Article Figures & Data
- Figure 1
OAC type at index haemorrhage based on major intracranial haemorrhage subtypes. DOAC, direct oral anticoagulant.
- Figure 2
The predicted ischaemic stroke rate in our cohort population based on weighted CHA₂DS₂-VASc score compared with the observed ischaemic stroke rate after LAAC. LAAC, left atrial appendage closure; RRR, relative risk reduction.
- Table 1
Baseline patient characteristics (n=146)
Age, mean±SD, years 75.66±7.61 Female, n (%) 42 (28.8) Hypertension, n (%) 143 (97.9) Diabetes mellitus, n (%) 37 (25.3) Dyslipidaemia, n (%) 123 (84.2) CAD, n (%) 65 (44.5) PVD, n (%) 18 (12.3) DVT/PE, n (%) 10 (6.8) Heart failure, n (%) 38 (26.0) Chronic renal disease, n (%) 36 (24.7) Smoking, n (%) 6 (4.1) Prior ischaemic strokes, n (%) 36 (24.7) CHA₂DS₂-VASc, mean±SD 5.23±1.52 HAS-BLED, mean±SD 3.58±1.00 Watchman or Watchman FLX, n (%) 145 (99.3%) Amplatzer Amulet, n (%) 1 (0.7%) CAD, coronary artery disease; DVT, deep vein thrombosis; LAAC, left atrial appendage closure; PE, pulmonary embolism; PVD, peripheral artery disease.
- Table 2
Classification of haemorrhagic pathologies that led to LAAC in our study population
Intracranial haemorrhage (ICH) 122 (83.6%) Intraparenchymal haemorrhage (IPH) 58 (47.5%) Lobar IPH 32 (55.2%) Deep IPH 23 (39.7%) Both deep and lobar IPH 3 (5.2%) Traumatic ICH 40 (32.8%) Non-traumatic subdural haemorrhage 18 (14.7%) primary intraventricular haemorrhage 3 (2.4%) Non-aneurysmal convexity subarachnoid haemorrhage 4 (3.3%) undetermined 2 (1.6%) Haemorrhagic imaging markers (CMB-group) 24 (16.4%) Total study population 146 (100%) *3 patients had separate events of IPH and Traumatic ICH and are included in both IPH and traumatic ICH groups.
CMB, cerebral microbleed; LAAC, left atrial appendage closure.
- Table 3
Presumed aetiology of IPH and of haemorrhagic imaging markers (CMB-group)
Etiologic considerations IPH (62)* CMB-group24 Cerebral amyloid angiopathy (CAA) Probable CAA 26 (41.9%) 10 (41.6%) Possible CAA 5 (8.1%) 2 (8.3%) Hypertensive cerebral small vessel disease (HTN-cSVD) Pure deep ICH/CMBs 18 (29.0%) 3 (12.5%) Mixed location ICH/CMBs, no cSS 8 (12.9%) 8 (33.3%) Mixed location ICH/CMBs/cSS (real mixed pathology) 2 (3.2%) 0 Others Brain metastasis 1 (1.6%) AVM related 1 (1.6%) Cavernous angiomas 1 (1.6%) Unknown distribution 1 (4.2%) *Including non-aneurysmal convexity subarachnoid haemorrhage.
.AVM, arteriovenous malformation; CMB, cerebral microbleed; cSS, cortical superficial siderosis; ICH, intracranial haemorrhage; IPH, intraparenchymal haemorrhage.
- Table 4
Burden of MRI markers of high intraparenchymal haemorrhage risk
Number of MRI markers of high brain bleeding risk in addition to IPH if present IPH
(n=50)CMB-group (n=23)* 0 0 0 1 4 (8%) 0 2 17 (34%) 5 (21.7%) 3 16 (32%) 9 (39.1%) 4 11 (22%) 8 (34.8%) 5 2 (4%) 1 (4.3%) *Total of 24 patients in the CMB-group, but one patient had no available MRI source images for cSVD imaging markers analysis.
CMB, cerebral microbleed; cSVD, cerebral small vessel disease; IPH, intraparenchymal haemorrhage.
- Table 5
Antithrombotic treatment after left atrial appendage closure (n=146)
Antithrombotic treatment Discharge 6 weeks p/LAAC 3 months p/LAAC 6 months p/LAAC 1 year p/LAAC AP monotherapy 1 (0.6%) 28 (19.2%) 96 (65.7%) 114 (78.1%) 110 (75.3%) DAPT 43 (29.5%) 85 (58.2%) 25 (17.1%) 6 (4.1%) 1 (0.6%) Warfarin 3 (2.0%) 0 0 1 (0.6%) 0 Warfarin+AP 8 (5.5%) 2 (1.4%) 1 (0.6%) 0 1 (0.6%) DOAC 42 (28.8%) 19 (13.0%) 8 (5.5%) 5 (3.4%) 6 (4.1%) DOAC+AP 49 (33.6%) 10 (6.8%) 2 (1.4%) 2 (1.4%) 3 (2.0%) None 0 1 (0.6%) 4 (2.8%) 6 (4.1%) 6 (4.1%) Died 0 1 (0.6%) 1 (0.6%) 1 (0.6%) 5 (3.4%) Lost to follow- up 0 0 9 (6.2%) 11 (7.5%) 14 (9.6%) AP, antiplatelet; DAPT, dual antiplatelet therapy; DOAC, direct oral anticoagulant; LAAC, left atrial appendage closure.
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