Rebound Increase in Thrombin Generation and Activity After Cessation of Intravenous Heparin in Patients With Acute Coronary Syndromes

Granger, Christopher B.; Miller, Julie M.; Bovill, Edwin G.; Gruber, András; Tracy, Russell P.; Krucoff, Mitchell W.; Green, Cindy; Berrios, Eric; Harrington, Robert A.; Ohman, E. Magnus; Califf, Robert M.

doi:10.1161/01.cir.91.7.1929

Cited by 192 publications

(91 citation statements)

References 20 publications

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“…Alternatively, prolonged heparin duration may cause more pronounced platelet activation or buildup of thrombin or identify a subset of patients with more unstable symptoms requiring prolonged heparin therapy. A prior study, however, found that the increase in thrombin generation and activation seen after heparin discontinuation was not associated with duration of heparin therapy, 8 which argues against this as a mechanism for the observed risk of prolonged therapy in our study. A repeat multivariate analysis in our population limited to those who were on study drug at the time of heparin withdrawal (data not shown) showed that prolonged heparin infusion actually provided a protective effect.…”

Section: Discussioncontrasting

confidence: 65%

Attenuation of Rebound Ischemia After Discontinuation of Heparin Therapy by Glycoprotein IIb/IIIa Inhibition With Eptifibatide in Patients With Acute Coronary Syndromes

Lauer

Houghtaling

et al. 2001

Circulation

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Background-A reactivation of ischemia after the discontinuation of intravenous heparin in acute coronary syndromes has been described. The effect of glycoprotein IIb/IIIa blockade on heparin rebound is unknown. Methods and Results-Patients with acute coronary syndromes who received heparin therapy but not initial revascularization in the Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial were analyzed. Rates of death or myocardial (re)infarction while on heparin therapy and in 12-hour periods in the 2 days after heparin discontinuation were compared between eptifibatide and placebo. There was no difference between study groups in event rates during heparin infusion. In the 12 hours after heparin discontinuation, there was a 2.5-fold increase in all events, an 8-fold increase in death, and a 2-fold increase in myocardial infarction. However, in the 12 hours after heparin discontinuation, there was a significantly lower rate of events (1.68% versus 2.53%, Pϭ0.03) and death (0.77% versus 0.21%, Pϭ0.002) in the eptifibatide group compared with the placebo group. When only considering patients who were on study drug at the time of heparin discontinuation, the reduction in the combined end point was marginally significant, but the difference in the rate of death remained significant (0.68% versus 0.06%, Pϭ0.004). In logistic regression analyses, the multivariate predictors of rebound events were the duration of heparin therapy, age, North American site, and lack of eptifibatide treatment. Conclusions-An increase in death or myocardial infarction occurs in the 12 hours after heparin discontinuation in patients with acute coronary syndromes. This rebound is attenuated by glycoprotein IIb/IIIa inhibition with eptifibatide.

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Section: Discussioncontrasting

confidence: 65%

Attenuation of Rebound Ischemia After Discontinuation of Heparin Therapy by Glycoprotein IIb/IIIa Inhibition With Eptifibatide in Patients With Acute Coronary Syndromes

Lauer

Houghtaling

et al. 2001

Circulation

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“…443, 444 The combination of UFH and ASA appears to mitigate this reactivation in part, 442,445 although there is hematologic evidence of increased thrombin activity after the cessation of intravenous UFH ("rebound") even in the presence of ASA. 446 Uncontrolled observations suggested a reduction in the "heparin rebound" by switching from intravenous to subcutaneous UFH for several days before the drug is stopped.…”

Section: Unfractionated Heparinmentioning

confidence: 99%

2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

Anderson¹,

Adams²,

Antman³

et al. 2011

Circulation

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682

367

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“…544, 545 The combination of UFH and ASA appears to mitigate this reactivation in part, 543,546 although there is hematologic evidence of increased thrombin activity after the cessation of intravenous UFH ("rebound") even in the presence of ASA. 547 Uncontrolled observations suggested a reduction in the "heparin rebound" by switching from intravenous to subcutaneous UFH for several days before the drug is stopped.…”

Section: Unfractionated Heparinmentioning

confidence: 99%

2012 ACCF/AHA Focused Update Incorporated Into the ACCF/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

Anderson¹,

Adams²,

Antman³

et al. 2013

Circulation

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204

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Rebound Increase in Thrombin Generation and Activity After Cessation of Intravenous Heparin in Patients With Acute Coronary Syndromes

Cited by 192 publications

References 20 publications

Attenuation of Rebound Ischemia After Discontinuation of Heparin Therapy by Glycoprotein IIb/IIIa Inhibition With Eptifibatide in Patients With Acute Coronary Syndromes

Attenuation of Rebound Ischemia After Discontinuation of Heparin Therapy by Glycoprotein IIb/IIIa Inhibition With Eptifibatide in Patients With Acute Coronary Syndromes

2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

2012 ACCF/AHA Focused Update Incorporated Into the ACCF/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

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