Supraventricular tachycardia
Supraventricular tachycardia (SVT) is a rhythm disturbance with a rate greater than 100 that requires tissue from above the His-Purkinje system to perpetuate. SVT can be regular (e.g., atrioventricular [AV] node reentry), irregular (e.g., atrial flutter [AFL] with variable AV conduction), or irregularly irregular (e.g., multifocal atrial tachycardia [MAT], atrial fibrillation [AF]). SVT can be associated with a narrow QRS complex, a wide QRS complex, or both. When it is associated with a wide QRS complex, preexisting bundle branch block (BBB), tachycardia-dependent (phase 3) BBB (aberrancy), or an accessory pathway will be present. Intermittently wide QRS complexes caused by the Ashman phenomenon are commonly seen in AF and usually have a right bundle branch block (RBBB) pattern due to the long refractoriness of the right bundle branch that is present after long–short RR cycles. There can be a one-to-one atrial to ventricular relationship (such as is commonly seen in AV node reentry tachycardia or AV reentry tachycardia) or a two-to-one or greater relationship (commonly seen in AFL or atrial tachycardia [AT]). SVTs can be sustained, recurrent, and intermittent and/or paroxysmal.
The differential diagnosis for SVT includes sinus tachycardia (appropriate and inappropriate), AF, AFL, AV node reentry tachycardia, AV reentry tachycardia, AT (including multifocal), accelerated junctional tachycardia (JT) (junctional ectopic tachycardia), and sinoatrial (SA) reentry tachycardia. It is important to recognize the type of tachycardia because the need for and type of acute and chronic treatment vary depending on the specific rhythm ( Algorithm 5.1 ).
Most SVTs are not life-threatening, but they can cause potential serious hemodynamic compromise, including presyncope and syncope, tachycardia-induced cardiomyopathy, congestive heart failure (CHF), and angina; palpitations and other rather nonspecific symptoms can have significant impact on quality of life. The aggressiveness of acute and long-term therapy depends on the perceived seriousness of the problem for the patient, based mainly on hemodynamic response to the arrhythmia. Before treatment, a precise rhythm diagnosis should be actively sought.
Atrial arrhythmias
Atrial Tachycardia
Description ( Algorithm 5.2A and B )
AT ( Fig. 5.1 ) is a less common type of SVT, responsible for 5% to 10% of cases of SVT. AT is suspected when there is a narrow QRS complex SVT with a long RP interval with variable coupling of the QRS to P wave interval or evidence for SVT with AV block. A long RP tachycardia can also occur in an atrioventricular reentrant tachycardia (AVRT) mediated by a slow or decrementally conducting accessory pathway, or atypical atrioventricular nodal reentrant tachycardia (AVNRT).
P-wave morphology differs from sinus but can help to predict the origin of the tachycardia. Focal AT can be difficult to distinguish from atrial reentrant tachycardia (ART) on the surface ECG, and an electrophysiology (EP) study may be necessary to distinguish the two.
Several mechanisms can be responsible for AT; it can be difficult to differentiate one mechanism from the others. They can be macroreentrant or of focal origin.
Focal ATs may be triggered by autonomic activity (sympathetic activation), increased automaticity, or triggered automaticity or may be microreentrant. Focal tachycardias may be characterized by their location (e.g., sinus nodal or ectopic to the sinus node). Automatic AT (AAT) is a focal AT that is characterized by a gradual onset (speeding up, warm-up) and gradual offset (slowing), in contrast with ARTs that may have sudden onset after a premature beat, and sudden offset. Triggered ATs may have sudden onset and offset. If they are catecholamine dependent, they may occur with exercise.
Specific pulmonary vein ectopic-triggered tachycardias may be related to effects from the parasympathetic and sympathetic nervous system and from ganglionated plexuses to initiate AF.
Whatever the mechanism of a focal AT, the approach to treatment is similar. If the tachycardia is focal, it can be ablated. Given the difficulty in mechanism differentiation, there is no specific approach to medical therapy should ablation not be first line for a specific patient and also for treatment in the acute phase of the tachycardia.
A unique and very rare form of AT is known as sinoatrial node reentrant tachycardia (SART) ( Fig. 5.2 ). SART appears because of a reentry circuit involving the SA node. The P-wave morphology is the same as or similar to the sinus P wave. This tachycardia tends to be nonsustained and somewhat irregular with a relatively normal PR interval and a consistent P-wave morphology. The tachycardia can respond to autonomic maneuvers, as well as drugs, in particular verapamil, adenosine, digoxin, and less commonly β-adrenergic blockers and amiodarone. SART can be ablated; the ablation point may be in the inferior portion of the SA node as it exits into the crista terminalis.
Reentrant ATs may be due to “macro” reentry around structural or functional barriers in the right and/or left atria, or due to microreentrant circuits. AV block can be present during AT and may result in variable or 2:1 AV conduction. It is useful to look for this because it helps to differentiate this tachycardia from AVNRT and AVRT.
Associated Conditions
Although AT may occur in normal, healthy adults, it can be associated with acute myocardial infarction (MI), acute alcohol intoxication, exacerbation of chronic obstructive pulmonary disease (COPD), electrolyte abnormalities, and digoxin toxicity (especially if accompanied by AV block); this last one is now uncommon given the doses of digoxin in current use. AT due to digoxin can occur with normal serum digoxin levels in older persons, especially if hypokalemia is present. AAT episodes are often transient in young patients but may be more persistent in older patients.
Clinical Symptoms and Presentation
As with other SVTs, symptoms range from mild palpitations to angina or symptoms of heart failure, depending on the presence and severity of underlying heart disease.
Approach to Management
AT can occur as an isolated episode related to, for example, infection and acute alcohol ingestion and does not necessarily require chronic therapy, or it may be frequent and/or recurrent, causing disabling symptoms so that long-term treatment is necessary. Chronic persistent AT can cause tachycardia-induced cardiomyopathy, a reversible form of systolic heart failure caused by chronic rapid heart rates and similar symptoms to other SVTs. Acute therapy generally consists of treating any precipitating factors and terminating with antiarrhythmic drugs. Prevention of recurrences over the long term is typically addressed with drugs or catheter ablation (success rate: 50% to 80%). Asymptomatic or minimally symptomatic patients can usually be managed as outpatients unless tachy-brady syndrome is suspected. If the P wave can be seen and is similar to that in sinus rhythm, SART could be present; the patient may respond acutely to carotid massage, adenosine, a β-adrenergic blocker, calcium channel blocker, or digoxin ( Table 5.1 ).
| Acute therapy, unstable (hypotension, angina, heart failure symptoms) |
|
| Digoxin toxicity |
|
| Stable ventricular rate < 120 bpm |
|
| Stable ventricular rate > 120 bpm |
|
| Prevention (for patients with persistent risk for AT) |
|
| MI |
|
| Preoperative/postoperative |
|
Automatic Atrial Tachycardia
Description
AAT is a rare type of SVT, responsible for less than 2% to 5% of cases. P-wave morphology differs from sinus but can help to predict the origin of the tachycardia. AAT can be difficult to distinguish from ART on the surface ECG, and an EP study may be necessary to distinguish the two. AAT is characterized by a gradual onset (speeding up) and offset (slowing), in contrast with reentrant tachycardias that may have sudden onset after a premature beat and sudden offset. AV block can be present during AAT and may result in variable or 2:1 AV conduction.
Associated Conditions
Although AAT may occur in normal, healthy adults, it is more often associated with acute MI, acute alcohol intoxication, exacerbation of COPD, electrolyte abnormalities, and digoxin toxicity (especially if accompanied by AV block); this last one is now uncommon given the lower doses of digoxin in current use. AAT can occur with normal serum digoxin levels in older patients, especially if hypokalemia is present. AAT episodes are often transient in young patients but may be more persistent in older patients.
Clinical Symptoms and Presentation
As with other SVTs, symptoms range from mild palpitations to angina or symptoms of heart failure, depending on the presence and severity of underlying heart disease.
Approach to Management
AAT can occur as an isolated episode related to, for example, infection and acute alcohol ingestion and does not require chronic therapy, or it may be frequent and/or recurrent, causing disabling symptoms. Chronic persistent AAT can cause tachycardia-induced cardiomyopathy, a reversible form of systolic heart failure caused by chronic rapid heart rates. Acute therapy generally consists of treating any precipitating factors and terminating with antiarrhythmic drugs. Prevention of recurrences over the long term is typically addressed with drugs or catheter ablation (a success rate of 50%). Asymptomatic or minimally symptomatic patients can be managed as outpatients unless severe tachy-brady syndrome is suspected ( Table 5.2 ).
| Acute therapy, unstable (hypotension, angina, heart failure symptoms) |
|
| Digoxin toxicity |
|
| Stable ventricular rate < 120 bpm |
|
| Stable ventricular rate > 120 bpm |
|
| Prevention (for patients with persistent risk for AAT) |
|
| MI |
|
| Preoperative/postoperative |
|
Atrial Reentrant Tachycardia
Description
ART ( Fig. 5.3 ) is an SVT that can be due to macroreentry (using large portions of the left or right atria) or microreentry. Macroreentrant ATs tend to occur around areas of scarring, including incisional scars from prior cardiac surgery, corrected congenital heart disease (“incisional or scar-related ART”), or trauma. ART causes 5% to 10% of SVTs. ART can be distinguished from AFL by discrete (nonsinus) P waves (which may be buried in the QRS complexes or T waves) and by their slower rate (170 to 220 bpm), but can be considered a slow atrial flutter. It can be distinguished from sinus tachycardia by its abrupt onset, persistence, and nonsinus P-wave morphology. Adenosine terminates ART in only approximately 15% of cases but can be used for diagnostic purposes because it causes transient AV block, uncovering the underlying P-wave rate and morphology. ART can be difficult to distinguish from AAT; an EP study may be needed.
Associated Conditions
ART is generally associated with structural heart disease. If ART is persistent, it can cause tachycardia-mediated cardiomyopathy or hemodynamic deterioration.
Clinical Symptoms and Presentation
Symptoms are similar to other SVTs but are also dependent on underlying heart disease.
Approach to Management
Terminating ART is the best first option, especially if the patient is symptomatic, unless ablation is planned, in which case mapping during tachycardia will be possible ( Table 5.3 ).
| Acute therapy in hemodynamically unstable patients |
|
| Subsequent therapy: Use oral antiarrhythmic drugs to prevent recurrence: Oral antiarrhythmic drugs are unlikely to cardiovert the rhythm to sinus (< 20%) but may help to maintain sinus rhythm after it is achieved. Consider oral antiarrhythmic drugs after cardioversion or if recurrent ART paroxysms. | |
| |
| Chronic therapy |
|
| MI |
|
| Preoperative |
|
| Postoperative |
|
| Pregnancy |
|
Multifocal Atrial Tachycardia
Description
MAT ( Fig. 5.4 ) is an SVT in which there are at least three distinct P-wave morphologies, indicating multifocality of the rhythm. The PP, PR, and RR intervals vary, and the ventricular rate is more than 100 bpm, usually ranging from 110 to 170 bpm. The multiple P-wave morphologies result from multiple depolarizing foci in the atria. The underlying mechanism may be enhanced automaticity or triggered activity. Whereas MAT is usually the predominant rhythm at a given time and does not occur in short bursts, on occasion other atrial arrhythmias (premature atrial complexes [PACs], AAT, sinus tachycardia, and even AFL and AF) may precede or follow a bout of MAT. The irregularly irregular ventricular rate can mimic AF. Differentiation from “coarse” AF can be made by the absence of isoelectric periods between P waves in AF. Distinction of MAT and AF is important because management strategies differ considerably.
Associated Conditions
The vast majority (approximately 60% to 85%) of cases occur in acutely ill older patients with severe COPD. However, in addition to COPD, MAT has been associated with severe coronary artery disease (CAD), cor pulmonale, pneumonia, sepsis, postoperative states, lung cancer, pulmonary embolism, congestive (usually systolic) heart failure, hypertensive heart disease, and other acute cardiac or pulmonary processes. Exacerbating factors include theophylline toxicity, catecholamine infusions, hypokalemia, hypomagnesemia, hypoxia, and acidosis. MAT usually lasts for days to weeks, especially in patients with exacerbations of COPD, and recurrences are common in acutely ill patients. Although MAT itself is rarely life-threatening (exception: rapid rate induces ischemia in those with severe coronary disease), acute mortality is approximately 30% to 40% because of the severity of the underlying disease, rather than the rhythm per se. MAT is rarely associated with acute MI.
Clinical Symptoms and Presentation
MAT is often asymptomatic but can be associated with rapid, irregular palpitations. Associated symptoms usually reflect the underlying illness (e.g., breathlessness in a COPD exacerbation).
Approach to Management
Primary treatment of MAT is extremely difficult and unrewarding because without effective treatment of the underlying disease the rhythm tends to persist; therapy should be directed at the acute illness. Electrolyte abnormalities should be corrected. Calcium channel blockers are preferable to β-adrenergic blockers, particularly if the underlying acute illness is COPD with bronchospasm ( Table 5.4 ).
| Acute therapy, stable and unstable |
|
| Chronic prevention |
|
| MI |
|
Atrial fibrillation
Description
AF is the most common SVT that requires long-term therapy. Depolarization of the atria occurs in rapid, multiple waves, with continuously changing pathways. Intraatrial activation can be recorded as irregular, rapid depolarizations, often at rates greater than 300 to 400 bpm. These depolarizations result in loss of coordinated atrial contraction and in irregular conduction to the ventricle due to irregular arrival and decremental conduction of impulses in the AV node. On the surface ECG, discrete P waves are absent and irregular fibrillatory waves are seen; the ventricular response is irregularly irregular and can be fast (> 100 bpm; Fig. 5.5 ), moderate (60 to 100 bpm; Fig. 5.6 ), or slow (< 60 bpm; Fig. 5.7 ), unless complete AV block is present, in which case the QRS rhythm results from a regularly firing escape focus ( Fig. 5.8 ). At times, the irregular fibrillatory waves are accompanied by more regular, but still varying, flutter-like waves ( Fig. 5.9 ); this still represents AF rather than AFL. MAT (see Fig. 5.4 ) and sinus with frequent PACs ( Fig. 5.10 ) can mimic AF with its irregularly irregular rhythm but are distinguished from AF by the presence of P waves preceding each QRS complex.
In the presence of an underlying BBB (or intraventricular conduction delay), AF can present as a wide QRS complex rhythm ( Fig. 5.11 ) that could mimic ventricular tachycardia (VT) (except that AF remains irregularly irregular). Intraventricular aberrancy with a BBB pattern can result in wide QRS complexes and occasionally mimic VT if the BBB pattern is not classic. Aberration is usually initiated by a long-short sequence (Ashman phenomenon) ( Fig. 5.12 ); RBBB aberration is more common than left bundle branch block (LBBB) aberration in the absence of structural heart disease. AF at extremely high ventricular rates (e.g., 200 to 300 bpm) should suggest the presence of a bypass tract ( Fig. 5.13 ), and the wide QRS complex is typically due to conduction down the bypass tract. Another instance of an irregularly irregular wide QRS complex tachycardia is AF in the setting of a dual-chamber pacemaker, in which the pacemaker tracks atrial activations at or near its upper rate limit.
Triggering sites, typically arising from the ostia of the pulmonary veins, have been recognized to initiate AF, particularly in lone AF (AF without structural heart disease). These triggers can potentially be ablated or isolated from atrial tissue using catheter-based or surgical pulmonary vein isolation, aiming for long-term cure.
Associated Conditions
AF occurs in normal, healthy adults (“lone” AF) but is often associated with structural heart disease (ischemic, valvular [especially mitral], rheumatic, cardiomyopathic, congenital). Other associated conditions include advancing age, hypertension, diabetes mellitus, postoperative states (especially after cardiac surgery with incidences after aortocoronary bypass procedures ranging from 15% to 40%, and after valve surgery, 40% to 60%), pericarditis, pulmonary embolism, chronic lung disease, thyrotoxicosis, acute alcohol ingestion (“holiday heart”), excessive caffeine, drugs (especially sympathomimetic drugs), autonomic fluctuation (vagal or sympathetic), hypokalemia or other metabolic derangements, systemic infection, sinus node dysfunction (tachy-brady syndrome), degenerative conduction system disease, and Wolff-Parkinson-White (WPW) syndrome. Long-term consequences include the risk of embolic stroke or transient ischemic attack (TIA) (with incidences in rheumatic AF of 10% to 12% per year; nonvalvular AF of 1% to 7% per year) and reduced exercise capacity due to reduction in stroke volume caused by loss of atrial kick and to left ventricular (LV) dysfunction (impaired diastolic filling during rapid ventricular response, tachycardia-mediated cardiomyopathy). There is a twofold increase in mortality in AF patients, possibly related to underlying heart disease and proarrhythmia rather than AF per se.
Clinical Symptoms and Presentation
Depending on the presence and severity of underlying heart disease, patients may be asymptomatic and have mild palpitations or significant symptoms, such as angina, CHF, syncope, or hemodynamic collapse. Symptoms may occur due to rapid rates, irregularity of the rhythm, and loss of AV synchrony and the atrial kick. AF is strongly associated with TIA, stroke, or other thromboembolic complications, which are not infrequently the initial manifestation of AF that has not been previously known to exist. AF is the most common cause of cardioembolic stroke and is a common cause of cryptogenic stroke.
AF may be categorized by its presentation into several types. Newly diagnosed AF characterizes patients presenting with AF for the first time, regardless of duration. Paroxysmal AF is AF that self terminates, usually within 48 hours after its onset (but sometimes up to 7 days). Persistent AF lasts more than 7 days or requires an intervention (pharmacologic or electrical) for cardioversion. Long-standing persistent AF is AF that has persisted continuously for more than 1 year. Permanent AF is AF that has been accepted to remain with either failure of rhythm control efforts and/or no additional efforts planned to restore sinus rhythm.
Approach to Management
The management of AF can be focused into three main aspects: (1) control of the ventricular rate (rate control), (2) control of the atrial rhythm (rhythm control), and (3) antithrombotic therapy to reduce the risk of stroke and other thromboembolic complications. For any patient with AF, all three aspects of management should be considered, but all are not necessarily required for a given patient.
Acute management of symptomatic AF with rapid ventricular rates includes consideration of urgent electrical cardioversion if there is evidence of hemodynamic instability, significant myocardial ischemia, or pulmonary edema. Electrical or pharmacologic cardioversion is also reasonable therapy for new-onset symptomatic AF. Ventricular rate control can usually be attempted while preparing for cardioversion, using intravenous (IV) or oral β-adrenergic blockers, diltiazem or verapamil, or digoxin (see Table 5.5 ). Rhythm control with intent to convert the AF to sinus rhythm can be begun with pharmacologic or electrical cardioversion. Anticoagulation strategies should be addressed before conversion. If the AF duration is more than 24-48 hours, anticoagulation with warfarin with international normalized ratios (INRs) therapeutic (between 2 and 3) or NOACs (e.g., dabigatran, rivaroxaban, apixaban, or edoxaban) for at least 3 weeks is needed and should be documented. Alternatively, if left atrial thrombus is not demonstrated by transesophageal echocardiography (TEE) and the patient is therapeutically anticoagulated (with heparin, warfarin with INR ≥ 2.0, or NOACs), cardioversion can be done and anticoagulation with warfarin or an NOAC initiated or continued for at least 3 to 6 weeks and indefinitely for many patients with risk factors. For AF duration of less than 48 hours, anticoagulation should still be considered, particularly if the patient has structural heart disease or risk factors for stroke or thromboembolism. Anticoagulation should be strongly considered for the postcardioversion period. Cardioversion can be attempted by electrical means or by antiarrhythmic drugs. The latter may include oral class I or class III antiarrhythmic drugs, such as IV ibutilide, procainamide, or amiodarone. A new drug, vernakalant, not yet approved, appears to also be highly effective to convert AF to sinus rhythm.
| Rate Control | Achievement and Maintenance of Sinus Rhythm | Antithrombotic Therapy | |
|---|---|---|---|
| Pharmacologic | β-adrenergic blockers Ca 2 + -channel blockers Digoxin | Antiarrhythmic drugs Class IA
Class IC
Class III
| Warfarin, heparin, LMWH NOAC
|
| Nonpharmacologic | AV junction ablation and pacing | Catheter ablation/PVI Surgical maze/PVI | LAA ligation, removal, or occlusion |
Long-term management should include all three aspects of management listed previously here, as well as evaluation for underlying structural heart disease, risk factors for stroke or thromboembolism, or other associated conditions associated with AF. However, appropriate management of associated conditions does not guarantee that AF will not recur. Evaluation includes an echocardiogram to assess for ventricular dysfunction, valve disease, and atrial size. Treadmill exercise testing and/or cardiac catheterization to assess coronary anatomy may be indicated in selected patients and/or patients considered for class IC (flecainide or propafenone) antiarrhythmic drugs. Patients with structural heart disease or CAD should not be treated with class IC drugs. Thyroid function tests should be checked at least once because hyperthyroidism can initiate AF. Anticoagulation using warfarin, a NOAC, aspirin, or aspirin plus clopidogrel should be considered in all patients. Ventricular rate control can be generally achieved with β-adrenergic blockers, diltiazem, or verapamil; digoxin can be used but is not a direct AV nodal blocker, and its AV nodal blocking effect will generally be lost with the vagolysis of activity. Rhythm control, with restoration and maintenance of sinus rhythm using cardioversion and/or antiarrhythmic therapy, should be considered; even though no significant overall survival benefit has been demonstrated for either approach, rhythm control is important in selected highly symptomatic patients (often with lone AF) in whom better survival in sinus rhythm and improved functional status and quality of life can be demonstrated. Because AF can be clinically silent, it is important that anticoagulation not be discontinued in patients at risk for thromboembolic complications, even if sinus rhythm appears during clinical follow-up to be maintained. Those patients who remain anticoagulated with warfarin or a NOAC have a lower risk of stroke. For new-onset AF or for those with continued symptoms despite rate control, a rhythm control strategy is still beneficial and is recommended ( Table 5.5 ).
Rate-Control Strategies
The mainstays of ventricular rate control are the β-adrenergic blockers, diltiazem or verapamil, and digoxin. IV AV nodal blocking drugs may be most efficacious and easily titrated during acute management of rapid ventricular rates. Digoxin is less effective, although it can be used in patients with CHF, but has a delayed onset, narrow therapeutic window, and less effect in hyperadrenergic states (e.g., in postoperative states, intensive care units). For patients in whom sinus rhythm cannot be maintained and who have continued difficulty with rapid ventricular rates despite medical therapies, AV junction ablation with implantation of a rate-responsive permanent ventricular pacemaker can improve symptoms and ventricular function. This approach can also be used in patients with paroxysmal AF (in whom dual-chamber pacing is recommended). AV junction ablation results in complete heart block (CHB) with a QRS rhythm originating in ventricular tissue, usually at rates in the 30s; the functional LBBB induced by RV apical pacing can lead to intraventricular dyssynchrony and reduced left ventricular ejection fraction (LVEF). In these cases, upgrading the pacing system to a biventricular one (cardiac resynchronization therapy) may be of benefit.
Rhythm-Control Strategies
Electrical cardioversion is the most effective way to terminate AF. One method to control AF is to perform cardioversion whenever AF episodes occur. This is appropriate if the AF episodes are not too closely spaced in time. Those patients who are most likely to have recurrence of AF after cardioversion include those who have large left atria, who are older, and who have had episodes of long duration.
Control of blood pressure and avoidance or treatment of any identified precipitating conditions or clinical triggers, such as stimulant use or hyperthyroidism, may be potentially helpful in reducing the risk of AF.
Pharmacologic cardioversion is less effective when there is long-standing AF. In some instances, after cardioversion, there is immediate or early return of AF; in these cases IV verapamil or IV ibutilide can help to maintain sinus rhythm after cardioversion. In addition, atropine IV may be useful in patients who have slow rates with their AF and may have high vagal tone that reinitiates the arrhythmia. Slow ventricular rates in AF (see Fig. 5.7 ) do not necessarily portend slow rates in sinus rhythm after cardioversion, but caution must be used, especially in patients who have been taking digoxin because they are at risk for malignant ventricular arrhythmias after cardioversion.
Antiarrhythmic drugs that can help to maintain sinus rhythm (and even help to stop AF in some instances) include class IA (quinidine, procainamide, disopyramide), class IC (flecainide, propafenone), and class III (sotalol, dofetilide, amiodarone, dronedarone) drugs.
The success rate of maintaining sinus rhythm is approximately 50% to 70%, depending on the drug and the definition of success; however, the goal of medical therapy to control the rhythm is to decrease the incidence of symptomatic AF, not necessarily to suppress the AF completely, which might require higher doses of antiarrhythmic drugs with their attendant side effects or toxicity. Thus recurrences are expected, and occasional recurrences do not necessarily constitute failure of this approach. Antiarrhythmic drug selection is individualized, based on the presence of structural heart disease or other individual factors, such as patient compliance with the regimen. In patients with no or minimal structural heart disease, flecainide, propafenone, sotalol, or dronedarone are first-line choices, followed by dofetilide and amiodarone. For these patients, flecainide or propafenone can be given intermittently on a pro rata nata (PRN) basis during episodes of AF (“pill in the pocket”). Dofetilide must be started in the hospital. For patients with hypertension and significant LV hypertrophy, amiodarone or dronedarone is recommended. For patients with CAD, IC drugs (flecainide, propafenone) must be avoided. First-line therapy for these patients includes sotalol, dronedarone, and dofetilide, followed by amiodarone. For patients with heart failure, amiodarone or dofetilide are first-line therapies and dronedarone should be avoided. Class IA antiarrhythmic drugs are rarely used because of high risk of toxicity and side effects.
The reason to use antiarrhythmic drug therapy is to reduce the risk of recurrent AF and in most cases to prevent symptoms. It is not clear how many patients have AF that remains undetectable or undetected, although implanted device interrogation suggests that up to 50% of AF episodes are unassociated with symptoms and therefore not detected clinically. Although symptom reduction is the main reason to treat AF, other reasons also are important to recognize, including the progression of ventricular dysfunction caused by tachycardia and symptomatic heart failure.
Another nonpharmacologic adjunctive therapy includes permanent pacemaker implantation for tachy-brady syndrome when long pauses and/or symptomatic bradycardia is present. Permanent pacemakers can be indicated in patients with symptomatic post-AF conversion pauses or other symptomatic bradyarrhythmias (including those due to ventricular rate control medications). Dual-chamber (DDD) pacing in which AV synchrony is preserved and the atria may be paced to avoid atrial bradycardia is associated with less AF recurrences than single chamber ventricular (VVI) pacing systems. Some pacemakers have an option of allowing atrial overdrive pacing just above the continuously sensed sinus rate to prevent irregularities of rate and pauses that may be related to the initiation or reinitiation of AF.
Potential curative catheter ablation directed toward electrical isolation of the pulmonary vein ostia and other arrhythmogenic atrial substrates can be considered for patients with symptomatic AF who have not responded to an antiarrhythmic drug. Radiofrequency (RF) or other energy or freezing (e.g., cryoablation) is applied segmentally or circumferentially to the antra of the pulmonary vein ostia to isolate the ostia. Fractionated electrical potentials, sites of vagal attachments, or ganglionated plexes or connecting areas between ostia may be targeted. The surgical maze or surgical pulmonary vein isolation procedure can be performed with minimally invasive or open cardiac surgical approaches. The maze procedure is performed by making incisions and resuturing the atria or by applying RF, cryo ablation, or other energy to create lines of conduction block. Much of the success of this approach has likely been due to the surgically created pulmonary vein antral isolation, and modifications of the maze procedure, including pulmonary vein isolation approaches, have been developed. Currently, surgical ablation is most commonly performed as a concomitant procedure during other cardiac operations.
Anticoagulation
Because stroke is one of the most important clinical consequences of and a source of major morbidity associated with AF, addressing anticoagulation is critical with each step in the management of AF. Multiple risk stratification schemes have been published. Two useful scoring systems for assessing thromboembolic risk are the CHADS 2 score ( Table 5.6A ), and the CHA 2 DS 2 -VASc score ( Table 5.6B ), which are two schemes for identifying patients at high and low risk for stroke. Recommended guidelines for long-term antithrombotic therapy are listed in Table 5.7 . Studies also suggest that for patients with AF who are at risk for stroke but who have contraindications to warfarin, aspirin plus clopidogrel may be beneficial. The magnitude of benefit is not as great as warfarin, and the magnitude of benefit over aspirin is relatively small. This combination therapy is associated with a higher risk of bleeding than with aspirin alone. Dabigatran, a direct thrombin inhibitor, and several factor Xa inhibitors, rivaroxaban, edoxaban, and apixaban (commonly, the group is known as non-vitamin K oral anticoagulants [i.e., “NOACs”]) were approved for reduction of the risk of stroke and systemic embolism in patients with nonvalvular AF. See Chapter 12 for further anticoagulation information. Left atrial appendage occlusion or resection is also an approach for reducing thromboembolic complications for those patients who cannot take an anticoagulant or refuse to take one but are at high risk of thromboembolic events ( Algorithm 5.3 ).
