Coronary artery calcification score and carotid intima–media thickness in patients with hemophilia

Zwiers, M.; Lefrandt, Johan; Mulder, Douwe J.; Smit, Andries J.; Gans, Rijk O. B.; Vliegenthart, Rozemarijn; Brands-Nijenhuis, A. V. M.; Kluin-Nelemans, Hanneke C.; Meijer, Karina

doi:10.1111/j.1538-7836.2011.04514.x

Cited by 47 publications

(42 citation statements)

References 34 publications

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“…8 Recently, 2 studies investigated whether hypocoagulability is associated with decreased atherogenesis by evaluating subclinical atherosclerosis and endothelial function in hemophilia patients and in matched unaffected controls. 6,7 The first study, a multicenter study from The Netherlands and Belgium compared 51 hemophilia A and B patients with obesity, as a proxy for increased cardiovascular risk, with 47 normal weight hemophiliacs and healthy age-matched controls with (42) and without (50) obesity. 6 The mean age of the subjects was 50 years and none had previous CVD.…”

Section: Atherosclerosis In Patients With Hemophiliamentioning

confidence: 99%

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Cardiovascular risk in patients with hemophilia

Kamphuisen

Cate

2014

Blood

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Patients with hemophilia, who have a lifelong hypocoagulability, seem to have a lower cardiovascular mortality than the general population. Nevertheless, the prevalence of cardiovascular risk factors in patients with hemophilia is as prevalent as in the general population, and hypertension is even more common. Furthermore, hemophiliacs have the same degree of atherosclerosis as the general population. The reduced cardiovascular mortality may be explained by reduced thrombus formation resulting from hypocoagulability. On the other hand, hemophilia, which is associated with reduced thrombin generation, may also increase atherosclerotic plaque stability, as has been shown in mice. Because treatment of these events is extremely challenging in patients with increased bleeding tendency, detection and aggressive treatment of risk factors is mandatory.

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Section: Atherosclerosis In Patients With Hemophiliamentioning

confidence: 99%

“…6,7 Furthermore, classical cardiovascular risk factors, such as hypertension, seem even more prevalent in hemophilia patients. Indeed, in clinical practice, an increasing number of hemophilia patients are diagnosed with CVD.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular risk in patients with hemophilia

Kamphuisen

Cate

2014

Blood

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“…13 However, although some clinical trials have shown a reduced incidence of myocardial infarction in patients with hemophilia A, 14,15 others have shown that the degree of atherosclerosis burden, as measured by different modalities such as intima–media thickness, degree of coronary artery calcification, plaque density of large vessels, and mode of endothelial vascular dilatation, is similar to that in the general population. 16,17 Nonetheless, reduced cardiovascular mortality 16,18 has been shown in hemophilic patients and is probably because of reduced fatal occlusive atherothrombosis.…”

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confidence: 99%

Factor XI Deficiency Protects Against Atherogenesis in Apolipoprotein E/Factor XI Double Knockout Mice

Ganor

Harats

Gailani

et al. 2016

ATVB

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Objective Atherosclerosis and atherothrombosis are still major causes of mortality in the Western world, even after the widespread use of cholesterol-lowering medications. Recently, an association between local thrombin generation and atherosclerotic burden has been reported. Here, we studied the role of factor XI (FXI) deficiency in the process of atherosclerosis in mice. Approach and Results Apolipoprotein E/FXI double knockout mice, created for the first time in our laboratory. There was no difference in cholesterol levels or lipoprotein profiles between apolipoprotein E knockout and double knockout mice. Nevertheless, in 24-week-old double knockout mice, the atherosclerotic lesion area in the aortic sinus was reduced by 32% (P=0.004) in comparison with apolipoprotein E knockout mice. In 42-week-old double knockout mice, FXI deficiency inhibited atherosclerosis progression significantly in the aortic sinus (25% reduction, P=0.024) and in the aortic arch (49% reduction, P=0.028), with a prominent reduction of macrophage infiltration in the atherosclerotic lesions. Conclusions FXI deprivation was shown to slow down atherogenesis in mice. The results suggest that the development of atherosclerosis can be prevented by targeting FXI.

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“…Results from clinical studies on the development of atherosclerosis in hemophilic patients using IMT or other imaging techniques were conflicting [74–79], although most studies did not demonstrate a protective effect of hemophilia [74–77]. The inconsistent results from studies comparing IMT of the carotid and femoral arteries of hemophilic patients and controls [77–79] might be attributable to differences in the progression of atherosclerosis between coronary, carotid and femoral arteries.…”

Section: Hypocoagulabilitymentioning

confidence: 99%

The impact of blood coagulability on atherosclerosis and cardiovascular disease

Loeffen

Spronk

Cate

2012

Journal of Thrombosis and Haemostasis

102

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Summary. Although the link between blood coagulation and atherogenesis has been long postulated, only recently, and through the extensive work on transgenic mice, crossbred on an atherogenic background, has the direction of this interaction become visible. In general, hypercoagulability in mice tends to increase atherosclerosis, whereas hypocoagulability reduces the atherosclerotic burden, depending on the mouse model used. The information on a direct relationship between coagulation and atherosclerosis in humans, however, is not that clear. Almost all coagulation proteins, including tissue factor, are found in atherosclerotic lesions in humans. In addition to producing local fibrin, a matrix for cell growth, serine proteases such as thrombin may be very important in cell signaling processes, acting through the activation of protease‐activated receptors (PARs). Activation of PARs on vascular cells drives many complex processes involved in the development and progression of atherosclerosis, including inflammation, angiogenesis, and cell proliferation. Although current imaging techniques do not allow for a detailed analysis of atherosclerotic lesion phenotype, hypercoagulability, defined either by gene defects of coagulation proteins or elevated levels of circulating markers of activated coagulation, has been linked to atherosclerosis‐related ischemic arterial disease. New, high‐resolution imaging techniques and sensitive markers of activated coagulation are needed in order to study a causal contribution of hypercoagulability to the pathophysiology of atherosclerosis. Novel selective inhibitors of coagulation enzymes potentially have vascular effects, including inhibition of atherogenesis through attenuation of inflammatory pathways. Therefore, we propose that studying the long‐term vascular side effects of this novel class of oral anticoagulants should become a clinical research priority.

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Coronary artery calcification score and carotid intima–media thickness in patients with hemophilia

Cited by 47 publications

References 34 publications

Cardiovascular risk in patients with hemophilia

Cardiovascular risk in patients with hemophilia

Factor XI Deficiency Protects Against Atherogenesis in Apolipoprotein E/Factor XI Double Knockout Mice

The impact of blood coagulability on atherosclerosis and cardiovascular disease

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