Use of a Direct Thrombin Inhibitor (Argatroban) during Pulse-Spray Thrombolysis in Experimental Thrombosis

Valji, Karim; Arun, K.; Bookstein, Joseph J.

doi:10.1016/s1051-0443(95)71067-3

Cited by 13 publications

(3 citation statements)

References 23 publications

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“…In contrast, the anticoagulant effect of argatroban is concentration dependent [6] and comprises both free and clot-bound thrombin. Specific antithrombin therapy using argatroban has been shown to be superior to heparin treatment in numerous experimental animal models of arterial thrombogenesis [7][8][9][10][11][12][13][14][15][16][17][18][19]. At doses causing comparable prolongation of activated partial thromboplastin time (aPTT), argatroban has been demonstrated to be significantly more effective than heparin for the prevention of platelet-rich thrombotic occlusion in an animal model [20].…”

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confidence: 99%

Argatroban during percutaneous transluminal coronary angioplasty: Results of a dose-verification study

Herrman¹,

Suryapranata²,

Heijer

et al. 1996

J Thromb Thrombol

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Background. Thrombin is a key enzyme in thrombogenesis. In animals, specific antithrombotic therapy at the time of coronary angioplasty reduced the incidence of subacute occlusion and inhibited the restenosis response. Argatroban is a highly selective synthetic thrombin antagonist that binds in a competitive manner. This is a report of a dose-verification study, assessing the safety and feasibility of intravenous Argatroban administration in patients undergoing percutaneous transluminal coronary angioplasty. Methods. Before angioplasty an intravenous bolus of 30 µg/kg argatroban was administered, followed by a continuous infusion of 3.5 µg/kg/min for 72 hours. Bolus injection was repeated, and the infusion rate was increased in order to achieve an activated coagulation time (ACT) of over 300 seconds. Following interim analysis, the bolus and initial infusion rate for the subsequent treatment groups was determined. Study endpoints were the occurrence of adverse events, coagulation tests, and qualitative angiogram reading. Patients were monitored by continuous 12-lead electrocardiographic recording over 24 hours, and underwent control angiography 18-24 hours following angioplasty. Results. Four treatment groups, comprised of 2, 8, 9, and 11 patients, respectively, were studied. The first two patients were excluded from analysis, since the initial dose was ineffective to attain an ACT-authorizing coronary angioplasty. The group with the highest dosage received a 250 µg/kg intravenous bolus of argatroban, followed by a 4 hour infusion of 15 µg/kg/min. At 4 hours the infusion rate was lowered to 3.8 µg/kg/min and was continued for 68 hours without adjustment for catheter removal. The adverse event profile included myocardial infarction, aortocoronary bypass graft, bailout procedures, and repeat coronary angioplasty. Thrombin-time (TT), activated partial thromboplastin time (APTT), and prothrombin time (PT) were significantly related to argatroban plasma concentration, as demonstrated by regression analyses (R-square 0.64, 0.71, and 0.84, respectively). Prothrombin fragments 1 and 2 and thrombin-antithrombin III complex did not fit into a mathematical model, but showed slightly increased levels after reduction or cessation of the infusion rate. Conclusions. This dose-verification study, including 30 patients at four dose levels, indicated that argatroban infusion in coronary angioplasty patients can be administered safely, and results in an adequate and predictable level of anticoagulation.

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confidence: 99%

Argatroban during percutaneous transluminal coronary angioplasty: Results of a dose-verification study

Herrman¹,

Suryapranata²,

Heijer

et al. 1996

J Thromb Thrombol

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“…The simultaneous use of alteplase and argatroban is documented minimally in the literature [5][6][7][8][9][10][11]. To our knowledge, there is only one case report describing the use of concomitant alteplase and argatroban for the treatment of acute thrombosis in lower extremities.…”

Section: Commentarymentioning

confidence: 99%

Argatroban and catheter‐directed thrombolysis with alteplase for limb‐ and graft‐threatening thromboses in a patient with a history of HIT

Maldonado

2009

American J Hematol

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A 73-year-old, 6 0 0@, 130 kg, white male who is selfemployed as a farmer presented to the hospital with a chief complaint of severe nausea, vomiting, and diarrhea accompanied by dizziness and diaphoresis occurring since that morning. His family and social history were noncontributory. On examination, the patient appeared comfortable and in no acute distress. The blood pressure was 92/56 mmHg, the pulse 68 beats per minute, the temperature 97.68F, the respiratory rate 18 breaths per minute, and the oxygen saturation 95% on room air. Lung sounds were diminished bilaterally in the bases. The remainder of a 10-point review of systems was negative except for an elevated serum creatinine (1.6, 1.2 mg/dL baseline), BUN (30 mg/dL), and white blood cell count (14.4 K/lL).The patient's initial presentation was consistent with a bacterial or viral gastroenteritis along with acute renal failure secondary to volume depletion. Other factors that predisposed him to gastrointestinal symptoms included longterm immunosuppression with mycophenolate mofetil as well as uremia.The patient has an extensive medical history that includes relevant disease states. The patient is 5 years post living donor kidney transplant secondary to chronic renal failure from ischemic nephropathy. His course immediately following transplant was complicated by deep venous thromboses in the right femoral and popliteal veins and pulmonary embolism secondary to hypercoagulability disorders including documented elevated anticardiolipin IgM antibody and protein S deficiency in the setting of a normal protein C level. Heparin and warfarin therapy had been initiated at the time of diagnosis. He developed thrombocytopenia and a heparin-induced thrombocytopenia (HIT) antibody test was reported in the record as weakly positive. He was subsequently treated with fondaparinux and warfarin but developed a diverticular bleed within 1 month. Anticoagulation was discontinued and an inferior vena cava filter was placed. The patient then opted against chronic anticoagulation. His current medications at the time of admission include alendronate, allopurinol, aspirin, calcium carbonate, carvedilol, ferrous sulfate, fish oil, furosemide, glipizide, multivitamins, mycophenolate mofetil, pantoprazole, prednisone, tacrolimus, and tamsulosin. His listed allergies include an unknown reaction to atenolol, itching with cephalexin, and heparin-induced thrombocytopenia.Upon admission, blood, stool, and urine cultures were obtained and subsequently were negative. FK506 and MMF levels were within normal limits making it unlikely that drug toxicity was causing his symptoms. An unenhanced abdominal CT demonstrated acute diverticulitis and the patient was started on ciprofloxacin and metronidazole for treatment.On the 2nd day of admission, the patient's serum creatinine continued to rise and he became oliguric. He also developed bilateral lower extremity edema, pain, cyanosis, and mottling. Due to his worsening renal function, the patient developed metabolic acidosis and because of this, ...

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“…4,5 Animal models of venous thrombosis, developed to address this problem, all alter one or more of "Virchow's Triad" of factors (stasis, hypercoagulability, and endothelial disturbance) to stimulate thrombus formation. Various methods, including complete occlusion of blood flow, 6 insertion of wool or silk threads, 7 and overt endothelial damage produced by mechanical, 8 electrical, 9 or chemical 10 means, have been used to induce thrombosis. These conditions seldom occur in patients who have deep vein thrombosis, and therefore, the experimental "thrombi" formed in these circumstances may be produced by different mechanisms and have a different composition and structure than human deep vein thrombi.…”

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confidence: 99%

A model of in vivo human venous thrombosis that confirms changes in the release of specific soluble cell adhesion molecules in experimental venous thrombogenesis

Quarmby¹,

Smith²,

Collins³

et al. 1999

Journal of Vascular Surgery

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Use of a Direct Thrombin Inhibitor (Argatroban) during Pulse-Spray Thrombolysis in Experimental Thrombosis

Cited by 13 publications

References 23 publications

Argatroban during percutaneous transluminal coronary angioplasty: Results of a dose-verification study

Argatroban during percutaneous transluminal coronary angioplasty: Results of a dose-verification study

Argatroban and catheter‐directed thrombolysis with alteplase for limb‐ and graft‐threatening thromboses in a patient with a history of HIT

A model of in vivo human venous thrombosis that confirms changes in the release of specific soluble cell adhesion molecules in experimental venous thrombogenesis

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