Coagulation Factors II, V, IX, X, XI, and XII, Plasminogen, and α-2 Antiplasmin and Risk of Coronary Heart Disease

Yamagishi, Kazumasa; Aleksic, Nena; Hannan, Peter J.; Folsom, Aaron R.

doi:10.5551/jat.3673

Cited by 27 publications

(33 citation statements)

References 14 publications

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“…32 In the prospective casecohort study of ARIC participants, the association of fXI:c with coronary heart disease was not significant when adjusted for Framingham risk factors. 33 In contrast, in the SMILE study, the risk of MI was increased for each quintile of fXI:c compared with the bottom quintile even after adjustment for cardiovascular risk factors and fXII:c levels. 31 Interestingly, although fXI:c and fXII:c levels were correlated, the opposite effects on risk for MI were also synergistic; therefore, the highest risk was found in men with both high fXI:c and low fXII:c. To explain this seeming paradox, the investigators suggested that any effect of fXII on risk of MI may not be mediated via fXI, but rather through some other mechanism.…”

Section: Fximentioning

confidence: 54%

“…No association was observed between fXII levels and coronary heart disease events, defined as hospitalized MI, a definite CHD death, proven silent MI, or a coronary vascularization. 33 It is evident from these studies that a firm conclusion on the role of fXII as a risk factor for MI is not established. It is possible that the discrepant results are explained by chance or other factors such as study design or case definitions.…”

Section: Fxiimentioning

confidence: 98%

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Epidemiologic and clinical data linking factors XI and XII to thrombosis

Key

2014

Hematology

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Currently available evidence supports the contention that elevated levels of factor XI (fXI) are associated with a greater risk of venous thromboembolism and ischemic stroke, but, less convincingly, with myocardial infarction. Conversely, reduced plasma levels of fXI seem to offer some protection from venous thromboembolism and stroke, but not myocardial infarction. Factor XI-deficient patients are at risk for certain types of bleeding, particularly posttraumatic hemorrhage on mucosal surfaces where there is a high endogenous fibrinolytic activity. In contrast, the situation with fXII in human thrombosis remains enigmatic. Deficiency of fXII is clearly not associated with any bleeding risk, but neither does it seem to be protective against thrombosis. The longstanding debate as to whether partial fXII deficiency represents a risk factor for thrombosis remains unresolved, with seemingly conflicting results depending on study design, type of assay used, and analyte evaluated. The possibility that elevated fXII levels represent a risk factor for thrombosis is not borne out in the literature.

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Section: Fximentioning

confidence: 54%

Section: Fxiimentioning

confidence: 98%

Epidemiologic and clinical data linking factors XI and XII to thrombosis

Key

2014

Hematology

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“…Prospective cohort and case–control studies have demonstrated both positive correlation and no correlation of plasminogen, tPA, or PAI-1 with incident CAD and MI [41–46]. Also, in the studies that found a positive correlation, the associations were not consistently independent of other cardiovascular risk factors [41, 43, 45, 46]. The relationship between OxPL-PLG and risk of future acute MI is less well studied.…”

Section: Discussionmentioning

confidence: 99%

Circulating levels of plasminogen and oxidized phospholipids bound to plasminogen distinguish between atherothrombotic and non-atherothrombotic myocardial infarction

DeFilippis

Chernyavskiy

Amraotkar

et al. 2015

J Thromb Thrombolysis

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Oxidized phospholipids (OxPL) are abundant in atherosclerotic plaques. They are also bound to circulating plasminogen after myocardial infarction (MI), and their binding to plasminogen may accentuate fibrinolysis. We sought to assess whether circulating levels of plasminogen and OxPL bound to plasminogen (OxPL-PLG) increase following acute MI and whether this increase differs between atherothrombotic (Type 1) and non-atherothrombotic (Type 2) MI. We measured circulating levels of plasminogen and OxPL-PLG at 0, 6, 24, 48 h, and >3 months (stable state) following acute MI and following an angiogram for stable coronary artery disease (CAD). Forty-nine subjects met the criteria for acute MI, of whom 34 had clearly defined atherothrombotic (n = 22) or non-atherothrombotic (n = 12) MI; 15 patients met the criteria for stable CAD. Mean baseline levels of plasminogen and OxPL-PLG were lower in the acute MI group than in the stable CAD group (9.75 vs 20.2, p < 0.0001 for plasminogen and 165.5 vs 275.1, p = 0.0002 for OxPL-PLG) and did not change over time or between time points, including the 3-month follow-up. Mean baseline levels of plasminogen and OxPL-PLG were also lower in atherothrombotic (Type 1) than in non-atherothrombotic (Type 2) MI subjects (8.65 vs 12.1, p < 0.03 for plasminogen and 164.5 vs 245.7, p = 0.02 for OxPL-PLG), and this relationship did not change over time or between time points. Plasminogen and OxPL-PLG were lower in patients presenting with an acute MI than in those with stable CAD and also in those with atherothrombotic MI (Type 1) vs. those with non-atherothrombotic MI (Type 2). These findings persisted at a median follow-up of 3 months post-MI. The association of plasminogen and OxPL-PLG with acute MI, particularly atherothrombotic MI (Type 1), could reflect a reduced fibrinolytic capacity, associated with an increased risk of atherothrombotic events differentiating stable CAD from unstable CAD and atherothrombotic MI (Type 1) from non-atherothrombotic MI (Type 2). Additional study with a larger sample size is warranted.

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“…However, evidence for an association between FXI levels in the general population and incident arterial thrombotic diseases has been inconsistent [4–7, 9–11, 13, 14]. Possible explanations for the discrepant results may include differences in study designs and assay methodologies, small sample sizes, inadequate control of confounding factors, reverse causation, or chance.…”

Section: Discussionmentioning

confidence: 99%

“…While elevated levels of FXI have been consistently positively associated with venous thromboembolism (VTE) [1–3] in epidemiologic studies, the relation of FXI to ischemic stroke (IS) [4–8], hemorrhagic stroke (HS) [7], myocardial infarction [4, 9–12], or coronary heart disease (CHD) [7, 13, 14] remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

Relation of coagulation factor XI with incident coronary heart disease and stroke

Appiah¹,

Fashanu

Heckbert

et al. 2017

Blood Coagulation &Amp; Fibrinolysis

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OBJECTIVES The role of coagulation factor XI (FXI) in the etiology of arterial thrombotic events remains uncertain. We examined the association of FXI with incident coronary heart disease (CHD), ischemic stroke (IS), and hemorrhagic stroke (HS). METHODS Data were from 3394 adults (mean age: 74.5 years) enrolled in the Cardiovascular Health Study who had FXI antigen from plasma samples drawn in 1992–1993 and were followed for cardiovascular events until June 30, 2013. RESULTS Approximately 63% of participants were women and 17% were black. FXI levels were higher in blacks and women, showed positive associations with HDL and total cholesterol, body mass index and diabetes, and negative associations with age and alcohol intake. During median follow-up of 13 years, we identified 1232 incident CHD, 473 IS, and 84 HS events. In multivariable Cox models adjusted for traditional CVD risk factors, the hazard ratio per 1 standard deviation (32.2 mg/dl) increment of FXI was 1.02 (95% CI: 0.96–1.08) for CHD; 0.94 (0.85–1.04) for IS and 0.85 (0.65–1.10) for HS. CONCLUSIONS In this prospective cohort of elderly adults, there was no statistically significant association of higher FXI levels with incident CHD and stroke.

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Coagulation Factors II, V, IX, X, XI, and XII, Plasminogen, and α-2 Antiplasmin and Risk of Coronary Heart Disease

Abstract: Aim:To examine whether plasma levels of coagulation factors , , , , , and , plasminogen, and -2 antiplasmin are associated with coronary heart disease (CHD) in a prospective case-cohort study. Methods

Cited by 27 publications

References 14 publications

Epidemiologic and clinical data linking factors XI and XII to thrombosis

Epidemiologic and clinical data linking factors XI and XII to thrombosis

Circulating levels of plasminogen and oxidized phospholipids bound to plasminogen distinguish between atherothrombotic and non-atherothrombotic myocardial infarction

Relation of coagulation factor XI with incident coronary heart disease and stroke

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