A paired difference test was used to assess changes over time within each group. We tested the association of GRS with family history, using t tests with significance set at P < .05. We compared the rate of statin initiation between participants with and those without a family history of CHD using logistic regression, also adjusting for allocation to GRS. 8 Continuous or dichotomous variables were compared between groups using a 2-sample t test or a χ 2 test, respectively. Participants returned at 3 and 6 months after risk disclosure for measurement of low-density lipoprotein cholesterol levels and assessment of statin use, dietary fat consumption (scores ranged between 0 to 110 indicative of very high dietary fat intake as measured by the fat screener 7), and physical activity levels (scores ranged between 7 and 1 based on the adapted version of telephonic assessment of a physical activity questionnaire).
All participants gave written informed consent financial compensation was provided. The study protocol was approved by the Mayo Clinic institutional review board. 6 The 10-year risk of CHD was disclosed by a genetic counselor informing participants of a 1.5- to 2.0-fold higher risk in the presence of family history, followed by shared decision making regarding statin therapy with a physician. A GRS was calculated based on genotypes at 28 CHD susceptibility loci. Family history was defined as the presence of CHD (ie, angina, myocardial infarction, or myocardial revascularization) in a first-degree male or female relative (ie, parents, siblings, and children) before age 55 or 65 years, respectively.
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