Table 2.

Details of competing mechanisms

Competing mechanism	All (N=685)*	DOAC (N=441)	VKA (N=244)
Large artery atherosclerosis, N (%)	415 (60.6)	255 (57.8)	160 (65.6)
Small vessel disease, N (%)	180 (26.3)	120 (27.2)	60 (24.6)
Coagulopathy†, N (%)	36 (5.3)	28 (6.3)	8 (3.3)
Peri-interventional stroke‡, N (%)	23 (3.4)	18 (4.1)	5 (2.0)
Endocarditis, N (%)	22 (3.2)	14 (3.2)	8 (3.3)
Other cardio-aortic causes§, N (%)	26 (3.8)	13 (2.9)	13 (5.3)
Cervical artery dissection, N (%)	9 (1.3)	6 (1.4)	3 (1.2)
Vasculitis, N (%)	4 (0.6)	2 (0.5)	2 (0.8)

*Details were available for 685/713 patients (96.1%) who had competing mechanism as stroke aetiology.

†Including suspected cancer-related coagulopathy, hereditary thrombophilia, myeloproliferative disorders and antiphospholipid syndrome.

‡Including percutaneous transluminal coronary angioplasty, transcatheter aortic valve implantation, pulmonary vein isolation, cardioversion and other cardiovascular procedures.

§Including intracardiac thrombus, aortic dissection, patent foramen ovale/atrial septal defect, heart valve fibroelastoma and other structural heart abnormalities.

DOAC, direct oral anticoagulant; VKA, vitamin K-antagonist.