Table 1 Mendelian randomization estimates for the effect of genetically determined levels of protein C on the risk of vascular diseases and traits.

From: Elucidating mechanisms of genetic cross-disease associations at the PROCR vascular disease locus

Exposure

Outcome

Number of SNPsa

MR causal estimate (IVW)

Heterogeneity

Odds ratio [95% CI]b

P value

Q-statistic

P value

Forward MR:

 Protein C

Coronary artery disease

19

0.88 [0.86, 0.90]

4.17 × 10−24

17.24

0.51

 Protein C

Deep venous thrombosis

18

1.34 [1.25, 1.44]

8.70 × 10−16

14.21

0.65

 Protein C

Venous thromboembolism

18

1.24 [1.17, 1.32]

1.05 × 10−11

17.80

0.40

 Protein C

Any stroke

18

0.90 [0.86, 0.94]

2.86 × 10−6

13.79

0.68

 Protein C

Ischemic stroke

18

0.90 [0.86, 0.95]

3.77 × 10−5

12.48

0.77

 Protein C

Pulmonary embolism

18

1.17 [1.06, 1.29]

2.65 × 10−3

19.01

0.33

 Protein C

Cardioembolic stroke

18

0.85 [0.77, 0.94]

2.10 × 10−3

17.83

0.40

 Protein C

Small-vessel stroke

18

0.94 [0.82, 1.07]

0.332

21.24

0.22

 Protein C

Large-artery stroke

18

0.94 [0.83, 1.07]

0.376

15.86

0.53

Reverse MR:

 Coronary artery disease

Protein C

157

0.99 [0.95, 1.02]

0.410

168.93

0.23

 Deep venous thrombosis

Protein C

20

1.05 [0.91, 1.21]

0.497

19.78

0.41

 Venous thromboembolism

Protein C

21

1.16 [1.00, 1.34]

0.050

15.04

0.77

  1. aNumber of SNPs as instrumental variants for PC.
  2. bRepresents increase/decrease of risk per SD increase in PC levels.
  3. Effect estimates and P values are provided for the inverse-variance weighting (IVW) method. Q-statistic and respective P values are shown from the Cochran’s Q-test for heterogeneity. Full details of the results from the different MR analyses, including details of data sources and number of cases, are reported in Supplementary Table 3.
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