Caroline Lind1, Kristin F Enga2, Ellisiv B Mathiesen2, Inger Njølstad2, Sigrid K Brækkan2, John-Bjarne Hansen2. 1. From the Department of Clinical Medicine, K.G. Jebsen Thrombosis Research and Expertise Center (TREC) (C.L., K.F.E., E.B.M., I.N., S.K.B., J.-B.H.), Department of Clinical Medicine, Hematological Research Group (C.L., K.F.E., S.K.B., J.-B.H.), Brain and Circulation Research Group, Department of Clinical Medicine (E.B.M.), Epidemiology of Chronic Diseases Research Group, Department of Community Medicine (I.N.), University of Tromsø, Tromsø, Norway; Department of Neurology and Clinical Neurophysiology (E.B.M.), Division of Internal Medicine (S.K.B., J.-B.H.), University Hospital of North Norway, Tromsø, Norway. caroline.lind@uit.no. 2. From the Department of Clinical Medicine, K.G. Jebsen Thrombosis Research and Expertise Center (TREC) (C.L., K.F.E., E.B.M., I.N., S.K.B., J.-B.H.), Department of Clinical Medicine, Hematological Research Group (C.L., K.F.E., S.K.B., J.-B.H.), Brain and Circulation Research Group, Department of Clinical Medicine (E.B.M.), Epidemiology of Chronic Diseases Research Group, Department of Community Medicine (I.N.), University of Tromsø, Tromsø, Norway; Department of Neurology and Clinical Neurophysiology (E.B.M.), Division of Internal Medicine (S.K.B., J.-B.H.), University Hospital of North Norway, Tromsø, Norway.
Abstract
BACKGROUND: A family history of myocardial infarction (FHMI) has been shown to increase the risk of venous thromboembolism (VTE). The mechanism underlying the association remains unclear. Therefore, we aimed to determine the risks of MI and VTE by FHMI using a cause-specific model and to explore whether atherosclerotic risk factors could explain the association between FHMI and VTE in a population-based cohort. METHODS AND RESULTS: The study included 21 624 subjects recruited from the Tromsø Study in 1994 to 1995 and 2001 to 2002. Incident MI and VTE events were registered from date of enrollment to end of follow-up, December 31, 2010. There were 1311 MIs and 428 VTEs during a median follow-up of 15.8 years. FHMI was associated with a 52% increased risk of MI (adjusted hazard ratio, 1.52; 95% confidence interval, 1.35-1.70) and a 26% increased risk of VTE (adjusted hazard ratio, 1.26; 95% confidence interval, 1.02-1.55) in the cause-specific Cox model. Similar results were found using the traditional Cox model. The risk estimates by status of FHMI were highest for unprovoked deep vein thrombosis (adjusted hazard ratio, 1.69; 95% confidence interval, 1.12-2.56), and the risk increased with increasing number of affected relatives. Modifiable atherosclerotic risk factors slightly altered the association between FHMI and MI but had a negligible effect on the association between FHMI and VTE. CONCLUSIONS: FHMI was associated with increased risk of both MI and VTE in a cause-specific model. Apparently, the association between FHMI and VTE applied to unprovoked deep vein thrombosis and was not explained by modifiable atherosclerotic risk factors.
BACKGROUND: A family history of myocardial infarction (FHMI) has been shown to increase the risk of venous thromboembolism (VTE). The mechanism underlying the association remains unclear. Therefore, we aimed to determine the risks of MI and VTE by FHMI using a cause-specific model and to explore whether atherosclerotic risk factors could explain the association between FHMI and VTE in a population-based cohort. METHODS AND RESULTS: The study included 21 624 subjects recruited from the Tromsø Study in 1994 to 1995 and 2001 to 2002. Incident MI and VTE events were registered from date of enrollment to end of follow-up, December 31, 2010. There were 1311 MIs and 428 VTEs during a median follow-up of 15.8 years. FHMI was associated with a 52% increased risk of MI (adjusted hazard ratio, 1.52; 95% confidence interval, 1.35-1.70) and a 26% increased risk of VTE (adjusted hazard ratio, 1.26; 95% confidence interval, 1.02-1.55) in the cause-specific Cox model. Similar results were found using the traditional Cox model. The risk estimates by status of FHMI were highest for unprovoked deep vein thrombosis (adjusted hazard ratio, 1.69; 95% confidence interval, 1.12-2.56), and the risk increased with increasing number of affected relatives. Modifiable atherosclerotic risk factors slightly altered the association between FHMI and MI but had a negligible effect on the association between FHMI and VTE. CONCLUSIONS: FHMI was associated with increased risk of both MI and VTE in a cause-specific model. Apparently, the association between FHMI and VTE applied to unprovoked deep vein thrombosis and was not explained by modifiable atherosclerotic risk factors.
Authors: Jennifer A Sumner; Laura D Kubzansky; Christopher Kabrhel; Andrea L Roberts; Qixuan Chen; Ashley Winning; Paola Gilsanz; Eric B Rimm; Maria M Glymour; Karestan C Koenen Journal: J Am Heart Assoc Date: 2016-05-12 Impact factor: 5.501
Authors: Joakim K Sejrup; Vania M Morelli; Maja-Lisa Løchen; Inger Njølstad; Ellisiv B Mathiesen; Tom Wilsgaard; John-Bjarne Hansen; Sigrid K Brækkan Journal: Res Pract Thromb Haemost Date: 2020-01-27