Ultrasound-accelerated Thrombolysis for the Treatment of Deep Vein Thrombosis: Initial Clinical Experience

Parikh, Sanjiv; Motarjeme, Amir; McNamara, Tom; Raabe, Rodney D.; Hagspiel, Klaus D.; Benenati, James F.; Sterling, Keith M.; Comerota, Anthony J.

doi:10.1016/j.jvir.2007.11.023

Cited by 179 publications

(115 citation statements)

References 29 publications

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“…CDT methods are currently available for the treatment of DVT as outlined by Pianta and Thomson (25). Motarjeme (26) and Parikh et al (11) were first to report the use of US-accelerated CDT for the treatment of DVT. They reported significantly higher complete clot lysis rates using US-accelerated CDT compared with standard CDT without an increase in the bleeding or thromboembolic risk.…”

Section: Discussionmentioning

confidence: 99%

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US-accelerated catheter-directed thrombolysis for the treatment of deep venous thrombosis

Dumantepe

Tarhan²,

Yurdakul³

et al. 2012

Diagn Interv Radiol

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Section: Discussionmentioning

confidence: 99%

“…Ultrasonography (US)-accelerated CDT has been developed to rapidly and completely resolve thrombi, thus decreasing the potential risk for PTS (11,12). This technique integrates high-frequency, low-intensity US with standard CDT to accelerate clot dissolution, which reduces treatment time and the incidence of thrombolysis-related complications.…”

mentioning

confidence: 99%

US-accelerated catheter-directed thrombolysis for the treatment of deep venous thrombosis

Dumantepe

Tarhan²,

Yurdakul³

et al. 2012

Diagn Interv Radiol

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“…FIBRINOLYSINS, INCLUDING tissue type (tPA) and urokinase (active two-chain enzyme; tcuPA), are plasminogen activators (PAs) that have long been used to treat a variety of thrombotic conditions including acute myocardial infarction (23; 44), deep vein thrombosis (33,40), ischemic stroke (1,3), acute respiratory distress syndrome (ARDS) (20,21), pulmonary emboli, and organizing pleural effusions (8,9,11,31,37,43). Although intrapleural fibrinolytic therapy (IPFT) has been in use for over 60 years, it has recently undergone reassessment in light of the disparate results seen in clinical trials (9,11,37).…”

mentioning

confidence: 99%

Active α-macroglobulin is a reservoir for urokinase after fibrinolytic therapy in rabbits with tetracycline-induced pleural injury and in human pleural fluids

Komissarov

Florova

Azghani

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

106

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Komissarov AA, Florova G, Azghani A, Karandashova S, Kurdowska AK, Idell S. Active ␣-macroglobulin is a reservoir for urokinase after fibrinolytic therapy in rabbits with tetracycline-induced pleural injury and in human pleural fluids. Am J Physiol Lung Cell Mol Physiol 305: L682-L692, 2013. First published August 30, 2013 doi:10.1152/ajplung.00102.2013.-Intrapleural processing of prourokinase (scuPA) in tetracycline (TCN)-induced pleural injury in rabbits was evaluated to better understand the mechanisms governing successful scuPA-based intrapleural fibrinolytic therapy (IPFT), capable of clearing pleural adhesions in this model. Pleural fluid (PF) was withdrawn 0 -80 min and 24 h after IPFT with scuPA (0 -0.5 mg/kg), and activities of free urokinase (uPA), plasminogen activator inhibitor-1 (PAI-1), and uPA complexed with ␣-macroglobulin (␣M) were assessed. Similar analyses were performed using PFs from patients with empyema, parapneumonic, and malignant pleural effusions. The peak of uPA activity (5-40 min) reciprocally correlated with the dose of intrapleural scuPA. Endogenous active PAI-1 (10 -20 nM) decreased the rate of intrapleural scuPA activation. The slow step of intrapleural inactivation of free uPA (t1/2 ␤ ϭ 40 Ϯ 10 min) was dose independent and 6.7-fold slower than in blood. Up to 260 Ϯ 70 nM of ␣M/uPA formed in vivo [second order association rate (kass) ϭ 580 Ϯ 60 M Ϫ1 ·s Ϫ1 ]. ␣M/uPA and products of its degradation contributed to durable intrapleural plasminogen activation up to 24 h after IPFT. Active PAI-1, active ␣2M, and ␣2M/uPA found in empyema, pneumonia, and malignant PFs demonstrate the capacity to support similar mechanisms in humans. Intrapleural scuPA processing differs from that in the bloodstream and includes 1) dose-dependent control of scuPA activation by endogenous active PAI-1; 2) two-step inactivation of free uPA with simultaneous formation of ␣M/uPA; and 3) slow intrapleural degradation of ␣M/uPA releasing active free uPA. This mechanism offers potential clinically relevant advantages that may enhance the bioavailability of intrapleural scuPA and may mitigate the risk of bleeding complications. fibrinolytic therapy; rabbit model; pleural injury; urokinase; ␣-macroglobulin; human FIBRINOLYSINS, INCLUDING tissue type (tPA) and urokinase (active two-chain enzyme; tcuPA), are plasminogen activators (PAs) that have long been used to treat a variety of thrombotic conditions including acute myocardial infarction (23; 44), deep vein thrombosis (33, 40), ischemic stroke (1, 3), acute respiratory distress syndrome (ARDS) (20, 21), pulmonary emboli, and organizing pleural effusions (8,9,11,31,37,43). Although intrapleural fibrinolytic therapy (IPFT) has been in use for over 60 years, it has recently undergone reassessment in light of the disparate results seen in clinical trials (9, 11, 37). The efficacy of IPFT in adults remains a subject of ongoing debate. Intrapleural streptokinase was ineffective in patients with complicated parapneumonic pleural effusions and empyema (EMP), whereas ...

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“…A total of 16 retrospective case studies have described the use of PMT with or without CDT in a little under 500 patients [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35]102], two of these studies were retrospective comparative studies comparing PMT plus CDT versus CDT alone. To date, there have been no randomized clinical trials of PMT compared with standard anticoagulation.…”

Section: Procedures Of Pmtmentioning

confidence: 99%

Thrombolysis versus thrombectomy in acute deep vein thrombosis

O’Sullivan

2011

Interventional Cardiology

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Thrombolysis versus thrombectomy in acute deep vein thrombosis reviewDeep vein thrombosis (DVT) is a significant health problem leading to the admission of over 250,000 Americans each year. Its most serious acute complication, namely pulmonary embolus kills approximately 100,000 each year, and is the third most common cardiovascular related mortality after myocardial infarction and stroke. Chronic leg problems following DVT include leg heaviness, tiredness, cramping and ulceration. These are termed the post-thrombotic syndrome. The current standard therapy of anticoagulation has changed little over 50 years. It does not remove or destroy thrombus, relying instead on the bodies own fibrinolytic mechanisms to do so. DVT needs to be more accurately categorized on an anatomical basis, and for a variety of reasons, the area of most importance is the iliofemoral region. The rationale for active, rather than passive, thrombus removal relies on multiple observations that, by doing so improves luminal patency, restores valvular function and has the potential to reduce the severity of post-thrombotic syndrome. Techniques of thrombus removal include catheter-directed thrombolysis, mechanical thrombectomy, and various combinations of both (pharmacomechanical catheter-directed thrombolysis). Although there no few direct trials comparing these directly, there is a reasonable body of evidence demonstrating their efficacy.

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Ultrasound-accelerated Thrombolysis for the Treatment of Deep Vein Thrombosis: Initial Clinical Experience

Cited by 179 publications

References 29 publications

US-accelerated catheter-directed thrombolysis for the treatment of deep venous thrombosis

US-accelerated catheter-directed thrombolysis for the treatment of deep venous thrombosis

Active α-macroglobulin is a reservoir for urokinase after fibrinolytic therapy in rabbits with tetracycline-induced pleural injury and in human pleural fluids

Thrombolysis versus thrombectomy in acute deep vein thrombosis

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