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Atrial fibrillation good


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recent updates about diagnosis and management of atrial fibrillation

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Atrial fibrillation good

  1. 1. Atrial fibrillation – Diagnosis and Management Dr K V pradeep babu. Post graduate , Internal Medicine, PSIMS &RF
  2. 2. Clinical features of AF
  3. 3. • It is estimated that approximately 25% of patients with AF are asymptomatic • Among those that are, symptoms associated with AF are variable. • Typical symptoms include palpitations, tachycardia, fatigue, weakness, dizziness, lightheadedness, reduced exercise capacity, increased urination, or mild dyspnea. • The history should focus on obtaining the following information: • A description of the symptoms: onset or date of discovery, the frequency and duration, severity, and qualitative characteristics.
  4. 4. • More severe symptoms include dyspnea at rest, angina, presyncope, or infrequently, syncope. • In addition, some patients present with an embolic event or the insidious onset of rightsided heart failure (as manifested by peripheral edema, weight gain, and ascites). • Precipitating causes: exercise, emotion, or alcohol. • Polyuria can occur because of release of atrial natriuretic hormone.
  5. 5. • Syncope is an uncommon symptom of AF, most often caused by a long sinus pause on termination of AF in a patient with the sick sinus syndrome. Less commonly, syncope occurs with a rapid ventricular rate either because of neurocardiogenic (vasodepressor) syncope that is triggered by the tachycardia a severe drop in blood pressure due to a sudden reduction in cardiac output, mostly in AS, HOCM.
  6. 6. • The presence of the following disease associations should be noted : • cardiovascular or cerebrovascular disease • Diabetes • Hypertension • Chronic obstructive pulmonary disease • potentially reversible causes (eg, hyperthyroidism, excessive alcohol ingestion).
  7. 7. Clinical findings in AF • The hallmark of AF on physical examination is an irregularly irregular pulse. • Short R-R intervals during AF do not allow adequate time for left ventricular diastolic filling, resulting in a low stroke volume and the absence of palpable peripheral pulse. • This results in a “pulse deficit,” during which the peripheral pulse is not as rapid as the apical rate. • Other manifestations of AF on the physical examination are irregular jugular venous pulsations and variable intensity of the first heart sound.
  8. 8. Clinical Evaluation of Atrial Fibrillation
  9. 9. • Minimum Evaluation :
  10. 10. The electrocardiogram in atrial fibrillation
  11. 11. Findings on ECG • Lack of discrete P waves. • Fibrillatory or f waves are present at a rate that is generally between 350 and 600 beats/minute • the f waves vary continuously in amplitude, morphology, and intervals. • The variability in the intervals between QRS complexes is often termed “irregularly irregular.”
  12. 12. • The ventricular rate usually ranges between 90 to 170 beats/min. • The QRS complexes are narrow unless AV conduction through the His Purkinje system is abnormal due to • Functional (rate-related) aberration • Pre-existing bundle branch or fascicular block • ventricular preexcitation with conduction down the accessory pathway.
  13. 13. AF is associated with the following changes on ECG AF with f waves
  14. 14. AF without f waves
  15. 15. ATRIAL ACTIVITY in AF • In AF there is no regular or organized atrial activity • Numerous micro-reentrant circuits within the atria generate multiple waves of impulses which often compete with or even extinguish each other. • No uniform activation of the atrial tissue and no distinctive P waves are generated or recognized on the surface ECG. • The sinus node is suppressed or not able to be expressed .
  16. 16. F waves • When the AF is of recent onset, the f waves are often coarse (>2 mm). • “Coarse” AF in which the amplitude of the f waves is large (especially in lead V1) is more common in recent onset AF and can be confused with atrial flutter or multifocal atrial tachycardia. • The f waves are usually fine (<1 mm) with AF of greater duration.
  17. 17. • The f waves are of greater amplitude when there is hypertrophy of left atrial myocardium and become smaller with increasing atrial scarring and fibrosis. • The amplitude of the fibrillatory waves does not correlate with the actual atrial size.
  18. 18. • In some cases, there are no recognizable deflections of the baseline in any ECG lead (more common in longstanding AF) . • AF is inferred because of the absence of P waves and the irregularly irregular ventricular rate. • If present, f waves are best seen in the inferior leads and in V1.
  19. 19. VENTRICULAR RATE in AF • The atrial rate is very rapid and depends upon the electrophysiologic characteristics of the atrial myocardium. • The ventricular response rate is dependent upon the properties of the atrioventricular node (AV) and His Purkinje system. • The ventricular rate (especially in the absence of nodal blockade) usually ranges from 90 to 170 beats/min. • However, many factors determine the rate at any moment in any individual.
  20. 20. Why irregular ventricular rate?? • Refractoriness of AV Node due to bombardment of the AV node with impulses in rapid succession. • The large number of atrial impulses arriving at the node compete with each other, interfering with their penetration into and through the node, leaving this tissue variably refractory. • The frequency of bombardment can lengthen conduction time, and these impulses that reach the AV node but do not conduct are said to lead to concealed conduction within the AV node.
  21. 21. When VR is increased ? Increases in the ventricular response rate to over 200 beats per minute may occur if the refractory period of the AV node is shortened: • With sympathetic stimulation • Increase in circulating catecholamines • conduction down an accessory pathway if present
  22. 22. When VR is decreased ? • A decrease in the ventricular response rate occurs when the refractory period of the node is increased . • Happens with aging. • Intrinsic AV nodal disease in combination with sympathetic blockade • Direct depression of the AV node with some drugs • Enhanced vagal tone.
  23. 23. Regularization of atrial fibrillation • Due to the complete blockade of AV nodal conduction . • Subsequently there will be development of a junctional (narrow QRS) or ventricular (wide QRS) escape rhythm. • Also, at very fast rates of conduction, the ventricular response rate can appear to be regular
  24. 24. • In some cases, regularization in rate is due to conversion of AF into atrial flutter with a fixed ratio of conduction. • Drugs that impair nodal conduction (such as digoxin, beta or calcium channel blockers) or AV nodal disease may result in the development of slowing and regularization of the ventricular response. • Digoxin is the most likely to do so.
  25. 25. Regular is not always right !!?? • So , regular rhythm in patient with AF after digoxin may be more ominous , for it may indicate complete Heart block !
  26. 26. AF in accessory pathway • When AF is associated with a preexcitation syndrome (ie, the presence of an antegrade conduction accessory pathway), the ventricular response rate may be very rapid, often in excess of 280 to 300 beats per minute. • Here impulse conduction bypasses the atrioventricular node, as conduction from the atria to the ventricles occurs by an accessory or intranodal pathway. • If the refractory period of this pathway is very short, impulse conduction can be very rapid
  27. 27. Why conduction is rapid in accessory tract ?? • The tissue of accessory pathways does not have the same characteristics as the AV node • It does not exhibit postrepolarization refractoriness • Conducts rapidly as the tissue is not dependent on calcium conduction • Rather it’s dependent on sodium conduction similar to atrial and ventricular muscle.
  28. 28. • In such cases, the QRS complex is usually aberrant (and wide) and may be confused with ventricular tachycardia, although the rhythm is still irregularly irregular. • This rhythm may also be confused with AF with aberrancy; but with standard aberration, the morphology is more typical of a left or right bundle branch block.
  29. 29. • Conduction via an accessory pathway often shows a slurred QRS upstroke (“Delta” wave) • This morphology depends on the location of the pathway and wherein inserts into the ventricular myocardium. • During so-called preexcitation syndromes, conduction can proceed through the AV node and/or the accessory pathway. • The more conduction proceeds through the accessory pathway, the more QRS appearance is “aberrant.” • A distinguishing feature of this entity of AF with preexcitation is the relationship between heart rate and QRS duration; the faster the rate, the wider the QRS width.
  30. 30. DIFFICULTIES IN DIAGNOSIS of ECG • The f waves may be inapparent on the standard and precordial leads . This is most likely to occur when AF is of long duration. • The f and u waves may have sufficient amplitude to look like P waves. • Extracardiac artifacts, such as those seen in patients with Parkinson disease and tremors, may simulate f waves
  31. 31. • Other rhythms in which the R-R intervals are irregularly irregular. These include : • • • • Multifocal atrial tachycardia (MAT) Wandering atrial pacemaker (WAP) Multifocal atrial premature beats Atrial tachycardia or atrial flutter with varying AV block.
  32. 32. • The R-R interval may be regular with AV dissociation or block, a setting in which a lower junctional, subjunctional, or ventricular pacemaker assumes control of the ventricles. Example : advancing digitalis toxicity .
  33. 33. • Atrial fibrillation with rapid ventricular rates may be misdiagnosed as paroxysmal supraventricular tachycardia patients are commonly treated with adenosine, which will not convert patients with AF . • AF with a wide QRS complex, as occurs in patients with either preexcitation or aberrancy, may make it difficult to determine if the rhythm is AF or ventricular tachycardia.
  34. 34. Morphology of the QRS complex • The QRS complex usually maintains its normal narrow configuration in AF, since activation through the infranodal conduction system is intact. • There are settings in which widening of the QRS complex occurs
  35. 35. • These include: • a pre-existing conduction defect (left or right bundle branch block) • Functional (generally rate-related) block in a portion of the infranodal conduction system that results in asynchronous or aberrant activation and, for example, a right bundle branch block (RBBB) pattern • Preexcitation through an atrioventricular (AV) bypass tract which is capable of antegrade conduction.
  36. 36. • Aberration following a long-short cycle in AF is often called the Ashman or Gouaux-Ashman phenomenon . • Ecg of ashman phenomena
  37. 37. Effect of high degrees of AV nodal block and exit block on ventricular response • May occur with digitalis toxicity or progressive AV nodal disease), impulses from the fibrillating atria fail to reach the infranodal conduction system. • As a result, a pacemaker below the level of the block assumes control of the ventricles. • The pacemaker is usually located in the AV junction above the bifurcation of the bundle branches. • Leads to a QRS complex that has the same morphology as if it had been conducted from the atria through the AV node. • This pacemaker has a characteristic rate of about 60 beats/min,unless it is accelerated or depressed due to pathology, ischemia, or drugs.
  38. 38. • Less commonly, the pacemaker is subjunctional or ventricular. • In this setting, the QRS complex will be wide and, unless accelerated, the ventricular rate will be relatively slow at 30 to 50 beats/min.
  39. 39. SUMMARY —ECG in AF • Absence of discrete P waves. • Fibrillatory or f waves are present at a rate that is generally between 350 and 600 beats/minute; the f waves vary in amplitude, morphology, and intervals. • The RR intervals follow no repetitive pattern; they have been labeled as “irregularly irregular.” • The ventricular rate usually ranges from 90 to 170 beats/min. • The QRS complexes are narrow unless AV conduction is abnormal due to functional (rate-related) aberration, pre-existing bundle branch or fascicular block, or ventricular preexcitation . • Although ECG findings described above usually allow the diagnosis of AF to be made easily, there are several pitfalls in correct identification of the rhythm.
  40. 40. Role of echocardiography in atrial fibrillation
  41. 41. Echo may be helpful in assessing … • Helpful in determining the conditions associated with AF • Risk for recurrent AF following cardioversion. • Identification of patients at increased risk for thromboembolic complications of AF before cardioversion and in patients with chronic AF
  42. 42. Two varieties of Echo • TTE : Transthoracic echocardiogram • TEE : Trans esophageal echocardiographic
  43. 43. Usually TTE is done It is useful for evaluating : • left atrial size • left ventricular systolic function • Mitral valve morphology and function.
  44. 44. Left atrial size • The normal left atrial dimension in adults is less than 4.0 cm (or <2.0 cm/m2 body surface area). • Left atrial enlargement is common in AF, particularly in patients with mitral valve disease, left ventricular dilation, annular calcification, or hypertension. • sustained AF itself can lead to a further increase in left atrial size, an effect that is reversible after cardioversion and maintenance of sinus rhythm.
  45. 45. Why LA status should be assessed ?? • Left atrial enlargement is important prognostically. • It decreases the probability that long-term maintenance of sinus rhythm will be successful . • Patients with chronic (more than one year) AF, rheumatic mitral valve disease, and severe left atrial enlargement (dimension greater than 6.0 cm) are at greatest risk for recurrent AF
  46. 46. Mitral valve function • Mitral stenosis in the adult may initially present with AF, often in the setting of acute thromboembolism. • In this setting, long-term anticoagulation with warfarin is indicated even if cardioversion to sinus rhythm is successful. • Long-term maintenance of sinus rhythm is unlikely unless the mitral stenosis is corrected (by surgery or percutaneous balloon mitral valvuloplasty).
  47. 47. • Moderate to severe mitral regurgitation appears to protect against clinical thromboembolism in chronic AF, presumably by minimized stasis in the left atrium and atrial appendage and less coagulation activity. • However, it does not appear to protect from the formation of left atrial appendage thrombus as identified on TEE
  48. 48. Left ventricular function • Assessment of left ventricular systolic function helps to guide the choice of pharmacologic therapy for ventricular rate control in chronic AF. • A beta blocker or a calcium channel blocker (diltiazem or verapamil)  patients with preserved left ventricular systolic function. • Patients with depressed left ventricular systolic function may be best treated  digoxin. • Patients with overt heart failure due to systolic dysfunction  both a beta blocker to improve survival and digoxin to control symptoms, independent of the presence or absence of AF.
  49. 49. • Left ventricular dysfunction, as determined from the TTE, independently predicts an increased risk of a stroke in patients with AF. • Analysis of 1066 patients entered into three prospective clinical trials evaluating the role of anticoagulation in nonvalvular AF (BAATAF, SPINAF, and SPAF) found that, the incidence of a stroke was 9.3 percent per year in patients with moderate to severe left ventricular dysfunction compared to 4.4 percent per year in those with normal or mildly abnormal left ventricular systolic function .
  50. 50. Left atrial thrombi • The ability of TTE to identify or exclude left atrial or atrial appendage thrombi is limited, with a reported sensitivity of 39 to 63 percent largely to poor visualization of the left atrial appendage.
  51. 51. TEE in a more selected subgroup • May benefit evaluation for left atrial thrombi to allow for early cardioversion, if no thrombi are identified. • The Stroke Prevention in Atrial Fibrillation (SPAF) investigators confirmed the usefulness of transesophageal echocardiography (TEE) for predicting thromboembolism, study involved 786 patients with nonrheumatic AF.
  52. 52. Results of SPAF study The rate of stroke was : 1. increased over threefold when TEE evidence of dense spontaneous echocontrast was present. 2. Increased by threefold for reduced left atrial appendage peak flow velocity and for left atrial appendage thrombus 3. Increased by fourfold by complex aortic plaque.
  53. 53. • TEE permits detection of thrombus in both the left atrium and the left atrial appendage • TEE evidence of left atrial thrombi is seen in approximately 13 percent of patients presenting with nonrheumatic AF of more than three days duration
  54. 54.  The prevalence is increased in high-risk patients with : • Mitral stenosis (33 percent in one series) • Left ventricular systolic dysfunction, enlargement of the left atrium or left atrial appendage • Spontaneous echo contrast, a recent thromboembolic event (43 percent in one report) , and high CHADS2 score
  55. 55. • The sensitivity and specificity of TEE for left atrial thrombi (in patients in whom the left atrium was directly examined at surgery) are 93 to 100 percent and 99 to 100 percent, respectively. • Cardioversion should not be attempted in patients with TEE evidence for atrial thrombi, even if thrombi appear "adherent" to the wall of the appendage. • Such patients are typically given warfarin therapy for at least four weeks before cardioversion as are patients who do not undergo TEE. • Resolution of thrombi occurs in approximately 75 percent of patients with nonrheumatic AF with no formation of new thrombi
  56. 56. Spontaneous echo contrast • Spontaneous echo contrast (SEC or "smoke") refers to the presence of dynamic, smoke-like echoes seen during TEE in the left atrium or atrial appendage . • SEC is thought to reflect increased erythrocyte aggregation caused by low shear rate due to altered atrial flow dynamics and uncoordinated atrial systole
  57. 57. • Erythrocyte aggregation is mediated by plasma proteins, especially fibrinogen, which promotes red cell rouleaux formation by moderating the normal electrostatic forces (due to negatively charged membranes) which keep erythrocytes from aggregating. • SEC is a strong risk factor for and may be the preceding stage to thrombus formation and thromboembolic events
  58. 58. Warfarin, which leads to thrombus resolution and a lower incidence of thromboembolism, does not affect the presence of SEC, since it does not change the underlying hemodynamic abnormality .
  59. 59. Mechanisms of thrombogenesis in atrial fibrillation
  60. 60. • Atrial fibrillation (AF) is associated with substantial mortality and morbidity, largely due to thrombo embolism, particularly stroke.
  61. 61. Risk factors • Pooled data from a meta-analysis have demonstrated that independent clinical risk factors for stroke in nonvalvular AF include a history of hypertension and diabetes . • Patients with heart failure are also at high risk, particularly those with left ventricular systolic dysfunction or aneurysm formation
  62. 62. Question we need to think over !!! Why the great majority of embolic events in patients occur within the first 10 days after cardioversion ??? Why even after the restoration of sinus rhythm ????
  63. 63. How cardioversion causes thromboembolism ?? • Risk  particularly if patients are not anticoagulated before, during, and after cardioversion. • In addition to dislodgement of pre-existing thrombi, embolization may result from de novo thrombus formation induced by impaired left atrial systolic function.
  64. 64. • The transient atrial contractile dysfunction is also known as atrial "stunning," and can occur whether sinus rhythm is restored spontaneously, by external or internal DC (electric) cardioversion, or by drugs.
  65. 65. • Pulsed Doppler studies have shown that the time to recovery of atrial mechanical function is directly related to the duration of AF • In Patients with AF for ≤2 weeks , mechanical recovery within 24 hours • In those with AF for more than six weeks, up to one month
  66. 66. Paroxysmal atrial fibrillation Is the incidence of stroke is higher with paroxysmal AF or Chronic AF ??? Is the risk of stroke is higher with paroxysmal AF or Paroxysmal supra ventricular tachycardia????
  67. 67. • Reports from the Framingham study and Montreal Heart study had suggested thromboembolic rates for paroxysmal AF that were intermediate between those associated with chronic atrial fibrillation and sinus rhythm.
  68. 68. Paroxysmal AF :abnormal haemostasis • Levels of beta-thromboglobulin and platelet factor 4 (markers of platelet activation) were significantly increased during episodes more than 12 hours in duration • There was also a trend toward an elevation in fibrinogen levels in these patients. • Intermediate values of fibrinogen and fibrin Ddimer between sinus rhythm and chronic AF.
  69. 69. Left ventricular dysfunction • Heart failure by itself confers a risk of stroke and thromboembolism • What is the percentage increase in risk of stroke for % decrease in ejection fraction ???
  70. 70. SAVE TRIAL • Every 5 percentage point decrease in left ventricular ejection fraction (LVEF) was associated with an 18 percent increase in the risk of stroke.
  71. 71. LV aneurysm • A left ventricular aneurysm has both diastolic and systolic bulging or dyssynergy which result in severe stasis of blood . • Patients with heart failure and left ventricular aneurysm, also demonstrate abnormalities of blood rheology, coagulation, and endothelial function. • As an example, both plasma fibrinogen and von Willebrand factor concentrations may be elevated in heart failure
  72. 72. paroxysmal supraventricular tachycardia • These patients retain active atrial contraction • Have a low risk of stroke • Had levels of hemostatic markers that were similar to controls in sinus rhythm.
  73. 73. Hypertension • It increases the risk of stroke associated with AF twofold. • Hypertension may be associated with a hypercoagulable state due in part to abnormalities in blood rheology and endothelial function
  74. 74. Valvular disease • Especially mitral stenosis, increases the risk of stroke in atrial fibrillation 17-fold. • some evidence that the presence of mitral regurgitation is protective against embolism. • SPAF trail :Even in the presence of left atrial enlargement, severe mitral regurgitation is associated with a lower incidence of embolism.
  75. 75. FACTORS PROMOTING THROMBOEMBOLISM in AF Almost 150 years ago, Virchow proposed that three conditions should be present for development of thrombosis [1]: • Abnormalities in blood flow • Abnormalities in the blood vessel wall • Interaction with blood constituents • Abnormalities in blood flow and vessels (the first two components of Virchow's triad) can be related to the presence of structural heart disease or extrinsic interventions such as cardioversion.
  76. 76. The third component ! Is AF a hypercoaguable state ???
  77. 77. IN patients with AF , the following observations suggesting hypercoaguable state are made : • Increased plasma concentrations of markers of platelet activation (beta-thromboglobulin and platelet factor 4) • Increased plasma markers of thrombogenesis (thrombin-antithrombin complexes, D-dimers) • Evidence of endothelial damage/dysfunction (elevated plasma and endocardial levels of von Willebrand factor, which is released from damaged endothelium)
  78. 78. Anticoagulation in AF alters the hypercoagulable state as illustrated by the following observations: • Fibrin D-dimer levels are increased in patients with AF. • In one study, fibrin D-dimer levels were highest in patients who were not receiving any antithrombotic therapy, intermediate in those on aspirin, and lowest in those treated with warfarin
  79. 79. In a substudy from the AFASAK trial • 100 patients with chronic AF were randomized to treatment with fixed minidose warfarin 1.25 mg daily alone  combination with aspirin 300 mg/day and conventional warfarin therapy with dose adjusted to maintain an International Normalized Ratio (INR) between 2.0 and 3.0 Aspirin 300 mg daily. • Patients treated with warfarin at any dose demonstrated a significant rise in the INR with a corresponding reduction in prothrombin fragment F1 + 2 [52].
  80. 80. The degree of anticoagulation with warfarin appears to be important! • In one report, ultra low-dose warfarin (1 mg/day) did not significantly alter plasma fibrin D-dimer or betathromboglobulin levels . • A second study found that treatment with aspirin (300 mg daily) plus low-dose warfarin (1 or 2 mg daily) or low-dose warfarin alone (2 mg daily) did not significantly reduce any of the hemostatic markers • In contrast, there was a significant reduction of fibrinogen and fibrin D-dimer with dose-adjusted warfarin .
  81. 81. Is AF a hypercoaguable state ??? yes. Beyond any doubt How and why it is a hypercoaguable state ??
  82. 82. Sluggish, slow flow within the atria Endothelial disturbance in the pulmonary vasculature stimulation of lung macrophages to produce hepatocyte stimulating factor ( IL-6) Increase in hepatic synthesis of fibrinogen, perhaps in a similar manner to smoking. Proposed mechanism of hypercoaguability in AF
  83. 83. SILENT CEREBRAL ISCHEMIA • Silent cerebral ischemia (SCI) is said to occur in a patient who has specific lesions on cerebral magnetic resonance imaging (or other tests) in the absence of clinical complaints or findings. • The prevalence of SCI and its potential relationship to cognitive performance in patients with AF was better studied in a registry that included 90 patients. • Cognitive impairment was significantly greater in persistent and paroxysmal AF patients compared to controls.
  84. 84. Antithrombotic therapy to prevent embolization in atrial fibrillation
  85. 85. Risk Vs benefit ratio • Embolization of atrial thrombi can occur with any form (ie, paroxysmal, persistent, or permanent) of atrial fibrillation (AF). • chronic antithrombotic therapy with either oral anticoagulation (ie, a vitamin K antagonist, direct thrombin inhibitor, or factor Xa inhibitor) or antiplatelet therapy is considered for most of these patients. • As antithrombotic therapy is associated with an increased risk of bleeding, its use must take both benefit and risk into account.
  86. 86. • Historically, the CHADS2 risk score is the most popular and has been best validated in different patient populations • The main advantage of the CHADS2 score compared to other risk models is its simplicity
  87. 87. • Using the CHADS2 or CHA2DS2-VASc (for those with CHADS2 of 0 or 1) score for evaluating risk of stroke and arterial embolization. • Antithrombotic prevention is recommended when the benefits outweigh the risks.
  88. 88. Prevention approach by CHADS2 score
  89. 89. • Warfarin is remarkably effective at reducing stroke risk in patients with AF. • This was clearly demonstrated by a metaanalysis by the AF Investigators of five randomized, controlled clinical trials comparing warfarin versus placebo in patients with AF
  90. 90. Break through RCT’s in AF
  91. 91. Effects of warfarin versus placebo on risk of stroke in six randomized, placebo-controlled clinical trials in nonvalvular AF
  92. 92. Annualized incidence of stroke or intracranial hemorrhage according to the INR. Note that when the INR decreases to <2.0, there is a steep rise in the odds ratio (OR) for stroke; but
  93. 93. Effects of aspirin versus placebo on risk of stroke in five randomized, placebo-controlled trials in nonvalvular AF. AFASAK I (1), The Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulant Therapy Study; CI, confidence interval; EAFT (9), European Atrial Fibrillation Trial; ESPS II (14), European Stroke Prevention Study; LASAF (13), Alternate-Day Dosing of Aspirin in Atrial Fibrillation Pilot Study Group; SPAF I (3), Stroke Prevention in Atrial Fibrillation; UK-TIA (16), United Kingdom Transient Ischaemic Attack Trial.
  94. 94. Effects of aspirin versus warfarin on risk of stroke in five randomized, controlled clinical trials in nonvalvular AF. AFASAK I (1) and AFASAK II (2), The Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulant Therapy Study; EAFT (9), European Atrial Fibrillation Trial; PATAF (15), Primary Prevention of Arterial Thromboembolism in Nonrheumatic Atrial Fibrillation; SPAF II (3), Stroke Prevention in Atrial Fibrillation.
  95. 95. Risk with warfarin • Bleeding risk — The major safety concern with the use of warfarin (and all oral anticoagulants) is the risk of major bleeding. • Major bleeding includes bleeding that requires hospitalization, transfusion, surgery, or involves particularly sensitive anatomic locations. • Intracranial hemorrhage (ICH) is the most serious bleeding complication with warfarin
  96. 96. Other anticoagulants • Overall, the trials, demonstrate equal or superior thromboembolism efficacy and major bleeding safety of these newer anticoagulants compared to warfarin. • Additional advantages of dabigatran, apixaban, rivaroxaban, and edoxaban (compared to warfarin) include no need for international normalized ratio monitoring and less susceptibility to dietary and drug interactions . • Disadvantages include twice-daily dosing (dabigatran, apixaban), higher pharmaceutical cost, lack of an antidote/reversingagent, the potential need for dose adjustment in patients with chronic kidney disease, and lack of long-term safety and “real world” data.
  97. 97. Dual anti platelet therapy • Dual antiplatelet therapy may be a reasonable alternative to therapy with aspirin alone in the occasional high-risk patient with AF who CANNOT be treated with anticoagulation . • It should be kept in mind that as dual antiplatelet therapy and oral anticoagulation have similar bleeding risks, a patient who would not be a candidate for oral anticoagulation because of bleeding risk is also not a candidate for dual antiplatelet therapy.
  98. 98. Management of new onset atrial fibrillation
  99. 99. • There is overlap between “new onset,” “acute,” and “first identified” atrial fibrillation, but each represents a distinct clinical presentation with unique features .
  100. 100. Decisions need to be made soon after a patient presents with new onset AF: • Is cardioversion indicated and if so should it be urgent? • When and how should rate control be carried out? • Who should be anticoagulated immediately and how? • Does the patient need hospitalization? • Are there any correctable causes of atrial fibrillation? • What should be done with the patient who spontaneously converts to sinus rhythm?
  101. 101. Important first steps • A complete history and physical examination should be performed in all patients with new onset AF. • Old records should be searched for evidence of a prior episode of AF or other atrial tachyarrhythmias
  102. 102. Is cardioversion indicated and if so should it be urgent?
  103. 103. Four circumstances for which urgent or emergent cardioversion may be needed: • Active ischemia (symptomatic or electrocardiographic evidence). • Evidence of organ hypoperfusion. • Severe manifestations of heart failure (HF) including pulmonary edema. • The presence of a preexcitation syndrome, which may lead to an extremely rapid ventricular rate due to the presence of an accessory pathway.
  104. 104. • In a patient with any of these indications for urgent cardioversion, the need for restoration of NSR takes precedence over the need for protection from thromboembolic risk.
  105. 105. Are there any correctable causes of atrial fibrillation?
  106. 106. • There should be a quick assessment for an underlying cause, such as heart failure (HF), pulmonary problems, poorly controlled blood pressure, or hyperthyroidism. • Therapy for a precipitating cause should be initiated prior to cardioversion in stable patients and may result in reversion to sinus rhythm.
  107. 107. What are the tests ,in addition to the electrocardiogram, should be performed on patients with new onset AF??
  108. 108. • Vital signs including oxygen saturation (in the ER setting and beyond) • Thyroid stimulating hormone (TSH) and free T4. (since the risk of AF is increased up to threefold in patients with subclinical hyperthyroidism ) • Serum electrolytes and assessment of renal function • Complete blood count • A transthoracic echocardiogram should be performed to screen for cardiac causes of new onset atrial fibrillation, even in the face of a normal physical examination. • Chest x-ray • Evaluation of myocardial infarction with serial troponin measurements, especially in patients with electrocardiogram (ECG) changes, hypotension, symptoms, history, or additional risk factors only .(AF rare manifestation of MI)
  109. 109. Who should be anticoagulated immediately and how?
  110. 110. • If the duration of AF is known to be less than 48 hours, cardioversion can be performed without anticoagulation • For most patients in whom the duration of new onset AF is suspected to be more than 48 hours (or when the duration is unknown), the risk of embolization is measurably increased. • If the time of onset of AF is unclear, for the sake of safety, the AF duration should be assumed to be more than 48 hours.
  111. 111. • Regardless of whether cardioversion is performed pharmacologically or electrically, therapeutic anticoagulation is necessary for 3 weeks or more before, if the AF has been ongoing for more than 48 hours. • These patients should be therapeutically anticoagulated for 4 weeks after cardioversion to prevent thromboembolic complications that may occur because of atrial stunning • When warfarin is chosen as the anticoagulant, the recommended target International Normalized Ratio (INR) is 2.5 (range 2.0 to 3.0)
  112. 112. When and how should rate control be carried out?
  113. 113. • In patients with mild to moderate symptoms, concurrent with the initiation of the appropriate anticoagulation treatment, the initial therapy includes slowing the ventricular rate without an immediate strategy to restore sinus rhythm. • Slowing the ventricular rate often results in significant improvement or even resolution of symptoms. • Attempting to get the rate below 110 beats per minute is reasonable.
  114. 114. • This can be achieved with beta blockers, calcium channel blockers ,verapamil and diltiazem • Occasionally, intravenous (IV) amiodarone may be needed for patients with poor left ventricular function. • The drug selected and the route of administration (oral versus intravenous) are dictated by the clinical presentation
  115. 115. • Beta blockers or verapamil or diltiazem are the preferred drugs in the absence of heart failure. • Intravenous amiodarone may help control rate when the other drugs are ineffective or cannot be given. • Digoxin is the preferred drug only in patients with AF due to HF.
  116. 116. Rate control in pre excitation • Procainamide IV is recommended for rate control and for attempt to cardiovert atrial fibrillation with preexcitation when urgent cardioversion is not available or recommended. • IV amiodarone is an alternative option. • IV AV nodal blockers in particular Beta blockers and CCB’s are contraindicated in AF with preexcitation .
  117. 117. Choice of drug for rate control • The choice between a beta blocker, diltiazem, and verapamil is frequently based upon physician preference and patients status. • Beta blockers are particularly useful when the ventricular response increases to inappropriately high rates during exercise, after an acute MI, and when exercise-induced angina pectoris is also present, especially after cardiac surgery. • a calcium channel blocker is preferred in patients with chronic lung disease • The use of both a beta blocker and calcium channel blocker is reasonable when rate control is not adequate with single therapy
  118. 118. Why it is recommended to control ventricular Rate immediately ???
  119. 119. The prevention of tachycardia-mediated cardiomyopathy is a principle reason for this recommendation.
  120. 120. Why rate control is prefered over rhythm control ???
  121. 121. Patient had rate control , haemodynamically stable , what is the next probable step ???
  122. 122. To decide whether an attempt will be made to cardiovert the patient and if so when. Most patients with symptomatic new onset atrial fibrillation should have at least one attempt at cardioversion (either electrical or chemical) to sinus rhythm, particularly after reversible causes have been identified and corrected. The rationale for cardioversion is that some patients will never have a second episode, or will have very infrequent episodes Cardioversion will likely improve symptom status, particularly in young people.
  123. 123. It is reasonable to not attempt cardioversion in a patient with new onset AF in : • Patients who are completely asymptomatic, particularly those who are very elderly (>80 years) with multiple comorbidities, where risks of undergoing cardioversion and/or pharmacologic rhythm control may outweigh the benefits of restoring sinus rhythm. • A patient with a high CHADS2 score who has a bleeding risk and cannot be anticoagulated during and after cardioversion.
  124. 124. Cardioversion --Electrical or pharmological ?? • The choice of electrical or pharmacologic cardioversion depends upon the comfort of the clinician to use one or the other approach. • Longer durations of the arrhythmia are less likely to respond to antiarrhythmic drug therapy for conversion • For patients with paroxysmal episodes of atrial fibrillation, drug therapy is preferred if they will have sinus rhythm maintained with long-term antiarrhythmic drug therapy • For persistent episodes, electrical cardioversion is preferred.
  125. 125. What should be done with the patient who spontaneously converts to sinus rhythm?
  126. 126. • New onset AF often spontaneously reverts to normal sinus rhythm, with the incidence of reversion related to the duration of the arrhythmia. • This was illustrated in a study of 1822 patients admitted to the hospital because of AF. • Two-thirds of those with spontaneous reversion had AF duration of less than 24 hours, which was the only predictor of spontaneous reversion • Choice of anticoagulation depending on CHADS2 score.
  127. 127. INDICATIONS for RHYTHM CONTROL There are three settings in which a rhythm control strategy for the maintenance of sinus rhythm should be considered • Persistent symptoms (palpitations, dyspnea, lightheadedness, angina, syncope, and heart failure) despite adequate rate control • An inability to attain adequate rate control (to prevent tachycardiamediated cardiomyopathy). • Patient preference. Some patients will strongly prefer to avoid either paroxysmal or persistent AF.
  128. 128. Paroxysmal AF
  129. 129. Survival in paroxysmal AF • Whether patients with paroxysmal AF have worse survival than the general population has been studied from the Stockholm cohort study of atrial fibrillation (SCAF) were followed for a mean of 4.6 years. • The standardized mortality ratio was significantly increased at 1.6 percent . • This excess mortality was principally from cardiovascular causes. • Patients treated with warfarin appeared to do better than those not treated.
  130. 130. MANAGEMENT OF THE ARRHYTHMIA • Acute therapy : same as in new onset AF • Prevention of recurrence : Catheter-based pulmonary vein isolation (PVI) is generally viewed as being more effective than antiarrhythmic medications. Surgical-based techniques such as the MAZE procedure are still being used and are often performed in conjunction with other cardiac surgical procedures.
  131. 131. Non pharmacological methods to prevent recurrent AF • . The two most common nonpharmacologic approaches are: • Radiofrequency catheter ablation (RFA) • surgery
  132. 132. Surgery and RAF are directed at • Elimination of the triggers of AF – Triggers are usually eliminated by disrupting the conduction of electrical activity between the tissues that contain these arrhythmogenic triggers . • Most commonly the ostial portion of the pulmonary veins, and the atrial myocardium. • Less commonly, triggers within the atrial myocardium can be directly ablated. • Modifying the atrial substrate(s) responsible for the maintenance of AF.
  133. 133. Recommendations for the use of radiofrequency catheter ablation (RFA) • The American College of Cardiology Foundation /American Heart Association /Heart Rhythm Society guidelines on the management of patients with atrial fibrillation (AF): • •A strong recommendation for RFA for patients with symptomatic, paroxysmal atrial fibrillation (AF) who have failed treatment with an antiarrhythmic drug. • •A weak recommendation for RFA for patients with symptomatic, persistent AF. • •A very weak recommendation was made for RFA for patients with symptomatic paroxysmal AF in patients with significant left atrial dilatation or with significant left ventricular dysfunction.
  134. 134. RFA • PULMONARY VEIN ISOLATION PROCEDURE • The pulmonary veins are the most common source for the initiation of AF • The LAA was the only source of the arrhythmia in about one third. • The two principal techniques are : • segmental ostial (PV) ablation • Circumferential ablation of left atrial tissue.
  135. 135. The three principal goals of surgical strategies • Interrupting the electrophysiologic substrate propagating the arrhythmia in both the right and left atria. • Reestablishment or maintenance of atrioventricular synchrony. • Restoration and preservation of atrial mechanical function in order to improve diastolic filling.
  136. 136. MAZE OPERATION • Developed in the 1990s • Aims to surgically create a “maze” of functional myocardium within the atrium • This allows for propagation of atrial depolarization while reducing the likelihood of microreentry
  137. 137. • The procedure has evolved over the last 20 years. • Originally involved several small incisions around the sino-atrial (SA) node as well as one to the atrial-superior vena caval junction (Maze I) • unintentionally resulted in chronotropic incompetence resulted in the Maze II procedure
  138. 138. • The final version (Maze III) reduced the frequency of chronotropic incompetence, improved atrial transport function, and shortened procedure times. • The maze procedure meets the three criteria for an ideal treatment of atrial fibrillation (AF)
  139. 139. Other surgical approaches • Radial approach • Pulmonary vein isolation • CORRIDOR OPERATION
  140. 140. Thank you !