A rise of troponin and/or von Willebrand factor over the first 48 h is associated with a poorer 1-year outcome in unstable angina patients

doi:10.1016/S0167-5273(99)00202-8

International Journal of Cardiology

Volume 72, Issue 3, 15 February 2000, Pages 293-294

https://doi.org/10.1016/S0167-5273(99)00202-8 Get rights and content

Abstract

The 1-year follow-up of the French population enrolled in the ESSENCE trial demonstrates that the combined evaluation of von Willebrand factor and troponin I during the first 48 h provides useful information on long-term prognosis of these patients with unstable angina.

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Cardiac specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes
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Platelet activation and endothelium dysfunction are determinants of atherothrombosis in acute coronary syndrome (ACS) patients. The aim of this study was to investigate the relationship between platelet and endothelial cell activation markers and mortality in patients presenting with ACS.
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In patients with ACS undergoing PCI, increased chronic endothelial cell activation and dysfunction is associated with an increased risk of long-term mortality.
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Whether low molecular weight heparin (LMWH) enoxaparin is equivalent to unfractionated heparin (UFH) in patients with non-ST-segment elevation myocardial infarction (NSTEMI) undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES) remains unclear.
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Enoxaparin group had similar incidences of cardiac death, total death, and total major adverse cardiac events (MACE) at 8 months compared with UFH group. The incidences of major and minor bleeding events were also similar between the two groups. Multivariable Cox regression analysis showed that enoxaparin group had similar incidences of cardiac death [adjusted odds ratio (OR) 1.16, 95% confidence interval (CI) 0.64–2.10, p = 0.620], total death (adjusted OR 1.08, 95% CI 0.66–1.76, p = 0.760), and total MACE (adjusted OR 0.94, 95% CI 0.69–1.28, p = 0.692) at 8 months as compared with UFH group.
Enoxaparin with reduced dose of UFH only during PCI as an adjunctive antithrombotic therapy in NSTEMI patients undergoing PCI with DES was safe and showed comparable 8-month clinical outcomes as compared with UFH alone.
Redefining Risk in Acute Coronary Syndromes Using Molecular Medicine
2007, Journal of the American College of Cardiology
Acute coronary syndromes represent a complex phenotype involving the interplay of many elements. The risk of developing an acute coronary syndrome and related complications has been defined by variables such as age, diabetes, smoking history, serum creatine phosphokinase, or electrocardiographic findings. However, in the past 5 years the wide-scale acceptance of a protein—troponin—has changed the diagnostic profile. With advances in molecular medicine, this protein is a segue to a panel of molecular assays that will improve screening and tailored intervention. We expound upon some of these factors and the potential they may carry in changing clinical medicine.
Enoxaparin versus tinzaparin in non-ST-segment elevation acute coronary syndromes: Results of the enoxaparin versus tinzaparin (EVET) trial at 6 months
2005, American Heart Journal
Citation Excerpt :
Apart from the differences in the antithrombotic effects of the 2 drugs, this can be attributed to their specific antiinflammatory effects. Previous studies have shown that increased plasma levels of von Willebrand factor is an independent predictor of early26 and late27 outcomes in NSTACS. Enoxaparin reduces the release of von Willebrand factor26 and thus possibly passivates the vulnerable plaques and prevents or reduces the severity of new ruptures.
We have previously reported significant benefits of using enoxaparin, compared to tinzaparin, in the 7- and 30-day incidence of the composite triple end point of death, myocardial infarction (MI), or recurrent angina in patients with non–ST-segment elevation acute coronary syndromes (NSTACS). In the present study, we aimed to determine whether the observed benefits of enoxaparin were maintained beyond the early phase and report the results of the 6-m follow-up of patients in the EVET study.
We recruited 438 patients with NSTACS. All patients received oral aspirin and were randomized to also receive enoxaparin, 100 IU/kg subcutaneously twice daily (equivalent to 1 mg/kg twice daily; n = 220), or tinzaparin, 175 IU/kg subcutaneously once daily (n = 218), for up to 7 days.
At 6 m, the incidence of the composite triple end point of death, MI, or recurrent angina was lower among patients receiving enoxaparin compared to those receiving tinzaparin (25.5% vs 44.0%, P < .001). A lower incidence of the secondary composite end point of death or MI was also found in the enoxaparin group compared to tinzaparin group (2.7% vs 6.9%, P = .046). The need for revascularization procedures was also lower in the enoxaparin group compared to tinzaparin group (23.2% vs 37.2%, P = .002).
In patients with NSTACS, enoxaparin significantly reduced the rates of recurrent ischemic events and therapeutic procedures in the short term, with sustained benefit at 6 m compared to tinzaparin.
Circulating endothelial cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute coronary syndromes
2005, Blood
Citation Excerpt :
We hypothesized that increased baseline plasma IL-6 and the numbers of CECs and/or increasing levels of these markers during the first 24 to 48 hours of presentation (ie, an “acute release” Δ) predict short- as well as long-term major adverse cardiovascular events (MACE) in patients with acute coronary disease. To test this hypothesis, we studied consecutive patients admitted with STEMI, non-STEMI, or UAP and used levels of VWF (previously shown to rise under these conditions8-10) as a comparator and positive control. A subhypothesis stated that there was a difference in the research indexes according to STEMI or non-STEMI status.
Markers of inflammation (eg, interleukin-6 [IL-6]), and endothelial perturbation (von Willebrand factor [VWF], circulating endothelial cells [CECs]) are altered in acute coronary syndromes (ACS). We hypothesized that CECs and IL-6 levels during the first 48 hours of ACS would predict 30-day and 1-year major cardiovascular end points (MACE). A total of 156 patients with ACS were included. Blood was drawn on admission (baseline) and 48 hours later for plasma VWF, IL-6 (both enzyme-linked immunosorbent assay [ELISA]), and CECs (CD146 immunomagnetic separation). CEC phenotyping was performed by indirect immunoperoxidase staining. At 30 days, 48 patients had a MACE, a predicted by baseline and 48-hour CECs and IL-6 levels, 48-hour VWF levels, and by the “admission–48 hour change” (Δ) in CECs, VWF, and IL-6 (all P = .002). On multivariate analysis, 48-hour CECs (P < .001) were the strongest predictor of MACE, followed by ΔIL-6 (P = .01) and ΔVWF (P = .048); 48-hour CECs were the only predictor of death (P = .007). At 1 year, 65 patients had MACE, predicted by 48-hour CECs and ΔIL-6 levels (P < .001); age (P = .046) and 48-hour CECs (P < .001) were the only predictors of death. CECs stained 93% positive for endothelial nitric oxide synthase (eNOS) but were less than 1% positive for CD34, CD36, and CD45 and less than 3% for CD31. Like raised VWF, abnormal CECs and IL-6 levels during the first 48 hours of ACS were strongly associated with 30-day MACE. CECs at 48 hours were the only independent predictor of both death and MACE at 30 days and 1 year, indicating the crucial role of endothelial/vascular damage in ACS pathophysiology.
Measurement of plasma von Willebrand factor in acute coronary syndromes and the influence of ABO blood group status [4]
2004, Journal of Thrombosis and Haemostasis

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Letter to the EditorA rise of troponin and/or von Willebrand factor over the first 48 h is associated with a poorer 1-year outcome in unstable angina patients

Abstract

J Am Coll Cardiol

Cardiac specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes

N Engl J Med

Letter to the Editor
A rise of troponin and/or von Willebrand factor over the first 48 h is associated with a poorer 1-year outcome in unstable angina patients