Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina

Montalescot, Gilles; Collet, Jean Philippe; Lison, Linda; Choussat, Rémi; Ankri, Annick; Vicaut, Éric; Perlemuter, Katy; Philippe, François; Thomas, Daniel

doi:10.1016/s0735-1097(00)00695-1

“…Enoxaparin also exhibits other important biological properties that may play significant roles in the prevention of recurrent ischemic events. [33][34][35][36] Although the present study provides important data on a diverse patient population, complementing the randomized trials that have more restrictive inclusion criteria, it must be noted that decisions regarding invasive management, treatment strategy, enoxaparin dosing, and timing of anti-Xa measurement were also less controlled than is usually the case in randomized trials. Our pharmacokinetic data must be interpreted with caution, especially in patients with severe renal dysfunction, and are applicable only to short-term treatments.…”

Section: Discussionmentioning

confidence: 99%

Anti-Xa Activity Relates to Survival and Efficacy in Unselected Acute Coronary Syndrome Patients Treated With Enoxaparin

Montalescot

¹

,

Collet

²

,

Tanguy

³

et al. 2004

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Background-Low-molecular-weight heparin (LMWH) is recommended in the treatment of unstable angina (UA)/non-ST-segment-elevation myocardial infarction (NSTEMI), but no relationship has ever been shown between anticoagulation levels obtained with LMWH treatment and clinical outcomes. Methods and Results-In all, 803 consecutive patients with UA/NSTEMI were treated with subcutaneous enoxaparin and were followed up for 30 days. The recommended dose of enoxaparin of 1 mg/kg BID was used throughout the population except when physicians decided on dose reduction because of a history of a recent bleeding event or because of a high bleeding risk. Anti-factor Xa activity was Ͼ0.5 IU/mL in 93% of patients; subtherapeutic anti-Xa levels (Ͻ0.5 IU/mL) were associated with lower doses of enoxaparin. The 30-day mortality rate was significantly associated with low anti-Xa levels (Ͻ0.5 IU/mL), with a Ͼ3-fold increase in mortality compared with the patients with anti-Xa levels in the target range of 0.5 to 1.2 IU/mL (Pϭ0.004). Multivariate analysis revealed low anti-Xa activity as an independent predictor of 30-day mortality at least as strong as age, left ventricular function, and renal function. In contrast, anti-Xa activity did not predict major bleeding complications within the range of anti-Xa levels observed in this study. Conclusions-In this large unselected cohort of patients with UA/NSTEMI patients, low anti-Xa activity on enoxaparin treatment is independently associated with 30-day mortality, which highlights the need for achieving at least the minimum prescribed anti-Xa level of 0.5 IU/mL with enoxaparin whenever possible.

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“…1 Previous reports have also shown that the release of these acute phase reactant proteins within the first hours of non-ST-elevation acute coronary syndromes predicts adverse clinical outcomes. 2,3 However, limited and incomplete information is available about these 2 markers in ST-elevation myocardial infarction (STEMI). Raised plasma levels of vWF and PAI-1 have been reported during the acute phase of STEMI, and some drug treatments have been shown to blunt the release of these markers.…”

mentioning

confidence: 99%

Acute Release of Plasminogen Activator Inhibitor-1 in ST-Segment Elevation Myocardial Infarction Predicts Mortality

Collet

¹

,

Montalescot

²

,

Vicaut

³

et al. 2003

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Background-A few studies have suggested that von Willebrand factor (vWF) or plasminogen activator inhibitor-1 (PAI-1) can be associated with outcomes of acute coronary syndromes. The present study was designed to assess the acute release of these markers in ST-segment elevation myocardial infarction (STEMI) and their relations to death. Methods and Results-In 153 consecutive patients with STEMI, vWF and PAI-1 antigens were measured on admission (H0) and 24 hours later (H24). At 30 days, the death rate was 7.2%. Heart failure (Killip stage Ն3) on admission was present in 13.7% of patients. The acute release of PAI-1 (H24ϪH0, in ng/mL) and of vWF (H24ϪH0, in %) was dramatically higher in patients who died than in those who survived (46.9Ϯ26.3 versus Ϫ0.6Ϯ2.8 ng/mL, Pϭ0.0001 and 65.8Ϯ20.0% versus 10.0Ϯ5.1%, Pϭ0.004 for PAI-1 and vWF, respectively) and in patients developing heart failure compared with those without (24.8Ϯ10.1 versus Ϫ1.1Ϯ3.3 ng/mL, Pϭ0.004 and 47.3Ϯ11.0% versus 8.1Ϯ5.6%, Pϭ0.005 for PAI-1 and vWF, respectively). The release of PAI-1 correlated weakly with the left ventricular ejection fraction (RϭϪ0.195, Pϭ0.01) and the peak of troponin (Rϭ0.149, Pϭ0.045). Postangioplasty TIMI-3 flow and the acute release of PAI-1 were the only 2 independent predictors of death at 30 days. Conclusions-The acute release of vWF and PAI-1 over the first 24 hours of STEMI is associated with death and heart failure. The acute rise of PAI-1 is also a strong independent predictor of death at 30 days.

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“…5,6 Similarly, various anticoagulant drugs have shown different abilities with regard to vWF release. 3,8 These observations suggest that these drugs may have multiple mechanisms of action to explain their clinical benefit.…”

Section: Discussionmentioning

confidence: 99%

“…1 Previous reports have also shown that the release of these acute phase reactant proteins within the first hours of non-ST-elevation acute coronary syndromes predicts adverse clinical outcomes. 2,3 However, limited and incomplete information is available about these 2 markers in ST-elevation myocardial infarction (STEMI). Raised plasma levels of vWF and PAI-1 have been reported during the acute phase of STEMI, and some drug treatments have been shown to blunt the release of these markers.…”

mentioning

confidence: 99%

ST‐Segment Elevation Myocardial Infarction

2017

Practical Cardiovascular Medicine

0

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Background-A few studies have suggested that von Willebrand factor (vWF) or plasminogen activator inhibitor-1 (PAI-1) can be associated with outcomes of acute coronary syndromes. The present study was designed to assess the acute release of these markers in ST-segment elevation myocardial infarction (STEMI) and their relations to death. Methods and Results-In 153 consecutive patients with STEMI, vWF and PAI-1 antigens were measured on admission (H0) and 24 hours later (H24). At 30 days, the death rate was 7.2%. Heart failure (Killip stage Ն3) on admission was present in 13.7% of patients. The acute release of PAI-1 (H24ϪH0, in ng/mL) and of vWF (H24ϪH0, in %) was dramatically higher in patients who died than in those who survived (46.9Ϯ26.3 versus Ϫ0.6Ϯ2.8 ng/mL, Pϭ0.0001 and 65.8Ϯ20.0% versus 10.0Ϯ5.1%, Pϭ0.004 for PAI-1 and vWF, respectively) and in patients developing heart failure compared with those without (24.8Ϯ10.1 versus Ϫ1.1Ϯ3.3 ng/mL, Pϭ0.004 and 47.3Ϯ11.0% versus 8.1Ϯ5.6%, Pϭ0.005 for PAI-1 and vWF, respectively). The release of PAI-1 correlated weakly with the left ventricular ejection fraction (RϭϪ0.195, Pϭ0.01) and the peak of troponin (Rϭ0.149, Pϭ0.045). Postangioplasty TIMI-3 flow and the acute release of PAI-1 were the only 2 independent predictors of death at 30 days. Conclusions-The acute release of vWF and PAI-1 over the first 24 hours of STEMI is associated with death and heart failure. The acute rise of PAI-1 is also a strong independent predictor of death at 30 days.

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Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina

Cited by 124 publications

References 22 publications

Anti-Xa Activity Relates to Survival and Efficacy in Unselected Acute Coronary Syndrome Patients Treated With Enoxaparin

Anti-Xa Activity Relates to Survival and Efficacy in Unselected Acute Coronary Syndrome Patients Treated With Enoxaparin

Acute Release of Plasminogen Activator Inhibitor-1 in ST-Segment Elevation Myocardial Infarction Predicts Mortality

ST‐Segment Elevation Myocardial Infarction

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