CHAPTER 17: SUPRAVENTRICULAR TACHYARRHYTHMIAS

Supraventricular tachyarrhythmias originate from or are dependent on conduction through the atrium or atrioventricular (AV) node to the ventricles. Most produce narrow QRS-complex tachycardia (QRS duration <120 ms) characteristic of ventricular activation over the Purkinje system. Conduction block in the left or right bundle branch or activation of the ventricles from an accessory pathway produces a wide QRS complex during supraventricular tachycardia that must be distinguished from ventricular tachycardia (Chap. 18). Supraventricular tachyarrhythmia may be divided into physiologic sinus tachycardia and pathologic tachycardia (Table 17-1). The prognosis and treatment vary considerably depending on the mechanism and underlying heart disease.

Supraventricular tachycardia can be of brief duration, termed nonsustained, or can be sustained such that an intervention, such as cardioversion or drug administration, is required for termination. Episodes that occur with sudden onset and termination are referred to as paroxysmal. Paroxysmal supraventricular tachycardia (PSVT) refers to a family of tachycardias including AV node reentry, AV reentry using an accessory pathway, and atrial tachycardia.

Symptoms of supraventricular arrhythmia vary depending on the rate, duration, associated heart disease, and comorbidities and include palpitations, chest pain, dyspnea, diminished exertional capacity, and occasionally syncope. Rarely, a supraventricular arrhythmia precipitates cardiac arrest in patients with the Wolff-Parkinson-White syndrome or severe heart disease, such as hypertrophic cardiomyopathy.

Diagnosis requires obtaining an electrocardiogram (ECG) at the time of symptoms. For transient arrhythmia, ambulatory ECG recording is warranted (see Table 18-1). Exercise testing is useful for assessing exercise-related symptoms. Occasionally an invasive electrophysiology study is warranted to provoke the arrhythmia with pacing, confirm the mechanism, and often, perform catheter ablation.

Physiologic sinus tachycardia

The sinus node is comprised of a group of cells dispersed within the superior aspect of the thick ridge of muscle known as the crista terminalis where the posterior smooth atrial wall derived from the sinus venosus meets the trabeculated anterior portion of the right atrium (Fig. 17-1). Sinus p waves are characterized by a frontal plane axis directed inferiorly and leftward, with positive p waves in leads II, III, and aVF; a negative p wave in aVR; and an initially positive biphasic p wave in V1. Normal sinus rhythm has a rate of 60–100 beats/min. Sinus tachycardia (>100 beats/min) typically occurs in response to sympathetic stimulation and vagal withdrawal, whereby the rate of spontaneous depolarization of the sinus node increases and the focus of earliest activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to normal sinus rhythm.

Sinus tachycardia is considered physiologic when it is an appropriate response to exercise, stress, or illness. Sinus tachycardia can be difficult to distinguish from focal atrial tachycardia (see below) that originates from a focus near the sinus node. A causative factor (such as exertion) and a gradual increase and decrease in rate favors sinus tachycardia, whereas an abrupt onset and offset favor atrial tachycardia. The distinction can be difficult and occasionally requires extended ECG monitoring or even invasive electrophysiology study. Treatment for physiologic sinus tachycardia is aimed at the underlying condition (Table 17-2).

Nonphysiologic sinus tachycardia

Inappropriate sinus tachycardia is an uncommon condition in which the sinus rate increases spontaneously at rest or out of proportion to physiologic stress or exertion. Affected individuals are often women in the third or fourth decade of life. Fatigue, dizziness, and even syncope may accompany palpitations, which can be disabling. Additional symptoms of chest pain, headaches, and gastrointestinal upset are common. It must be distinguished from appropriate sinus tachycardia and from focal atrial tachycardia, as discussed above. Misdiagnosis of physiologic sinus tachycardia with an anxiety disorder is common. Therapy is often ineffective or poorly tolerated. Careful titration of beta blockers and/or calcium channel blockers may reduce symptoms. Clonidine and serotonin reuptake inhibitors have also been used. Ivabradine, a drug that blocks the I_f current causing sinus node depolarization, is promising but is not approved for use in the United States. Catheter ablation of the sinus node has been used, but long-term control of symptoms is usually poor, and it often leaves young individuals with a permanent pacemaker.

When symptomatic sinus tachycardia occurs with postural hypotension, the syndrome is called postural orthostatic tachycardia syndrome (POTS). Symptoms are often similar to those in patients with inappropriate sinus tachycardia. POTS is sometimes due to autonomic dysfunction following a viral illness and may resolve spontaneously over 3–12 months. Volume expansion with salt supplementation, oral fludrocortisone, compression stockings, and the α-agonist midodrine, often in combination, can be helpful. Exercise training has also been purported to improve symptoms.

Focal atrial tachycardia

Focal atrial tachycardia (AT) can be due to abnormal automaticity, triggered automaticity, or a small reentry circuit confined to the atrium or atrial tissue extending into a pulmonary vein, the coronary sinus, or vena cava. It can be sustained, nonsustained, paroxysmal, or incessant. Focal AT accounts for approximately 10% of PSVT referred for catheter ablation. Nonsustained AT is commonly observed on 24-h ambulatory ECG recordings, and the prevalence increases with age. Tachycardia can occur in the absence of structural heart disease or can be associated with any form of heart disease that affects the atrium. Sympathetic stimulation is a promoting factor such that AT can be a sign of underlying illness. AT with AV block can occur in digitalis toxicity. Symptoms are similar to other supraventricular tachycardias (SVTs). Incessant AT can cause tachycardia-induced cardiomyopathy.

AT typically presents as an SVT either with 1:1 AV conduction or with AV block that can be Wenckebach type conduction or fixed (e.g., 2:1 or 3:1) block. Because it is not dependent on AV nodal conduction, AT will not terminate with AV block, and the atrial rate will not be affected, which distinguishes AT from most AV nodal–dependent SVTs, such as AV nodal reentry and AV reentry using an accessory pathway (see below). An accelerated warm-up phase after initiation or cool-down phase prior to termination also favors AT rather than AV nodal–dependent SVT. P waves are often discrete, with an intervening isoelectric segment, in contrast to atrial flutter and macroreentrant AT (see below). When 1:1 conduction to the ventricles is present, the arrhythmia can resemble sinus tachycardia typically with a P-R interval shorter than the R-P interval (Fig. 17-2). It can be distinguished from sinus tachycardia by the p-wave morphology, which usually differs from sinus p waves depending on the location of the focus. Focal AT tends to originate in areas of complex atrial anatomy, such as the crista terminalis, valve annuli, atrial septum, and atrial muscle extending along cardiac thoracic veins (superior vena cava, coronary sinus, and pulmonary veins) (Fig. 17-3), and the location can often be estimated by the P-wave morphology. AT from the right atrium has a positive P-wave morphology in lead I and biphasic P-wave morphology in lead V₁. AT from the atrial septum will frequently have a narrower P-wave duration than sinus rhythm. AT from the left atrium will usually have a monophasic, positive P wave in lead V₁. AT that originates from superior atrial locations, such as the superior vena cava or superior pulmonary veins, will be positive in the inferior limb leads II, III, and aVF, whereas AT from a more inferior location, such as the ostium of the coronary sinus, will inscribe negative P waves in these same leads. When the focus is in the superior aspect of the crista terminalis, close to the sinus node, however, the p wave will resemble that of sinus tachycardia. Abrupt onset and offset then favor AT rather than sinus tachycardia. Depending on the atrial rate, the P wave may fall on top of the t wave or, during 2:1 conduction, may fall coincident with the QRS. Maneuvers that increase AV block, such as carotid sinus massage, Valsalva maneuver, or administration of AV nodal–blocking agents, such as adenosine, are useful to create AV block that will expose the p wave (Fig. 17-4).

Acute management of sudden-onset, sustained AT is the same as for PSVT (see below), but the response to pharmacologic therapy is variable, likely depending on the mechanism. For AT due to reentry, administration of adenosine or vagal maneuvers may transiently increase AV block without terminating tachycardia. Some ATs terminate with a sufficient dose of adenosine, consistent with triggered activity as the mechanism. Cardioversion can be effective in some, but fails in others, suggesting automaticity as the mechanism. Beta blockers and calcium channel blockers may slow the ventricular rate by increasing AV block, which can improve tolerance of the arrhythmias. Potential precipitating factors and intercurrent illness should be sought and corrected. Underlying heart disease should be considered and excluded.

For patients with recurrent episodes, beta blockers, the calcium channel blockers diltiazem or verapamil, and the antiarrhythmic drugs flecainide, propafenone, disopyramide, sotalol, and amiodarone can be effective, but potential toxicities and adverse effects often warrant avoiding these agents (Tables 17-3, 17-4, and 17-5). Catheter ablation targeting the AT focus is effective in more than 80% of patients and is recommended for recurrent symptomatic AT when drugs fail or are not desired or for incessant AT causing tachycardia-induced cardiomyopathy.

Atrioventricular nodal reentry tachycardia

AV nodal reentry tachycardia (AVNRT) is the most common form of PSVT, representing approximately 60% of cases referred for catheter ablation. It most commonly manifests in the second to fourth decades of life, often in women. It is often well tolerated, but rapid tachycardia, particularly in the elderly, may cause angina, pulmonary edema, hypotension, or syncope. It is not usually associated with structural heart disease.

The mechanism is reentry involving the AV node and likely the perinodal atrium, made possible by the existence of multiple pathways for conduction from the atrium into the AV node (Fig. 17-5). In the most common form, a slowly conducting AV nodal pathway extends from the compact AV node near the bundle of His, inferiorly along the tricuspid annulus, adjacent to the coronary sinus os. The reentry wavefront propagates up this slow pathway to the compact AV node and then exits from the fast pathway at the top of the AV node. The path back to the slow pathway to complete the circuit is not defined. The conduction time from the compact AV node region to the atrium is similar to that from the compact node to the His bundle and ventricles, such that atrial activation occurs at about the same time as ventricular activation. The p wave is therefore inscribed during, slightly before, or slightly after the QRS and can be difficult to discern. Often the P wave is seen at the end of the QRS complex as a pseudo-r´ in lead V₁ and pseudo-S waves in leads II, III, and aVF (Fig. 17-5A). The rate can vary with sympathetic tone. Simultaneous atrial and ventricular contraction results in atrial contraction against a closed tricuspid valve that produces cannon a waves visible in the jugular venous pulse and that the patient often perceives as a fluttering sensation in the neck. Elevated venous pressures may also lead to release of natriuretic peptides that cause posttachycardia diuresis. Less frequently, the AV nodal reentry circuit revolves in the opposite direction and gives rise to a tachycardia with an R-P interval longer than the P-R interval, similar to AT. The p wave will have the morphology noted above, and in contrast to ATs, maneuvers or medications that produce AV block terminate the arrhythmia.

Acute treatment is the same as for PSVT (discussed below). Whether ongoing therapy is warranted depends on the severity of symptoms and frequency of episodes. Reassurance and instruction as to performance of the Valsalva maneuver to terminate episodes are sufficient for many patients. Administration of an oral beta blocker, verapamil, or diltiazem at the onset of an episode has been used to facilitate termination. Chronic therapy with these medications or flecainide is an option if prophylactic therapy is needed. Catheter ablation of the slow AV nodal pathway is recommended for patients with recurrent or severe episodes or when drug therapy is ineffective, not tolerated, or not desired by the patient. Catheter ablation is curative in over 95% of patients. The major risk is heart block requiring permanent pacemaker implantation, which occurs in less than 1% of patients.

Junctional tachycardia

Junctional ectopic tachycardia (JET) is due to automaticity within the AV node. It is rare in adults and more frequently encountered as an incessant tachycardia in children, often in the perioperative period of surgery for congenital heart disease. It presents as a narrow QRS tachycardia, often with ventriculoatrial (VA) block, such that AV dissociation is present. JET can occur as a manifestation of increased adrenergic tone and may be seen after administration of isoproterenol. It may also occur for a short period of time after ablation for AVNRT.

Accelerated junctional rhythm is a junctional automatic rhythm between 50 and 100 beats/min. Initiation may occur with gradual acceleration in rate, suggesting an automatic focus, or after a premature ventricular contraction, suggesting a focus of triggered automaticity. VA conduction is usually present, with p-wave morphology and timing such that it resembles slow AVNRT.

Accessory pathways (APs) occur in 1 in 1500–2000 people and are associated with a variety of arrhythmias including narrow-complex PSVT, wide-complex tachycardias, and, rarely, sudden death. Most patients have structurally normal hearts, but APs are associated with Ebstein’s anomaly of the tricuspid valve and forms of hypertrophic cardiomyopathy including PRKAG2 mutations, Danon’s disease, and Fabry’s disease.

APs are abnormal connections that allow conduction between the atrium and ventricles across the AV ring (Fig. 17-6). They are present from birth and are due to failure of complete partitioning of atrium and ventricle by the fibrous AV rings. They occur across either an AV valve annulus or the septum, most frequently between the left atrium and free wall of the left ventricle, followed by posteroseptal, right free wall, and anteroseptal locations. If the AP conducts from atrium to ventricle (antegrade) with a shorter conduction time than the AV node and His bundle, then the ventricles are preexcited during sinus rhythm, and the ECG shows a short P-R interval (<0.12 s), slurred initial portion of the QRS (delta wave), and prolonged QRS duration produced by slow conduction through direct activation of ventricular myocardium over the AP (Fig. 17-6A). The morphology of the QRS and delta wave is determined by the AP location (Fig. 17-7) and the degree of fusion between the excitation wavefronts from conduction over the AV node and conduction over the AP. Right-sided pathways preexcite the right ventricle, producing a left bundle branch block–like configuration in lead V₁, and often show marked preexcitation because of relatively close proximity of the AP to the sinus node (Fig. 17-7). Left-sided pathways preexcite the left ventricle and may produce a right bundle branch–like configuration in lead V₁ and a negative delta wave in aVL, indicating initial depolarization of the lateral portion of the left ventricle that can mimic q waves of lateral wall infarction (Fig. 17-7). Preexcitation due to an AP at the diaphragmatic surface of the heart, typically in the paraseptal region, produces delta waves that are negative in leads III and aVF, mimicking the q waves of inferior wall infarction (Fig. 17-7). Preexcitation can be intermittent and disappear during exercise as conduction over the AV node accelerates and takes over ventricular activation completely.

Wolff-Parkinson-White (WPW) syndrome is defined as a preexcited QRS during sinus rhythm and episodes of PSVT. There are a number of variations of APs, which may not cause preexcitation and/or arrhythmias. Concealed APs allow only retrograde conduction, from ventricle to atrium, so no preexcitation is present during sinus rhythm, but SVT can occur. Fasciculoventricular connections between the His bundle and ventricular septum produce preexcitation but do not cause arrhythmia, nor do fibers such as atrio-Hisian connections, probably because the circuit is too short to promote reentry. Atriofascicular pathways, also known as Mahaim fibers, probably represent a duplicate AV node and His-Purkinje system that connect the right atrium to fascicles of the right bundle branch and conduct slowly only in the anterograde direction.

Av reentry tachycardia

The most common tachycardia caused by an AP is the PSVT designated orthodromic AV reentry. The circulating reentry wavefront propagates from the atrium anterogradely over the AV node and His-Purkinje system to the ventricles and then reenters the atria via retrograde conduction over the AP (Fig. 17-6B). The QRS is narrow or may have typical right or left bundle branch block, but without preexcitation during tachycardia. Because excitation through the normal AV conduction system and AP are necessary, AV or VA block results in tachycardia termination. During sinus rhythm, preexcitation is seen if the pathway also allows anterograde conduction (Fig. 17-6A). Most commonly, during tachycardia the R-P interval is shorter than the P-R interval and can resemble AVNRT (Fig. 17-1). Unlike typical AVNRT, P-wave timing is never simultaneous with a narrow QRS complex because the ventricles must be activated before the reentry wavefront reaches the AP and conducts back to the atrium. The morphology of the P wave is determined by the pathway location, but can be difficult to assess because it is usually inscribed during the ST segment. The p wave in posteroseptal APs is negative in leads II, III, and aVF, similar to that of AV nodal reentry, but P-wave morphology differs from AV nodal reentry for pathways in other locations (Fig. 17-7).

Occasionally, an AP conducts extremely slowly in the retrograde direction, which results in tachycardia with a long R-P interval, similar to most ATs. These pathways are usually located in the septal region and have negative p waves in leads II, III, and aVF. Slow conduction facilitates reentry, often leading to nearly incessant tachycardia, known as paroxysmal junctional reciprocating tachycardia (PJRT). Tachycardia-induced cardiomyopathy can occur. Without an invasive electrophysiology study, it may be difficult to distinguish this form of orthodromic AV reentry from atypical AV nodal reentry or AT.

Preexcited tachycardias

Preexcitated tachycardia occurs when the ventricles are activated by antegrade conduction over the AP (Fig. 17-6C). The most common is antidromic AV reentry in which activation propagates from atrium to ventricle via the AP and then conducts retrogradely to the atria via the His-Purkinje system and the AV node (or rarely a second AP). The wide QRS complex is produced entirely via ventricular excitation over the AP because there is no contribution of ventricular activation over more rapidly conducting specialized His-Purkinje fibers. This tachycardia is often indistinguishable from monomorphic ventricular tachycardia. The presence of preexcitation in sinus rhythm suggests the diagnosis.

Preexcitated tachycardia also occurs if an AP allows antegrade conduction to the ventricles during AT, atrial flutter, atrial fibrillation (Fig. 17-8), or AV nodal reentry. Atrial fibrillation and atrial flutter are potentially life threatening if the AP allows very rapid repetitive conduction. Approximately 25% of APs causing preexcitation allow minimum R-to-R intervals of less than 250 ms during atrial fibrillation are therefore associated with a risk of inducing ventricular fibrillation and sudden death. Preexcited atrial fibrillation presents as a wide-complex, very irregular rhythm. During atrial fibrillation, the ventricular rate is determined by the conduction properties of the AP and AV node. The QRS complex can appear quite bizarre and change on a beat-to-beat basis due to the variability in the degree of fusion from activation over the AV node and AP, or all beats may be due to conduction over the AP (Fig. 17-8). Ventricular activation from the Purkinje system may depolarize the ventricular end of the AP and prevent 1:1 atrial wavefront conduction over the AP. Slowing AV nodal conduction can thereby facilitate AP conduction and dangerously accelerate the ventricular rate. Administration of AV nodal–blocking agents including oral or intravenous verapamil, diltiazem, beta blockers, intravenous adenosine, and intravenous amiodarone are contraindicated. Preexcited tachycardias should be treated with electrical cardioversion or intravenous procainamide or ibutilide, which may terminate or slow the ventricular rate.

Management of patients with accessory pathways

Acute management of orthodromic AV reentry is discussed below for PSVT. Patients with WPW syndrome may have wide-complex tachycardia due to antidromic AV reentry, orthodromic AV with bundle branch block, or a preexcited tachycardia, and treatment depends on the underlying rhythm.

Initial patient evaluation should include assessment for aggravating factors, including intercurrent illness and factors that increase sympathetic tone. Examination should focus on excluding underlying heart disease. An echocardiogram is reasonable to exclude Ebstein’s anomaly and hypertrophic cardiomyopathy.

Patients with preexcitation who have symptoms of arrhythmia are at risk for developing atrial fibrillation and sudden death if they have an AP with high-risk properties. The risk of cardiac arrest is in the range of 2 per 1000 patients in adults but is likely greater in children. An invasive electrophysiology study is warranted to determine if the AP is high enough risk to warrant potentially curative catheter ablation. For patients with concealed APs or known low-risk APs causing orthodromic AV reentry, chronic therapy is guided by symptoms and frequency of events. Vagal maneuvers may terminate episodes, as may a dose of beta blocker, verapamil, or diltiazem taken at the onset of an episode. Chronic therapy with these agents or flecainide can reduce the frequency of episodes in some patients. Catheter ablation is warranted for recurrent arrhythmias when drugs are ineffective, not tolerated, or not desired by the patient or if the AP is considered high risk (Fig. 17-8). Efficacy is in the range of 95% depending on the location of the AP. Serious complications occur in fewer than 3% of patients, but can include AV block, cardiac tamponade, thromboemboli, coronary artery injury, and vascular access complications. Mortality occurs in less than 1 in 1000 patients.

Adults who have preexcitation but no arrhythmia symptoms have a risk of sudden death estimated to be 1 per 1000 patient-years. Electrophysiology study is usually advised for people in occupations for which an arrhythmia occurrence would place them or others at risk, such as police, military, and pilots, or for individuals who desire evaluation for risk. Routine follow-up without therapy is reasonable in others. Children are at greater risk of sudden death, approximately 2 per 1000 patient-years.

Macrorrentrant atrial tachycardia is due to a large reentry circuit, often associated with areas of scar in the atria. Common or typical right atrial flutter is due to a circuit that revolves around the tricuspid valve annulus, bounded anteriorly by the annulus and posteriorly by functional conduction block in the crista terminalis. The wavefront passes through an isthmus between the inferior vena cava and the tricuspid valve annulus, known as the sub-Eustachian or cavotricuspid isthmus, where it is susceptible to interruption by catheter ablation. Thus, common atrial flutter is cavotricuspid isthmus-dependent atrial flutter. This circuit most commonly revolves in a counterclockwise direction (as viewed looking toward the tricuspid annulus from the ventricular aspect), which produces the characteristic negative sawtooth flutter waves in leads II, III, and aVF and positive P waves in lead V₁ (Fig. 17-10). When the direction is reversed, clockwise rotation produces the opposite P-wave vector in those leads. The atrial rate is typically 240–300 beats/min but may be slower in the presence of atrial disease or antiarrhythmic drugs. It often conducts to the ventricles with 2:1 AV block, creating a regular tachycardia at 150 beats/min, with p waves that may be difficult to discern. Maneuvers that increase AV nodal block will typically expose flutter waves, allowing diagnosis.

Common right atrial flutter often occurs in association with atrial fibrillation and with atrial scar from senescence or prior cardiac surgery. Some patients with atrial fibrillation that is treated with an antiarrhythmic drug, particularly flecainide, propafenone, or amiodarone, will present with atrial flutter rather than fibrillation.

Macroreentrant ATs that are not dependent on conduction through the cavotricuspid isthmus are referred to as atypical atrial flutters. They can occur in either atrium and are usually associated with areas of scar. Left atrial flutter and perimitral left atrial flutter are commonly seen after extensive left atrial ablation for atrial fibrillation or atrial surgery. The clinical presentation is similar to common atrial flutter, but with different P-wave morphologies. They can be difficult to distinguish from focal AT, and in most cases, the mechanism can only be confirmed by an electrophysiology study.

Multifocal AT (MAT) is characterized by at least three distinct P-wave morphologies with rates typically between 100 and 150 beats/min. Unlike atrial fibrillation, there are clear isoelectric intervals between P waves (Fig. 17-11). The mechanism is likely triggered automaticity from multiple atrial foci. It is usually encountered in patients with chronic pulmonary disease and acute illness.

Atrial fibrillation (AF) is characterized by disorganized, rapid, and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction (Fig. 17-12). In an untreated patient, the ventricular rate also tends to be rapid and variable, between 120 and 160 beats/min, but in some patients, it may exceed 200 beats/min. Patients with high vagal tone or AV nodal conduction disease may have slow rates.

AF is the most common sustained arrhythmia and is a major public health problem. Prevalence increases with age, and more than 95% of AF patients are older than 60 years of age. The prevalence by age 80 is approximately 10%. The lifetime risk of developing AF for individuals 40 years old is approximately 25%. AF is slightly more common in men than women and more common in whites than blacks. Risk factors for developing AF in addition to age include hypertension, diabetes mellitus, cardiac disease, and sleep apnea. AF is a marker for heart disease, the severity of heart disease, and age, and it is therefore difficult to determine the extent to which AF itself contributes to associated increased mortality and morbidity. AF is associated with increased risk of developing heart failure. AF increases the risk of stroke by fivefold and is estimated to be the cause of 25% of strokes. It also increases the risk of dementia.

AF is occasionally associated with an acute precipitating factor such as hyperthyroidism, acute alcohol intoxication, or an acute illness including myocardial infarction or pulmonary embolism. AF occurs in up to 30% of patients recovering from cardiac surgery, associated with inflammatory pericarditis.

The clinical type of AF suggests the underlying pathophysiology (Fig. 17-12). Paroxysmal AF is defined as episodes that start and stop spontaneously. It is often initiated by small reentrant or rapidly firing foci in sleeves of atrial muscle along the pulmonary veins. Catheter ablation that isolates these foci usually abolishes the AF. Persistent AF has a longer duration, exceeding 7 days, and, in many cases, will continue unless cardioversion is performed. Cardioversion can be followed by prolonged periods of sinus rhythm. Episodes may be initiated by rapidly firing foci, but persistence of the arrhythmia is likely due to single or multiple areas of reentry facilitated by structural and electrophysiologic atrial abnormalities. In patients with long-standing persistent AF (>1 year), significant structural changes are present in the atrium that support reentry and automaticity, making it difficult to restore and maintain sinus rhythm. Some patients progress over years from paroxysmal to persistent AF. Fibrosis that develops with aging and atrial hypertrophy in response to hypertension and other cardiac disease may be an important promoting factor, although electrophysiologic changes to conduction and refractoriness occur as well in response to chronic tachycardia in the atrium.

Clinical consequences are related to rapid ventricular rates, loss of atrial contribution to ventricular filling, and predisposition to thrombus formation in the left atrial appendage with potential embolization. Presentations vary with the ventricular rate and underlying heart disease and comorbidities. Many patients are asymptomatic. Rapid rates may cause hemodynamic collapse or heart failure exacerbations particularly in patients with impaired cardiac function, hypertrophic cardiomyopathy, and heart failure with preserved systolic function. Exercise intolerance and easy fatigability are common. Occasionally, dizziness or syncope occurs due to pauses when AF terminates to sinus rhythm (Fig. 17-13).

Acknowledgment

Portions of this chapter were retained from the work of the previous author, Francis Marchlinski.