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Atrial fibrillation
1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat. 2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and decreased quality of life. 3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment depending on factors like symptoms, age, and stroke risk level.
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Atrial fibrillation
- 1. ATRIAL FIBRILLATION Dr SYED RAZA MD,MRCP(UK),CCT(UK),MESC,Dip.Card(UK),FCCP Consultant Cardiologist
- 3. OBJECTIVES • Introduction • Classification • Burden of the problem • Diagnosis • Management
- 4. What is it? • Abnormal electrical wavelets originate from left atrium • Propagating in different directions • Disorganized atrial depolarisation without effective atrial contraction
- 6. DIAGNOSIS • Pulse palpation •12 lead ECG • Holter monitoring • Others • Echocardiogram, CXR • TFT, Electrolytes, Clotting, LFT,CBC
- 8. ECG Diagnosis • OnECG p waves are absent and RR interval is variable. • f waves 350-600 beats /min. • ventricular response is grossly irregular at 100-160 beats /min. • Rate : No. of R waves x 10 ( 6 sec strip)
- 11. Prevalance • 2.2 Million people in the US • 6.5 cases/1000 examinations • 4% > 60yrs • 8 % > 80 yrs • 25% of individuals aged 40 yrs and older will develop AF in their life time.
- 12. Prevalence of AFin the Renfrew- Paisley study Cohort of men and women aged 45–64 years (n = 15,406) Reproduced with permission of the BMJ Publishing Group from Stewart S et al, Heart 2001: 86:516-21
- 13. Clinical events (outcomes)affected by AF Outcome Parameter Relative change in AF patients 1.Death 1.Death rate is doubled 2.Stroke 2.Stroke risk increases 5 times 3.Hospitalisation 3.More frequent 4.Quality of life and 4.Can be markedly exercise capacity decreased 5.LV function 5.Tachycardiomyopathy/ heart failure
- 14. Classification of AF Terminology Clinical features Initial event (first Symptomatic Rhythm/Rate detected episode) Asymptomatic Onset unknown Paroxysmal Spontaneous termination Rhythm <7 days and most often Control <48 hours Persistent Not self-terminating Rhythm or Lasting >7 days or prior Rate control cardioversion Permanent Not terminated Rate Control (‘accepted’) Terminated but relapsed No cardioversion attempt
- 16. Etiologies of AF CARDIAC Hypertensive heart disease Valvular heart disease Ischaemic heart disease Cardiomyopathy Pericarditis Congenital heart disease Post Cardiac surgery
- 17. Etiologies of AFcontd: NON CARDIAC 1. Pulmonary : Pneumonia, COPD,PE 2. Hyperthyroidism 3. Excess catecholamine /sympathetic activity 4. Drugs and alcohol 5. Significant electrolyte imbalance
- 18. LONE ATRIAL FIBRILLATION • Younger patients < 60 • No underlying cause • Usually not much symptoms • Normal heart structure • No associated co-morbidities
- 19. Why AF managementis important? • extremely common • Can lead to symptoms • potentially serious consequences: – embolism – impaired cardiac output – increased mortality
- 20. Management of AcuteAF (<48 hrs) • Haemodynamically unstable : hypotension/heart failure/chest pain/syncope Use DC Cardioversion Haemodynamically stable : Rate control : If significant tachycardia Rhythm control : Flecainide, Propafenone (cl- I) Amiodarone, Sotalol (cl-III) Anticoagulant : LMWH
- 21. Treatment for permanentAF • Heart Rate control minimise symptoms associated with excessive heart rates prevent tachycardia-associated cardiomyopathy • Anticoagulation
- 22. Rhythm control aspreferred therapy – ? First episode afib – Reversible cause (alcohol) – Symptomatic patient despite rate control – Patient unable to take anticoagulant (falls, bleeding, noncompliance) – CHF precipitated or worsened by afib – ? Young afib patient (to avoid chronic electrical and anatomic remodeling that occurs with afib)
- 23. Rate control aspreferred therapy – Age > 65, less symptomatic, hypertension – Recurrent afib – Previous antiarrhythmic drug failure – Unlikely to maintain sinus rhythm (enlarged LA)
- 24. Cardioversion • Cardioversion isperformed as part of a rhythm-control treatment strategy • There are two types of cardioversion: electrical (ECV) and pharmacological (PCV) • Cardioversion of AF is associated with increased risk of stroke in the absence of antithrombotic therapy.
- 26. AFFIRM : 5Year Outcomes Survival Rhythm Control Rate Control 1 year 96% 96% 3 year 87% 89% 5 year 76% 79% p = 0.058 NO Difference : death, disabling stroke, major bleed, or cardiac arrest Sinus rhythm maintained in only 63% of rhythm control group NEJM 2002;347:1825
- 28. Rate Control Options •Beta blocker • Calcium channel blocker • Verapamil, diltiazem . Digoxin • AV junction ablation plus pacemaker
- 29. STROKE RISK Without AF <60 yrs : 0.5% > 80 yrs : 3 yrs With AF < 60 yrs : 3% > 80 yrs : 30%
- 33. Lip Y, etal. Chest 2010, 137(2):263
- 34. How do wedetermine stroke risk ? – 0 points – low risk (1.2-3.0 strokes per 100 patient years) – 1-2 points – moderate risk (2.8-4.0 strokes per 100 patient years) – > 3 points – high risk (5.9-18.2 strokes per 100 patient years)
- 36. Atrial fibrillation 2009 Target INR 2-3
- 37. ACC AHA HRSAfib Focused Update (Dabigatran), March 2011 • Non-inferior to warfarin re thromboembolism (afib) • Caution when CrCl < 30ml/min • Increased dabigatran levels with amiodarone, verapamil • Half life 12-17 hours • No reversal re hemorrhage – dialysis • Coagulation testing ??? aPTT, dilute thrombin time
- 38. Who should remainon warfarin? • Patient already receiving warfarin and stable whose INR is easy to control • If dabigatran, rivaroxaban, apixaban not available • Cost • If patient not likely to comply with twice daily dosing (Dabigatran, Apixaban) • Chronic kidney disease (GFR < 30 ml/min)
- 39. Bleeding Risk • Assessmentof bleeding risk should be part of the clinical assessment of AF patients prior to starting anticoagulation • Antithrombotic benefits and potential bleeding risks of long-term coagulation should be explained and discussed with the patient • Aim for a target INR of between 2.0 and 3.0 • Forms of monitoring include point of care or near patient testing and patient self- monitoring
- 40. From Hart RG,et al. Stroke. 2005;36:1588
- 41.
- 42. Substrate for Substrate for Triggering events initiation perpetuation
- 43. When to considerablation? • Antiarrhythmic therapy ineffective • Antiarrhythmic therapy not tolerated • Symptomatic afib
- 46. Others in whomablation may be a first strategy • Patient very symptomatic in AF and refuses antiarrhythmic drug therapy • Young patient whose only effective antiarrhythmic drug is amiodarone • Patient with significant bradycardia for whom antiarrhythmic drug therapy will require pacemaker
- 47. Summary • AF isthe commonest arrhythmia • High prevalence • Stroke is one of the most dreadful complications . • Different management strategies,
Editor's Notes
- #13 NOTES FOR PRESENTERS Refer to the full guideline – page 13, table 1.01. Renfrew-Paisley UK study, cohort of men and women aged 45-64 years (n = 15,406) there were 100 documented cases of AF. Prevalence of AF increased with age and more cases were detected in men.
- #15 NOTES FOR PRESENTERS For more details, refer to the full guideline, pages 11 and 12, section 1.2 AF is considered recurrent when a patient develops two or more episodes. These episodes may be paroxysmal if they terminate spontaneously, defined by consensus as terminating within seven days, or persistent if the arrhythmia requires electrical or pharmacological cardioversion for termination. Successful termination of AF does not alter the classification of persistent AF in these patients. Longstanding AF (defined as over 1 year) not successfully terminated by cardioversion, or when cardioversion is not pursued, is classified as permanent. Without treatment, AF can result in some degree of disruption to the circulation of blood around the body. In some cases of AF, the degree of haemodynamic instability can represent a critical condition that requires immediate intervention. The next slide sets out why we need this guideline.
- #17 NOTES FOR PRESENTERS There are many risk factors for developing AF. In the Framingham study, the development of AF was associated with increasing age, diabetes, hypertension and valve disease. It is also commonly associated with, and complicated by, congestive heart failure and strokes. Dietary and lifestyle factors have also been associated with AF, such as excessive alcohol and caffeine, as well as emotional and physical stress. Cardiac causes of AF Common cardiac causes: Ischaemic heart disease Rheumatic heart disease Hypertension Sick sinus syndrome Pre-excitation syndromes (e.g. Wolff-Parkinson-White syndrome) Less common cardiac causes: Cardiomyopathy or heart muscle disease Pericardial disease (including effusion and constrictive pericarditis) Atrial septal defect Atrial myxoma Non-cardiac causes of AF Acute infections, especially pneumonia Electrolyte depletion Lung carcinoma Other intrathoracic pathology (e.g. pleural effusion) Pulmonary embolism Thyrotoxicosis Refer to the full guideline – page 89, section 10 Post-op AF is associated with a greater risk of mortality and morbidity, and evidence is emerging that post-op AF predisposes people to a significantly increased risk of stroke and thromboembolism. The next slide highlights the classification of AF, which is based on the temporal pattern of the arrhythmia.
- #22 NOTES FOR PRESENTERS In patients with permanent AF who need treatment for rate-control: - beta-blockers or rate-limiting calcium antagonists should be the preferred initial monotherapy in all patients In patients with permanent AF where monotherapy is inadequate: to control the heart rate during normal activities only, beta-blockers or rate-limiting calcium antagonists should be administered with digoxin to control the heart rate during both normal activities and exercise, rate-limiting calcium antagonists should be administered with digoxin
- #25 NOTES FOR PRESENTERS For further details, refer to the NICE guideline – page 27. Patients undergoing PCV are usually admitted to hospital
- #40 NOTES FOR PRESENTERS Refer to NICE guideline – pages 22 and 23 In order to provide adequate thromboprophylaxis with minimal risk of bleeding, current clinical practice aims for a target INR of between 2.0 and 3.0; INRs higher than 3.0 are associated with increases in bleeding, and INRs lower than 2.0 are associated with increases in stroke risk.