More than the half number of the severe CAD patients without features of metabolic syndrome had hyperlipoprotein(a)-emia

Abstract

Abstract Background It was reported that insulin suppresses apolipoprotein(a) synthesis in primary cultures of cynomolgus monkey hepatocytes (Neele DM. Diabetologia 1999). Therefore, there is a possibility that inverse association exists between lipoprotein(a); Lp(a) and metabolic syndrome (Mets) with insulin resistance/ hyperinsulinemia for the coronary atherosclerosis. Purpose The purpose is to examine the association between Lp(a) and Mets on the CAD patients. Method 847 male subjects with angiographically demonstrated CAD were enrolled. The subjects were divided into the five groups according to the scored numbers by the counting of Mets components shown below (presence 1, absence 0); 1. BMI ≥25kg/m2, 2. comorbidity of hypertension, 3. triglyceride ≥150mg/dL and/or HDL cholesterol <40mg/dL, 4. fasting plasma glucose ≥110mg/dL and/or comorbidity of diabetes mellitus (Group 0; without any Mets components, Group 4; with all Mets component). The insulin levels (μU/mL) and the prevalence of hyperLp(a)-emia (≥30 mg/dL) were compared between in Group 0 and in Group 4. The blood samples for laboratory tests were collected after an over night fast. Result As the scored numbers increased, the insulin levels increased (Group 0; 5.1 μU/mL versus Group 4; 11.4 μU/mL: p<0.0001) and the prevalence of hyperlipoprotein(a)-emia decreased (Group 0; 41.6% versus Group 4; 21.4%: p<0.01). The prevalence of hyperLp(a)-emia increased as the severity of coronary atherosclerosis aggravated (Figure 1; one vessel disease 21.5%, two vessel disease 27.0% three vessel disease 32.1%: one vessel disease versus three vessel disease p<0.01). Especially to limited the three vessel disease subjects (Figure 2), the prevalence of hyperlipoprotein(a)-emia in Group 0 was markedly high (56.7%). Conclusion More than the half number of severe CAD patients without features of Mets had hyperLp(a)-emia. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2