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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.