Comparison of the Prevalence of APC-resistance in Vascular Patients and in a Normal Population Cohort in Western Germany

Aleksic, M.; Jahn, Philipp; Heckenkamp, J.; Wielckens, Klaus; Brunkwall, Jan

doi:10.1016/j.ejvs.2005.03.008

Cited by 8 publications

(4 citation statements)

References 30 publications

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“…We revealed an increased APC sensitivity in young women with a history of MI compared with controls. Previous studies on APC resistance in relation to arterial thrombosis provided contradictory results, with some studies showing an increased APC resistance in patients with arterial thrombosis and in other studies no effect of APC resistance on arterial thrombosis [21–23]. A possible explanation for the differences found in the literature may lie in differences in patient selection criteria and assays used to determine APC resistance.…”

Section: Discussionmentioning

confidence: 99%

“…A possible explanation for the differences found in the literature may lie in differences in patient selection criteria and assays used to determine APC resistance. In the present study, APC resistance was measured using a thrombin generation‐based test rather than an APTT‐based test [21,24]. These assays have different determinants: the CAT test is primarily dependent on free TFPI and protein S, whereas the APTT‐based test is mainly determined by FVIII levels [12,25].…”

Section: Discussionmentioning

confidence: 99%

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Increased tissue factor pathway inhibitor activity is associated with myocardial infarction in young women: results from the RATIO study

Winckers

Siegerink

Duckers

et al. 2011

Journal of Thrombosis and Haemostasis

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Summary. Background: The tissue factor pathway inhibitor (TFPI)/protein S anticoagulant system is a potent inhibitor of blood coagulation. TFPI and protein S are major determinants of thrombin generation (TG) tests determined at low tissue factor (TF) and at high TF concentrations in the presence of activated protein C (APC). Both TFPI and protein S protect against venous thrombosis, but the importance of the TFPI/protein S system in arterial thrombosis remains unclear. Objectives: To investigate the influence of the TFPI/protein S anticoagulant system on the risk of myocardial infarction (MI) in young women. Methods: The RATIO study is a case-control study in women under 50 years of age, including 205 patients and 638 controls. TFPI and protein S were quantified using ELISA. The TFPI/ protein S activity (nTFPIr) and the APC sensitivity ratio (nAPCsr) were determined using TG tests. Odds ratios (ORs) adjusted for putative confounders and corresponding 95% confidence intervals (95% CI) were determined. Results: Women with MI had higher TFPI levels than controls (135.9 ± 40% vs. 124.2 ± 41%), resulting in increased TFPI/protein S activities and increased APC sensitivity. Furthermore, an increased TFPI activity was associated with MI [nTFPIr: adjusted OR Q1 vs. Q4 = 2.1 (95%CI 1.1-4.1)]. Additionally, an increased APC sensitivity was associated with MI [nAPCsr: adjusted OR Q1 vs. Q4 = 1.7 (95% CI 0.9-3.2)] Conclusion: Women with MI had increased TFPI levels compared with controls. Consequently, the TFPI/protein S activity and APC sensitivity are increased in women with MI. Whether this increase in TFPI activity acts as a compensating mechanism for an increased procoagulant state or is a marker of endothelial damage remains to be investigated.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased tissue factor pathway inhibitor activity is associated with myocardial infarction in young women: results from the RATIO study

Winckers

Siegerink

Duckers

et al. 2011

Journal of Thrombosis and Haemostasis

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“…In contrast, Sampram and Lindblat 24 suggested that an FVL mutation was associated with a doubled rate of failure for infrainguinal procedures both at one month and one year (37 versus 22% and 46 versus 27%). In contrast, Evans et al 25 only reported one APC resistant patient in 116 claudicants, while Aleksić et al 26 showed neither an increased prevalence of APCR in patients with PAOD nor a firm association between the presence of APCR and previous bypass occlusion or postoperative failure of the vascular reconstruction. Variations in reported figures and even opposing findings of various studies may be explained by the preferential use of DNA analysis or APC ratio to define FVL; variations in the lower value of the normal range for defining the normal APC ratio; and the severity of the presenting PAOD.…”

Section: Discussionmentioning

confidence: 95%

Vascular graft thrombosis secondary to activated protein C resistance: a case report and literature review

Pejkić¹,

Savić²,

Paripović³

et al. 2013

Vascular

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Hypercoagulability is a well-documented and prominent risk factor for venous thromboembolism. The role of thrombophilia in arterial thrombotic events is less well defined. A 52-year-old male patient with multiple atherogenic risk factors was admitted for non-healing pedal ulcer and absent distal pulses. Based on the clinical presentation, Doppler ultrasound and angiography findings, the patient underwent elective in situ bypass arterial reconstruction. The saphenous vein graft was of satisfactory quality and the procedure went routinely. Acute graft thrombosis on postoperative day 0 was recognized immediately and prompted an emergent surgical revision. No technical errors or anatomical/mechanical causes for failed reconstruction were found and the graft was successfully thrombectomized using a Fogarty balloon-catheter. Graft rethrombosis, however, ensued after several hours. Considering the absence of threatening limb ischemia and the idiopathic recurrent thrombosis, raising suspicion of prothrombotic state, conservative treatment was pursued. Postoperative thrombophilia testing proved positive for activated protein C resistance, mandating introduction of chronic oral anticoagulation. Six months later, the operated extremity is viable. Inexplicable vascular graft thrombosis, particularly if early and recurrent, should raise suspicion of underlying thrombophilia. If confirmed by laboratory testing, long-term secondary antithrombotic prophylaxis may be required.

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“…17 But in contrast to a solid association between FVL and venous thrombosis, the data relating FVL and arterial events remain controversial. Nevertheless, some clinical studies suggest an increased risk of thrombosis after arterial revascularization, [18][19][20][21][22][23][24][25] implicating vessel wall injury during the revascularization procedure as the triggering event. Not unexpectedly, the relationship between FVL and failure of arterial reconstructive procedures appears especially high in homozygotes.…”

Section: Discussionmentioning

confidence: 99%

Arterial Thrombosis in Mice with Factor V Leiden Mutation

Sampram

Saad²,

Ouriel³

2008

Vascular

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The factor V Leiden (FVL) mutation has been demonstrated to be associated with the development of venous thrombosis in humans. Whether such a propensity also exists in the arterial circulation remains controversial. In an effort to minimize the variability that clouds the clinical study of arterial thrombosis, we studied FVL-associated arterial thrombosis in an experimental model of homozygous, heterozygous, and wild-type mice. Heterozygous FVL mice were crossbred to C57BL/6J mice over several generations. The genotypes of the resulting three genotype groups (wild type, heterozygous FVL, and homozygous FVL) were blinded to the investigators. Arterial injury was produced with the injection of ferric chloride into an isolated segment of carotid artery. Arterial thrombosis was assessed with an ultrasonic flow probe and the time to occlusion (TTO) was recorded. The carotid artery occluded within 60 minutes of injury in 72 of the animals studied (97.3%). The carotid artery remained patent at 60 minutes in the remaining two animals, both of whom were subsequently found to be genotypically wild type. There was a statistically significant relationship between TTO and genotype (p = .002). TTO was greatest in the wild-type mice (p < .001 vs heterozygous, < .001 vs homozygous) and least in the homozygotes (p < .001 vs heterozygotes). Increased thrombogenicity is present in mice with the FVL mutation and is more prolonged in homozygotes than heterozygotes. These findings provide some corroboration to the clinical studies that suggest an increased risk of arterial events in patients with the FVL mutation.

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Comparison of the Prevalence of APC-resistance in Vascular Patients and in a Normal Population Cohort in Western Germany

Cited by 8 publications

References 30 publications

Increased tissue factor pathway inhibitor activity is associated with myocardial infarction in young women: results from the RATIO study

Increased tissue factor pathway inhibitor activity is associated with myocardial infarction in young women: results from the RATIO study

Vascular graft thrombosis secondary to activated protein C resistance: a case report and literature review

Arterial Thrombosis in Mice with Factor V Leiden Mutation

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