Myocardial infarction, prothrombotic genotypes, and venous thrombosis risk: The Tromso Study

被引:5
作者
Sejrup, Joakim K. [1 ]
Morelli, Vania M. [1 ]
Lochen, Maja-Lisa [2 ]
Njolstad, Inger [2 ]
Mathiesen, Ellisiv B. [3 ]
Wilsgaard, Tom [2 ]
Hansen, John-Bjarne [1 ,4 ]
Braekkan, Sigrid K. [1 ,4 ]
机构
[1] UiT Arctic Univ Norway, Dept Clin Med, KG Jebsen Thrombosis Res & Expertise Ctr TREC, Tromso, Norway
[2] UiT Arctic Univ Norway, Dept Community Med, Epidemiol Chron Dis Res Grp, Tromso, Norway
[3] UIT Arctic Univ Norway, Dept Clin Med, Brain & Circulat Res Grp, Tromso, Norway
[4] Univ Hosp North Norway, Div Internal Med, Tromso, Norway
关键词
epidemiology; genetics; myocardial infarction; pulmonary embolism; risk factors; thromboembolism; venous; FAMILY-HISTORY; SUBCLINICAL ATHEROSCLEROSIS; CAROTID ATHEROSCLEROSIS; PULMONARY-EMBOLISM; FUTURE RISK; PROTEIN-C; THROMBOEMBOLISM; ARTERIAL; POPULATION; METAANALYSIS;
D O I
10.1002/rth2.12306
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background The risk of venous thromboembolism (VTE) is increased after a myocardial infarction (MI). Some prothrombotic genotypes associated with VTE have also been associated with risk of MI. Whether prothrombotic single-nucleotide polymorphisms (SNPs) further increase the risk of VTE in MI patients is scarcely investigated. Aim To study the combined effect of MI and prothrombotic SNPs on the risk of VTE. Methods Cases with incident VTE (n = 641) and a randomly sampled subcohort weighted for age (n = 1761) were identified from the 4 to 6 surveys of the Tromso Study (1994-2012). DNA was genotyped for rs8176719 (ABO), rs6025 (F5), rs1799963 (F2), rs2066865 (FGG), and rs2036914 (F11). Hazard ratios (HRs) for VTE with 95% confidence intervals (CIs) were estimated by categories of risk alleles and MI status. Results Patients with MI had a 1.4-fold increased risk of VTE, and adjustments for the 5 SNPs, either alone or in combination, did not affect this relationship (adjusted HR, 1.52; 95% CI, 1.12-2.07). In subjects without MI, an increased risk of VTE was observed for each of the individual SNPs (>= 1 vs. 0 risk alleles), and the risk increased linearly with increasing number of risk alleles in the 5-SNP score. The combination of MI and prothrombotic genotypes, either as individual SNPs or in the 5-SNP score, did not result in an excess risk of VTE. Conclusion The relationship between MI and VTE was not explained by these 5 prothrombotic genotypes. Prothrombotic genotypes did not yield an excess risk of VTE in patients with MI.
引用
收藏
页码:247 / 254
页数:8
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