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Table 1 Baseline characteristics of GENOA and FHS

From: The relationship between diastolic blood pressure and coronary artery calcification is dependent on single nucleotide polymorphisms on chromosome 9p21.3

  GENOA FHS P
N = 974 N = 1,140
Age, years 58.41 (±10.17) 59.28 (±8.98) 0.67
Women, % 59.02% 54.35% 0.03
Participants with detectable CAC, % 68.60% 68.39% 0.92
 ln(CAC score + 1) 2.88 (±2.56) 3.15 (±2.66) 0.16
Hypertension, % 72.17% 37.84% <0.0001
 Anti-hypertensive medication use, % 67.58% 27.83% <0.0001
 Systolic blood pressure, mmHg 131.20 (±16.87) 125.04 (±17.59) <0.0001
 Diastolic blood pressure, mmHg 74.26 (±9.16) 74.56 (±9.37) 0.60
Diabetes, % 13.96% 7.46% <0.0001
 Fasting glucose, mg/dL* 97.27 (±10.71) 96.66 (±9.78) 0.43
Past or Active tobacco use, % 45.26% 56.19% 0.0001
 ln(Pack years + 1) 1.28 (±1.58) 2.56 (±1.01) 0.03
Statin Use, %† 24.57% 15.59% <0.0001
 LDL:HDL ratio 2.55 (±1.04) 2.56 (±1.01) 0.71
  1. GENOA = Genetic Epidemiology Network of Arteriopathy; FHS = Framingham Heart Study Offspring cohort; CAC = coronary artery calcification; HDL = high density lipoprotein; LDL = low density lipoprotein; ln = natural logarithm; Statin = HMG-CoA Reductase Inhibitor.
  2. *Fasting glucose mean and standard deviation calculated in subset of non-diabetics (GENOA: N = 844, FHS: N = 1054).
  3. †Statin use was missing for 5 FHS participants.
  4. P-value from a linear mixed effects model to test the difference between the two cohorts’ means (quantitative traits) or the difference between the two cohorts’ frequencies (qualitative traits), accounting for sibship structure.