TABLE 1 Clinical Classification of AF. New onset AF (first detected) Paroxysmal (<7 days, mostly < 24 hours)

Transcription

1 Clinical Practice Guidelines for the Management of Patients With Atrial Fibrillation Deborah Ritchie RN, MN, Robert S Sheldon MD, PhD Cardiovascular Research Group, University of Calgary, Alberta Partly supported by grants from the Canadian Institutes of Health Research, Ottawa, Canada to Dr RS Sheldon. Introduction Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia seen in clinical practice. Its incidence increases with age and the presence of structural heart disease. For patients over the age of 65, the prevalence of AF is 6%. The causes of AF are diverse with hypertension being the most common. Significant mortality, morbidity and cost arise from the thromboembolic and hemodynamic consequences of AF. It is a major cause of stroke, particularly in the elderly. The American College of Cardiology (ACC), the American Heart Association (AHA) and the European Society of Cardiology (ESC) created a committee of experts to establish guidelines for the management of this arrhythmia. The reader is referred to the full text guidelines available on the ACC ( AHA ( ESC ( and NASPE ( web sites and published in the European Heart Journal in October 2001 for a complete description of the rationale and evidence supporting these recommendations. Definition AF is a supraventricular arrhythmia characterized by uncoordinated atrial activation with deterioration of atrial mechanical function. On the electrocardiogram (ECG), regular p waves are replaced by rapid fibrillatory waves varying in size, shape and timing and are associated with an irregular, often rapid ventricular response. The ventricular response depends on the electrophysiological characteristics of the AV node, vagal and sympathetic tone, and drug actions. Figure 1 Regular RR intervals are sometimes seen in the presence of AV block or interference by ventricular or junctional tachycardia. When a rapid, irregular, sustained, wide QRS complex tachycardia is seen, it suggests AF with underlying bundle branch block or AF with conduction via an accessory pathway. Classification of AF The Guidelines recommend a new classification scheme for AF (Table 1) that is simpler

2 and more clinically relevant. The pattern in a particular patient usually cannot be determined until AF recurs. Paroxysmal and persistent AF may be recurrent and may progress to permanent AF over time. TABLE 1 Clinical Classification of AF New onset AF (first detected) Paroxysmal (<7 days, mostly < 24 hours) Persistent (> 7 days) Permanent (cardioversion failed or not attempted) Causes of Atrial Fibrillation The autonomic nervous system can trigger AF through heightened vagal or adrenergic tone. AF may also occur secondary to a precipitating event (Table 2). In these cases, management of the arrhythmia along with treatment of the underlying disorder usually eliminates the AF. Acute MI Cardiac surgery Hyperthyroidism TABLE 2 Reversible Causes of AF Pulmonary disease/ pulmonary embolism Acute alcohol intoxication Non-cardiac surgery Diagnostic tests Myocarditis Electrocution Epidemiology and Prognosis Atrial fibrillation is the most common rhythm disturbance seen in clinical practice and accounts for close to one third of hospitalizations for cardiac arrhythmias. This is expected to increase as the Canadian population ages. The median age of patients with atrial fibrillation is about 75 years. The overall number of men and women with AF is about equal, but approximately 60% of AF patients over age 75 are female. Patients may be reassured that AF is not life threatening but may pose an increased risk of stroke (Table 3). The rate of ischemic stroke among those with nonrheumatic AF averages about 5% per year, which is 2 to 7 times the rate for people without AF. One of every six strokes occurs in patients with AF. Atrial fibrillation doubled the risk of

3 stroke in the Manitoba Follow Up Study independently of other risk factors. The total mortality rate is close to double in patients with AF compared with patients in normal sinus rhythm and is linked with the severity of underlying heart disease. TABLE 3 Risk Factors For Stroke Previous stroke or TIA History of hypertension Congestive heart failure Advancing age Diabetes mellitus Coronary artery disease Fuster V, Ryden LE, Asinger RW, Cannom DS, Crijns HJ, Frye RL, Halperin JL, Kay GN, Klein WW, Levy S, McNamara RL, Prystowsky EN, Wann LS, Wyse DG. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2001;38:1266i-lxx. Antithrombotic Therapy Although the pathophysiology of thromboembolism in patients with AF is unclear, its prevention is essential. A number of randomized clinical trials of antithrombotic therapy in AF have addressed the use of long-term anticoagulation in reversing the increased risk of stroke. From these trials, it is evident that oral anticoagulation, particularly with warfarin, dramatically reduces the risk of stroke in AF (Table 4). Currently, it is felt that ASA may be prescribed in patients with AF who are less than 60 years and have no other risk factors for stroke. Despite its efficacy, warfarin is often an unattractive therapy for doctors and patients. Patients who are feeling well are reluctant to pursue a lifelong regimen of a risky therapy that requires frequent blood tests and ongoing concern about drug and diet interactions. The anticoagulation of patients in AF undergoing chemical or electrical cardioversion is another issue. Patients must be anticoagulated (INR 2-3) for at least 3-4 weeks if the AF has lasted more than 48 hours or is of unknown duration. Following successful cardioversion, patients should remain anticoagulated for an additional 3-4 months and then be reassessed, based on risk factors for stroke. Immediate cardioversion without anticoagulation may be performed in patients with acute (recent onset) AF accompanied by hemodynamic instability resulting in angina, MI, shock or pulmonary edema. Many patients with CAD and bypass surgery are prescribed ASA for maintaining vessel patency. These patients may also take warfarin for AF, if necessary. TABLE 4 Recommendations For Antithrombotic Therapy in Patients With AF Patient Features Antithrombotic Therapy

4 <60 yrs, no heart disease ASA 325 mg OD or no therapy < 60 yrs, heart disease but no stroke risk factors > 60 yrs with no stroke risk factors ASA 325 mg OD ASA 325 mg OD > 60 yrs with diabetes or CAD Oral anticoagulation (INR 2-3) > 75 yrs, especially women Oral anticoagulation (INR 2-3) Heart failure, EF = 35%, thyrotoxicosis hypertension Rheumatic mitral stenosis, prosthetic Oral anticoagulation (INR 2-3) Oral anticoagulation (INR or heart valves, prior thromboembolism, higher) persistent atrial thrombus on TEE Fuster V, Ryden LE, Sanger RW, Cannom DS, Crijns HJ, Frye RL, Halperin JL, Kay GN, Klein WW, Levy S, McNamara RL, Prystowsky EN, Wann LS, Wyse DG. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2001;38:1266i-lxx. Pathophysiology of AF Atrial factors The atria of patients with AF have structural abnormalities in addition to those caused by heart disease. Fibrosis or fatty infiltration of the atrial fibers and of the sinus node likely affects atrial refractoriness. Inflammation may play a role in the pathogenesis of AF. Atrial fiber hypertrophy and progressive atrial dilatation are seen echocardiographically and can be either a cause or a consequence of persistent AF. It is postulated that 2 processes drive AF: enhanced automaticity in 1 or several foci, and reentry involving one or more circuits. Rapidly firing atrial foci, found in one or more of the superior pulmonary veins initiates AF in most people. Foci can also occur in the right atrium, the superior vena cava, and the coronary sinus. AV node factors The AV node ordinarily limits conduction during AF. Patients with Wolff-Parkinson-White syndrome accessory pathways between the atrium and the ventricle have the ability to conduct rapidly. If this occurs during AF, a very rapid ventricular response may occur that can be fatal. Myocardial and hemodynamic consequences of AF Hemodynamic function is affected by 3 factors during AF: loss of synchronous atrial mechanical activity, irregularity of ventricular response, and inappropriately rapid heart rate. A decrease in cardiac output can occur with the loss of atrial contraction, especially in patients with impaired diastolic ventricular filling, congestive heart failure, hypertension, or mitral stenosis. A persistently rapid atrial rate can adversely affect atrial mechanical function leading to tachycardia-induced atrial cardiomyopathy. Similarly, a persistently elevated ventricular rate during AF can produce a dilated cardiomyopathy. Clinical Evaluation

5 AF can be symptomatic or asymptomatic, even in the same patient. Common symptoms include palpitations, awareness of the heart beat, chest heaviness or discomfort, lightheadedness, sweatiness, fatigue, reduced exercise capacity, shortness of breath and feeling generally unwell or anxious. Syncope is uncommon but may occur in patients with sinus node dysfunction, aortic stenosis or other conditions. The treatment chosen hinges on the information obtained from the patient history, physical exam and investigation results. The minimum evaluation of the patient with atrial fibrillation includes a history and physical examination. The history should include questioning to determine the symptoms, if any, associated with AF; the clinical type of AF (new onset, paroxysmal, persistent or permanent); the onset of the episode or the date the AF is discovered; the frequency, duration, precipitating factors and modes of termination of AF (if any); response to any drugs given and the presence of heart disease or reversible conditions. Investigations include an ECG to identify the rhythm, left ventricular hypertrophy, P wave morphology, preexcitation, bundle branch block and prior MI. A chest Xray should be done if the clinical exam suggests a pulmonary abnormality. An echocardiogram will determine the presence of valvular heart disease, atrial size, left ventricular (LV) size and function, LV hypertrophy and LA thrombus. Blood tests should be done for thyroid function, particularly for a first episode of AF. Additional testing may be needed. Exercise testing is completed to try to reproduce exercise induced AF, to determine the adequacy of rate control or to exclude ischemia prior to selecting a Class 1C antiarrhythmic drug. Holter monitoring may be carried out if the diagnosis is in question or to evaluate rate control. Transesophageal echocardiography (TEE) is completed to determine the presence of LA thrombus and to guide cardioversion. An electrophysiology study may be necessary to identify the mechanism of a wide complex tachycardia, to identify another atrial arrhythmia or as part of a curative radiofrequency ablation. Pharmacological Management Whether AF is paroxysmal or persistent, AF is a chronic disorder and recurrence is likely with most patients. In persistent AF, the 4 year arrhythmia-free survival was less than 10% after electrical cardioversion without antiarrhythmic drug therapy. However, the recurrence of AF is not equivalent to treatment failure. A reduction of the arrhythmia burden may be considered a partial success by some patients, but in others, any recurrence may be intolerable. The major issues in the management of patients with AF are the prevention of thromboembolism, the reduction of symptoms and the prevention of tachycardiainduced cardiomyopathy. The Guidelines outline the pharmacological management algorithms for each possible presentation of AF: new onset, recurrent paroxysmal AF, and recurrent persistent or permanent AF. New onset or first detected episode of AF It is not always known if the initial presentation of AF is actually the patient's first episode, particularly in patients with minimal or no symptoms. Therefore, both are considered together. Paroxysmal AF In patients with paroxysmal AF, antiarrhythmic drugs to prevent recurrences are usually

6 unnecessary unless the AF is associated with severe symptoms. The decision for short or long-term anticoagulation should be based on the individual patient. Persistent AF In persistent AF, there are two ways to manage the arrhythmia: to restore and maintain sinus rhythm or to control the ventricular rate leaving the patient in AF. The potential toxicity of antiarrhythmic drug therapy must be weighed against the benefit of restoration of sinus rhythm. If the decision is made to attempt to restore and maintain sinus rhythm, anticoagulation and rate control must be considered prior to cardioversion. Rate control may be assessed by the Six Minute Walk Test, Exercise Treadmill Test, or by Holter Monitor, if the patient is unable to walk adequately. Generally, heart rate control is defined as = 80 beats per minute at rest in AF and = 110 beats per minute (in AF) during a Six Minute Walk Test. Recurrent Paroxysmal AF If the episodes are brief and minimally symptomatic, it is reasonable to avoid antiarrhythmic drugs. Rate control and anticoagulation are appropriate. The initial selection of an antiarrhythmic drug is based on patient safety. For patients with no or minimal structural heart disease, flecainide, propafenone and sotalol are recommended. If one or other of these drugs is ineffective or associated with side effects, other choices include amiodarone, disopyramide, procainamide and quinidine, all of which have a greater potential for adverse reactions. A non-pharmacological approach is appropriate for some patients and may be considered prior to the initiation of amiodarone. TABLE 5 Rate Control Drugs Digoxin Diltiazem Beta blocker Verapamil Combination of above drugs Rhythm Control Drugs Propafenone Quinidine Procainamide Dofetilide Flecainide Sotalol Disopyramide Amiodarone For patients with heart failure, safety data support the use of amiodarone or dofetilide to maintain sinus rhythm. Patients with ischemic heart disease often require beta-blocker therapy. Sotalol is considered first with these patients, unless the patient has heart failure, followed by amiodarone and dofetilide. Dofetilide is not generally available in Canada. Hypokalemia should be avoided in all patients taking an antiarrhythmic drug. In patients with hypertension without LVH, flecainide and propafenone are

7 recommended first. If these are ineffective or cause side effects, then amiodarone, dofetilide and sotalol are reasonable second choices. Amiodarone is suggested as first line therapy in patients with LVH. TABLE 6 Antiarrhythmic Drug Contraindications Coronary artery disease Elderly women CHF Lung disease Disopyramide, procainamide, quinidine (Ia) Flecainide, propafenone (Ic) Sotalol Sotalol Amiodarone Recurrent Persistent AF Patients with few symptoms, who have had at least one attempt to restore sinus rhythm, can remain in AF with appropriate therapy for rate control and prevention of thromboembolism. Patients with troubling AF symptoms should be treated with an antiarrhythmic drug, before cardioversion. The antiarrhythmic drug selection should be based on the same algorithm for patients with recurrent paroxysmal AF. Permanent AF This term applies to patients in whom sinus rhythm cannot be maintained after cardioversion of AF or when the patient and physician decide to allow AF to continue without further attempts to restore sinus rhythm. Control of ventricular rate and anticoagulation is necessary for all these patients. The recent (March 2002) summary of results of the AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management) Trial, indicated that the management of AF with rhythm control offered no advantage over rate control for patients with AF at high risk for stroke who require long-term therapy, predominantly drug therapy. Given these findings, rate control should be given more consideration as primary therapy. The rate control strategy is often simpler, may be less costly due to a reduction in hospitalizations, and may offer a survival benefit after one year. Continuous anticoagulation seems to be warranted in all patients with AF and risk factors for stroke, regardless of treatment. Summary The assessment and treatment of AF is complex, however, this article has provided the tools to assist you in the management of your atrial fibrillation patients. The following are guidelines to evaluation of AF patients: Try to determine if the AF is new or old, paroxysmal, persistent or permanent. If the AF is relatively new, is there a precipitating factor? Is the AF causing some clinical deterioration in your patient or is the AF due to a condition causing clinical deterioration? Is the patient anticoagulated and if so, is the INR therapeutic? Once you have assembled the above information along with a rhythm strip or 12 lead

8 ECG, you have to decide who to notify and how urgently. Follow your Cardiac Rehabilitation Program's protocol for notification of adverse patient events. Your patient may need to be treated immediately or may be able to wait to see a physician. Find out which strategy has been selected for patient treatment, rate or rhythm control, and be familiar with any medications prescribed so that you may counsel your patient.

9 Copyright 2002 Canadian Association of Cardiac Rehabilitation. All rights reserved The materials contained in the publication are the views/findings of the author(s) and do not represent the views/findings of CACR. The information is of a general nature and should not be used for any purpose other than to provide readers with current knowledge in the area. For more information please contact: Executive Director CACR 1390 Taylor Avenue Winnipeg, MB R3M 3V8 Canada