Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

Andreotti, Felicita; Hackett, D.; Haider, Ahmed; Roncaglioni, Maria Carla; Davies, Graham; Beacham, J; Kluft, C.; Maseri, Attilio

doi:10.1055/s-0038-1646343

Cited by 21 publications

(9 citation statements)

References 23 publications

(31 reference statements)

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“…Patients with a patent infarct-related artery showed a highly significant fall in VWF as compared to those with an occluded artery. 108 Consistently, a protracted elevation in VWF levels has been observed in patients with occluded infarct-related artery for whom rescue PCI was required. 109 Although the clinical benefits of thrombolytic therapy in the management of STEMI are well established, concerns have been raised that further myocardial damage via endothelial activation may occur after reperfusion therapy.…”

Section: Vwf and Thrombolysissupporting

confidence: 48%

Von Willebrand Factor in Cardiovascular Disease

2008

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Abstract-von Willebrand factor (VWF) plays a pivotal role in platelet adhesion and aggregation at sites of high shear rates (eg, in coronary arteries that have stenotic or ruptured atherosclerotic plaque lesions). Numerous studies have investigated the relationship between VWF plasma levels and thromboembolic cardiovascular events. In contrast to the rather weak association in the general population, in patients with preexisting vascular disease, VWF is significantly predictive for adverse cardiac events, including death. Likewise, VWF typically rises during the course of acute coronary syndrome, and the extent of this VWF release is an independent predictor of adverse clinical outcome in these patients. Key Words: coronary disease Ⅲ myocardial infarction Ⅲ platelets Ⅲ thrombosis Ⅲ von Willebrand factor F or Ͼ150 years, it has been known that alterations in blood flow, vascular wall, and blood components, the so-called Virchow's triad, 1 may progressively lead to thrombus formation. Yet, a more complete understanding of the complex interactions among the vascular endothelium, platelet adhesion, activation, aggregation, and clotting factor activation involved in this process is still emerging from contemporary research.Under physiological conditions, the vascular endothelium produces many substances that contribute importantly to hemostasis, fibrinolysis, and regulation of vessel tone and permeability. One such substance is the multimeric glycoprotein von Willebrand factor (VWF), which is produced almost exclusively by endothelial cells. 2 Plasma levels of VWF are raised in different states of endothelial damage and have therefore been proposed as useful markers of endothelial dysfunction. 3 Along this line, blockade of nitric oxide enhances the stimulated release of VWF in humans. 4,5 Furthermore, VWF plays a crucial role in platelet adhesion and aggregation under high shear conditions. 6 Finally, VWF supports the third component of Virchow's triad, clotting factor activation, by acting as a carrier protein and stabilizer for factor VIII. 7 Almost all acute coronary syndromes (ACS) result from thrombus formation in preexisting coronary atherosclerosis. As a result of plaque rupture and exposure of prothrombotic subendothelial matrix, local thrombus formation occurs, which subsequently leads to coronary artery occlusion and acute myocardial infarction (AMI). The presence of VWF has been shown to play a pivotal role in platelet aggregation at sites of high shear, eg, at the sites of lesions in the coronary arteries. 8 Accordingly, VWF is a well-characterized marker of cardiovascular risk, and VWF plasma levels are increased in patients with ACS. 9 Considering the central role of VWF in thrombogenesis, therapies that specifically inhibit VWF are of particular interest as potential new antiplatelet drugs.

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Section: Vwf and Thrombolysissupporting

confidence: 48%

Von Willebrand Factor in Cardiovascular Disease

2008

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“…several days after the acute event, C-reactive protein levels return to the control range again [28,31] . The elevation of C-reactive protein in acute myocardial infarction seems to be independent of the underlying atherosclerotic process and may be triggered, for example, by soluble inflammatory factors such as interleukin-1beta and tumour necrosis factor-alpha, which are related to the extent of myocardial necrosis [32] . The clear-cut association between C-reactive protein concentration and the degree of clinically manifest, generalized atherosclerosis contributes to the findings of prospective studies which show that coronary heart disease patients with elevated blood C-reactive protein concentrations have a worse prognosis than those whose C-reactive protein concentrations are not elevated.…”

Section: Discussionmentioning

confidence: 99%

C-reactive protein and the severity of atherosclerosis in myocardial infarction patients with stable angina pectoris

Tataru

Heinrich²,

Junker³

et al. 2000

European Heart Journal

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Background Recent findings provide evidence for the importance of inflammatory processes in the pathogenesis of atherosclerosis. C-reactive protein was elevated in patients with peripheral artery disease, coronary heart disease and myocardial infarction compared to normal subjects. MethodsIn 1112 male and 299 female survivors of myocardial infarction (mean age SD, men, 50·4 9·5, women, 56·1 9·3), we investigated whether plasma C-reactive protein concentration is associated with the severity of coronary heart disease and generalized pre-clinical or clinically manifest arteriopathy. The control group consisted of 326 male and 138 female individuals matched for age without clinical symptoms of coronary disease. The severity of arteriosclerotic changes was determined for the extra-cranial brain-supplying arteries, abdominal aorta, pelvis and leg arteries. In myocardial infarction patients coronary angiography was performed. Laboratory analyses included determination of C-reactive protein, fibrinogen, D-dimer, HDL-cholesterol, LDL-cholesterol and triglycerides. ResultsThe following ranking of C-reactive protein concentrations was found: controlscpatients after myocardial infarction without atherosclerosiscpatients with myocardial infarction and pre-clinical atherosclerosiscpatients with myocardial infarction and clinically manifest atherosclerosis. Additionally, our data showed a significant association between C-reactive protein concentrations and the angiographically detected degree of coronary heart disease.Conclusions As C-reactive protein is a marker of inflammatory processes, our results in patients with clinically manifest and early pre-clinical atherosclerosis support the hypothesis that inflammatory processes in the vessel wall participate in atherogenesis. Moreover, they support the hypothesis of a causal relationship between an acute phase reaction and the pathogenesis of atherosclerosis in coronary arteries and other parts of the arterial vessel system.

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“…13,14 A high CRP after MI predicts infarct expansion, cardiac rupture, and mortality. 14 -16 Reduction of cardiac rupture by ␤-blockers is associated with a decrease in the rise in CRP after MI.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory and Profibrinolytic Effect of Insulin in Acute ST-Segment–Elevation Myocardial Infarction

et al. 2004

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Background-The clinical benefits of insulin previously observed in acute ST-segment-elevation myocardial infarction (STEMI) may be partially explained by an anti-inflammatory effect. We assessed this potential effect of insulin in STEMI patients treated with fibrinolytics. Methods and Results-Thirty-two patients receiving reteplase were randomly assigned infusions of either insulin at 2.5 U/h, dextrose, and potassium (GIK) or normal saline and potassium (C) for 48 hours. Plasma concentrations of high-sensitivity C-reactive protein (CRP), serum amyloid A (SAA), plasminogen activator inhibitor-1 (PAI-1), creatine kinase (CK), and CK-MB were measured at baseline and sequentially for 48 hours. Total p47 phox protein in mononuclear cells was measured in a subgroup of 13 subjects. Baseline CRP and SAA were significantly increased (2-to 4-fold) at 24 and 48 hours in each group (PϽ0.01). However, in the insulin group, there was a significant (PϽ0.05) attenuation of the absolute rise in concentration of CRP and SAA from baseline. The absolute increase of CRP and SAA was reduced by 40% (CRP) and 50% (SAA) at 24 hours and at 48 hours compared with the control group. The absolute increase in PAI-1 from baseline and the percentage increase in p47 phox over 48 hours were significantly (PϽ0.05) lower in the insulin-treated group. CK-MB peaked earlier and tended to be lower in insulin-treated subjects, especially in patients with inferior MI. Conclusions-Insulin

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Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

Cited by 21 publications

References 23 publications

Von Willebrand Factor in Cardiovascular Disease

Von Willebrand Factor in Cardiovascular Disease

C-reactive protein and the severity of atherosclerosis in myocardial infarction patients with stable angina pectoris

Anti-Inflammatory and Profibrinolytic Effect of Insulin in Acute ST-Segment–Elevation Myocardial Infarction

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