Effect of hirudin vs heparin on haemostatic activity in patients with acute coronary syndromes

Kottke‐Marchant, Kandice; Granger, C.B.; Zoldhelyi, Pierre; Ardissino, Diego; Brooks, Linda; Griffin, John H.; Potthoff, Richard F.; Werf, Frans Van de; Califf, Robert M.; Topol, Eric J.

doi:10.1053/euhj.2001.3074

Cited by 11 publications

(7 citation statements)

References 23 publications

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“…This is supported by data from the Clopidogrel forH igh Atherothrombotic Risk and Ischemic Stabilisation, Management and Avoidance( CHARISMA), indicatingt hat therewas no benefit amongthe groups of patients whohad risk factorsbut no prior events, whereas a12% reduction in events wasobservedinthe groups of prior coronary, cerebrovascularor peripheral arterial disease (33).I na ddition, clopidogrel or GPIIb/IIIa antagonistsdid not suppresscoagulation activation in patients with acuteC AD (34)(35)(36). The fact thatc onventional anticoagulants failedtosuppress thrombin generation in patients with establishedCAD in some studies (37,38) alsosuggests a degree of overactivity of the blood coagulation system in these patients.…”

Section: Discussionmentioning

confidence: 99%

Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test

Orbe¹,

Zudaire²,

Serrano³

et al. 2008

Thromb Haemost

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SummaryAtherosclerosisi st he most commonp athophysiologics ubstrateofcoronaryarterydisease (CAD).Whereasplaque progression anda rterial remodeling arec ritical components in chronic CAD, intracoronarythrombosis over plaque disruption is causally related to acute CAD. It wast he objectiveo ft his study to investigate thed ifferencesb etween priora cute CAD and chronic CADbyasimple global coagulation assaymeasuring thrombin generation.A cross-sectional study involving 15 healthyc ontrols,35p atientsw ith chronic stable CAD, and 60 patientsa fter an episodeo fa cute myocardial infarction (AMI) was performed. Thrombin generation wasm easuredb etween three and 11 monthsafter the initialdiagnosis (mean6months) by acommerciallya vailable fluorogenic assay(Te chnothrombin TGA). In each patient the lag phase,v elocityi ndex and peak thrombin were obtained from the thrombogram profile.TradiKeywords Thrombin,acute myocardial infarction, coronarysyndrome tional cardiovascular risk factors were recorded, andthe inflammatorymarkers, fibrinogen and hs-C-reactive proteinweredetermined. Compared with stable CADpatients, showing normal thrombograms, those with previous AMIs howede arlierl ag phase (p<0.05) and significant increase of botht he velocity index (p<0.001) and peak thrombin (p<0.05),indicating faster and higherthrombin generation in theAMI group.Differencesin thrombin generation between stable and acute CADp atients remaineds ignificant (p<0.001) after adjusting forc onventional CADriskfactors (age,gender, diabetes,hypertension,smoking, andh ypercholesterolemia). In conclusion, patients with ap revious historyo fa cute CADs howede arlier, faster and higher thrombin generation than stable chronic CADp atients. The thrombin generation test maybeofclinical value to monitor hypercoagulable/vulnerable blood and/or guide therapyinCAD.

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Section: Discussionmentioning

confidence: 99%

Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test

Orbe¹,

Zudaire²,

Serrano³

et al. 2008

Thromb Haemost

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“…These findings suggest that the accumulation of prothrombotic factors during antithrombin therapy leads to a relative hypercoagulable state after drug withdrawal. 7 One of the strongest predictors of rebound events in the multivariate analysis was prolonged duration of heparin infusion. Because the infusion of eptifibatide was limited to 72 hours and the mean heparin infusion duration was Ͼ94 hours, a long heparin infusion may simply be a surrogate for heparin discontinuation without the protective effects of eptifibatide.…”

Section: Discussionmentioning

confidence: 99%

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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“…A DTI inhibits thrombin activity better than heparin, and offers better protection against reactivation of thrombin after cessation of treatment. 7 While clot bound thrombin is protected from inactivation by the heparin-antithrombin III complex, it can still be inactivated by DTI. 8 Unlike warfarin, ximelagatran exerts its anticoagulant effect almost immediately, has no known drug or food interactions, and does not require frequent laboratory monitoring.…”

Section: Oral Direct Thrombin Inhibitormentioning

confidence: 99%

Will oral antithrombin agents replace warfarin?

Sinnaeve

2004

Heart

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Effect of hirudin vs heparin on haemostatic activity in patients with acute coronary syndromes

Cited by 11 publications

References 23 publications

Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test

Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test

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

Will oral antithrombin agents replace warfarin?

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