Frequently Asked Questions — Atrial Fibrillation Anticoagulation (CHA₂DS₂-VA / NOAC)
1) What is CHA₂DS₂-VA and how does it differ from CHA₂DS₂-VASc?
The CHA₂DS₂-VA score is a variation of CHA₂DS₂-VASc that excludes sex as a variable. It maintains a similar predictive value for thromboembolic risk and may perform better in individuals aged ≥ 75 years.
2) How are points assigned in CHA₂DS₂-VA?
1 point: heart failure/reduced ejection fraction, hypertension, age 65–74, diabetes, vascular disease (peripheral/coronary/aortic).
2 points: age ≥ 75, prior stroke/TIA/embolism.
3) When should I anticoagulate according to CHA₂DS₂-VA?
≥ 2 points: indicate oral anticoagulation (preferably a NOAC).
1 point: individualized decision based on thrombotic/bleeding risk and patient preference.
0 points: do not anticoagulate.
4) Is HAS-BLED used to contraindicate anticoagulation?
No. HAS-BLED identifies modifiable bleeding risk factors (e.g., uncontrolled hypertension, alcohol, medications, labile INR on VKA). A high score indicates closer monitoring and risk correction, not automatic withholding of anticoagulation.
5) NOAC or vitamin K antagonist (VKA)?
In non-valvular AF, prefer NOACs for efficacy/safety. Use VKAs in mechanical valves, moderate–severe rheumatic mitral stenosis, antiphospholipid syndrome, pregnancy, Child-Pugh C, or when a NOAC is contraindicated/unavailable.
6) How to choose a NOAC and adjust the dose?
Base the choice on renal and hepatic function, age, and weight. Dose adjustments follow creatinine clearance and drug-specific labeling (e.g., apixaban is reduced with ≥2 of: age ≥80, weight ≤60 kg, serum creatinine ≥1.5 mg/dL). Also review interactions (P-gp/CYP3A4).
7) Does antiplatelet therapy replace anticoagulation in AF?
No. Single antiplatelet therapy does not prevent stroke in AF. Combining an anticoagulant + antiplatelet is reserved for another formal indication (e.g., recent ACS/PCI) and for the minimum necessary time.
8) What are the absolute and relative contraindications to NOACs?
Absolute: large esophageal varices, platelets < 50×109/L, drug hypersensitivity, major surgery < 72 h with high bleeding risk.
Relative: prior intracranial hemorrhage, recent GI bleeding without a clear cause, active/recent peptic ulcer, frequent falls with high bleeding risk, dementia/poor adherence — require individualized assessment.
9) How should patients on NOACs be monitored?
Assess renal function (at least annually; if CrCl 15–60 mL/min or in elderly/frail patients, every 3–6 months), periodic liver function/CBC, adherence, bleeding events, and new interactions (e.g., azoles, amiodarone, dronedarone, verapamil, rifampin, antiepileptics, immunosuppressants).
10) What to consider in patients at high bleeding risk?
Do not stop routinely. Optimize BP, treat GI ulcer disease, reduce alcohol, review NSAIDs/antiplatelets, choose a NOAC with a more favorable GI profile (e.g., apixaban/edoxaban), and use the correct labeled dose.
11) What about cardioversion?
If AF lasts > 48 h or duration is unknown, ensure ≥ 3 weeks of anticoagulation before and ≥ 4 weeks after cardioversion (or a TEE-guided strategy to exclude thrombus with periprocedural anticoagulation).
12) How to manage procedures and surgery?
Interrupt the NOAC according to the procedure’s bleeding risk and renal function (typically 24–72 h beforehand). No bridging with heparin in most cases. Restart when hemostasis is secured.
13) What if bleeding occurs while on a NOAC?
Provide supportive care, localize the source, and consider specific reversal when available (e.g., idarucizumab for dabigatran; procoagulant agents/specific factor Xa reversal where applicable) according to severity and the agent involved.
14) Are there alternatives when anticoagulation is unfeasible?
In selected cases with a persistent contraindication to anticoagulation and high thrombotic risk, left atrial appendage occlusion may be considered after multidisciplinary discussion.
