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

Res Pract Thromb Haemost. 2020 Jan 27;4(2):247-254. doi: 10.1002/rth2.12306. eCollection 2020 Feb.

Abstract

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 Tromsø 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.

Keywords: epidemiology; genetics; myocardial infarction; pulmonary embolism; risk factors; thromboembolism; venous.