Skip to main content
. Author manuscript; available in PMC: 2016 Nov 3.
Published in final edited form as: J Am Coll Cardiol. 2015 Nov 3;66(18):2053–2055. doi: 10.1016/j.jacc.2015.08.866

Table 1.

Association of APOC3 Loss-of-Function Mutation Carrier Status with Blood Lipid Levels and Subclinical Atherosclerosis

Non-Carriers (N=6,331) Carriers (N=64) Effect Estimate 95% CI P-value
Blood Lipids
 Triglycerides (mg/dL)* 166.1 ± 96.2 91.2 ± 44.1 −43.7% −36.6, −49.9 1.83 × 10−21
 HDL Cholesterol (mg/dL) 55.6 ± 15.2 66.6 ± 15.0 +11.1 7.6, 14.6 3.55 × 10−10
 LDL Cholesterol (mg/dL) 130.3 ± 36.4 131.6 ± 35.8 +1.5 −7.4, 10.3 0.75

Subclinical Atherosclerosis
 Coronary Arterial Calcification (Agatston Units) 46.0 (0.0, 245.0) 29.0 (0.0, 227.5) −27.9 −51.1, −4.7 0.019
 Carotid Plaque (mm2) 183.8 (0.0, 555.9) 112.8 (0.0, 367.2) −8.7 −73.5, 56.0 0.79
 Carotid Intima Media Thickness (mm)* 0.76 ± 0.16 0.74 ± 0.13 −1.7% −6.3, 3.0 0.47

HDL = high-density lipoprotein; LDL = low-density lipoprotein; CI = confidence interval

Values are represented as effect estimates (95% confidence intervals) between APOC3 loss-of-function mutation carriers and non-carriers after adjustment for covariates. Covariates used were age, sex, ancestry, and principal components of ancestry.

*

Effect estimates for triglycerides and carotid intima media thickness were derived from natural log transformation and are expressed as percent difference in carriers compared with non-carriers.

Effect estimates for coronary arterial calcification and carotid plaque derived from median quantile regression and represent differences in medians. Therefore, summary statistics of the distributions in non-carriers and carriers are represented as median (interquartile range).