Plasma fibrinopeptide A levels in patients with acute myocardial infarction treated with alteplase. Correlation with concomitant heparin, coronary artery patency, and recurrent ischemia. The European Cooperative Study Group.

Rapold, Hans J.; Bono, David de; Arnold, Alfred; Arnout, Jozef; Cock, F De; Collen, D.; Verstraete, Marc

doi:10.1161/01.cir.85.3.928

Cited by 85 publications

(21 citation statements)

References 38 publications

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“…Comparing the results obtained with the different therapies we found that more thrombin is generated in the patients treated with thrombolytics+heparin than in those receiving heparin only. This finding is in keeping with previous studies that showed an increase in thrombin generation and activity during thrombolysis with either SK or rt-PA [11,13,16,18,27]. The increase in F1+2 plasma levels observed in the SK+heparin and rt-PA+ heparin groups despite concomitant administration of intravenous heparin may relate to the reexposure of the ruptured plaque to blood flow, which might lead to the generation of more factor Xa and thrombin.…”

Section: Discussionsupporting

confidence: 91%

Increase in Thrombin Generation after Coronary Thrombolysis with rt-PA or Streptokinase with Simultaneous Heparin versus Heparin Alone

Regañón¹,

Ferrando²,

Vila³

et al. 1998

Pathophysiol Haemos Thromb

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This study compares the extent of inhibition of thrombin generation and activity achieved in patients with acute myocardial infarction receiving fibrinolytic treatment (streptokinase SK, or rt-PA) and concomitant intravenous heparin treatment adjusted to the patients’ weight with that achieved with the same heparin regimen but without fibrinolytic therapy. The study involved 90 patients, grouped according to their treatment: SK+heparin; rt-PA+heparin, and heparin without thrombolytic agents. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), fibrinopeptide A (FPA) and activated partial thromboplastin time were measured. Patients treated with SK+heparin or rt-PA+heparin and higher F1+2 plasma levels than the patients treated with heparin alone at 12, 48 and 72 h in the case of SK+heparin, and at 12, 24, 48 and 72 h in that of rt-PA+heparin. Compared to baseline, the plasma levels of FPA were decreased in the three treatment groups at 24–48 h. There were no significant changes in TAT and FPA plasma levels among the three treatment groups at the different times. After thrombolytic therapy with both SK and rt-PA, there was an increase in thrombin generation, although high-dose intravenous heparin inhibited the different increases in thrombin associated with the thrombolytic agents to the same extent.

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Section: Discussionsupporting

confidence: 91%

Increase in Thrombin Generation after Coronary Thrombolysis with rt-PA or Streptokinase with Simultaneous Heparin versus Heparin Alone

Regañón¹,

Ferrando²,

Vila³

et al. 1998

Pathophysiol Haemos Thromb

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“…These results are consistent with prior studies that show an increase in some of these hemostatic markers several days after the onset of an acute coronary syndrome [1,11,16,17]. These hematological markers of the hypercoagulable state were found to relate to the subsequent risk of thrombotic events [2,11,18].…”

Section: Discussionsupporting

confidence: 91%

Elevated Thrombotic Activity after Myocardial Infarction: A 2-Year Follow-Up Study

Martínez‐Sales¹,

Vila²,

Regañón³

et al. 1998

Pathophysiol Haemos Thromb

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This study examines the evolution of the thrombotic activity in patients with myocardial infarction (MI) treated with aspirin (200 mg/day) for 2 years after MI. Plasma samples of 10 patients were collected at 7, 30, 60, 90, 120, 150, 180, 360 and 720 days. In all the samples we measured fibrinogen (Fg), high molecular weight Fg (HMW-Fg), fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2), β-thromboglobulin (β-TG), von Willebrand factor (vWF), tissue factor (TF) and TF pathway inhibitor (TFPI). The plasma Fg, HMW-Fg, FPA, F1+2, β-TG and vWF levels were significantly elevated in the patients at the beginning of the study as compared to the normal group. The 95% confidence intervals were Fg 277–333 mg/dl, HMW-Fg 200–244 mg/dl, FPA 5.3–16.5 ng/ml, F1+2 1.4–1.8 nmol/l, β-TG 110–118 IU/ml and vWF 139–195%. At thirty days Fg and HMW-Fg returned to normal levels, whereas the increase in FPA and F1+2 levels persisted throughout the study. At 120 and 150 days, respectively, β-TG and vWF returned to normal levels. The increase in thrombin generation and activity pointed to a persistent hypercoagulable state 2 years after MI. Plasma levels of TF and TFPI showed no statistically significant variations with respect to the normal values over the 2-year period studied. In conclusion, these results suggest a persistent generation and activity of thrombin and cellular activation in these patients after MI.

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“…These results are consistent with observations of procoagulant tendencies (eg, increase in fibrinopeptide A) induced by thrombolysis for myocardial infarction. [13][14][15] Interestingly, control subjects with vascular risk factors exhibited a significant activation of hemostasis compared with control subjects without such risk factors. Compared with risk factor-matched subjects, patients with acute ischemic stroke exhibited a significant increase in hemostatic indicators.…”

Section: Discussionmentioning

confidence: 97%

Changes in Coagulation and Fibrinolysis Markers in Acute Ischemic Stroke Treated With Recombinant Tissue Plasminogen Activator

Faßbender

Dempfle

Mielke

et al. 1999

Stroke

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Background and Purpose-Shifts of the balance between coagulation and fibrinolysis play a crucial role in pathogenesis and treatment of cerebral ischemia. In this study, we characterized the kinetics of hemostatic abnormalities induced by acute ischemic stroke and its thrombolytic (recombinant tissue plasminogen activator [rtPA]) or anticoagulant (heparin) treatment. Methods-Systemic generation of molecular markers of hemostasis (fibrin monomer, D-dimer, thrombin-antithrombin complex, and fibrinopeptide 1.2) was monitored in acute ischemic stroke, and the effects of thrombolytic and anticoagulant treatments were analyzed. Results-Thrombolysis with rtPA induced a massive response of markers of coagulation activation and fibrin formation that peaked after 1 to 3 hours and persisted for up to 72 hours. In contrast, only minor hemostatic changes were induced by acute ischemic stroke itself. Administration of heparin did not significantly affect these hemostatic abnormalities. Conclusions-This first characterization of the coagulation activation induced by rtPA treatment for acute ischemic stroke and the failure to abolish such hemostatic abnormalities by heparin may be of value for further refinement of the currently discussed thrombolytic therapy and the controversial adjunctive anticoagulant prophylaxis in stroke patients.

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Plasma fibrinopeptide A levels in patients with acute myocardial infarction treated with alteplase. Correlation with concomitant heparin, coronary artery patency, and recurrent ischemia. The European Cooperative Study Group.

Cited by 85 publications

References 38 publications

Increase in Thrombin Generation after Coronary Thrombolysis with rt-PA or Streptokinase with Simultaneous Heparin versus Heparin Alone

Increase in Thrombin Generation after Coronary Thrombolysis with rt-PA or Streptokinase with Simultaneous Heparin versus Heparin Alone

Elevated Thrombotic Activity after Myocardial Infarction: A 2-Year Follow-Up Study

Changes in Coagulation and Fibrinolysis Markers in Acute Ischemic Stroke Treated With Recombinant Tissue Plasminogen Activator

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