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We undertook genetic and biochemical assays in patients with arterial (n = 146) and venous (n = 199) thromboembolism and survivors of pulmonary embolism (n = 58) to study causation and gene-life style interactions. In the clinical material from North Western Russia,  factor V Leiden  was found to be a risk factor in venous thrombosis (OR = 3.6), while the methylenetetrahydrofolate reductase  (MTHFR) C677T  mutation was a significant variable in both venous (p = 0.03) and arterial thrombosis (p = 0.004). Homocysteine levels were determined (n = 84) and hyperhomocysteinemia correlated with the  T  allele of the  MTHFR  gene, and with smoking and coffee consumption. Vitamin supplementation reduced homocysteine levels dependent on  MTHFR  genotype (36% TT, 25% CT, 22% CC). In pulmonary embolism patients, frequency of the − 455G/A  β- fibrinogen  dimorphism was studied. Carriers of this allele were significantly underrepresented (p &lt; 0.02) among pulmonary embolism survivors (34.5%) compared to controls (56.7%). Additionally, − 455AA homozygotes  were found in 11.7% controls but only 1.7% of pulmonary embolism patients (p = 0.006). In venous and arterial thrombosis cases,  MTHFR  and homocysteine data led to effective dietary supplementation with a reduced risk of disease progression. Results from the pulmonary embolism study may indicate that screening tests for the − 455G/A  β- fibrinogen  genetic variation could be of prognostic value, and may point the way for novel anticoagulation strategies.

Genetic Variations Observed in Arterial and Venous Thromboembolism – Relevance for Therapy, Risk Prevention and Prognosis