A nationwide family study of venous thromboembolism and risk of arterial vascular disease

Zöller, Bengt; Li, Xinjun; Sundquist, Jan; Sundquist, Kristina

doi:10.1136/heartjnl-2015-308892

Cited by 5 publications

(6 citation statements)

References 26 publications

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“…Family history of VTE is related to different venous thromboembolic manifestations and varicose veins but not to coronary heart disease, ischemic stroke, cancer, preeclampsia, aortic aneurysm, or peripheral artery disease to any major degree. The only two other conditions except VTE associated with family history in the Swedish population are varicose veins and peripheral arterial embolism and thrombosis [47,50,54]. It is therefore surprising that no association was observed between family history of VTE and RVO.…”

Section: Discussionmentioning

confidence: 96%

Venous thromboembolism does not share familial susceptibility with retinal vascular occlusion or glaucoma: a nationwide family study

Zöller

Sundquist

et al. 2016

J Thromb Thrombolysis

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Inherited hypercoagulable states (i.e. thrombophilia) have been suggested to be involved in retinal vascular occlusion but results are divergent. Vascular micronutrition and ischemia have been hypothesised to be involved in the pathogenesis of glaucoma. This nationwide study determines the importance of family history of venous thromboembolism (VTE) as a risk factor for retinal vein occlusion (RVO), retinal artery occlusion (RAO), primary open angle glaucoma (POAG) and primary angle-closure glaucoma (PACG). A total of 6,007,042 Swedish individuals were studied. Data from the Swedish Multigeneration Register for subjects aged 0-78 years old for the period 1997-2010 were linked to the Swedish Hospital Discharge Register and the Hospital Outpatient Register. Main exposure measure was family history of VTE in first-degree relatives (parents and/or siblings). Main outcomes were hazard ratios (HRs) for RVO, RAO, POAG, and PACG. During follow-up 9036 individuals developed RVO, 2137 individuals developed RAO, 29,176 individuals developed POAG and 1498 individuals developed PACG. There was no association between family history of VTE and risk of RVO (HR = 1.04, 95 % CI 0.98-1.10), RAO (HR = 1.00, 95 % CI 0.89-1.13), POAG (HR = 0.96, 95 % CI 0.93-0.99), and PACG (HR = 0.92, 95 % CI 0.80-1.06) in the crude age and sex adjusted model. The results were similar in the fully adjusted model: RVO (HR = 1.04, 95 % CI 0.99-1.11), RAO (HR = 1.01, 95 % CI 0.89-1.13), POAG (HR = 0.97, 95 % CI 0.94-1.00), and PACG (HR = 0.91, 95 % CI 0.79-1.05). Family history of VTE is not a risk factor for RVO, RAO, POAG and PACG. Thus, it is unlikely that strong and common genetic variants associated with VTE are of importance for these disorders.

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Section: Discussionmentioning

confidence: 96%

Venous thromboembolism does not share familial susceptibility with retinal vascular occlusion or glaucoma: a nationwide family study

Zöller

Sundquist

et al. 2016

J Thromb Thrombolysis

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“…Of special interest is the finding that FH of VTE was related to increased risk of ATE. 69 Thus, there could be common gene variants that both increase VTE risk and ATE. However, for most investigated conceivable pleiotropic associations for VTE and other diseases the familial shared risks were weak or inconsistent.…”

Section: Discussionmentioning

confidence: 99%

“…[65][66][67] A slight to moderate association has been found between FH of VTE and varicose veins (FRR for one affected sibling ¼ 1.30, and FRR for two affected siblings ¼ 1.70) and arterial thrombosis and embolization (FRR for 1 or more affected sibling ¼ 1.61), suggesting partially shared familial susceptibility. 68,69 In contrast family history of VTE is only weakly or not consistently associated with ischemic stroke (similar risk in spouses and first-degree relatives), myocardial infarction and coronary heart disease (CHD), aortic aneurysm, peripheral artery disease, retinal vein occlusion, retinal artery occlusion, primary open angle glaucoma, primary angle-closure glaucoma, cancer, and preeclampsia/eclampsia. [69][70][71][72][73][74][75][76][77] These studies suggest that it is not probable that strong and common shared disease-causing variants exist in the Swedish population for VTE and several conditions.…”

Section: Hill's Third Criterion: Specificitymentioning

confidence: 99%

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Epidemiology of Familial Aggregation of Venous Thromboembolism

Zöller

et al. 2016

Semin Thromb Hemost

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Familial aggregation (clustering) of venous thromboembolism (VTE) is the clustering of VTE within a family. Though several genes, such as antithrombin, protein C, protein S, factor V, and prothrombin are associated with the familial clustering of VTE, these loci only partially explain the familial aggregation of VTE. The epidemiology of the familial aggregation of VTE exhibits typical characteristics of complex traits. The family history of VTE in first-degree relatives is associated with a two to three times increased familial relative risk (FRR). The FRR of VTE is higher in younger individuals, increases with a number of affected relatives, decreases as the familial relationship becomes more distant, increases with severity (unprovoked), and exhibits slightly stronger male transmission (Carter effect). High FRR is observed in individuals with two or more affected siblings (FRR > 50). Because familial aggregation represents the sum of shared family environmental and genetic factors, one should not assume that evidence of familial aggregation implies genetic effects. However, studies in twins, extended families, adoptees, and spouses indicate a weak involvement of shared environmental factors to the familial aggregation of VTE. Moreover, familial aggregation of VTE fulfills the Hill's criteria for causation. In conclusion, familial aggregation of VTE signals a clinically relevant inherent predisposition for VTE.

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“…2 Interestingly, these findings are also in agreement with previous nationwide epidemiological register-based family studies in Sweden. [3][4][5] Family history of VTE is a strong risk factor for VTE in Sweden as determined using the world's largest family database-the Swedish Multi-generation Register. 6 However, family history of VTE is not a strong risk factor for CAD or ischemic stroke in Sweden.…”

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confidence: 99%

Reactome Pathway Analysis of Venous Thromboembolism, Peripheral Artery Disease, Stroke, and Coronary Artery Disease

et al. 2020

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A nationwide family study of venous thromboembolism and risk of arterial vascular disease

Abstract: VTE shares only weak familial susceptibility with AA and PAD in the Swedish population. However, ATE partially shares a moderate familial susceptibility and possibly genetic factors with VTE. Moreover, familial non-genetic factors may contribute to the observed familial associations.

Cited by 5 publications

References 26 publications

Venous thromboembolism does not share familial susceptibility with retinal vascular occlusion or glaucoma: a nationwide family study

Venous thromboembolism does not share familial susceptibility with retinal vascular occlusion or glaucoma: a nationwide family study

Epidemiology of Familial Aggregation of Venous Thromboembolism

Reactome Pathway Analysis of Venous Thromboembolism, Peripheral Artery Disease, Stroke, and Coronary Artery Disease

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