Guideline AFibrilliationzz- Trisnha.pptx

Guideline

1. Guideline Afib (ESC 2020) dr. Romadhana Trisnha Yomara

2. Hemostasis Physiology

3. Virchow Triad

4. Definition

5. Diagnostic

6. Risk Factors

7. Risk Factors

8. Clinical Presentation

9. Classification

10. Classification (pathophysiology)

11. Characterization of AF

12. Stroke risk and Bleeding Risk (Characterization)

13. Characterization

14. Management A – Anticoagulant / Avoid Stroke Stroke risk assessment and Bleeding Risk assessment Stroke Prevention Therapies B – Better Symptoms Control Rate Control Rhythm Control C – Cardiovascular Risk Factors and Concomitant Diseases: Detection and Management Lifestyle Intervention Specific Cardiovascular risk factors/ comobirdites

15. A – Anticoagulants 10.1.1 Stroke risk assessment Non Paroxysmal AF > Paroxysmal AF in stroke risk Patients with CHA2DS2VaSc score 0-1 don’t need any treatment Cardiac biomarker is not specific for AF, but could define risk differentiation in low risk patients Authors concluded that theCHADS2 (CHF history, Hypertension history, Age>_75y, Diabetes mellitus history, Stroke or TIA symptoms previously), CHA2DS2-VASc, and ABC risk scores have the best evidence for predicting thrombo-embolic risk(moderate strength of evidence for limited prediction ability of each score

16. A - Anticoagulants 10.1.2 Bleeding risk assessment Need to assess bleeding risk before giving treatment (HASBLED-score) Biomarkers are non-specific in predicting stroke, death, HF, etc High bleeding score should not lead to withholding OAC, as the clinical benefit is greater amongst patients Focus attention on modifiable risk factors, and should be reassessed in every time contact with patients Patients with high-risk and non-modifiable risk factors should be assessed more often ( eg : every 4 weeks rather than 4-6 months)

17. A- Anticoagulants

18. A - Anticoagulants 10.1.3 Absolute contraindications to oral anticoagulants Serious bleeding Severe thrombocytopenia Severe anemia ICH

19. A- Anticoagulants 10.1.4 Stroke prevention therapies - VKa (Warfarin) used in AF patients with RHD and/or with artificial heart valve -> needs to watch INR (2-3) Needs to have good TTR in counting effectiveness of therapy

20. A- Anticoagulants 10.1.4 Stroke prevention therapies Non-Vitamin K Antagonists oral anticoagulants (NOACs) Better in preventing bleeding risks than Warfarin if INR control was poor Standard-dose NOACs are better than Warfarin in Asians Apixaban 5mg b.i.d. reduced the risk of stroke/systemic embolism with no reduced in major bleeding ICH compared with aspirin Xa inhibitors are safer amongst vulnerable patients (elderly, renal dysfunction, previous stroke, etc ) Reduce dose regimens are feasible options for severe CKD ( Crcl 15-30mL/min)

21. A – Anticoagulants

22. A – Anticoagulants Anti-thrombotic therapy DAPT is less effective than warfarin with a similar rate of major bleeding SAPT is ineffective for stroke prevention and is potentially harmful 10.1.5.1 Strategies to minimize the risk of bleeding VKA treatment -> needs good TTR (>70%) Selecting the appropriate NOAC dose is important Bleeding risk profile is a stronger predictor in predicting bleeding risk in the first 3 months

23. A – Anticoagulants

24. A – Anticoagulants

25. B – Better Symptoms To target the optimal ventricular rate range -> rest <80 and activity <110 bpm Therefore lenient heart rate is acceptable initial approach regardless HF status -> drugs Drugs -> Beta Blocker, Non-Dihydropyridine CCB, Digoxin

26. B – Better Symptoms Beta Blocker Often first-line rate-controlling agents, better acute rate control (usually B-1 antagonists are better options( Non- Dihydropiridine CCB Verapamil and Diltiazem are mainly the choice, can improve AF-related symptoms Digoxin Not mainly used, lower doses of digoxin associated with better prognosis Amiodarone

27. B – Better Symptoms

28. B – Better Symptoms

29. B – Better Symptoms Rhythm Control

30. B – Better Symptoms Rhythm Control Mechanical Cardioversion Pharmacological Cardioversion

31. B- Better Symptoms

32. B – Better Symptoms

33. B – Better Symptoms Peri-cardioversion management of stroke risk Increased of TE risk in patients >12h Afib (maybe difficult to ascertain because usually asymptomatic and seek help when symptoms occur) Afib patients >12h should be managed with OAC peri-cardioversion Peri-cardioversion with VKA is recommended, but hard to manage INR 2.0-3.0 in 3 weeks before cardioversion may be difficult -> can be replaced by NOAC TOE pre-cardioversion to see TE pre-cardioversion then introduced -> if no TE, proceed with heparin and give OAC post-cardioversion If TOE identified a thrombus, give patients OAC for 3 weeks before reassessment of cardioversion, repeat TOE before cardioversion Long term OAC should be given not based on the return of SR, but based on CHA2DS2VASC score and HASBLED

34. B – Better Symptoms

35. B – Better Symptoms Long-term AAD therapy for rhythm control Aim of AAD -> improve AF-related symptoms -> QOL AAD less effective than catheter ablation, but AADs can be continued post PVI to reduce recurrent Afib Short-term AAD therapy is also used to prevent early AF recurrences post catheter ablation Concomitant management of underlying cardiovascular conditions is important to reduce Afib symptoms and facilitate the maintenance of SR

36. C – Cardiovascular Diseases (concomitant)

37. ABC Pathway in specific Patients Afib with Hemodynamic Instability:

38. ABC Pathway in specific Patients Afib with ACS and periprocedural PCI:

39. Intinyadehhhh Fibrinolysis halal jika INR tidak mencapai target (INR <2.0) Jika fibrinolysis, lanjut dengan NOAC + Clopi Jika mau fibrinolysis, harus cek INR (pada VKA) atau cek aPTT (NOAC) Jika mau triple therapy, akan menurunkan thrombotic risk namun meningkatkan bleeding risk, tapi jika dual therapy, akan meningkatkan thrombotic risk namun menurunkan bleeding risk

40. Afib in VHD

41. NOA

42. Summary

43. RHYTHM CONTROL FARMACOLOGIC MECHANIC