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Myocardial infarction under the age of 36: prevalence of thrombophilic disorders
Loukianos S Rallidis1, Chrusula I Belesi, Helen S Manioudaki
1General Hospital of Nikea, Department of Cardiology, 74 Thermopylon, Argiroupolis, 16451, Greece. rallidis@ath.forthnet.gr
Insights
The G20210A prothrombin gene mutation significantly increases the risk of myocardial infarction (MI) in young adults. This genetic factor, especially combined with smoking, elevates MI risk substantially.
Area of Science:
- Cardiovascular Genetics
- Thrombosis and Hemostasis
- Molecular Cardiology
Background:
- Thrombotic tendency is a known risk factor for myocardial infarction (MI).
- Genetic thrombogenic disorders may contribute to premature MI.
- Investigating specific genetic mutations and deficiencies is crucial for understanding young-onset MI risk.
Purpose of the Study:
- To assess the association between genetic thrombogenic disorders and the risk of MI in individuals under 36 years old.
- To evaluate the role of the G20210A prothrombin gene mutation, G1691A factor V gene mutation, and deficiencies in protein C, S, and antithrombin III.
- To determine the combined effect of genetic factors and traditional cardiovascular risk factors on premature MI.
Main Methods:
- A case-control study was conducted with 70 young MI survivors (under 36) and 260 healthy controls.
- Genotyping was performed for the G20210A prothrombin mutation and G1691A factor V mutation.
- Prevalence of protein C, protein S, and antithrombin III deficiencies was assessed.
- Statistical analysis included odds ratios (OR) and confidence intervals (CI), adjusting for cardiovascular risk factors.
Main Results:
- The G20210A prothrombin gene mutation was significantly more prevalent in young MI patients (11.4%) compared to controls (3.1%), yielding an OR of 4.
- The adjusted OR for MI, considering major cardiovascular risk factors, was 4.3.
- Combined G20210A mutation and smoking dramatically increased MI risk (OR, 58).
- No significant association was found for the G1691A factor V mutation or deficiencies in protein C, S, or antithrombin III.
Conclusions:
- The G20210A mutation in the prothrombin gene is a significant genetic risk factor for myocardial infarction in individuals under 36 years old.
- Smoking acts synergistically with the G20210A mutation to further elevate the risk of premature MI.
- Other investigated genetic thrombophilic factors do not appear to play a substantial role in this population.
Abstract:
It has been suggested that thrombotic tendency increases the risk of myocardial infarction (MI). To investigate the association between the risk of MI at a young age and genetic thrombogenic disorders (G20210A mutation in the prothrombin gene, G1691A mutation in the factor V gene and deficiencies of protein C, protein S and antithrombin III) we conducted a case-control study among 70 survivors of MI who had experienced the event before the age of 36 and 260 healthy subjects. The G20210A mutation in the prothrombin gene was found more often in young patients with MI than among controls (11.4 versus 3.1%). The odds ratio (OR) for MI for carriers versus non-carriers was 4 (95% confidence interval [CI], 1.5 to 11.3). The adjusted OR for major cardiovascular risk factors (smoking, hypecholesterolaemia, diabetes mellitus, hypertension and obesity) was 4.3 (95% CI, 1.3 to 14). The simultaneous presence of both G20210A mutation in the prothrombin gene and smoking further increased the risk of MI compared with nonsmokers and non-carriers (OR, 58; 95% CI, 11.4-294). The G1691A mutation in factor V gene was not associated with an increased relative risk for MI (OR, 0.87; 95% CI, 0.26 to 2.5). Finally, there was no significant difference in the prevalence of deficiencies of protein C, protein S and antithrombin III between cases and controls. In conclusion, our data indicate that the G20210A mutation in the prothrombin gene was the only genetic prothrombotic risk factor associated with the risk of developing MI under the age of 36 years.
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