Laila Staerk1, Emil Loldrup Fosbøl2,3, Morten Lamberts1,2, Anders Nissen Bonde1, Kasper Gadsbøll1, Caroline Sindet-Pedersen1, Ellen A Holm4, Thomas Alexander Gerds5, Brice Ozenne5, Gregory Y H Lip6,7, Christian Torp-Pedersen8,9, Gunnar Hilmar Gislason1,3,10,11, Jonas Bjerring Olesen1. 1. Department of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Kildegaardsvej 28, 2900 Hellerup, Denmark. 2. Department of Cardiology, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark. 3. The Danish Heart Association, Vognmagergade 7, 1120 Copenhagen K, Denmark. 4. Department of Internal Medicine, Nykøbing F. Hospital, Fjordvej 15, 4800 Nykøbing Falster, Denmark. 5. Department of Public Health, Section of Biostatistics, University of Copenhagen, Øster Farimagsgade 5, 1353 Copenhagen K, Denmark. 6. Institute of Cardiovascular Sciences, University of Birmingham, Birmingham B15 2TT, UK. 7. Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Fredrik Bajers vej 5, 9100 Aalborg, Denmark. 8. Department of Cardiology and Clinical Epidemiology, Aalborg University Hospital, Hobrovej 18-22, 9100 Aalborg, Denmark. 9. Department of Health, Science and Technology, Aalborg University, Fredrik Bajers vej 5, 9100 Aalborg, Denmark. 10. Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark. 11. The National Institute of Public Health, University of Southern Denmark, Øster Farimagsgade 5, 1353 Copenhagen K, Denmark.
Abstract
Aims: We examined the risks of all-cause mortality, stroke, major bleeding, and recurrent traumatic injury associated with resumption of vitamin K antagonists (VKAs) and non-VKAs oral anticoagulants (NOACs) following traumatic injury in atrial fibrillation (AF) patients. Methods and results: This was a Danish nationwide registry-based study (2005-16), including 4541 oral anticoagulant (OAC)-treated AF patients experiencing traumatic injury (defined as traumatic brain injury, hip fracture, or traumatic torso or abdominal injury). Within 90 days following discharge from traumatic injury, 60.6% resumed VKA (median age = 80, CHA2DS2-VASc = 4, HAS-BLED = 2), 16.7% resumed NOAC (median age = 81, CHA2DS2-VASc = 4, HAS-BLED = 2), and 22.7% did not resume OAC treatment (median age = 81, CHA2DS2-VASc = 4, HAS-BLED = 3). Switch from VKA to NOAC occurred among 9.5%. Since 2009, the trend in OAC resumption increased (P-value <0.0001), in particular with NOACs (P-value <0.0001). Follow-up started 90 days after discharge, and time-varying multiple Cox regression analyses were used for comparisons. Compared with non-resumption, VKA and NOAC resumption were associated with lower hazard [95% confidence interval (CI)] of all-cause mortality [hazard ratio (HR) 0.48 (0.42-0.53) and HR 0.55 (0.47-0.66), respectively] and ischaemic stroke [HR 0.56 (0.43-0.72) and HR 0.54 (0.35-0.82), respectively], increased major bleeding hazard [HR 1.30 (1.03-1.64) and HR 1.15 (0.81-1.63), respectively], and similar hazard of recurrent traumatic injury [HR 0.93 (0.73-1.18) and HR 0.87 (0.60-1.27), respectively]. Conclusion: AF patients resuming VKA and NOAC treatment following traumatic injury have lower hazard of all-cause mortality and ischaemic stroke, increased hazard of major bleeding but without additional hazards of recurrent traumatic injury. Withholding OAC following a traumatic injury in AF patients may not be warranted.
Aims: We examined the risks of all-cause mortality, stroke, major bleeding, and recurrent traumatic injury associated with resumption of vitamin K antagonists (VKAs) and non-VKAs oral anticoagulants (NOACs) following traumatic injury in atrial fibrillation (AF) patients. Methods and results: This was a Danish nationwide registry-based study (2005-16), including 4541 oral anticoagulant (OAC)-treated AFpatients experiencing traumatic injury (defined as traumatic brain injury, hip fracture, or traumatic torso or abdominal injury). Within 90 days following discharge from traumatic injury, 60.6% resumed VKA (median age = 80, CHA2DS2-VASc = 4, HAS-BLED = 2), 16.7% resumed NOAC (median age = 81, CHA2DS2-VASc = 4, HAS-BLED = 2), and 22.7% did not resume OAC treatment (median age = 81, CHA2DS2-VASc = 4, HAS-BLED = 3). Switch from VKA to NOAC occurred among 9.5%. Since 2009, the trend in OAC resumption increased (P-value <0.0001), in particular with NOACs (P-value <0.0001). Follow-up started 90 days after discharge, and time-varying multiple Cox regression analyses were used for comparisons. Compared with non-resumption, VKA and NOAC resumption were associated with lower hazard [95% confidence interval (CI)] of all-cause mortality [hazard ratio (HR) 0.48 (0.42-0.53) and HR 0.55 (0.47-0.66), respectively] and ischaemic stroke [HR 0.56 (0.43-0.72) and HR 0.54 (0.35-0.82), respectively], increased major bleeding hazard [HR 1.30 (1.03-1.64) and HR 1.15 (0.81-1.63), respectively], and similar hazard of recurrent traumatic injury [HR 0.93 (0.73-1.18) and HR 0.87 (0.60-1.27), respectively]. Conclusion:AFpatients resuming VKA and NOAC treatment following traumatic injury have lower hazard of all-cause mortality and ischaemic stroke, increased hazard of major bleeding but without additional hazards of recurrent traumatic injury. Withholding OAC following a traumatic injury in AFpatients may not be warranted.
Authors: Grace M Turner; Christel McMullan; Olalekan Lee Aiyegbusi; Danai Bem; Tom Marshall; Melanie Calvert; Jonathan Mant; Antonio Belli Journal: Int J Stroke Date: 2021-04-04 Impact factor: 5.266
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