Abstract
The objective of our study was to examine the contribution of elevated Lp(a) to 10-year mortality in 140 CAD patients, depending on gender, baseline lipid levels, ApoA-I, ApoB, and the ApoA1, ApoE, and ApoB gene polymorphisms. Methods and Results: The study included 140 patients (75 men and 65 women) of the Uzbek population, hospitalized with diagnosis “CAD, unstable angina (IIB class, E. Braunwald et al., 1989)” (main group) in the period between January 2009 and February 2011. The endpoints at 10-year follow-up were death from cardiovascular causes (fatal myocardial infarction and sudden cardiac death). In the studied cohort of CAD patients, Lp(a) distribution was skewed to the right, the median was 16.9mg/dL, and the mean was 34.3mg/dL. At the same time, Lp(a) value greater than the 75th percentile was >41mg/dL. In this regard, we compared the baseline values in 2 groups of patients: Group 1 (Lp(a)<41mg/dL) and Group 2 (Lp(a)>41mg/dL). The 10-year cardiovascular mortality rate was higher significantly in Group 2 (RR =3.67; 95% CI: 1.67-8.11; P=0.0013). Cardiovascular mortality was significantly higher (P<0.001) in men of Group 2 than in men of Group 1 (RR=5.31; 95% CI: 2.03-13.88; P<0.001), while in women, the 10-year mortality in the compared groups did not differ significantly. Cardiovascular mortality was lower in patients with ApoA-1≥140mg/dL, the majority of whom were women. Conclusion: In the absence of targeted Lp(a) therapy, long exposure to a level of Lp(a) of >41mg/dL is a factor that increases 10-year mortality in CAD patients. Highlights • 10-year cardiovascular mortality was higher in CAD patients with Lp(a)>41mg/dL. • However, the increase in mortality due to high Lp(a) was statistically significant in men than in women. • The ApoA-I level was higher in women than in men. • Cardiovascular mortality was lower in patients with ApoA-I≥140mg/dL, most of whom were women.
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