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AUTHOR AND EDITOR INFORMATION

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Author: Shubhayan Sanatani, MD, Assistant Professor, Department of Pediatrics, University of British Columbia at Vancouver; Consulting Staff, Division of Pediatric Cardiology, Children's and Women's Health Center of British Columbia

Shubhayan Sanatani is a member of the following medical societies: Alpha Omega Alpha, British Columbia Medical Association, Canadian Cardiovascular Society, Canadian Heart Rhythm Society, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Heart Rhythm Society, and Royal College of Physicians and Surgeons of Canada

Coauthor(s): Robert Murray Hamilton, MD, MSc, FRCPC, Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto, Canada

Editors: Charles Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Hugh D Allen, MD, Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine; Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Author and Editor Disclosure

Synonyms and related keywords: supraventricular tachycardia, atrial ectopic tachycardia, AET, ectopic atrial tachycardia, automatic atrial tachycardia, arrhythmia, tachycardia-induced cardiomyopathy, bundle branch block, sinus tachycardia, first-degree atrioventricular block, AV block, second-degree atrioventricular block, congenital heart disease, exercise intolerance, congestive heart failure, hyperthyroidism, anemia, catecholamine-producing malignancy, hepatic congestion, pulmonary congestion, respiratory syncytial virus

INTRODUCTION

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Background

Atrial ectopic tachycardia (AET) is a rare arrhythmia; however, it is the most common form of incessant supraventricular tachycardia (SVT) in children. AET is believed to be secondary to increased automaticity of nonsinus atrial focus or foci. This arrhythmia, which is also known as ectopic atrial tachycardia or automatic atrial tachycardia, has a high association with tachycardia-induced cardiomyopathy. AET is often refractory to medical therapy and is not usually responsive to direct current (DC) cardioversion.

The diagnosis of AET is based on the presence of a narrow complex tachycardia (in the absence of aberrancy or preexisting bundle branch block) with visible P waves at an inappropriately rapid rate. The rates range from 120-300 beats per minute (bpm) and are typically higher than 200 bpm, although physiologic rates may be observed. The P-wave axis is usually abnormal, although a focus near the sinus node can be mistaken for sinus tachycardia. Similarly, the P-wave morphology may be abnormal. Onset of the tachycardia occurs with a P wave identical to the subsequent P waves. The tachycardia may exhibit a "warming up," which refers to a progressively shortening P-P interval for the first few beats of the arrhythmia. Similarly, a "cooling down" may be observed at its termination. First-degree atrioventricular (AV) block is typical and second-degree AV block is common. The tachycardia cycle length and degree of AV block are influenced by the autonomic tone.

Pathophysiology

Spontaneous depolarization is a phenomenon of automatic myocardium. The sinus node is usually the pacemaker of the heart because it has the most rapid spontaneous rate of firing. A small cluster of cells with abnormal automaticity is presumed to be responsible for AET. The conduction spreads from this cluster to the surrounding atrium and to the ventricles via the AV node. A conduction delay from atrium to ventricle often occurs, with most patients demonstrating first-degree AV block and some showing second-degree block.

Because AET is often incessant, tachycardia-induced cardiomyopathy is commonly observed. Although the exact underlying mechanism of the development of cardiac dysfunction in the setting of chronic arrhythmias is unknown, numerous reports have documented improved cardiac function following ventricular rate control and treatment of the arrhythmia.

Frequency

International

Although the exact incidence is unknown and few large series have been reported, AET is reported to comprise 5-10% of pediatric SVTs. Although estimates of the incidence of pediatric SVTs widely vary, AET likely occurs with an incidence of approximately 1 case per 10,000 children.

Mortality/Morbidity

Tachycardia is generally well tolerated. Syncope is unusual, and cardiac arrest is rare, except when encountered as a complication of treatment. Tachycardia-induced cardiomyopathy is the most significant sequela of AET and may be insidious. The time to development depends on the rate and duration of the tachycardia; however, ventricular dilatation may be present on initial presentation. This can also be reversed with successful treatment of the arrhythmia.

Age

The arrhythmia is predominantly observed in infants and children; this accounts for a peak of 11-16% of tachycardias for which a mechanism is determined in young childhood. A review from Texas Children's Hospital suggests that children younger than 3 years have a better response to medication and a higher rate of spontaneous resolution of the arrhythmia.1 The adult form of AET may have a different etiology and natural history than the pediatric form.


CLINICAL

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History

Although atrial ectopic tachycardia (AET) is occasionally encountered in patients following surgery for congenital heart disease, most patients have structurally normal hearts and are symptomatic. Palpitations, chest pain, lightheadedness, presyncope, and dyspnea are the most common symptoms.

Asymptomatic or preverbal patients may be noted to be tachycardic or dyspneic on routine evaluation. Difficulty feeding or diaphoresis may accompany the tachycardia in infants.

Exercise intolerance and congestive heart failure are late manifestations of secondary cardiac dysfunction.

The history must be sufficiently broad to rule out causes of persistently elevated heart rates, such as hyperthyroidism, anemia, or catecholamine-producing malignancy. The family history is rarely positive for AET.

Physical

The heart rate is inappropriately elevated for the degree of activity. If second-degree AV block is present, the heart rate may be irregular. The patient may be tachypneic. In advanced cardiomyopathy, pulses and perfusion are poor and evidence of cardiac enlargement is present. Hepatic and pulmonary congestion may be present.

Causes

AET is usually idiopathic. Occasionally, mycoplasmal or viral infections, such as respiratory syncytial virus, may trigger this arrhythmia, although more complex atrial tachycardias, such as chaotic atrial tachycardia, are more frequently found in this scenario. Atrial tumors have been reported to be associated with AET. Reports of familial cases with an autosomal dominant inheritance are present in the literature.


DIFFERENTIALS

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Atrial Flutter

Other Problems to be Considered

The differential diagnosis for a narrow complex tachycardia is extensive, and the term supraventricular tachycardia (SVT) is nonspecific. Differentiation of automatic versus reentrant mechanisms may be determined by the presence of a warm-up or cool-down period at onset and termination and by the response to vagal maneuvers or adenosine. A right-sided atrial ectopic tachycardia (AET) focus in the presence of tachycardia-induced cardiomyopathy must be differentiated from idiopathic dilated cardiomyopathy with a secondary compensatory sinus tachycardia; the degree of dysfunction and heart rate are higher and second-degree AV block is more common in patients with AET. AET must also be differentiated from atypical AV node reentry, permanent junctional reciprocating tachycardia, and inappropriate sinus tachycardia. The former 2 usually respond to adenosine with abrupt termination.

Inappropriate sinus tachycardia typically occurs in association with exercise intolerance and a mild elevation of a sinus rate, more commonly in females. Approximately one half of patients with AET demonstrate transient atrial slowing with adenosine, whereas the others demonstrate only transient AV block. Aberrantly conducting AET must be differentiated from ventricular tachycardia (VT).


WORKUP

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Lab Studies

  • Assess electrolyte levels, hematocrit levels, and thyroid function.
  • Consider thyroid studies or urine collections in some patients for assessment of possible pheochromocytoma.

Imaging Studies

  • Perform echocardiography with focus on cardiac function and dimensions to rule out cardiomyopathy and associated congenital heart disease. The earliest manifestation of cardiomyopathy may be ventricular dilatation. A decreased shortening fraction follows. Reversal of these findings after treatment follows a reciprocal pattern. Diastolic function abnormalities may also occur in tachycardia-induced cardiomyopathy and may be the last parameter to correct after therapy.
  • Atrial angiography may occasionally be helpful as a roadmap during radiofrequency (RF) catheter ablation.

Other Tests

  • During the arrhythmia in stable patients, 12-lead electrocardiography (ECG) is necessary.
    • Inspect the ECG for P-wave axis and morphology, ventricular rate, and conduction block. Ectopic atrial tachycardia usually creates a P wave that is at least slightly different from sinus rhythm, first-degree AV block, and possible periods of second-degree AV block without termination of tachycardia.
    • To differentiate atrial ectopic tachycardia (AET) from sinus tachycardia secondary to cardiomyopathy, Gelb and colleagues demonstrated that negative late terminal P-wave forces in lead V2 occur more commonly in AET.2 The rate is also usually higher in AET.
    • Algorithms to determine the site of the ectopic focus based on P-wave morphology are known. A negative or biphasic (positive, then negative) P wave in lead V1 indicated a right atrial tachycardia. A positive or biphasic (negative, then positive) P wave in ECG lead V1 indicated a left atrial tachycardia.3
  • Patients should undergo Holter monitoring to determine the time spent in tachycardia and the ventricular rates. Holter monitoring is particularly useful in identifying and analyzing onsets and offsets of tachycardia.
  • The Holter monitor findings often facilitate the diagnosis by (1) revealing an elevated average heart rate over a 24-hour period, with reduced circadian variability; (2) revealing a higher peak heart rate than normally encountered in sinus rhythm; or (3) revealing periods of AV block, demonstrating 2 consecutive P waves at an elevated rate without an intervening QRS complex.
  • Exercise testing may occasionally unmask an intermittent AET.

Procedures

  • Although invasive studies are not usually necessary to make a diagnosis of AET, in some patients, an esophageal electrophysiology recording may be useful to assist confirmation of the diagnosis; the response to overdrive pacing can also be assessed. Many automatic foci transiently suppress when overdrive pacing is performed.
    • An invasive electrophysiology study can also be performed for these indications, but this is usually performed in patients undergoing attempt at RF ablation.
    • In patients with ectopic atrial tachycardias arising from the pulmonary veins, an esophageal recording may also be helpful in localizing the site of tachycardia.
  • The response of AET to adenosine may be persistent in the setting of AV block or a transient slowing of the tachycardia; it rarely terminates. DC cardioversion usually does not terminate the arrhythmia.

Histologic Findings

  • Endomyocardial biopsy findings often reveal vacuolized myocytes in the setting of tachycardia-induced cardiomyopathy.


TREATMENT

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Medical Care

  • Acute atrial ectopic tachycardia (AET)
    • For patients who present in cardiac arrest or with hemodynamic compromise, establish ABCs (as is standard); provide appropriate monitoring; make sure that a defibrillator is available; and attempt conversion with a defibrillator if necessary.
    • Patients with AET may present with circulatory collapse similar to patients with cardiomyopathy. Although these patients may benefit from afterload reduction and inotropy, primary therapy aimed at reversing their tachycardia is usually more successful.
    • Immediate rate control is desired in the child who requires significant ICU support, including intubation. This can often be achieved without resorting to negatively inotropic antiarrhythmic agents. Digitalization and the use of intravenous amiodarone may quickly achieve rate control relatively. An additional maneuver involves the use of atrial pacing (eg, esophageal, transthoracic, transvenous) to overdrive the atrial tachycardia to a point of consistent 2:1 AV block, thus lowering the ventricular response rate. In the era of RF ablation, most patients who require this degree of support undergo an attempt at ablation of the focus, particularly if it is an incessant tachycardia.
    • More frequently, patients are evaluated in the clinical setting, and hospitalization is often only necessary for initiation of certain antiarrhythmic medications.
  • Chronic AET
    • Three options are available for treatment of patients with AET, including medication to suppress the arrhythmia or control the ventricular response, surgery, or RF ablation. Long-term oral medication is the mainstay of therapy in patients not undergoing RF ablation. Class IC and III antiarrhythmic agents are generally the most effective, and a staged approach is recommended. Medical therapy may be effective in as many as 75% of patients, but more than one medication is usually needed.
    • RF ablation has been very successful in curing AET, with success rates ranging from 75-100%. The complication rates are similar to other RF ablation procedures, with a higher risk of recurrence. The encircling technique uses 2 catheters capable of delivering RF energy as mapping catheters, alternating the reference and roving catheters until no site provides an earlier signal than the reference. This early reference catheter is then used to deliver ablation.
    • Noncontact mapping systems have gained an increasing role in the ablation of AET.4 The ability to localize the focus, including a nonsustained focus, with accuracy is an advantage of this technique. A limitation in the pediatric population is the size of the equipment and duration of the procedures.

Surgical Care

  • Although surgical cryoablation has previously been used to treat patients with AET, this has been primarily supplanted by catheter RF ablation techniques.

Diet

  • Historically, patients have been advised to avoid caffeine and chocolate. The role of these dietary elements must be assessed in the individual patient; most cases are not related to these dietary elements.


MEDICATION

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Drugs with some effect in atrial ectopic tachycardia (AET) include digoxin (used predominantly for rate control), amiodarone, propafenone, flecainide, procainamide, and esmolol. Only digoxin and oral amiodarone are devoid of negative inotropic effect. Adequate control may not require the complete abolition of all atrial ectopic beats or runs.

Drug Category: Antiarrhythmic agents

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Drug NameDigoxin (Lanoxin, Lanoxicaps)
DescriptionCardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. Used to control ventricular rate when administering propafenone, flecainide, or procainamide.
Adult Dose0.125-0.375 mg PO qd
Pediatric DoseDigitalizing dose (administer one half of the total digitalizing dose [TDD] initially, then one fourth of TDD at 6- and 12-h intervals):
1 month to 2 years: 35-60 mcg/kg PO
2-5 years: 30-40 mcg/kg PO
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: Use 25-35% of PO loading dose
ContraindicationsDocumented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
InteractionsMedications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (eg, carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsHypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patients to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are within the reference range; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Drug NameAmiodarone (Cordarone)
DescriptionMay inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Before administration, control ventricular rate and CHF (if present) with digoxin.
Adult DoseLoading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk, then decrease to 600-800 mg/d in 1-2 doses for 1 mo
Alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h, then 540 mg over next 18 h
Maintenance dose: 400 mg PO qd
Pediatric DoseLoading dose: 10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained, reduce to 5 mg/kg/d or 200-400 mg/1.73 m2/d for several wk (limited data available for IV loading dose)
Maintenance dose: 2.5 mg/kg/d PO or lowest effective dose following loading dose
ContraindicationsDocumented hypersensitivity; complete AV block; intraventricular conduction defects
InteractionsIncreases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and further decrease myocardial contractility; cimetidine may increase levels
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in breastfeeding women; caution in thyroid or liver disease; may cause proarrhythmic effect, optic neuritis, CNS toxicity, hypothyroidism, hepatotoxicity, interstitial pneumonitis, or pulmonary fibrosis

Drug NameEsmolol (Brevibloc)
DescriptionExcellent drug for use in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
Adult DoseLoading dose: 250-500 mcg/kg/min IV for 1 min followed by a 4-min maintenance infusion of 50 mcg/kg/min IV; if adequate therapeutic effect (ie, decreased HR and BP) not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 100 mcg/kg/min for 4 min; sequence may be repeated q5-10min, increasing maintenance infusion by 50 mcg/kg/min with each sequence; not to exceed 200 mcg/kg/min
Pediatric DoseInfants and children: Limited information available; suggested dose is 100-500 mcg/kg IV over 1 min initial; followed by 200 mcg/kg/min IV; titrate upward by 50-100 mcg/kg/min q5-10min until heart rate or BP decreases by >10%; typical dose 550 mcg/kg/min (range is 300-1000 mcg/kg/min)
ContraindicationsDocumented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
InteractionsAluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsBeta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; slowly withdraw drug and closely monitor patient

Drug NamePropafenone (Rythmol)
DescriptionTreats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period.
Adult Dose150 mg PO q8h initial; may increase q3-4d; not to exceed 300 mg q8h
Pediatric DoseInfants and children: Not established, the following doses have been suggested:
150-400 mg/m2/d PO divided tid/qid; may increase by 100 mg/m2/d q2-3d to achieve adequate control; not to exceed 600 mg/m2/d
Alternatively, 8-10 mg/kg/d PO divided tid/qid; may increase by 2 mg/kg/d to achieve adequate control; not to exceed 20 mg/kg/d
ContraindicationsDocumented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure; coadministration with ritonavir or amprenavir
InteractionsInhibits CYP2D6 and may decreases serum levels of isoenzyme substrates (eg, rifampin, cimetidine, quinidine, warfarin); inhibitors of CYP2D6 (eg, beta-blockers, amiodarone, paroxetine, fluoxetine, ritonavir), CYP1A2 (eg, cimetidine, ritonavir), or CYP3A4 (eg, amprenavir, ritonavir, erythromycin, amiodarone, fluoxetine) may increase blood levels
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsShould only be used for life-threatening arrhythmias; caution in congestive heart failure, myocardial infarction, or hepatic dysfunction (adjust dose)

Drug NameFlecainide (Tambocor)
DescriptionTreats life-threatening ventricular arrhythmias. Causes a prolongation of refractory periods and decreases action potential without affecting duration. Blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart with greatest effect on the His-Purkinje system (H-V conduction). Effects upon AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.
Adult Dose100 mg PO q12h; may increase by 100 mg/d q4d until adequate response achieved; not to exceed 400 mg/d
Pediatric DoseInitial dose: 1-3 mg/kg/d or 50-100 mg/m2/d PO divided tid; may increase gradually by 50 mg/m2/d q5d until adequate response achieved; not to exceed 8 mg/kg/d (200 mg/m2/d); children <6 mo initiate at lowest dose
Maintenance dose: Typical dose is 3-6 mg/kg/d or 100-150 mg/m2/d PO divided tid
ContraindicationsDocumented hypersensitivity; third-degree AV block; right bundle branch block when associated with left hemiblock (bifascicular block) if pacemaker not in place; cardiogenic shock
InteractionsBeta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; may increase digoxin serum levels; CYP2D6 inhibitors (eg, ritonavir, amiodarone, cimetidine) may increase serum levels and cardiotoxicity
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsBecause of proarrhythmic effect and associated deaths, should only be used for life-threatening arrhythmias; caution in renal or hepatic impairment (adjust dose), CHF, and post-MI

Drug NameProcainamide (Procan, Pronestyl)
DescriptionClass IA antiarrhythmic used for PVCs, ventricular tachycardias, and SVTs. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult Dose0.5-1 g PO q6h (as SR)
Loading dose: 30 mg/min IV at continued infusion rates until arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered
Once arrhythmia is suppressed, may infuse at continuous rate of 1-4 mg/min
Pediatric DoseNot established; the following doses have been suggested:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
Loading dose: 3-6 mg/kg/dose IV infused over 5 min; not to exceed 100 mg/dose; may repeat q5-10h to a maximum of 15 mg/kg per loading dose
Maintenance dose: 20-80 mcg/kg/min IV; not to exceed 2 g/d
ContraindicationsDocumented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker not in place; torsade de pointes; systemic lupus erythematosus
InteractionsIncreased levels of procainamide metabolite NAPA when coadministered with cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; coadministration with sparfloxacin may increase risk of cardiotoxicity
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMonitor for hypotension; plasma concentrations of procainamide and active metabolite (NAPA) may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency (adjust dose)


FOLLOW-UP

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Complications

  • Atrial ectopic tachycardia (AET) is one of the incessant tachycardias, which may become associated with myocardial dysfunction if the average ventricular rate remains elevated over a long term.

Prognosis

  • Several reports have documented the spontaneous remission of AET in the pediatric population and in young adults.5 This may occur in as many as one third of patients following withdrawal of medication.

Patient Education


MISCELLANEOUS

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Special Concerns

  • Patients with atrial ectopic tachycardia (AET) should be monitored by a cardiologist.
  • RF ablation can be curative and performed with a high degree of success, a low complication rate, and a low recurrence rate.


REFERENCES

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  1. Salerno JC, Kertesz NJ, Friedman RA, Fenrich AL Jr. Clinical course of atrial ectopic tachycardia is age-dependent: results and treatment in children or =3 years of age. J Am Coll Cardiol. Feb 4 2004;43(3):438-44. [Medline].
  2. Gelb BD, Garson A Jr. Noninvasive discrimination of right atrial ectopic tachycardia from sinus tachycardia in "dilated cardiomyopathy". Am Heart J. 1990;120:886-91. [Medline].
  3. Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. Sep 5 2006;48(5):1010-7. [Medline].
  4. Higa S, Tai CT, Lin YJ, et al. Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation. Circulation. Jan 6 2004;109(1):84-91. [Medline]. [Full Text].
  5. Bauersfeld U, Gow RM, Hamilton RM, Izukawa T. Treatment of atrial ectopic tachycardia in infants <6 months old. Am Heart J. Jun 1995;129(6):1145-8. [Medline].
  6. Case CL, Gillette PC. Automatic atrial and junctional tachycardias in the pediatric patient: strategies for diagnosis and management. Pacing Clin Electrophysiol. Jun 1993;16(6):1323-35. [Medline].
  7. Dagres N, Gutersohn A, Wieneke H, et al. A new hereditary form of ectopic atrial tachycardia with autosomal dominant inheritance. Int J Cardiol. Feb 2004;93(2-3):311-3. [Medline].
  8. Dhala AA, Case CL, Gillette PC. Evolving treatment strategies for managing atrial ectopic tachycardia in children. Am J Cardiol. Aug 1 1994;74(3):283-6. [Medline].
  9. Fishberger SB, Colan SD, Saul JP, et al. Myocardial mechanics before and after ablation of chronic tachycardia. Pacing Clin Electrophysiol. Jan 1996;19(1):42-9. [Medline].
  10. Haas NA, Fox S, Skinner JR. Successful use of an intravenous infusion of flecainide and amiodarone for a refractory combination of postoperative junctional and ectopic tachycardias. Cardiol Young. Aug 2005;15(4):427-30. [Medline].
  11. Janousek J, Paul T. Safety of oral propafenone in the treatment of arrhythmias in infants and children (European retrospective multicenter study). Working Group on Pediatric Arrhythmias and Electrophysiology of the Association of European Pediatric Cardiologists. Am J Cardiol. May 1 1998;81(9):1121-4. [Medline].
  12. Koike K, Hesslein PS, Finlay CD, et al. Atrial automatic tachycardia in children. Am J Cardiol. 1988;61:1127-30. [Medline].
  13. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharmacologic management of supraventricular tachycardias in children. Part 2: Atrial flutter, atrial fibrillation, and junctional and atrial ectopic tachycardia. Ann Pharmacother. Nov 1997;31(11):1347-59. [Medline].
  14. Markowitz SM, Stein KM, Mittal S, Slotwiner DJ, Lerman BB. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol. Apr 1999;10(4):489-502. [Medline].
  15. Naheed ZJ, Strasburger JF, Benson DW Jr, Deal BJ. Natural history and management strategies of automatic atrial tachycardia in children. Am J Cardiol. Feb 15 1995;75(5):405-7. [Medline].
  16. Perry JC, Fenrich AL, Legras MD, et al. Acceleration of atrial ectopic tachycardia as a guide to successful radiofrequency ablation. Pacing Clin Electrophysiol. Oct 1993;16(10):2007-11. [Medline].
  17. Walsh EP, Saul JP, Hulse JE, et al. Transcatheter ablation of ectopic atrial tachycardia in young patients using radiofrequency current. Circulation. Oct 1992;86(4):1138-46. [Medline].

Supraventricular Tachycardia, Atrial Ectopic Tachycardia excerpt

Article Last Updated: Jul 16, 2008