Arterial cardiovascular risk factors and venous thrombosis: results from a population-based, prospective study (the HUNT 2)

Quist‐Paulsen, Petter; Næss, Inger Anne; Cannegieter, Suzanne C.; Romundstad, Pål Richard; Christiansen, Sverre Christian; Rosendaal, Frits R.; Hammerstrøm, Jens

doi:10.3324/haematol.2009.011866

Cited by 94 publications

(127 citation statements)

References 41 publications

(53 reference statements)

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“…30 Only 1 other article has studied the relationship between family history of stroke and risk of VTE. 12 In that study, which was smaller than the present one, an association (adjusted OR, 1.5; 95% CI, 1.1-2.1) was observed but only for family history of stroke in idiopathic VTE patients, that is, VTE without major provoking factors. 12 The reverse association was not studied, that is, risk of stroke when family history of VTE was present.…”

Section: Discussioncontrasting

confidence: 42%

See 1 more Smart Citation

Venous Thromboembolism Does Not Share Strong Familial Susceptibility With Ischemic Stroke

Zöller

Li²,

Sundquist³

et al. 2011

Circ Cardiovasc Genet

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Background-Coagulation allelic variants associated with venous thromboembolism (VTE) have been suggested to be involved in the pathogenesis of ischemic stroke. This nationwide study aimed at determining whether VTE shares familial susceptibility with ischemic stroke. Method and Results-The Swedish Multigeneration Register of 0-to 75-year-old subjects was linked to the Swedish Hospital Discharge Register and the Cause of Death Register for the period 1987 to 2007. Odds ratios (ORs) for VTE and ischemic stroke were determined in 2 ways: odds of ischemic stroke in offspring whose parents had been diagnosed with VTE, and odds of VTE in offspring whose parents had been diagnosed with ischemic stroke. The analyses were repeated for siblings and spouses. Offspring of parents with VTE (nϭ25 929) were at increased risk for ischemic stroke (nϭ5595): OR, 1.10 (95% confidence interval [CI], 1.06 -1.14). Siblings of probands with VTE (nϭ45 132) had no increased risk of ischemic stroke (nϭ1716): OR, 1.05 (95% CI, 1.00 -1.11). Spouses of probands with VTE (nϭ24 106) were at increased risk for ischemic stroke (nϭ940): OR, 1.18 (95% CI, 1.10 -1.27). The risks for VTE in relatives of probands with ischemic stroke were OR, 1.15; 95% CI, 1.10 -1.21 (offspring); OR, 1.07; 95% CI, 1.02-1.12 (siblings); and OR, 1.21; 95% CI, 1.11-1.32 (spouses). Conclusions-VTE does not share strong familial susceptibility with ischemic stroke in the Swedish population. Moreover, familial nongenetic factors contribute to the observed weak familial associations. The present study suggests that it is unlikely that strong shared disease-causing mutations exist to a large extent in the Swedish population. (Circ Cardiovasc Genet. 2011; 4:484-490.)

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Section: Discussioncontrasting

confidence: 42%

“…Only 1 case-control study has investigated the link between familial history of ischemic stroke and risk of VTE. 12 In that study family history of stroke was a risk factor for idiopathic VTE (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.1-2.1).…”

Section: Clinical Perspective On P 490mentioning

confidence: 99%

Venous Thromboembolism Does Not Share Strong Familial Susceptibility With Ischemic Stroke

Zöller

Li²,

Sundquist³

et al. 2011

Circ Cardiovasc Genet

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show abstract

“…In a recently published study, common causative factors, including genetic thrombophilia and procoagulant markers, explained the increased risk of arterial cardiovascular disease after VTE. 27 A family history of MI has been shown to be associated with both arterial thrombotic disease 28,29 and VTE, 30,31 which suggests a common genetic component for both diseases. Concordantly, some inherited thrombophilias have also been associated with arterial thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Impact of Incident Venous Thromboembolism on Risk of Arterial Thrombotic Diseases

et al. 2014

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Background-Growing evidence supports an association between venous thromboembolism (VTE) and arterial thrombotic diseases (ie, myocardial infarction and ischemic stroke). We aimed to study the association between VTE and future arterial events and to determine the population attributable risk of arterial events by VTE in a large prospective cohort recruited from the general population. Methods and Results-In 1994 to 1995 and 1993 to 1997, 81 687 subjects were included in the Tromsø Study and in the Diet, Cancer and Health Study and followed up to the date of incident venous and arterial events (myocardial infarction or ischemic stroke), death or migration, or to the end of the study period (2010 and 2008, respectively). There were 1208 cases of VTE and 90 subsequent arterial events during a median follow-up of 12.2 years. An association between VTE and future arterial events was found in all women and men aged <65 years but not in men aged >65 years. Women <65 years old with VTE had 3.3-fold higher risk of arterial disease (adjusted hazard ratio, 3.28; 95% confidence interval, 1.69-6.35) compared with women of the same age without VTE. The corresponding hazard ratio in men aged <65 years was 2.06 (95% confidence interval, 1.32-3.20). Only 0.9% of the arterial events were attributed to VTE, and the VTE explained 63.8% of the risk of arterial events among VTE patients. Conclusions-Our findings imply that women and young men with VTE have higher risk of arterial thrombotic disease than those without VTE. However, only 1% of the arterial thrombotic events in the population are attributed to VTE. (Circulation. 2014;129:855-863.)

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“…3 Thus, the highest levels of high sensitivity (hs) CRP doubled the risk of thrombosis, 3 being in accordance with results of several prospective studies. 30 The highest levels of PTX3 were associated with a lower thrombosis rate, 3 implying PTX3 to exert a protective effect against thrombosis. Indeed, deficiency of PTX3 has been shown to promote vascular inflammation and atherosclerosis and elevated levels of PTX3 to be associated with a reduced risk of cardiovascular disease and thrombosis.…”

Section: Does Chronic Inflammation Contribute To Cardiovascular Morbimentioning

confidence: 99%

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Hasselbalch

2012

Blood

272

301

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The morbidity and mortality of patients with the chronic Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascular diseases, thrombohemorrhagic complications, and bone marrow failure because of myelofibrosis and leukemic transformation. In the general population, chronic inflammation is considered of major importance for the development of atherosclerosis and cancer. MPNs are characterized by a state of chronic inflammation, which is proposed to be the common denominator for the development of "premature atherosclerosis," clonal evolution, and second cancer in patients with MPNs. Chronic inflammation may both initiate clonal evolution and catalyze its expansion from early disease stage to the myelofibrotic burnt-out phase. Furthermore, chronic inflammation may also add to the severity of cardiovascular disease burden by accelerating the development of atherosclerosis, which is well described and recognized in other chronic inflammatory diseases. A link between chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the time of diagnosis (statins and interferon-␣2), the aims being to dampen chronic inflammation and clonal evolution and thereby also diminish concurrent diseasemediated chronic inflammation and its consequences (accelerated atherosclerosis and second cancer).

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Arterial cardiovascular risk factors and venous thrombosis: results from a population-based, prospective study (the HUNT 2)

Cited by 94 publications

References 41 publications

Venous Thromboembolism Does Not Share Strong Familial Susceptibility With Ischemic Stroke

Venous Thromboembolism Does Not Share Strong Familial Susceptibility With Ischemic Stroke

Impact of Incident Venous Thromboembolism on Risk of Arterial Thrombotic Diseases

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

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