Table 3.
Model | Risk factor | PAR % | 95% confidence interval |
---|---|---|---|
Genetic |
|
22.16% | (20.44–23.88) |
Clinical |
|
21.91% | (18.19–25.63) |
Combined: clinical and genetic |
|
35.99% | (33.31–38.68) |
Population attributable risk (PAR) models using (1) genetic, (2) clinical, and (3) combined clinical and genetic risk factors were constructed to describe the percent likelihood a FHHD can be explained by each of the above variables. The PAR analytic framework compares exposed to unexposed, and as such, continuous variables were converted to polychotomous variables. The lowest risk level for all variables was compared to any elevation in risk. Thus for polychotomous variables quintiles 2–5 are compared to the lowest quintile (reference). A combined approach using both clinical and genetic risk factors explained a larger proportion of the likelihood of having a FHHD. Each model was controlled for age, sex, and cholesterol medication use.
ApoB:ApoAI, apolipoprotein B-to-apolipoprotein AI ratio [2nd–5th quintiles vs. 1st quintile (reference)]; HeFH, heterozygous familial hypercholesteremia; hsCRP, high sensitivity C-reactive protein mg/L [2nd–5th quintiles vs. 1st quintile (reference)ntile]; Lp(a), Lipoprotein(a) nmol/L [2nd–5th quintiles vs. 1st quintile (reference)]; PRSCAD, polygenic risk score for coronary artery disease [2nd–5th quintiles vs. 1st quintile (reference)]; WHR, waist to hip ratio [2nd–5th quintiles vs. 1st quintile (reference)].