Genetically Reduced Antioxidative Protection and Increased Ischemic Heart Disease Risk
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Discussion
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Implication
Prospective cohort study shows increased ischemic heart disease risk in EC-SOD-R213G carriers, suggesting reduced arterial antioxidant defense accelerates cardiovascular disease.
Key Points
- To determine whether the extracellular superoxide dismutase (EC-SOD) R213G variant predisposes individuals to ischemic heart disease and offers predictive utility beyond plasma EC-SOD and oxidized LDL autoantibodies.
- Followed 9,188 participants from The Copenhagen City Heart Study over 23 years (956 incident IHD events) in a prospective, population-based cohort design.
- Retested findings cross-sectionally using independent cohorts of patients with IHD (n=943) or ischemic cerebrovascular disease (ICVD, n=617) against 7,992 disease-free controls.
- Conducted a nested case-control study with 956 age- and gender-matched pairs, adjusting for plasma EC-SOD levels and autoantibodies against oxidized LDL.
- Heterozygosity for EC-SOD-R213G (2.4%, n=221 vs noncarriers n=8,965) yielded an age- and gender-adjusted relative risk for IHD of 1.5 (95% CI, 1.1 to 2.1).
- Cross-sectional retesting demonstrated an age- and gender-adjusted odds ratio of 1.4 (95% CI, 1.0 to 2.0) for IHD and 1.7 (95% CI, 1.1 to 2.7) for ICVD.
- Further adjustment for plasma EC-SOD generated an IHD odds ratio of 9.2 (95% CI, 1.2 to 72), while adjustment for oxLDL autoantibodies resulted in an odds ratio of 2.5 (95% CI, 1.2 to 5.3).
Cite This Study
Juul et al. (2003) studied this question.