Effect of LPA gene on CAD risk among diabetic patients

Abstract Introduction Previous research reported that LPA gene is a strong and independent predictor of CAD in non-diabetic patients but not in patients with type 2 diabetes. These results suggest that LPA gene might contribute less to CAD risk in patients with T2DM than in general population. Objective Investigate, in our population, the association between LPA gene CT variant and CAD risk among diabetic patients. Methods 3050 individuals (1619 coronary patients and 1431 controls) were genotyped for LPA rs3798220 TT/CT. Pearson's chi-squared test was applied to evaluate the association between LPA variants and CAD, firstly, in the general population and, secondly, in the group of patients with T2DM (n=735). Multivariate logistic regression was performed with LPA CT variant and 6 traditional risk factors (TRF) (smoking, dyslipidemia, diabetes, hypertension, family history of CAD and physical inactivity) in both general and diabetic population. Results In total population, LPA CT variant was found to be strongly and significantly associated with CAD with an OR of 2.32 (95% CI: 1.56–3.45; p<0.0001). However, this association was less pronounced in the diabetic population with a CAD risk of 1.38 (95% CI: 0.56–3.43) without statistical significance (p=0.485). In the presence of 6 major TRF, multivariate analysis showed that LPA CT remained a strong and independent predictor of CAD risk (OR= 2.34; 95% CI: 1.52–3.62; p<0.0001). In diabetic population, LPA was no longer an independent predictor for CAD by multivariate analysis. Conclusions Our results show that the effect of LPA gene on CAD risk among diabetic patients might be different from that in the general population. Diabetes status is such a strong risk factor that may attenuate the genetic effects of LPA on CAD risk. This may indicate a complex role of Lp (a) and diabetes interaction in cardiometabolic diseases.