thrombolysis depends on the plasminogen activator concentration, the intensity of ultrasound waves, the duty cycles, and the frequency. A successful thrombolytic effect has been reported for urokinase, 25,26,28 rtPA, 25,48 tPA, 27 reteplase, 35 and streptokinase 25,28,34,36 at intensities ranging from 0.125 to 4 W/cm 2 . The lytic effect of streptokinase and reteplase, however, disappeared at intensity levels of $4 W/cm 2 , indicating that the balance between ultrasound waves and pharmacological treatment is crucial.…”
Section: In Vitro Studiesmentioning
confidence: 99%
“…The lytic effect of streptokinase and reteplase, however, disappeared at intensity levels of $4 W/cm 2 , indicating that the balance between ultrasound waves and pharmacological treatment is crucial. [34][35][36] In addition, Soltani et al 90 demonstrated that ultrasound with a frequency of 1 MHz and intensities of 2.5 to 3.1 W/cm 2 had no statistically significant effect on the enzymatic activity of the plasminogen activators urokinase, reteplase, alteplase, and streptokinase. Nevertheless, only limited data is available on the ideal concentrations of plasminogen activators necessary for optimal ultrasoundenhanced thrombolysis.…”
Ultrasound enhanced thrombolysis seems to be a promising concept in the treatment of various thromboembolic conditions. The technique has shown to be safe and efficacious in vitro, in vivo, and in clinical studies. Randomized controlled trials are warranted and should be awaited before considering catheter-directed ultrasound-accelerated thrombolysis as a new standard treatment.
“…PEG-gelatin nanocarriers also prolonged the circulation of tPA and released it in an ultrasound-responsive fashion, improving recanalization of occlusive clots in rabbits. 29 Further refinements of the ELIP approach are warranted, as potent ultrasound may inactivate PAs 30 and cause vascular damage. Some clots may not be amenable to this approach due to unknown location or risk of hemorrhage.…”
Section: Ata Carriers Sensitive To Ultrasound and Hydrodynamic Forcesmentioning
Despite continued achievements in antithrombotic pharmacotherapy, difficulties remain in managing patients at high risk for both thrombosis and hemorrhage. Utility of antithrombotic agents (ATAs) in these settings is restricted by inadequate pharmacokinetics and narrow therapeutic indices. Use of advanced drug delivery systems (ADDSs) may help to circumvent these problems. Various nanocarriers, affinity ligands, and polymer coatings provide ADDSs that have the potential to help optimize ATA pharmacokinetics, target drug delivery to sites of thrombosis, and sense pathologic changes in the vascular microenvironment, such as altered hemodynamic forces, expression of inflammatory markers, and structural differences between mature hemostatic and growing pathological clots. Delivery of ATAs using biomimetic synthetic carriers, host blood cells, and recombinant fusion proteins that are activated preferentially at sites of thrombus development has shown promising outcomes in preclinical models. Further development and translation of ADDSs that spare hemostatic fibrin clots hold promise for extending the utility of ATAs in the management of acute thrombotic disorders through rapid, transient, and targeted thromboprophylaxis. If the potential benefit of this technology is to be realized, a systematic and concerted effort is required to develop clinical trials and translate the use of ADDSs to the clinical arena.
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