Table 12.

 Prospective and retrospective cohort studies (sample size ≥100) of peri-procedural oral anticoagulation in atrial fibrillation patients undergoing cardiac rhythm device procedures

Study	Design	Subjects (n)	Age (years), mean	Continued OAC (%)	Interrupted OAC (%)	Timing of OAC Interruption (h), mean or median	Timing of OAC resumption	Antiplatelet therapy (%)	Clinically significant haematoma (%)	Other device-related bleeding (%)	Thromboembolic and other complications (%)
Birnie et al.16	BRUISE CONTROL 1 prospective randomized control trial	Warfarin 681	72 years	50.3%	Heparin bridging 49.7%	NA	NA	Warfarin Aspirin: 38.2% P2Y12: 6.2% Heparin bridging aspirin: 40.5% P2Y12: 6.1%	Warfarin: 3.5% Heparin bridging: 16.0%	Pericardial effusion Warfarin: 0% Heparin bridging: 0.3%	Stroke/TIA Warfarin: 0.6% Heparin bridging: 0% MI Warfarin: 0% Heparin bridging: 0.3%
Black-Meier et al.7,23	Retrospective analysis of ORBIT-AF	Warfarin 284 NOAC 60	Warfarin 77 years NOAC 70.5 year	Warfarin 36% NOAC 35%	Warfarin 64% NOAC 65%	NA	NA	Warfarin Aspirin: 35% P2Y12: 7.4% NOAC Aspirin: 51.7% P2Y12: 8.3%		Major bleeding −ve warfarin: 1% +ve warfarin: 3% −ve NOAC: 0% +ve NOAC: 0%	Stroke/TIA −ve warfarin: 1% +ve warfarin: 1% −ve NOAC: 0% +ve NOAC: 0%
Essebag et al.19	Post-hoc analysis of RE-LY trial	VKA 201 Dabigatran 410	73 years	0%	100%	VKA: 144 h (total pre + post) NOAC: 53 h	NOAC: 34 h	Aspirin: 44% P2Y12: 8%	VKA, bridging: 10.8% VKA, no bridging: 2.4% NOAC: 2.2%	Major bleeding VKA, bridging: 2.7% VKA, no bridging: 0.6% NOAC: 1.0%	Stroke VKA, bridging: 0% VKA, no bridging: 0.6% NOAC: 0.2%
Leef et al.20	Post-hoc analysis of ROCKET-AF trial	VKA 211 Rivaroxaban 242	75 years	25%	75%	VKA: 5 days NOAC: 3 days	VKA: 3 days NOAC: 2 days	—	NOAC: 0.4% VKA: 2.9% −ve OAC: 1.2% +ve OAC: 2.7%	Major bleeding NOAC: 1.2% VKA: 1.0% −ve OAC: 1.2% +ve OAC: 0.9%	Stroke/SE NOAC: 1.3% VKA: 0.5% −ve OAC: 0.6% +ve OAC: 1.8%
Ricciardi et al.24	Prospective randomized pilot trial	NOAC 101 (Dabigatran = 37, Rivaroxaban = 33, Apixaban = 31)	76 years	49.5%	50.5%	Dabigatran: 24–48 h Rivaroxaban/ apixaban: 24 h	≥24 h	Aspirin: 15.8% P2Y12: 5.9% Both: 3%	−ve NOAC: 0% +ve NOAC: 2%	Any haematoma −ve NOAC: 4% +ve NOAC: 3.9% Loss of Hb > 2 g/dL −ve NOAC: 6% +ve NOAC: 9.8%	Pocket infection +ve NOAC: 1%
Birnie et al.18	BRUISE CONTROL 2 prospective randomized control trial	NOAC 647 (Dabigatran = 96, Rivaroxaban = 106, Apixaban = 125)	74	49.3%	50.5%	Dabigatran: 24–48 h Rivaroxaban/ apixaban: 48 h	≥24 h	Aspirin 17.4% P2Y12: 3.6%	−ve NOAC: 2.1% +ve NOAC: 2.1%	Any haematoma −ve NOAC: 4.8% +ve NOAC: 5.5% Pericardial effusion −ve NOAC: 0.3% +ve NOAC: 0.3%	Stroke −ve NOAC: 0.3% +ve NOAC: 0.3%
Tsai et al.22	Retrospective analysis	NOAC 100 (Dabigatran = 28, Rivaroxaban = 61, Apixaban = 10, Edoxaban = 1)	78 years	100%	0%	NA	NA	Aspirin: 6% P2Y12: 2%	+ve NOAC: 1%	Pericardial effusion +ve NOAC: 1%	0%
Steffel et al.21	Post-hoc analysis of ENGAGE AF trial	VKA 324 Edoxaban 549	74 years	26%	74%	median 7 days (pre + post)	NA	Aspirin: 32% P2Y12: 2.5%	NA	Major bleeding −ve VKA: 0% +ve VKA: 0% −ve NOAC: 0% +ve NOAC: 0.5%	Stroke +ve VKA: 1.1% −ve VKA: 0.9% +ve NOAC: 0.5% −ve NOAC: 0.4%

−ve , interrupted; +ve, continued; MI, myocardial infarction; NA, not available; NOAC, non-vitamin K antagonist oral anticoagulant; OAC, oral anticoagulant; SE , systemic embolism; TIA, transient ischaemic attack; VKA , vitamin K antagonist.