Theoretic and Practical Considerations on Laboratory Monitoring of Thrombolytic Therapy

Conard, J.; Samama, M

doi:10.1055/s-2007-1003495

Cited by 18 publications

(3 citation statements)

References 43 publications

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“…However, although commonly used during thrombolysis, the Clauss method may give spuriously low fibrinogen values by defective fibrin polymerization in presence of high levels of fibrin(ogen) degradation products. 49,50 Postlytic Fibrinopeptide A and Reocclusion…”

Section: Clinical and Angiographic Results Of Thrombolytic Therapymentioning

confidence: 99%

Monitoring of fibrin generation during thrombolytic therapy of acute myocardial infarction with recombinant tissue-type plasminogen activator.

et al. 1989

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Fibrinopeptide A (FPA) is a very sensitive marker of fibrin generation in vivo. Because an imbalance between thrombogenic and thrombolytic forces may be responsible for the failure to recanalize and for reocclusion of coronary arteries, such a marker could be of eminent value during thrombolytic treatment of acute myocardial infarction. Thirty-four consecutive patients with acute myocardial infarction (peak creatine kinase level, 1,869±+1,543 IU/l) were treated with 100 mg recombinant tissue-type plasminogen activator (rt-PA) 3.1±1.1 hours after onset of chest pain. Angiography 12.5+±6.1 days later revealed an 81% patency rate of the infarct-related vessel. FPA plasma levels (normal, 1.9±0.5 ng/ml) were 34±46 ng/ml on admission and 93+86 ng/ml (538 ±674% with respect to each patient's admission level) after 90 minutes of rt-PA infusion (p <0.01). In patients without evidence of reocclusion (including three primary failures), FPA levels fell under continuous heparin infusion to 6.7 +9.7 ng/ml (24+33%,p

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Section: Clinical and Angiographic Results Of Thrombolytic Therapymentioning

confidence: 99%

Monitoring of fibrin generation during thrombolytic therapy of acute myocardial infarction with recombinant tissue-type plasminogen activator.

et al. 1989

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“…Congenital plasminogen deficiency rarely appears (205), however, it may be more common than formerly thought with the availability and use of reliable and simple plasminogen assays by synthetic substrate methods (206)(207)(208)(209). It is estimated that congenital plasminogen deficiency may account for about 2% to 3% of unexplained DVT in young patients (210).…”

Section: Congenital Plasminogen Deficiencymentioning

confidence: 99%

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

Bick

Kaplan

1998

Clin Appl Thromb Hemost

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This article stresses the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects apear to be APC-R, SPS, antithrombin, protein C, and protein S deficiency, and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant (antiphospholipid antibodies). Therefore, these are the defects that should first be looked for in an individual with unexplained thrombosis. If these more common defects are not found, then the rarer defects including HC II, plasminogen or TPA deficiency, dysfibrinogenemia, el evated PAI-1 and hyperhomocysteinemia should be sought. The importance of finding these defects has significant impli cations for therapy of the individual patient and for institutions of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipopro tein (a) or defects of extrinsic (tissue factor) pathway inhibitor (EPI, TFPI), may be associated with enhanced risks of throm bosis. Finally, it must be recalled that a diagnosis of thrombo sis, like that of anemia, is only a generic and partial diagnosis; just as in the anemic patient, the etiology must be clearly de fined. Only in this manner can cost-effective and appropriate therapy for both primary treatment and secondary prevention be designed. In addition, the demonstration of a hereditary defect will allow primary prevention in afflicted family mem bers by allowing the choice of appropriate therapy.

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“…204 However, this deficiency may be more common than formerly thought with the availability of reliable and simple plasminogen assays by synthetic substrate methods. [205][206][207][208] It is estimated that congenital plasminogen deficiency may account for as many as 2 to 3% of unexplained deep vein thrombosis in young patients. 209 The disorder is inherited by autosomal dominance.…”

Section: Congenital Plasminogen Deficiencymentioning

confidence: 99%

Syndromes of Hypercoagulability and Thrombosis: A Review

Bick

Pegram

1994

Semin Thromb Hemost

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This review has stressed the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects appear to be antithrombin, protein C, and protein S deficiency and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant. Therefore these are the defects that should first be looked for in an individual with unexplained thrombosis. If these more common defects are not found, then the rarer defects, including heparin cofactor II, plasminogen or tissue plasminogen activator deficiency, dysfibrinogenemia, or elevated PAI-1 should next be sought. The importance of finding these defects has significant implications for therapy of the individual patient and for institution of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipoprotein(a) or defects of extrinsic (tissue factor) pathway inhibitor may be associated with enhanced risks of thrombosis.

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Theoretic and Practical Considerations on Laboratory Monitoring of Thrombolytic Therapy

Cited by 18 publications

References 43 publications

Monitoring of fibrin generation during thrombolytic therapy of acute myocardial infarction with recombinant tissue-type plasminogen activator.

Monitoring of fibrin generation during thrombolytic therapy of acute myocardial infarction with recombinant tissue-type plasminogen activator.

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

Syndromes of Hypercoagulability and Thrombosis: A Review

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