The bene ts of ischemic stroke reduction generally outweigh the risk of harm from serious bleeding with OAC use; one estimate was that Modi able bleeding risk factors Potentially modi able bleeding risk factors Nonmodi able bleeding risk factors Biomarkers Hypertension/elevated SBP INR control (target 2.0-3.0)a ; target TTR 65% Concomitant APTs and NSAIDs Excessive alcohol intake Nonadherence to OAC/APT Avoidance of hazardous hobbies/occupations Avoidance of bridging therapy with OAC Appropriate choice of OAC and correct doseb Extreme frailty excessive falls riskc VKA management strategyd Anemia Reduced platelet count or function Renal impairment (CrCI >30 mL/min) Age (>65 y) Previous major bleeding Severe renal impairment (dialysis or renal transplant) Severe hepatic disease (cirrhosis) Malignancy Genetic factors (eg, CYP 2C9 polymorphisms) Previous stroke, small vessel disease etc Diabetes mellitus Cognitive impairment/dementia Cystatin C/CKD-EPI cTnT-hs vWF (plus other coagulation markers) Figure 2 Risk factors for bleeding with oral anticoagulation and antiplatelet therapy. a For patients receiving VKA treatment. b Dose adaptation based on patient s age, body weight, and serum creatinine level. c Walking aids; appropriate footwear; home review to remove trip hazards; neurologic assessment where appropriate. d Increased INR monitoring, dedicated OAC clinicals, self-monitoring/self-management, educational/behavioral in- terventions. APTs antiplatelets; CKD-EPI Chronic Kidney Disease Epidemiology Collaboration; CrCl creatinine clearance; cTnT-hs high- sensitivity troponin T; CYP cytochrome P450; GDF-15 growth differentiation factor-15; INR international normalized ratio; NSAIDs nonsteroidal antiin ammatory drugs; SBP systolic blood pressure; vWF von Willebrand factor. See Figure 1 legend for expansion of other abbreviations. 