Atrial fibrilation


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atrial fibrillation, classification, pathophysiology

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Atrial fibrilation

  1. 1. Atrial fibrillation (Classification, Mechanism &Management)
  2. 2. Introduction… AF is characterised by wavelets propagating in different directions causing disorganized atrial depolarization without effective atrial contraction Electrical activity of atrium can be detected in ECG as small irregular baseline undulations of variable amplitude & morphology (f waves) at rate of 350 to 600 Ventricular response is irregularly irregular, & in untreated patients with normal AV conduction, is usually between 100 to 160 WPWsyndrome ventricular rate may be rapid >300 due to conduction over accessory pathway( short antegrade refractory periods)
  3. 3. Introduction… ventricular rate during AF is altered due to Autonomic tone Property of AV node Effect of drugs on AV conduction
  4. 4. Introduction Atrial fibrillation is the most common arrhythmia & the incidence & prevalence increases with the age The incidence <0.5% below 50Yrs 2% in age 60-69 4.6% in age 70-79 8.8% in age 80-89 Men were 1.5 times more likely to develop AF than women Whites were more likely to develop AF than blacks
  5. 5. Framingham heart study ---cardiac factor predicting AF• CHF• RHD• HT• Stroke• Left atrial enlargement• Increased LV wall thickness• Decreased LV fractional shortening
  6. 6. Relative risk of stroke - 6 fold in non rheumatic AF Relative risk of stroke - 17 fold in rheumatic AF Annual risk of stroke in pt aged 50- 59:1.5% Annual risk of stroke in aged 80-89:23.5%
  7. 7. Underlying causes of AF CVS  Tumors Rheumatic heart disease  WPW syndrome ASD  Systemic Cardiac surgery  Alcohol (holiday heart Cardiomyopathy syndrome) Hypertrophic  CVA Idiopathic Infiltrative  COPD Hypertension  Defibrillation CAD (Acute & chronic)  Effort MVPS  Electrocution Non rheumatic mitral or tricuspid valve disease  Electrolyte abnormalities Pericarditis  Fever Tacycardia-bradycardia syndrome  Hypothermia
  8. 8. Underlying causes of AF… Pneumonia  Congenital Pulmonary embolism  Multiple sclerosis Sudden emotion  Muscular dystrophy Thyrotoxicosis  Pheochromocytoma Trauma  Right atrial cold injections Rare  Swallowing Acute hypovolemia  Tyramine foods
  9. 9. of Atrial fibrillation
  10. 10. Classification of Atrial fibrillation First detected AF -usually <48hr in AF during diagnosis Paraoxysmal AF - last < 7days (most<24hrs) self-terminating episodes Persistent AF - last >7days requires electrical or pharmacologic cardioversion Permanent AF - sustained >1yr & failed cardioversion
  11. 11. Mechanisms It was first thought that irregular contractions of the atria are caused by either single or multiple foci In 1924, Garry had suggested reentry to be the mechanism behind the AF In 1960, Moe suggested the “multiple wavelet hypothesis ” AF is characterized by fragmentation of a wavefront into multiple, independent daughter wavelets that move randomly throughout the atrium, giving rise to new wavelets that collide with each other & mutually annihilate, or that give rise to new wavelets in a perpetual activity that resembles Brownian motion
  12. 12. Mechanisms Stability of AF is a function of several factors Non-uniform distribution of refractory periods Specially large tissue area Either a relatively brief refractory period or a relatively slow conduction velocity of the impulse, or both Average no. of the wavelets Allessie et al, estimated the critical no. of wavelets to sustain AF was approximately 4 - 6
  13. 13.
  14. 14. Mechanisms Trigger factor - self-terminating AF Perpetuating factor - AF does not terminate spontaneously Paraoxysmal AF - 95% of Triggering foci are mapped in pulmonary vein Other foci - within SVC ,coronary sinus
  15. 15. distribution of focal trigger in Paraoxysmal AF
  16. 16. Mechanisms Waldo et al divided AF into 4 types according atrial electrogram• Type – I --- ECG showed discrete complexes of variable morphology separated by a clear isoelectric baseline• Type – II --- ECG characterized by discrete atrial complexes with variable cycle lengths and morphology, the baseline is not isoelectric• Type – III --- ECGs were highly fragmented, showing no discrete complexes or isoelectric intervals• Type – IV --- Fibrillation was characterized by
  17. 17. Mechanisms “ f” waves They do not represent total atrial activity but depict only the larger vectors generated by the multiple wavelets of depolarization that occur at any given time Why ventricular response is irregularly irregular? Large no. of atrial impulses that penetrate the AV node, makes it partially refractory to subsequent impulses These effect of non conducted atrial impulses to influence the response of subsequent atrial impulse is called as “concealed conduction”
  18. 18. Mechanisms Electrical remodelling It means long term changes in refractory periods resulting from prolonged changes in atrial rate EPS --- ↓ERP,↓Action potential, ↓ amplitude of AP plateau Mechanisms --- Structural , cellular or ion channels It encompasses diverse structural changes in the myocardium -interstitial fibrosis Alteration in quantity or properties of ion channel proteins in sarcolemma Microscopic changes in cell size , content & extra cellular matrix leads to irreversible macroscopic changes
  19. 19. Mechanisms Maladoptations of atrial refractionaries – cause of chronic AF Atrial remodelling Caused by atrial ischemia & stretch leads to AF due to ↑ automaticity & reentry After AF has continued for a long time, atria are not only electrically remodelled, but atrial contractile function is also disturbed Recovery of atrial transport function may depend upon duration of AF After sinus rhythm is restored, it may take several weeks before atrial contractility fully returns
  20. 20. Mechanisms Modulating factors The onset & persistence of AF may be modulated by autonomic nervous system Coumel et al distinguished vagal & adrenergic AF (distinction is not clear) Vagally mediated AF Occurs more frequently in men than in women Usually younger age group (30 – 50 years)
  21. 21. Mechanisms Predominantly occurs in the absence of structural heart disease Rarely progresses to permanent AF Attacks occur at night, end of the morning Neither emotional stress nor exertion trigger the arrhythmia Rest, postprandial state, & alcohol are other precipitating factors Mechanism may relate to vagally induced shortening of the atrial refractory period
  22. 22. Mechanisms Adrenergic AF More frequently associated with structural heart disease (IHD) Occurs during the day time, & it is precipitated by stress, exercise, tea, coffee or alcohol The underlying mechanism is unknown
  23. 23. Hemodynamic effect Loss of atrial contraction Rapid ventricular rate - ↓duration of diastole & ventricular filling irregular ventricular rhythm - ↓ CO & coronary blood flow Loss of AV synchrony - ↓LVEDP - ↓SV AF causes hypotension or pulmonary oedema in the setting of restrictive physiology
  24. 24. Antiarrhythmic therapy of atrial fibrillation Three antiarrhythmic strategies Acute pharmacologic termination Prevention of recurrence after cardioversion Control of ventricular rate Acute conversion of paroxysmal AF Pharmacologic cardioversion Most effective if initiated within 7 days after onset of AF Restoration of sinus rhythm can be achieved in 70% of the patients First choice : Propafenone & flecainide (po & iv), ibutilide, dofetilide Second choice : Amaiodarone (high dose, iv +oral) & Qunidine (po)
  25. 25. to maintain sinus rhythm in AF
  26. 26. Antiarrhythmic therapy of atrial fibrillation Class IC drugs – Restore sinus rhythm with in a short period of time ( 1 hour) – conversion rate up to 90% (PAFIT-3) Ibutilide It acts twice more effectively for conversion of atrial flutter than atrial fibrillation (63% v 31%) Efficacy decreased significantly with AF of >7 days Studies, enrolled patients with mild to moderate underlying disease, so these results may not be generalizable to patients with markedly depressed LVF
  27. 27. Antiarrhythmic therapy of atrial fibrillation Dofetilide DIAMOND-CHF Study of 1518 patients with symptomatic heart failure (EF <35%) Therapy with 1000mic.g was associated with a greater rate of conversion to sinus rhythm (44% v14%) SAFIRE-D Study of 325 patients with persistent AF &/or atrial flutter Cardioversion rates were 6.1%,9.8% & 29.9% for 125, 250 & 500mic.g bid compared with 1.2% of conversion with placebo
  28. 28. Antiarrhythmic therapy of atrial fibrillation Amiodarone Produce sinus rhythm in 80% within 24hours (late conversion) Advantages It lowers ventricular rate before conversion (IC drugs increase the rate) Recommended in hemodynamically compromised patients since it is less negatively inotropic Prefered in pts with LVF, LVH, IHD IV amiodarone is moderately effective in converting AF compared with placebo (63% v 44%), with maximum effect at 24hours (74% v 55%) --- 12 meta-analysis Higher than usual dose & combination of IV & oral administration may enhance the cardioversion rate
  29. 29. Antiarrhythmic therapy of atrial fibrillation Quinidine Usually administered in conjunction with B-Blocker Cumulative dose of up to 1350mg has shown to cardiovert 50- 77% of patients with recent onset AF Sotalol It is ineffective in acute conversion It is effective for the prevention of AF This discrepancy relates to its property to prolong the refractory period predominantly at lower atrial rates, but not during rapid AF
  30. 30. Antiarrhythmic therapy of atrial fibrillation Availability of studies on the efficacy of procainamide & disopyramide is limited, precluding definite conclusions Digitalis, B-Blockers, & CCBs are ineffective for acute conversion of AF DAAF study (Digoxin in acute AF) There was no difference in cardioversion rates at 16 hours between IV digoxin & placebo (51% v 46%) Digoxin can facilitate AF due to its cholinergic effects which may cause a non-uniform reduction in conduction velocity & effective refractory periods of the atria, and to delay the reversal of remodelling after restoration of sinus rhythm
  31. 31. of paroxysmal AF(<3days)
  32. 32. Antiarrhythmic therapy of atrial fibrillation Prevention of paroxysmal AF No need for prophylactic AAD After first episode of AF which may self terminate or require electrical or pharmacologic cardioversion Patients with infrequent, self limiting & well tolerated paroxysms of AF Prophylactic AAD are recommended if Occurs frequently (1 episode per 3 months) Associated with significant symptoms
  33. 33. Antiarrhythmic therapy of atrial fibrillation Prophylactic AAD are recommended if… Worsening of LV function In the presence of left atrial enlargement, LVD, underlying CVS pathology, long duration of AF, advanced age B-blockers Effective in adrenergic dependent AF (class IA & IC are ineffective) It prevents the recurrence of persistent AF after cardioversion
  34. 34. Antiarrhythmic therapy of atrial fibrillation Control of ventricular rate during paroxysmal AF Digitalis, B-blockers, CCBs are useful Addition of rate controlling drugs is necessary with class IA & IC drugs (not needed with amiodarone or sotalol) Control of ventricular rate in the setting of SSS may be impossible without implanting pacemaker In WPW syndrome complicated by AF – acute rate control & conversion to SR may be achieved by procainamide or flecainide
  35. 35.
  36. 36. Antithrombotic therapy Whether AF is persistent or intermittent --- Predisposes to stroke Non valvular AF Most common cardiac disease associated with cerebral embolism The risk of stroke is 5-7 times greater when compared to control group Risk factors that predicts stroke Previous stroke or TIA Diabetes mellitus Systemic hypertension Increasing age CAD CHF
  37. 37. Antithrombotic therapy LV dysfunction & left atrial size > 2.5cm/sq.m --- associated with thromboembolism Age - 60-65, normal echo, no risk factors --- Extremely low risk for stroke (1% per year) Results from 5 large anticoagulation trails Annual rate of stroke in control group --- 4.5% Annual rate of stroke in warfarin-treated group --- 1.4% (68% risk reduction) Aspirin 325mg/d produced a risk reduction of 44%
  38. 38. Antithrombotic therapy Annual rate of major hemorrhage Control group --- 1% Aspirin group --- 1% Warfarin group --- 1.3% No difference was noted in stroke risk, when patients with paroxysmal (intermittent) AF were compared with chronic AF Anticoagulation was 50% more effective than aspirin in preventing ischemic stroke
  39. 39. Antithrombotic therapy Risk factors for stroke Prior stroke or TIA Significant valvular heart disease Hypertension Diabetes mellitus Age >65 years Left atrial enlargement CAD Congestive heart failure
  40. 40. Antithrombotic therapy Lone AF Age <60years, no risk factors ---No antithrombotic therapy Age - 60-75 years (risk-2%per year) ---Aspirin Age > 75 years --- Anticoagulation (INR – 2.0) Any patients with AF + Risk factors for stroke --- Treated with warfarin anticoagulation (INR – 2 to 3) Patients with contraindication to anticoagulation (or) unreliable individual (or) no risk factors --- Aspirin
  41. 41. Antithrombotic therapy Risk of embolism after cardioversion Risk --- 0 -7% Risk is independent of mode of cardioversion High risk patients are Prior embolism, Mechanical valve prosthesis, Mitral stenosis In AF (>2d) --- Warfarin for 3 weeks before cardioversion + 3-4 weeks after reversion to sinus rhythm Alternate strategy --- TEE (to exclude LA thrombus) + heparin before cardioversion + followed by warfarin for 4weeks
  42. 42. Antithrombotic therapy Risk of embolism after cardioversion… For emergency cardioversion (TEE cannot be obtained) --- heparin before cardioversion + followed by warfarin for 4weeks Low risk patients Age <65 years without risk factor for stroke in nonvalvular AF Anticoagulation may not be necessary before cardioversion but aspirin is indicated It is important to emphasize that suggestions must be individualized for a given patient Absolute contraindication for anticoagulation - ICH,SDH,GI bleed
  43. 43. Non – pharmacologic therapies Rhythm control strategies Device therapy Single site pacing --- High right atrial & septal In many patients with SSS, atrial pacmaker allows higher dose of AAD since sinus node dysfunction is treated In patients with paroxysmal AF, there is evidence for intraatrial conduction delay Atrial pacing may decrease the frequency of recurrent AF in patients who have SSS
  44. 44. Non – pharmacologic therapies Incidence of AF is lower in patients treated by atrial pacing than ventricular pacing (prospective studies) Multisite pacing --- Biatrial synchronous & Dual site atrial pacing In addition to the high RA lead, another atrial lead is placed just outside the CS ostium for stability & LA synchronization These pacing cause resynchronization of atrial depolarisation & helpful in patients with intra atrial conduction delay
  45. 45. Non – pharmacologic therapies Usually performed in patients with recurrent, symptomatic & drug refractory AF ECG showed biphasic ‘p’ wave in inferior leads with abbreviation of ‘P’ wave duration Implantable atrial defibrillator Automatic atrial defibrillator• It detect AF by means of implanted RA, CS & RV leads
  46. 46. Non – pharmacologic therapies• It delivers ‘R’ wave synchronization shock of 6J after a minimal preceding R-R interval of 500 ms• Unfortunately this device in its current form is not in use Atrial-ventricular defibrillator/pacemaker• It has dual chamber algorithm-based arrhythmia detection• Pacing & defibrillation therapies for treatment of AF & atrial tachycardias
  47. 47. Non – pharmacologic therapies Ablation therapy --- surgical His bundle ablation (surgical ligation, mechanical, cryothermia) + Pace maker implantation Corridor surgery Creating an isolated strip of muscle to isolate the SA & AV nodes, thus driving ventricular rate via AV node-His bundle complex But, atrial areas outside of narrow RA corridor continued to fibrillate with persistent loss of atrial transport function & persistent risk of thromboembolism
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  49. 49. Non – pharmacologic therapies Maze procedure The principle is compartmentalize both atria so that AF cannot be maintained Right & left atrial appendages were resected, pulmonary vein ostia are isolated, linear RA & LA lesions are connected to anatomic structures to form an “electrical maze” --- “Maze 3” Appropriately placed atrial incisions not only interrupt the conduction routes of reentrant circuits, but they also direct the sinus impulse from SA to AV along a
  50. 50. Indication for maze procedure Symptomatic AF Refractory to AAD Recurrent systemic embolism despite anticoagulation
  51. 51. Maze procedure 90% pt cured of AF with operative mortality <1 <10% requires PPI due to sinus node dysfunction Transient fluid retention due to ↓atrial natriuretic peptide must be treated with diuretics The entire atrial myocardium was electrically activated & atrial transport function is preserved
  52. 52. – pharmacologic therapies
  53. 53. Non – pharmacologic therapies Tans catheter ablation therapy Linear atrial ablation (Radiofrequency) It is employed in LA & RA for substrate compartmentalization Trigger ablation (Radiofrequency) Focal pulmonary vein Pulmonary vein isolation - transseptal puncture followed by pulmonary venography to define anatomy Adverse effect Stroke Phrenic nerve injury Pericardial effusion & tamponade Pulmonary vein stenosis
  54. 54. Indication for ablation Symptomatic AF Refractory to AAD Without structural heart disease
  55. 55. Non – pharmacologic therapies Rate control strategy Catheter AV junctional modification (radiofrequency) Principle --- Posterior inputs of AV node have shorter ERP, their ablation slows the ventricular response during AF Patient who becomes symptomatic due rapid ventricular response will benefit Currently, AV node modification is usually reserved for patients who require non-pharmacologic control but are opposed to pacemaker implantation
  56. 56. Non – pharmacologic therapies Catheter ablation (DC shock or radiofrequency) + Pacemaker It is performed in patients with unmanageable symptoms related to rapid ventricular response DC current ablation is highly dangerous --- produce electrical arcing & barotrauma ( cardiac perforation, tamponade, acute depression of LV, proarrhythmia & sudden death Radiofrequency ablation ---avoid complications Disadvantages Dependence on pacemaker Atria will continue to fibrillate --- need long term
  57. 57. Non – pharmacologic therapies Choice of pace maker type --- determined by the current phase of AF Chronic AF --- VVIR + AV nodal ablation Paroxysmal AF ( usually in sinus rhythm between episodes) --- Dual-chamber pacemaker with mode switching Stroke prevention strategy Percutaneous LA appendage transcatheter occlusion (PLAATO) Involves insertion of an occlusion device by catheter into the LA appendage via trans septal puncture
  58. 58. circular mapping catheter is in the ostium of the left lower PV and an ablation catheter with a large-tip electrode is recording a PV potential from the nearby strand.
  59. 59. During radiofrequency ablation near Lasso-8 recording, the sharp PVPs are seen in the first two beats but are absent during the last two beats
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  61. 61. you
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  68. 68. Introduction Paroxysmal AF Short lasting < 1 hour Long lasting >1; < 48 hours AF interspersed with periods of sinus rhythm & usually terminates spontaneously Persistent AF Occur between 2days - weeks Intervention is needed to restore the sinus rythum Chronic or permanent AF Persists for months to years No spontaneous conversion Interventions to restore sinus rythum are either ineffectual or
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  70. 70. Mechanisms Type – I --- Activation consisted of single, broad wavefronts propagating without conduction delay & either only short arcs of conduction block or small areas of slow conduction that did not disrupt the main course of propagation Type – II --- Activation consisted of either the presence of 2 wavelets or of single wave (with either considerable conduction block or slow conduction or both) Type – III --- Activation was characterized by 3 or more wavelets combined with areas of slow conduction & multiple arcs of conduction block As the fibrillation changed from type I to III, AFs frequency & irregularity increased, creating a higher incidence of continuous electrical activity & reentry
  71. 71. Mechanisms Familial AF• Genetic predisposition – is a hypothesis• Defect linked to chromosome 10q (21 of 49 members from 3 spanish families presented with AF)• Missense mutation in the lamin A/C gene (In DCM – associated with AF)• Missense mutation Arg663His ( In specific phenotype of HCM – associated with 47% of AF)
  72. 72. control in atrial fibrillation
  73. 73. control in atrial fibrillation
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  75. 75. therapy of atrial fibrillation
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  77. 77. 30%