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Cardiac Arrhythmia: Current Therapy MICHAEL R. GOLD and MARK E. JOSEPHSON University of Maryland and Harvard University |
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Rhythm disturbances can range from the harmless to the life-threatening, and treatment varies accordingly, from watchful waiting to emergency intervention. Traditional antiarrhythmic medications have largely been supplanted by newer agents; pharmacologic therapy is giving way to device-based treatment, including pacemakers, defibrillators, and catheter ablation.
Dr. Gold is Director, Cardiac Electrophysiology Service, and Associate Professor of Medicine, University of Maryland School of Medicine, Baltimore. Dr. Josephson is Professor of Medicine, Harvard Medical School, and Director, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Boston.
During the past few years, the treatment of many cardiac arrhythmias has tended to move away from drug therapy and toward device-based therapy. The latter may involve pacemakers, implantable defibrillators, or catheter ablation, depending on the type of arrhythmia. When drug therapy is the preferred route, the agents used are different from those selected several years ago. The treatment changes affect the management of the most common arrhythmias seen in primary care practice, including atrial fibrillation, atrial flutter, supraventricular tachycardia, and ventricular arrhythmia.
Atrial FibrillationThe prevalence of atrial fibrillation increases with age; this arrhythmia is most often seen in patients older than 65 years. Atrial fibrillation is typically associated with some form of cardiovascular disease, such as hypertension, coronary artery disease, or valvular heart disease, but it can also occur secondary to metabolic disorders such as thyrotoxicosis. In a minority of young patients, there is no obvious cause, a condition known as lone atrial fibrillation. Anticoagulation. Since disruption of normal atrial blood flow with stasis can promote thrombus formation, leading to stroke or peripheral embolization, first-line therapy for patients with atrial fibrillation is anticoagulation. The drug of choice is warfarin, typically in conjunction with heparin until warfarin reaches therapeutic levels. Multiple studies have demonstrated that anticoagulation with warfarin prevents strokes much better than with any other therapy, including aspirin. The value of long-term anticoagulation has been questioned only in the small group of patients with lone atrial fibrillation, who have a low risk of stroke. It is clear that even elderly patients with paroxysmal atrial fibrillation--in whom atrial fibrillation occurs for relatively short periods followed by a spontaneous return to sinus rhythm--have a high risk of stroke and should receive more than merely acute anticoagulation therapy. The recommended duration of anticoagulation therapy is longer now than in the past. Previously, the rule was to anticoagulate for four weeks or so after cardioversion had restored sinus rhythm. It is now clear that many patients will revert to atrial fibrillation after that time and may present with a stroke if anticoagulation has been discontinued. Consequently, many physicians will continue anticoagulation indefinitely in patients at risk for atrial fibrillation. The consensus is to maintain anticoagulation until the patient has had at least six months of documented sinus rhythm. Even when the episode of atrial fibrillation is the patient's first and sinus rhythm is readily restored, long-term anticoagulation is recommended in those with risk factors for atrial fibrillation (e.g.,older than 65 years with hypertension or coronary artery disease). It is especially important to maintain anticoagulation in patients who are asymptomatic during episodes of atrial fibrillation since they may not seek medical attention. This new approach to anticoagulation therapy has, admittedly, been shaped more by experience than by data from controlled clinical trials. Rate Control. In addition to anticoagulation, the acute management of atrial fibrillation includes rate control. This can be achieved with beta-blockers, calcium channel blockers, or digoxin. Traditionally, digoxin has been the first-line drug, but studies have shown it to be less effective over a 24-hour period than are drugs from the other two classes. While digoxin may be effective for controlling ventricular response when patients are at rest, it is relatively ineffective during activity or exercise. Because calcium channel blockers and beta-blockers are about equally effective treatments for rate control, the choice between them often depends on other factors, such as side effects and concomitant clinical conditions. In patients with asthma or another contraindication to beta-blockade, we administer a calcium channel blocker. In those who have had a myocardial infarction, a beta-blocker would be the drug of choice, especially when the patient has left ventricular dysfunction. Even if conversion to sinus rhythm is successful and fibrillation does not recur, we usually keep patients on a rate-control drug indefinitely. Beta-blockers are the preferred agents because they may help to prevent the recurrence of atrial fibrillation and also reduce the ventricular rate and symptoms if fibrillation does recur. The only patients who do not require long-term drug therapy for rate control are those in whom atrial fibrillation develops after cardiac surgery. Their risk is limited to the first couple of weeks postoperatively. After that, they require no further treatment, provided that sinus rhythm has been restored. Acute Rhythm Control. When patients present with persistent atrial fibrillation (>48 hours in duration), we attempt to restore sinus rhythm with an antiarrhythmic drug or electrical cardioversion. Before proceeding with either of those, however, it is necessary to minimize the risk of embolism that may be caused by terminating atrial fibrillation. One way to do that is to provide adequate anticoagulation therapy for at least three weeks--adequate is defined as a warfarin dosage sufficient to produce a prothrombin time with an international normalized ratio (INR) of greater than 2.0. If it is important to restore sinus rhythm sooner or anticoagulation therapy is contraindicated, a transesophageal echocardiogram can be performed to look for evidence of thrombus in the left atrial appendage. If anticoagulation is adequate or there is no evidence of thrombus, pharmacologic or electrical cardioversion can be performed safely (i.e., with extremely low risk). It should be noted that even if a transesophageal echocardiogram shows no thrombus in the left atrial appendage, the patient should receive heparin anticoagulation at the time of cardioversion because the procedure leads to atrial dysfunction and potential clot formation. In addition, oral anticoagulation with warfarin should be initiated after cardioversion when feasible. Acutely, a number of intravenous drugs can be used to terminate atrial fibrillation. Amiodarone or procainamide have been the traditional choices. A newer drug, ibutilide, a type III antiarrhythmic that is available only in intravenous form, has been effective in terminating new-onset atrial fibrillation (and even more effective in terminating atrial flutter). However, the efficacy rates are still only about 30% for atrial fibrillation and 50% for atrial flutter. Several factors determine the choice between pharmacologic and electrical cardioversion. If the patient already has been hospitalized, we often treat with an antiarrhythmic drug. We also tend to use pharmacologic cardioversion in patients who probably will require chronic treatment with an antiarrhythmic agent. In general, however, we favor electrical cardioversion, since it is a simple outpatient procedure and faster and more effective than pharmacologic cardioversion. Chronic Rhythm Control. Once sinus rhythm has been restored, physicians must decide whether to attempt to maintain sinus rhythm with antiarrhythmic drug therapy. The use of antiarrhythmic drugs for atrial fibrillation has fallen somewhat out of favor recently because of consistently disappointing study results and a high incidence of adverse effects. Regardless of the drug selected, at least 50% of patients revert to atrial fibrillation within about six months. The National Institutes of Health is conducting the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) trial, comparing rate control to rhythm control in more than 4,000 patients with atrial fibrillation. The goal of the AFFIRM trial is to determine whether maintaining sinus rhythm with antiarrhythmic drugs improves survival and quality of life. Results of the trial will not be available for several years. In the meantime, it is our practice to attempt to restore and maintain sinus rhythm in nearly every patient with atrial fibrillation. Patients first are cardioverted. If atrial fibrillation recurs, subsequent therapy depends on the patient's status. We aggressively treat with antiarrhythmic drugs if the patient has symptoms or if we believe that the arrhythmia may be deleterious over the long term, either because the patient is not a good candidate for prolonged anticoagulation (e.g., a history of peptic ulcer disease) or has active angina or congestive heart failure. Occasionally, we will leave patients in atrial fibrillation, provided that they are asymptomatic, demonstrate good rate control, and have no complicating cardiac disorders. At present, the most successful drugs for maintaining sinus rhythm appear to be the type III antiarrhythmics, particularly amiodarone and sotalol. Despite amiodarone's potential for toxicity, we have found that if patients are monitored closely and the drug is used in low doses, treatment is safe and effective. Among cardiologists, and certainly amongelectrophysiologists, amiodaroneis rapidly becoming the most frequently used antiarrhythmic agent. Traditionally, type IA antiarrhythmic drugs were employed for preventing atrial fibrillation. However, quinidine, the one most commonly used, has a high risk for provoking ventricular arrhythmia and is less efficacious than the type III drugs. In patients who do not have coronary artery disease, type IC drugs flecainide and propafenone can be useful to prevent atrial fibrillation. It is mandatory to use rate control drugs in conjunction with these agents because type IC drugs can convert atrial fibrillation to atrial flutter with a very rapid ventricular response. AV Node Ablation and Pacemakers. A small subset of patients with chronic or paroxysmal atrial fibrillation have poorly controlled rates, despite treatment with multiple rate-slowing drugs. In these cases, we often recommend ablation of the AV node (thereby severing the connection between the atria and ventricles) and implantation of a permanent pacemaker. Although it is generally considered a therapy of last resort, AV node ablation effectively reduces symptoms, improves cardiac function, and improves quality of life. It is an especially useful technique in patients with obstructive lung disease or severe congestive heart failure and in them, it should be considered earlier than usual. In addition, in some patients, AV node ablation is preferred to chronic multiple-drug therapy. Patients with atrial fibrillation and sick sinus syndrome, who tend to have bradycardia or long pauses while in sinus rhythm, usually need a pacemaker to help prevent bradyarrhythmia. A dual chamber pacemaker alone can sometimes prevent atrial fibrillation; in other cases it must be combined with antiarrhythmic drugs.
Atrial FlutterAtrial flutter occurs in the same patient population as does atrial fibrillation. Atrial flutter is a much more regular, organized rhythm than is atrial fibrillation. The flutter typically produces an atrial rate of 300 bpm and has a sawtooth ECG pattern, seen best in lead II (Figure 1). There are also atypical forms of atrial flutter that have different ECG morphologies. |
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Although ibutilide, as mentioned, can effectively terminate atrial flutter, preventing recurrences with medical treatment can be frustrating. However, atrial flutter readily responds to radiofrequency catheter ablation. A series of ablation lines is created within the right atrium to interrupt the circuit that sustains flutter. Patients generally do very well after ablation. The complication rate is low and the initial success rate is almost 100%. Unfortunately, the recurrence rate is about 20%, higher than with other supraventricular tachycardias. Nevertheless, given the limited efficacy of antiarrhythmic drugs, we have begun to recommend catheter ablation earlier in the course of typical atrial flutter. Newer methods to validate the formation of critically placed lesions will reduce recurrence rates. A small subgroup of patients with atrial fibrillation experience conversion to atrial flutter after treatment with antiarrhythmic agents. They can be given combination therapy with ablation and an antiarrhythmic drug. Ablation eliminates flutter and the drug prevents fibrillation.
Supraventricular TachycardiaSupraventricular tachycardia (SVT) comprises a group of arrhythmias in which the atria or AV node is a critical part of the circuit. SVT is typically a rapid, regular rhythm with QRS complexes identical to those of sinus rhythm. The two most common forms are AV-node reentrant tachycardia and AV reciprocating tachycardia. AV reentrant tachycardia results from reentry through two functionally distinct pathways within the AV node, while AV reciprocating tachycardia involves a bypass tract or accessory pathway. Accessory pathways from the atria to the ventricles that bypass the AV node cause Wolff-Parkinson-White (WPW) syndrome. Affected patients will show evidence of preexcitation on the ECG (i.e., delta-waves and a short PR interval), although in some cases the accessory pathway is concealed and conducts impulses retrograde from the ventricle to the atrium. In this latter situation, patients may still have SVT, but the ECG will be normal and not show preexcitation. The position of the P wave is a useful tool to help differentiate SVT mechanisms. A P wave that occurs during the QRS complex (which will not be discernible or will be visible only as a slight deformity at the terminal part of the QRS complex) suggests AV-node reentrant tachycardia (Figure 2). P waves within the ST segment point to a bypass tract. P waves that come after the T wave and precede the next QRS suggest atrial tachycardia, although some forms of AV-nodal and bypass-tract tachycardia can also present this way. Although these guidelines are useful, electrophysiologic testing is needed for definitive diagnosis. |
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SVTs tend not to be dangerous arrhythmias, but they can cause distressing symptoms. For acute management, patients should be taught maneuvers to terminate the arrhythmia. The Valsalva maneuver or carotid massage is often successful. In patients who present to the emergency department because they cannot terminate their arrhythmias, treatment with intravenous adenosine usually is effective within seconds. Asymptomatic patients whose ECG shows a WPW pattern do not need treatment. Patients with recurrent symptomatic episodes of SVT can be treated with drugs that inhibit conduction through the AV node--calcium channel blockers and beta-blockers. Catheter ablation is a very effective treatment in those who continue to have symptomatic episodes despite drug therapy. Ablation is now an outpatient procedure that can cure standard SVT in about 95% of patients. The complication rate is low and patients are spared repeated emergency department visits. In patients with WPW and ventricular preexcitation, we tend to perform catheter ablation earlier, because there is a small risk that dangerous, rapid arrhythmias can be transmitted through the bypass tract. In patients who do not want to undergo ablation, the class IC drugs flecainide and propafenone are probably the best choices for preventing the arrhythmia.
SyncopeSyncope can result from a variety of causes. Some are relatively harmless; however, syncope can also signal the presence of significant cardiac disease and be a harbinger of more serious events. Vasovagal Syncope. The most common cause of syncope is neurocardiogenic syncope, the fainting spell that may occur when a person is having blood drawn or receives bad news. In some patients, the vasovagal reflex that causes this form of syncope is more developed than usual. Episodes most often occur when patients are exposed to hot weather or when they become dehydrated, and almost always while they are standing. The usual warning signs are diaphoresis and nausea. Falls resulting from loss of consciousness rarely result in serious injury. In patients suspected of having neurocardiogenic syncope, symptoms can be elicited with tilt-table testing, which is routinely available in electrophysiology laboratories. Most affected patients require no treatment other than reassurance and maintenance of good hydration. Many patients are young and healthy; however, they may be on a low-salt diet (despite the absence of hypertension), or they may not be eating regularly because of hectic schedules. Simply advising them to increase their dietary salt intake and to maintain good hydration will usually suffice. If not, the drugs traditionally used to treat this condition have been volume expanders and beta-blockers. In extreme cases, pacemakers may be useful to help prevent episodes, but this is very rarely needed in young, healthy patients. Cardiac Syncope. More worrisome is the patient who has syncope and underlying heart disease, particularly left ventricular dysfunction. Unlike vasovagal syncope, episodes of syncope caused by arrhythmia tend to feature sudden loss of consciousness without warning. Cardiac syncope can result from bradycardia (including intermittent complete heart block and sinus node dysfunction) or tachycardia. The ECG often shows significant conduction abnormalities, particularly bundle branch block. In patients with left ventricular dysfunction, particularly those with previous myocardial infarctions, ventricular tachycardia is thought to be a leading cause of syncope. Patients who experience syncope without warning and have either bundle branch block or known or suspected left ventricular dysfunction need to be admitted immediately for evaluation. Depending on the presentation, the evaluation may include an echocardiogram to rule out severe aortic stenosis and hypertrophic cardiomyopathy as well as to evaluate left ventricular function. An electrophysiology study is often indicated to assess cardiac conduction or the inducibility of ventricular arrhythmia. Carotid massage is also a routine part of the evaluation. Carotid hypersensitivity is common cause of syncope, particularly in patients older than 70 years. In this group, massaging the carotid can cause long periods of asystole and reproduce the symptoms. Massage is done after ruling out carotid bruits and is performed on both sides sequentially. Treatment for most arrhythmic causes of syncope is now nonpharmacologic. Patients with bradycardia, whether from carotid hypersensitivity, sinus node dysfunction, or intermittent heart block, receive permanent pacemakers. Patients with left ventricular dysfunction and sustained ventricular arrhythmias receive implantable defibrillators. The technology of implantable defibrillators has changed dramatically since the first model was approved by the Food and Drug Administration in 1985. In the early days, implantation required opening the chest cavity and placing patches on the heart; patients were hospitalized for seven to 10 days. Today, implantation is similar to pacemaker placement. The defibrillator is placed subcutaneously below the clavicle and a single transvenous lead is threaded into the heart. The procedure takes about an hour, and in selected cases can be performed on an outpatient basis.
Ventricular ArrhythmiaVentricular arrhythmias are a leading cause of sudden death in the United States. An estimated 350,000 persons die from cardiac arrest each year, and most of these deaths involve ventricular tachycardia or fibrillation. Until recently, diagnosis and treatment of ventricular arrhythmia was limited to patients in whom the condition was suspected or known--those who survived a cardiac arrest, presented in sustained ventricular tachycardia, or had documented syncope with structural heart disease or left ventricular dysfunction (Figure 3). |
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In patients with a cardiac arrest or sustained ventricular tachycardia of irreversible cause (i.e., acute myocardial infarction or severe electrolyte abnormalities), the treatment of choice is an implantable defibrillator. The largest study evaluating this group of patients was the Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial, which compared defibrillation with drug therapy (amiodarone or sotalol). Mortality was reduced in patients who received early defibrillator implantation. The defibrillator is also recommended as first-line therapy in patients with syncope, left ventricular dysfunction, and inducible sustained ventricular tachycardia on electrophysiologic testing. One of the major goals in the prevention of sudden death is to identify patients with a high risk before sustained ventricular arrhythmia occurs. Studies have demonstrated that in the subset of patients who have had a myocardial infarction and have reduced left ventricular ejection fraction and evidence of high-grade ventricular arrhythmia (particularly spontaneous, nonsustained ventricular tachycardia), electrophysiologic testing can identify those who will benefit from prophylactic defibrillator implantation. The Multicenter Unsustained Tachycardia Trial (MUSTT) and Multicenter Automatic Defibrillator Implantation Trial (MADIT) have confirmed that defibrillator implantation can reduce mortality by as much as 50% in coronary artery disease patients with ejection fractions of less than 0.40, spontaneous nonsustained ventricular tachycardia, and inducible sustained ventricular tachycardia on electrophysiologic studies. Other trials are evaluating additional factors that may identify patients at risk who would benefit from therapy. One large study, the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), is comparing amiodarone and defibrillator use with placebo in patients with clinical congestive heart failure and ejection fractions of less than 0.35. Results will not be available for several years. Dilated cardiomyopathy also increases the risk for ventricular arrhythmia. However, risk stratification is more difficult in these patients than in those with coronary artery disease. Electrophysiologic studies are unreliable, and our ability to predict and prevent arrhythmias is less well developed. In summary, the treatment of choice for patients at risk of ventricular arrhythmia is an implantable defibrillator. Multiple studies have documented that defibrillators are more efficacious than any antiarrhythmic drug currently available, including amiodarone. Indeed, studies of patients with coronary artery disease and left ventricular dysfunction have shown that type I drugs tend to increase mortality. Amiodarone and sotalol appear to be less harmful, but no trial has convincingly shown that prophylactic use of these agents decreases mortality.
 Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators: A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med 337:1576, 1997 Jackman WM et al: Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med 324:1605, 1991 Kapoor W: Evaluation and management of syncope. JAMA 268:2553, 1992 Moss AJ et al: Improved survival with an implanted defibrillator in patients with coronary artery disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial. N Engl J Med 335:1933, 1996 Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation: Analysis of pooled data from five randomized controlled trials. Arch Intern Med 154:1449, 1994
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