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Table of Contents

Published
December 11, 2003

Fredrick J.
Jaeger, DO

Department of
Cardiovascular
Medicine

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Definition

Prevalence

Pathophysiology

Signs and
Symptoms

Diagnosis

Therapy

Outcomes

References

Broadly defined, cardiac arrhythmias comprise any abnormality or pertubation in the normal activation sequence of the myocardium. The sinus node, displaying properties of automaticity, normally spontaneously depolarizes sending a depolarization wave over the atrium, depolarizing the atrioventricular (AV) node, then propagating over the His-Purkinje system, depolarizing the ventricle in a systematic fashion. There are literally hundreds of different types of cardiac arrhythmias. The normal rhythm of the heart, so-called "normal sinus rhythm," can be disturbed through either failure of automaticity, such as in sick sinus syndrome, or through overactivity as in inappropriate sinus tachycardia. Ectopic foci prematurely exciting the myocardium as an isolated event or on a continual basis results in premature atrial contractions (PACs) and premature ventricular contractions (PVCs). Sustained tachyarrhythmias in the atria, such as atrial fibrillation, paroxysmal atrial tachycardia, and supraventricular tachycardia (SVT), originate because of micro-level or macro-level re-entry. In general, the seriousness of a cardiac arrhythmia depends upon the presence or absence of structural heart disease.

The most common example of a relatively benign arrhythmia is atrial fibrillation, which is discussed elsewhere in this series. Similarly common are PACs and PVCs, which, although a nuisance, are generally benign in the absence of structural heart disease. In contrast, the presence of non-sustained ventricular tachycardia (VT) or syncope in patients with coronary artery disease or severe left ventricular (LV) dysfunction may be harbingers of sudden cardiac death and must not be ignored.

This section assumes a basic knowledge of the myriad types of cardiac arrhythmias and will not focus on specific aspects of arrhythmia identification and diagnosis except to discuss in broad terms the various treatment options for the many commonly encountered types. There are excellent texts available that provide core curricular material for the identification of cardiac arrhythmias, rate determination, interval measurement, and identification of normal and abnormal P-, QRS-, and T-wave morphology. Cardiac arrhythmias are very common, and dizziness, palpitations, and syncope are symptoms frequently encountered by family physicians, internists, and cardiologists. In contrast to these ubiquitous complaints that are generally benign, sudden cardiac death remains an important public health concern. The latest statistics from the Centers for Disease Control put sudden cardiac death rates at over 600,000 per year. Up to one-half of patients have sudden death as the first manifestation of cardiac disease (Figure 1). Efforts at decreasing this alarming number have obviously focused on primary prevention, such as cardiac risk factor reduction, but have also led to the proliferation of automatic external defibrillators. These devices have been shown to reduce mortality when used within the first few minutes of an arrest.

Regardless of the specific arrhythmia, the pathogenesis of arrhythmias falls into one of three basic mechanisms. These include enhanced or suppressed automaticity, triggered activity, or re-entry. Automaticity is a natural property of all myocytes. Ischemia, scarring, electrolyte disturbances, medications, advancing age, and other factors may suppress or enhance automaticity in various areas. Suppression of automaticity of the sinoatrial node can result in sinus node dysfunction and sick sinus syndrome. Sick sinus syndrome is still the most common indication for permanent pacemaker implantation (Figure 2).

In contrast to suppressed automaticity, enhanced automaticity can result in multiple arrhythmias, both atrial and ventricular. Triggered activity occurs when early afterdepolarizations and delayed afterdepolarizations initiate spontaneous multiple depolarizations precipitating ventricular arrhythmias. Examples of this include torsades de pointes (Figure 3) and ventricular arrhythmias due to digitalis toxicity.

Finally, probably the most common mechanism of arrhythmogenesis results from re-entry. Requisites for re-entry include bi-directional conduction and uni-directional block. "Micro-" level re-entry occurs with VT from conduction around the scar of myocardial infarction and "macro-" level re-entry occurs via conduction through manifest (Wolff-Parkinson-White syndrome—WPW) or concealed accessory pathways.

The signs and symptoms of cardiac arrhythmias can range from completely asymptomatic to loss of consciousness or sudden cardiac death. In general, more severe symptoms are more likely to occur in the presence of structural heart disease. For example, sustained monomorphic VT, particularly in a normal heart, may be hemodynamically tolerated without syncope. In contrast, even non-sustained VT may be poorly tolerated and cause marked symptoms in patients with severe LV dysfunction. Complaints such as lightheadedness, dizziness, quivering, shortness of breath, chest discomfort, heart fluttering or pounding, and forceful or painful extra beats are commonly reported with a variety of arrhythmias. Frequently patients notice their arrhythmia only after checking peripheral pulses. Certain symptoms raise the index of suspicion and can give clues to the type of arrhythmia. The presence of sustained regular palpitations or heart racing in young patients without any evidence of structural heart disease suggests the presence of an SVT due to atrioventricular nodal re-entry, or SVT due to an accessory pathway. Such tachycardias may frequently be accompanied by chest discomfort, diaphoresis, neck fullness, or a vasovagal type of response with syncope, diaphoresis, and nausea. It has been shown that the hemodynamic consequences of SVT and VT can have an autonomic basis, recruiting vasodepressor reflexes similar to that observed in neurocardiogenic syncope. Isolated or occasional premature beats suggest PACs or PVCs and are benign in the absence of structural heart disease.

Syncope in the setting of noxious stimuli such as pain, prolonged standing, and venepuncture, particularly when preceded by vagal-type symptoms (diaphoresis, nausea, vomiting), suggests neurocardiogenic (vasovagal) syncope. Occasionally, patients may report abrupt syncope without prodromal symptoms, suggesting the possibility of the "malignant" variety of neurocardiogenic syncope. Malignant neurocardiogenic syncope denotes syncope in the absence of a precipitating stimulus, with a short or absent prodrome, often resulting in injuries, and is associated with marked cardioinhibitory and bradycardic responses spontaneously or provoked by head-up tilt-table testing.² The presence of sustained or paroxysmal sinus tachycardia, frequently associated with chronic fatigue syndrome and fibromyalgia, suggests the possibility of POTS (postural orthostatic tachycardia syndrome). This syndrome, which may be a form of autonomic dysfunction, is currently unexplained. It is characterized by a markedly exaggerated chronotropic response to head-up tilt-table testing and stress testing. POTS frequently has associated systemic signs such as muscle aches (fibromyalgia), cognitive dysfunction, and weight loss. Inappropriate sinus tachycardia syndrome is similar in presentation, but probably represents a separate disorder with alternative etiology, possibly due to atrial tachycardias in the sinus node area or dysregulation of sinus node automaticity.

Since there are multiple tests available for the diagnosis of cardiac arrhythmias, it is important to proceed with a stepwise approach. The goal is finding a correlation between symptoms and the underlying arrhythmia, and initiation of appropriate therapy. Additional testing is usually advisable to identify patients with arrhythmias due to ischemia or who are at risk for sudden cardiac death.

Assessment of Structural Heart Disease
The initial assessment of structural heart disease obviously begins with the history and physical examination. Careful attention to coronary artery disease or previous myocardial infarctions, risk factors for coronary artery disease, and family history of sudden cardiac death are extremely important. Careful scrutiny of the electrocardiogram (ECG) is imperative to look for conduction system delays, QRS widening, previous myocardial infarctions, or PVCs. Cardiac auscultation may detect irregular rhythm or premature beats. Stress testing, usually with imaging (stress echocardiogram, or stress thallium and echocardiography), can demonstrate significant coronary artery disease, LV dysfunction, or valvular disease.

Frequently, patients may present with a wide-complex tachycardia, possibly VT or SVT with aberrancy. Various algorithms have been described to facilitate the differentiation of wide-complex tachycardias. Brugada et al synthesized the various schemes into one simple and convenient protocol (Figure 4). The rule of thumb, however, is that sustained or non-sustained wide-complex tachycardia in a patient with known coronary artery disease or previous myocardial infarction is VT until proven otherwise.³ Obviously, the initial approach to sustained wide-complex tachycardia is to cardiovert if the patient is hemodynamically unstable. In stable patients, assume VT and treat empirically with intravenous medications (amiodarone, procainamide, lidocaine). If SVT with aberrancy is strongly suspected, diagnostic maneuvers such as adenosine can be cautiously employed.

Holter Monitoring
Ambulatory Holter monitoring has been available for several decades and has proved invaluable in identifying underlying ambient rhythm abnormalities.⁴ Generally, 24- to 48-hour baseline Holter monitoring is useful in quantitating and qualifying underlying arrhythmias in patients with frequent symptoms (Figure 5).

Event Recording
In patients who have less frequent symptoms occurring on a weekly or monthly basis, Holter monitoring may not aid in the diagnosis unless the patient has an event during recording. Event recording monitoring systems, also called loop recorders (eg, King of Heart, Instromedix; Milwaukee, WI), can be worn for longer intervals (usually a month) and can document infrequent arrhythmia episodes and obtain symptom-arrhythmia correlation. These devices are either automatically activated or patient activated, and utilize telephone modem technology to transmit the ECG rhythm strips. These devices use continuous loop technology (retrograde memory) so that in the event of a symptom, the patient activates the device by pushing a button and starts recording the ECG rhythm strip several minutes prior to the event. When prolonged, external ambulatory event monitors fail to document an arrhythmia; an implantable device (Reveal, Medtronic; Minneapolis, MN) can be used in patients with recurrent enigmatic syncope or arrhythmias in whom conventional testing has not yielded a diagnosis. This device, with a battery life of 14 to 22 months, is implanted subcutaneously and continuously scans for arrhythmias (Figure 6). The device automatically records and stores tachycardia or bradycardia events, and can be patient activated. Insurance reimbursement for the Reveal device requires extensive preliminary traditional and conventional diagnostic testing, including negative event monitors, tilt-table testing, and electrophysiologic studies. Preliminary studies of the implantable event monitor studies have shown a significant reduction in time to diagnose as well as overall costs when used in patients with syncope and no structural heart disease.

Signal-Averaged ECG and T-Wave Alternans
Although initially touted as an important screening test for patients with syncope or ventricular arrhythmic risk, the signal-averaged ECG now has a limited role in the evaluation of patients with enigmatic palpitations.⁵ The presence of low-amplitude late potentials indicating a positive signal-averaged ECG suggests an underlying abnormality in ventricular repolarization seen with a discrete scar and can be associated with ventricular ectopy and spontaneous VT (Figure 7). However, signal-averaged ECG may be abnormal in patients with no evidence of structural heart disease and in patients with conduction disturbances (eg, right bundle branch block) and, therefore, a "positive" study has an uncertain specificity and sensitivity. In contrast, the signal-averaged ECG can be very helpful in screening patients or family members for arrhythmogenic right ventricular dysplasia. Similarly, T-wave alternans may have an important role for risk stratification in patients with LV dysfunction and complex ventricular arrhythmias. It has been recognized for many years that abnormalities in the ST segment and T wave may precede the onset of ventricular arrhythmias. Presumably, changes in autonomic activity as well as repolarization may facilitate the provocation of lethal ventricular arrhythmias in susceptible individuals. Rosenbaum et al reported that abnormal T-wave alternans may be an important marker for assessing patients and determining their risk for sudden cardiac death.⁶ T-wave alternans is available on stress testing and ambulatory monitors (Figure 8).

In the last several years, wireless technologies have been introduced that are capable of long-term cardiac telemetric monitoring for cardiac arrhythmias, both in the home environment and on an ambulatory basis. External monitoring systems can be worn continuously by the patient and utilize hard wire telephone modem connections or wireless cellular network technology. These monitors can automatically detect cardiac arrhythmias and transmit the telemetry strip to a central cardiac monitoring station, which alerts the patient, physician, or emergency response systems. The devices can be patient activated, but also have automatic logic algorithms for detection of arrhythmias similar to those incorporated in defibrillators. This wireless technology has recently become available in implant devices such as pacemakers and defibrillators (Biotronik). These devices monitor for arrhythmias and detect pacemaker or defibrillator activity or device malfunction. Ambulatory cardiac monitoring provides an attractive alternative to prolonged hospitalization and may ultimately lower health care costs and reduce mortality.

Electrophysiologic Testing
Electrophysiologic testing has become the gold standard for identification of high-risk patients with non-sustained VT such as those with previous myocardial infarction and LV dysfunction (Figure 9).^5,7 Inducible sustained monomorphic VT indicates a high risk for spontaneous clinical sustained VT and ventricular fibrillation. Electrophysiologic testing is also the gold standard for evaluation of patients with recurrent syncope and can help identify underlying His-Purkinje disease, inducible sustained monomorphic VT, SVT, and sinus node dysfunction (Table 1).⁸

Pacemakers and Defibrillators:

Implantation of a permanent pacemaker requires specific levels of evidence and indications based upon the ACC/AHA guidelines.⁹ Class I and Class II indications are appropriate for the implantation of a permanent pacemaker. Correlation of symptoms with underlying bradyarrhythmias and heart block are required. Rarely, the decision to implant a pacemaker is made empirically. The implantable cardioverter defibrillator (ICD) is indicated for sustained VT or ventricular fibrillation, survivors of aborted sudden cardiac death (AVID study—secondary prevention),¹⁰ or for inducible sustained monomorphic VT (MADIT I—primary prevention).¹¹ Based on the results of the MADIT II study, ICDs will also routinely be implanted in patients with LV dysfunction, ejection fraction less than 35%, and a previous myocardial infarction.¹² Emerging indications for ICDs include syncope in the presence of dilated cardiomyopathy and hypertrophic obstructive cardiomyopathy in high-risk patients (non-sustained VTs, syncope, and family members who have experienced sudden cardiac death).

Since their introduction 40 years ago, pacemakers have advanced in sophistication, reliability, and longevity. Pacemakers are now expected to last at least 10 years and leads much longer. Although lead technology is continuously undergoing improvement, leads still fail due to material breakdown, fatigue, and manufacturing defects and may require removal and replacement (Figure 10). Leads and devices may also need to be removed secondary to infection. Chronic leads are frequently heavily fibrosed by endovascular tissue. Lead extraction requires sophisticated equipment, such as lasers, and very experienced operators to be safely removed. ICD life is currently 5 to 7 years and continues to improve. Follow-up for a permanent pacemaker or ICD is usually every 6 to 12 months with comprehensive testing of pacing and sensing thresholds. Pacemakers can be dual chamber and have rate-response capability. Rate responsiveness simulates the chronotropic response of the sinus node and uses either minute ventilation or, more commonly, motion to estimate the needed heart rate. Pacemakers and ICDs have extensive telemetric capacity, allowing for retrieval of events, trends, battery, and lead data. Permanent pacemakers and ICDs can also transmit limited data via the telephone. An ICD can obviously terminate VT or ventricular fibrillation with a shock (Figure 11), but it can also terminate sustained VT with anti-tachycardic pacing (Figure 12).

Chest x-ray of pacemaker and atrial and ventricular leads. Note fracture of ventricular lead.

Figure 10

Defibrillators can be single chamber or dual chamber and can have rate responsiveness as well (Figure 13). Recently, the results of the DAVID study demonstrated that dual-chamber pacing ICDs in patients with decreased LV function led to an increased incidence of congestive heart failure and death.¹³ The presumed mechanism is by creating a "functional" left bundle branch block, which can lead to cardiac desynchronization and heart failure. In contrast, restoring cardiac resynchronization with bi-ventricular pacing can improve congestive heart failure symptoms and has led to an explosion of referrals to implant patients with chronic heart failure, Functional Class II-IV, and severe LV dysfunction.¹⁴ Therefore, dual-chamber ICDs should be reserved for those with a normal left ventricle, or those with frequent supraventricular arrhythmias such as atrial fibrillation (to avoid spurious shocks secondary to rapid ventricular responses). If dual-chamber pacing is required and the LV dysfunction is severe, consideration should be given to a bi-ventricular pacemaker.

Radiofrequency Ablation:

Radiofrequency catheter ablation (RFA) is a revolutionary advance in the treatment of cardiac arrhythmias.^7,8,15,16 For the first time, RFA provides the opportunity to completely cure a cardiac disease. Introduced over two decades ago as Direct current (DC) ablation, and then in the late 1980s with radiofrequency, ablation has proved to be a safe, efficacious, and cost-effective treatment for specific cardiac arrhythmias such as atrioventricular nodal re-entry tachycardia (AVNRT); orthodromic reciprocating tachycardia associated with WPW and concealed accessory pathways; normal heart VT, particularly right ventricular outflow tract tachycardia or fascicular tachycardia; and atrial flutter. In addition, RFA can provide adjuvant therapy for ischemic VT when the patient is experiencing frequent ICD shocks or failing antiarrhythmic therapy. Finally, pulmonary vein isolation as a treatment option for very symptomatic, drug refractory, paroxysmal or persistent atrial fibrillation is gaining widespread acceptance and is undergoing intense clinical scrutiny.¹⁷ However, rate control and chronic anticoagulation are acceptable alternatives for asymptomatic or mildly symptomatic patients with atrial fibrillation according to the results of the recently released AFFIRM study.¹⁸

AVNRT is the most common of the SVTs (Figure 14). Onset is usually in the third to fifth decades of life, and the patient may present with sustained rapid tachycardia rates of 180 to 240 bpm. AVNRT originates from a micro re-entry around the fast and slow pathways of the AV node. Typically, AVNRT shows a narrow-complex tachycardia without apparent P waves. Vagal maneuvers or adenosine can terminate AVNRT. RFA has proved extremely effective at curing AVNRT, with success rates above 95%. Complication rates are low, and with successful modification of the AV node, specifically ablation of the slow pathway, the need for a permanent pacemaker in this condition is almost a thing of the past.

The presence of an accessory pathway (Kent bundle) in various locations around the tricuspid or mitral annulus results in a characteristic delta wave pattern on ECG (Figure 15). Macro re-entry tachycardia, called ORT (orthodromic reciprocating tachycardia or AVRT (atrioventricular reciprocating tachycardia) occurs when the AV node is used in an antegrade direction and the accessory pathway is used in a retrograde direction. Typically, AVRT is a narrow-complex tachycardia, but a small retrograde P wave may be visible between the QRS and T wave. When the accessory pathway is used in an antegrade direction—called antidromic reciprocating tachycardia—a wide-complex tachycardia occurs that mimics VT. Atrial fibrillation is also very common with WPW. It is speculated that constant retrograde re-entry into the atrium during ventricular depolarization is responsible. Because of the potential for rapid conduction over an accessory pathway with atrial fibrillation and WPW, extreme caution must be exercised with AV nodal blocking agents, particularly digoxin, and calcium channel blockers. Although rare, atrial fibrillation with rapid ventricular response over an accessory pathway can initiate ventricular fibrillation leading to sudden death. Acute treatment of atrial fibrillation and WPW consists of cardioversion and occasionally intravenous procainamide. The most common location for accessory pathways is the LV free wall, but it also can be posteroseptal or right sided. RFA has been successful in ablating and curing WPW. Success rates approaching 97% have been safely achieved in experienced centers. For symptomatic WPW, particularly in young patients, RFA is considered to be the treatment of choice.

RFA has also been extremely useful for cure of typical atrial flutter (Figure 16). Typical flutter is identified by an atrial rate of 240 bpm or greater and characteristic negative saw-tooth flutter waves identified on the ECG, classically in inferior leads (II, III, aVF). Mapping studies have revealed that typical flutter occurs with a counter-clockwise rotation of atrial activation descending on the right atrial free wall, traversing the isthmus (zone between the coronary sinus orifice and tricuspid leaflet) and ascending the atrial septum. Disruption of conduction over the isthmus by RFA can successfully eliminate the potential for typical flutter. Many patients, however, can continue to have atrial tachyarrhythmias, especially atrial fibrillation, in up to 25% of cases. Nevertheless, RFA is an acceptable first therapy for symptomatic atrial flutter.

Antiarrhythmic Medications:

The CAST study (Cardiac Arrhythmia Suppression Trial), published in 1989, completely and radically changed the utilization of antiarrhythmic medications.¹⁹ CAST was designed to test the hypothesis that antiarrhythmic medication suppression of PVCs and non-sustained VT would improve mortality in patients following a myocardial infarction who had decreased LV function. The medications selected—moricizine, flecainide, and encainide—were known to have very significant ventricular arrhythmia suppression properties. However, CAST demonstrated an increase in mortality in patients treated with antiarrhythmic medications compared with placebo (Figure 17). It was suspected that the increased mortality resulted from the proarrhythmic effects of these drugs, especially in the presence of ischemia and LV dysfunction.²⁰ Therefore, these type IC drugs (Table 2) are contraindicated in patients with coronary artery disease and ischemia. Because of CAST's findings, there is concern that this increased mortality could be extended to other antiarrhythmics, especially when administered for relatively benign arrhythmias (atrial fibrillation, PVCs). Quinidine was subsequently shown to increase mortality when administered to patients with atrial fibrillation.²¹ Since publication of the CAST study, many other studies have confirmed the proarrhythmic effects of antiarrhythmic medication when used injudiciously. This has led to specific guidelines for the use of antiarrhythmic medications, especially those that prolong the QT interval and increase proarrhythmia.²⁰ For the most part, type I A and type III medications are initiated in the hospital with telemetry monitoring. Type IC agents, however, are relatively safe when used in a normal heart. Similarly, amiodarone, because of its long half-life (43 days to months) and very low incidence of proarrhythmia, can usually be initiated at low doses in an outpatient setting in the absence of severe LV dysfunction or bradycardia.

Increased arrhythmic mortality in patients receiving antiarrhythmic medication versus placebo in the CAST study. Adapted from reference 19.

Figure 17

Because of the results of the CAST study, the Food and Drug Administration and the pharmaceutical industry took unprecedented measures to ensure appropriate prescription practices and credentialing of ordering physicians when the new antiarrhythmic medication, dofetilide (Tikosyn, Pfizer), was released for use in patients with atrial fibrillation.

Specific Arrhythmias:

Normal Heart Ventricular Tachycardia
Occasionally, sustained and non-sustained VT can occur in the absence of structural heart disease—so called "normal heart" VT. In general, the prognosis is good with a low risk for sudden cardiac death. Examples include right ventricular outflow tract VT and left ventricular outflow tract VT, fascicular VT, idiopathic left VT, repetitive monomorphic VT, sinus of Valsalva VT, and others (Figure 18).²² Treatment is usually with beta blockers or calcium channel blockers and, if refractory, RFA. Treatment is aimed at symptom suppression.

Arrhythmogenic Right Ventricular Dysplasia
Arrhythmogenic right ventricular dysplasia is a genetic disease in which right ventricular normal architecture is disrupted by progressive infiltration and transformation to fatty, fibrous material. This creates the potential for chaotic depolarization and VT. Symptoms include palpitations, VT, and sudden cardiac death. The diagnosis should be suspected in patients with an abnormal ECG showing right bundle branch block or juvenile T-wave pattern, and epsilon waves (Figure 19). Signal-averaged ECG often is abnormal with low-amplitude late potentials. Echocardiography may reveal right ventricular dysfunction and aneurysms. The diagnosis is confirmed with an abnormal CT or magnetic resonance image showing the typical fatty infiltration (Figure 20). Symptomatic patients are screened for ventricular arrhythmias with electrophysiologic studies and, if positive, receive an ICD.

Long QT Syndrome
Long QT syndrome is a genetically transmitted disorder causing metabolic abnormalities of cardiac myocyte sodium- and potassium-channel depolarization (so-called channelopathy) leading to prolongation of the QT interval. This prolongation leads to susceptibility to spontaneous polymorphic VT and torsades de pointe and VT (Figure 21). Treatment consists of atrial pacing, beta blockers, specific antiarrhythmics to improve repolarization, and ICDs in high-risk patients.

Brugada Syndrome
Brugada syndrome is a relatively rare cause of VT and fibrillation characterized by an abnormal ECG exhibiting a right bundle branch block pattern and ST-segment elevation in the precordial leads (Figure 22). Treatment requires implantation of an ICD in patients with syncope and complex ventricular arrhythmias.

Bundle Branch Re-entry Ventricular Tachycardia
In bundle branch re-entry VT, re-entry around components of the His-Purkinje system and one of the bunch branches results in a VT that can resemble the native QRS. This type of VT is often seen in dilated cardiomyopathy. The major prerequisite is baseline sinus conduction delays, usually left bundle branch block. Confirmation of this type of VT requires an electrophysiologic study demonstrating His-bundle participation in the VT. Bundle branch re-entry VT can be eliminated by right bundle branch block ablation and usually does not result in complete heart block. Patients still require an ICD as other morphologies of VT are usually present or probable.

In the absence of structural heart disease, benign arrhythmias such as PACs, SVTs, PVCs, and atrial fibrillation have been shown to have an excellent prognosis. 18 RFA for SVT has been shown to have a greater than 95% success rate with no long-term untoward side effects. The use of ICDs has been shown to improve survival both in primary and secondary prevention trials. Secondary prevention trials, such as the AVID study, enrolled patients who had a life-threatening arrhythmia and were successfully resuscitated.¹⁰ The defibrillator proved superior to medical therapy (in most cases amiodarone) in preventing recurrence with sudden death. Primary prevention trials focus on high-risk groups of patients who have not already experienced an untoward ventricular arrhythmia. The MADIT and MUST trials confirmed the superiority of the ICD in survival of patients who had inducible sustained monomorphic VT during an electrophysiologic study and a history of coronary artery disease and myocardial infarction.^11,23 The MADIT II study recently suggested that an electrophysiologic study was superfluous for risk stratification for patients with LV dysfunction (ejection fraction less than 35%) and a history of coronary artery disease, regardless of whether ventricular arrhythmias were present or absent.¹² Patients who received an "empiric" ICD had a significant survival benefit. The findings of this study will have a tremendous impact on public health care costs. Further primary prevention trials will focus on prevention of sudden death in patients with valvular heart disease, hypertrophic obstructive and non-obstructive cardiomyopathies, and dilated cardiomyopathy.

Return to Medicine Index

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