Table 4

Use of NOACs in relation to baseline characteristics for patients on AC at baseline (n=20 167)

VariableOR‡ (95% CI)
Gender
 Female1
 Male1.08 (1.01 to 1.15)
Ethnicity
 Caucasian/Hispanic/Latino1
 Asian1.28 (1.19 to 1.37)
 Other1.08 (0.87 to 1.35)
Age, years
 651
 65–801.10 (1.02 to 1.18)
 80–851.19 (1.08 to 1.32)
 >851.32 (1.16 to 1.50)
Medical history*
 CHF0.94 (0.87 to 1.01)
 Hypertension (history or >140/90 mm Hg)0.90 (0.83 to 0.97)
 Diabetes0.82 (0.77 to 0.88)
 CAD0.85 (0.77 to 0.94)
 Vascular disease0.87 (0.79 to 0.97)
 Dementia1.46 (1.13 to 1.88)
 Moderate-to-severe CKD†0.84 (0.76 to 0.92)
 NSAID usage1.27 (1.06 to 1.53)
 Bleeding1.19 (0.96 to 1.48)
Smoking
 Never1
 Ex-smoker1.05 (0.98 to 1.13)
 Current smoker1.16 (1.05 to 1.29)
Previous stroke/TIA/SE (reference: no previous stroke/TIA/SE)
  In cohort 2 (2011–2013)1.08 (0.91 to 1.28)
  In cohort 3 (2013–2014)0.76 (0.65 to 0.89)
  In cohort 4 (2014–2015)0.95 (0.82 to 1.10)
Patients without stroke/TIA/SE
  Cohort 2 (2011–2013)1
  Cohort 3 (2013–2014)2.33 (2.14 to 2.53)
  Cohort 4 (2014–2015)3.82 (3.52 to 4.15)
Patients with previous stroke/TIA/SE
  Cohort 2 (2011–2013)1
  Cohort 3 (2013–2014)1.64 (1.32 to 2.03)
  Cohort 4 (2014–2015)3.37 (2.74 to 4.15)
  • *Reference group is patients with no medical history.

  • †Includes NKF KDOQI stages III to V; none or mild (reference group) includes all other patients.

  • ‡An OR >1 implies that NOACs are more frequent than VKAs, while an OR <1 means that VKAs are more frequent than NOACs. Only the interaction between cohort and stroke/TIA/SE was statistically significant (p=0.01).

  • AC, anticoagulant; CAD, coronary artery disease; CHF, congestive heart failure; CKD, chronic kidney disease; NKF KDOQI, National Kidney Foundation's Kidney Disease Outcomes Quality Initiative; NOAC, non-vitamin K antagonist oral anticoagulant; NSAID, non-steroidal anti-inflammatory drug; SE, systemic embolism; TIA, transient ischaemic attack; VKA, vitamin K antagonist.