Multifocal atrial tachycardia

INTRODUCTION — 

Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety of clinical disorders [1]. The characteristic electrocardiographic (ECG) features of MAT are ventricular rate greater than 100 beats per minute (bpm) and multiple P-wave morphologies. (See 'Definition of MAT' below and 'Diagnosis' below.)

This topic will review the definition, pathogenesis, etiology, and treatment of MAT in adults. Other tachycardias of atrial origin, as well as the discussion of this arrhythmia in children, are reviewed separately. (See "Focal atrial tachycardia" and "Atrial tachyarrhythmias in children" and "Atrioventricular nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

TERMINOLOGY

Definition of MAT — The heart rate in MAT exceeds 100 bpm, as for all tachyarrhythmias. The key feature distinguishing MAT from other tachyarrhythmias of atrial origin is the presence of organized atrial activity yielding P waves with three or more different morphologies (waveform 1) with distinct isoelectric interval between P waves. The term MAT became commonplace in the late 1960s [2]. (See 'Diagnosis' below.)

Arrhythmias that may be confused with MAT are discussed below. (See 'Differential diagnosis' below.)

Issues regarding terminology — A more accurate term for this arrhythmia is probably "multiform" as there is no proof that the arrhythmia is actually multifocal, although multifocal remains the commonly used term [1]. A number of authors have used the term "chaotic" to describe MAT [3-5]. However, chaos in modern usage in nonlinear dynamics and mathematics implies there is order in what appear to be random events [6].

The tachycardic threshold for MAT has traditionally been set at 100 bpm, but a review of 60 patients with multifocal atrial arrhythmias found a stronger association between the incidence of chronic obstructive pulmonary disease exacerbations and the diagnosis of MAT if a threshold of 90 bpm was used [7].

MECHANISMS — 

The changing morphology of the P waves and the variable PR interval suggests that the atrial pacemaker activity arises from different atrial locations. However, the variable PR interval is probably more likely a result of the variable atrial rate. Alternatively, a single focus with different exit pathways or abnormalities in intraatrial conduction could produce identical ECG findings. There have only been a few invasive electrophysiologic investigations of MAT. A study found abnormal intraatrial and atrioventricular (AV) nodal conduction in many individuals with MAT [5]. A case report demonstrated origin of multiform premature atrial complex (PACs) from adjacent areas in the right pulmonary veins [8]. However, this patient did not have the typical setting in which MAT is seen.

Automaticity refers to spontaneous pacemaker activity. Triggered activity, on the other hand, results from a normal stimulus giving rise to afterdepolarization, which, if threshold is attained, can result in regenerative action potentials (resulting in tachycardia) in any cardiac tissue. Reentry refers to a circuit in which previously excited tissue is re-excited, producing an extra beat or a sustained rhythm. The occasional responsiveness of MAT to verapamil suggests intracellular calcium overload causing afterdepolarizations leading to triggered activity as the underlying mechanism [9,10].

It is thought that some MAT results from right atrial hypertension and distension, either from secondary pulmonary hypertension from advanced chronic obstructive pulmonary disease or left ventricular dysfunction caused by comorbid processes such as coronary heart disease, systemic hypertension, or aortic stenosis [11,12].

A report described a human-induced pluripotent stem cell model that recapitulated MAT [13]. This model identified upregulation of genes regulating calcium handling. Ivabradine exhibited therapeutic effects in this model.

EPIDEMIOLOGY

Associated arrhythmias — MAT is commonly accompanied by premature atrial complexes (PACs) and can itself be considered a prolonged sequence of PACs [1]. The majority of episodes of MAT are self-limited and nonsustained.

MAT may be associated with or precede atrial fibrillation [2,14]. In one report of 31 patients, for example, 55 percent developed atrial fibrillation or flutter [15].

CLINICAL MANIFESTATIONS AND DIAGNOSIS

Clinical manifestations — In most cases, the clinical manifestations of MAT differ from those of other tachyarrhythmias in that symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia [16]. (See 'Associated clinical conditions' below.)

Patients have paroxysms of irregular heart rate greater than 100 bpm. The arrhythmia is usually recognized by ECG monitoring, as the majority of patients are acutely ill and on continuous ECG monitoring. Patients rarely present with symptoms such as palpitations. Presyncope or syncope is generally not associated with this arrhythmia. Given that the majority of patients with MAT are concurrently affected by advanced or decompensated pulmonary disease, many patients have typical symptoms related to the underlying lung disease (eg, shortness of breath, wheezing, productive cough, etc) or acute metabolic derangements.

Most episodes of MAT do not precipitate hemodynamic compromise or limiting symptoms [16]. However, higher heart rates associated with MAT can sometimes worsen systemic oxygenation in patients with advanced pulmonary disease. Additionally, in patients with coexistent advanced cardiac disease, namely those with severe multivessel obstructive coronary artery disease or decompensated heart failure, the faster heart rates associated with MAT can exacerbate heart disease, leading to signs and symptoms of cardiac decompensation (eg, angina, dyspnea, orthopnea). Symptomatic decompensation of underlying cardiac or pulmonary disease is an indication for pharmacologic therapy aimed specifically at the tachycardia rather than therapy to control the underlying disease process. (See 'Pharmacologic therapy' below.)

Diagnosis — The diagnosis of MAT can be suspected from the presence of an irregular rapid pulse and heartbeat on physical examination, usually in a patient with underlying, often poorly controlled, cardiac or pulmonary disease, or sepsis. The diagnosis cannot be confirmed, however, without an ECG.

A diagnosis of MAT requires the following be present on the ECG (waveform 1) [1,2]:

●Discrete P waves with at least three different morphologies (excluding the normal sinus P wave).

●An atrial rate greater than 100 bpm, which is the classic definition of MAT [2]. However, based upon data from a series of patients with chronic obstructive pulmonary disease, a threshold of 90 bpm has been proposed [7].

●P waves that return to the baseline and thus are separated by isoelectric intervals.

●P-P intervals, P-R duration, and R-R intervals that vary. It should be recognized that the primary abnormality is the variability in P-P intervals. The variation in P-R intervals follows because of the physiologic response of the AV node to changing atrial rate. The variation in R-R intervals follows as a physiologic consequence of the variation in the P-P and P-R intervals.

Differential diagnosis — The differential diagnosis for MAT is similar to that of other narrow QRS complex tachycardias with an irregular rhythm (assuming there is normal AV conduction without bundle branch block) and includes:

●Sinus tachycardia with frequent premature beats – The premature beats may be premature atrial complexes (PACs) or ventricular premature beats (VPBs).

●Atrial tachycardias (including atrial flutter) with variable AV conduction – MAT can usually be differentiated from both atrial flutter with variable AV conduction and sinus tachycardia with PACs/VPBs by the regular P-P interval seen in both atrial flutter and sinus tachycardia, which is not present in MAT. (See "Electrocardiographic and electrophysiologic features of atrial flutter", section on 'Electrocardiographic features'.)

●Atrial fibrillation – MAT, with its organized atrial activity resulting in P waves on surface ECG, can be readily distinguished from atrial fibrillation, which lacks any discernible P waves. However, MAT can and does degenerate into atrial fibrillation in some patients. (See "The electrocardiogram in atrial fibrillation".)

●Wandering atrial pacemaker – Patients with multiple P-wave morphologies but a normal heart rate (60 to 100 bpm) are considered to have a wandering atrial pacemaker or multifocal atrial rhythm, since the heart rate does not meet criteria for a tachycardia. Also, wandering atrial pacemaker usually occurs in individuals who are asymptomatic or less ill than individuals with MAT [1].

A more in-depth discussion of the differential diagnosis of narrow QRS complex tachycardias is presented separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

ASSOCIATED CLINICAL CONDITIONS

Pulmonary disease — MAT is associated with significant lung disease in roughly 60 percent of cases [1,16]. Furthermore, this arrhythmia has been identified in up to 20 percent of patients hospitalized for acute respiratory failure [17]. Chronic obstructive pulmonary disease is the most common pulmonary disorder associated with MAT, but this arrhythmia can also occur with pneumonia and pulmonary embolism. Hypoxia, hypercapnia, acidosis, autonomic imbalance, right atrial enlargement, and therapy with aminophylline or theophylline may contribute to the enhanced ectopic atrial activity [2,9,18]. (See "Arrhythmias in COPD".)

MAT has also been identified in patients with coronavirus disease 2019 (COVID-19) [19]. In this setting, the presence of MAT was reported to not be associated with increased mortality [19]. (See "COVID-19: Arrhythmias and conduction system disease".)

Cardiac disease — MAT can occur in the presence of coronary, valvular, hypertensive and other types of heart disease, particularly when associated with heart failure and/or underlying lung disease. Affected patients tend to have elevated pulmonary capillary wedge and pulmonary end-diastolic pressures as well as a low-normal cardiac index [2,14].

Interactions between cardiac and pulmonary disease — In advanced cases of cardiac and pulmonary disease, MAT may be part of a complicated pathophysiologic complex in which several conditions (eg, pulmonary hypertension, elevated left ventricular filling pressures, and MAT) contribute to the progression and persistence of each other [12,20,21]. Illustrations of these relationships include:

●Severe pulmonary arterial hypertension has been associated with and may cause LV diastolic dysfunction [20,21]. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)".)

●Theoretically, the rapid heart rate associated with MAT decreases diastolic filling time and can result in increased LV diastolic pressure, which in turn increases pulmonary artery pressure that encourages MAT [12]. However, the vast majority of episodes of MAT are brief and not associated with symptoms or recognizable hemodynamic compromise. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".)

●Prolonged episodes of tachycardia can cause a cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".)

Miscellaneous — MAT is also associated with a number of other disorders:

●Hypokalemia – MAT has been associated with hypokalemia, most often induced by diuretic use [1-3]. Hypokalemia may predispose to MAT by increasing the rate of phase 4 depolarization in atrial tissues. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)

●Hypomagnesemia – The administration of magnesium can suppress MAT in hypomagnesemic and, at times, in apparently normomagnesemic patients [22]. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion".)

●Drugs – Isoproterenol, aminophylline, and theophylline can induce or exacerbate MAT, particularly in the presence of pulmonary disease [2,9,18]. By comparison, digitalis is generally not considered to be a cause of MAT, although some reports suggest that such an association may exist [2,3,14,15,23,24]. One case report implicates risperidone (a second-generation antipsychotic medication) [25].

●Chronic kidney failure – Approximately 15 percent of patients with MAT have chronic kidney failure [3,23]. It is unclear, however, if this represents a cause-and-effect relationship.

●Other – MAT also can occur in sepsis and after recent surgery, particularly if the patient has pulmonary compromise and/or heart failure [1,2].

MAT in children and young adults — The association of MAT with serious illness is generally less in children than in adults. Information on multifocal (or chaotic) atrial tachycardia in children is presented separately. (See "Atrial tachyarrhythmias in children", section on 'Chaotic atrial tachycardia'.)

TREATMENT — 

Most episodes of MAT are nonsustained and do not precipitate hemodynamic compromise or symptoms. Thus, therapy in patients with MAT should be aimed at the inciting underlying disease [16,26,27]. Amelioration of MAT generally parallels improvement in severe pulmonary or cardiac disease or sepsis. Not infrequently, medication used for the treatment of pulmonary disease, such as theophylline, induces or exacerbates MAT [2,9,18]. In many cases, MAT is precipitated by poor oxygenation and/or acid-base disturbances.

In addition to treatment for the underlying pathologic condition associated with MAT, specific therapies for the tachycardia are sometimes used (usually only if the arrhythmia is so frequent or sustained as to compromise oxygenation or cause hemodynamic compromise). In patients with electrolyte disturbances, maintaining magnesium and potassium levels in the normal range is important. Pharmacologic therapy to slow the ventricular heart rate, using either verapamil or a beta blocker, is administered for patients with signs or symptoms felt to be related to their tachycardia. While rate control therapy is often very effective, there is no role for electrical cardioversion or antiarrhythmic drug therapy in patients with MAT.

Magnesium and potassium repletion — Patients with MAT and associated hypokalemia or hypomagnesemia should undergo electrolyte repletion prior to the initiation of additional medical therapy for MAT [26].

Magnesium repletion — Hypomagnesemia appears to promote the development of some atrial and ventricular arrhythmias. The administration of magnesium has been reported to suppress MAT in the hypomagnesemic patient and, at times, in patients with normal plasma magnesium levels [22,28]. As an example, one study randomized 14 patients with chronic obstructive pulmonary disease and MAT to magnesium therapy (2 grams over five minutes and 10 grams over five hours) or placebo [28]. At five hours, patients treated with magnesium had a slowing of heart rate from 130 to 99 bpm, while there was no change in the placebo group. Sinus rhythm was present at the end of the infusion in seven of nine patients treated with magnesium versus one of five receiving placebo. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion".)

Management of hypomagnesemia (algorithm 1) is discussed in detail separately. (See "Hypomagnesemia: Evaluation and treatment", section on 'Treatment'.)

Potassium repletion — Potassium repletion in the hypokalemic patient may also control MAT, with or without magnesium supplementation [22,29]. In an observational study of eight patients, the combined use of magnesium and potassium was associated with conversion to sinus rhythm in seven [22].

Management of hypokalemia is discussed in detail separately. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Treatment'.)

Pharmacologic therapy — The use of antiarrhythmic drugs in the treatment of MAT has generally been disappointing [1,26]. Additionally, administration of antiarrhythmic agents to acutely ill patients with kidney and/or hepatic dysfunction increases the risk of toxic reactions to these agents. There is, however, evidence of benefit with agents to control the ventricular heart rate, namely verapamil and beta blockers.

Medical therapy for MAT is indicated only if MAT causes a sustained rapid ventricular response that causes or worsens myocardial ischemia, heart failure, peripheral perfusion, or oxygenation [16,30]. For patients with symptomatic MAT requiring ventricular rate control, we recommend therapy with verapamil or a beta blocker (table 1).

Nondihydropyridine calcium channel blockers — While both diltiazem and verapamil can be effective agents for slowing AV nodal conduction and controlling ventricular heart rates, verapamil has been most commonly used in MAT, and the response in some cases (suppression of the MAT) suggests that triggered activity may initiate the arrhythmia. (See 'Mechanisms' above.)

Verapamil decreases the ventricular rate by reducing the degree of atrial ectopy and/or by limiting the transmission of beats through the AV node [1,31-34]. In an analysis of pooled data, verapamil lowered the ventricular rate by an average of 31 bpm, but only 43 percent of patients reverted to a sinus rhythm [1]. Furthermore, MAT may recur if verapamil is discontinued.

The following regimen, given with continuous ECG and blood pressure monitoring, has been suggested for intravenous verapamil (table 1) [10]. A 5 to 10 mg IV bolus over two minutes; if no response, an additional 10 mg IV bolus may be administered 15 to 30 minutes following the initial dose. A lower initial dose (eg, 2.5 mg IV) may be chosen in patients who are older or who have multiple comorbidities, in whom there are concerns about potential hypotension or other side effects. If MAT reverts to sinus rhythm, oral verapamil is given at an initial dose of 80 mg every six hours and subsequently titrated as blood pressure and heart rate allow (total daily dose range 120 to 480 mg).

Beta blockers — Beta blockers can suppress ectopic foci and decrease transmission through the AV node, thereby slowing the ventricular response. Their use in MAT has been limited because of the risk in patients with underlying heart failure or chronic obstructive pulmonary disease, particularly when bronchospasm is part of the picture. However, several studies showing a benefit have been performed, particularly with the relatively cardioselective agent metoprolol [35-37]. Esmolol and acebutolol have also been used in small numbers of patients [38-40].

The pooled data from the metoprolol studies revealed an average decrease in ventricular rate of 51 bpm, with 79 percent of patients reverting to sinus rhythm [1]. Side effects were few, but long-term therapy is required in approximately one-quarter of patients [37].

We use the following protocol for intravenous (IV) metoprolol (table 1) [36].

●Metoprolol – 2.5 to 5 mg IV bolus over two to five minutes; if no response, an additional 2.5 to 5 mg IV bolus may be administered every 10 minutes to a total dose of 15 mg.

In patients who are unable to receive oral medications, subsequent doses of IV metoprolol can be administered every 4 to 6 hours with the patient in a monitored setting. An advantage of metoprolol is the ease of switching to an oral preparation (typically long-acting metoprolol at a dose of 50 mg once daily or short-acting metoprolol 25 mg twice daily, with titration as needed based on heart rate and blood pressure). Beta blockers should generally not be given to patients with acute decompensated heart failure, severe reactive pulmonary disease, hypotension, drug hypersensitivity, and a history or ECG showing greater than first-degree heart block, bifascicular block, or serious sinus node dysfunction (unless a pacemaker is implanted).

Precautions with verapamil and beta blockers — Verapamil and beta blockers should not be given to patients with sinus node dysfunction or preexisting second- or third-degree block unless a temporary or permanent pacemaker has been implanted. Verapamil should be administered cautiously in patients with preexisting heart failure or hypotension as it has both negative inotropic and peripheral vasodilator activity, potentially leading to a reduction in blood pressure or even significant hypotension [31,34]. Beta blockers should also be administered cautiously in patients with acutely decompensated heart failure. Verapamil and beta blockers should either be avoided or used at lower doses and with caution in patients already treated with a beta blocker, verapamil or another calcium channel blocker, or digoxin. (See "Major side effects of beta blockers" and "Major side effects and safety of calcium channel blockers".)

Which to use first: Calcium channel blocker or beta blocker? — The decision to use a nondihydropyridine calcium channel blocker or a beta blocker is most often determined by the presence or absence of acute decompensated heart failure with reduced left ventricular ejection fraction and severe bronchospasm. We prefer metoprolol before verapamil in patients without these complications. In a randomized, double-blind study of 13 patients, the incidence of benefit was 89 percent with metoprolol versus 44 percent with verapamil [30]. (See "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Secondary therapy (MRA)' and "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Beta blocker'.)

By contrast, we prefer to begin with verapamil (or diltiazem) in patients with severe bronchospasm. Beta blockers may be used cautiously in some patients with heart failure, but active bronchospasm is a contraindication. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Beta blocker'.)

In either case, repletion of electrolyte deficiencies (hypomagnesemia and hypokalemia) should occur simultaneously. (See 'Magnesium and potassium repletion' above.)

Antiarrhythmic drugs — For patients with symptomatic MAT that remains inadequately rate-controlled following treatment of the underlying disorder and initiation of rate controlling therapy, we do not use an antiarrhythmic drug. This is based on extensive literature showing a general lack of efficacy of standard antiarrhythmic drugs in treating MAT as well as increased risk of toxicity in this setting [26]. Ineffective drugs include quinidine, procainamide, lidocaine, and phenytoin, among others [1]. Digitalis also appears to have little benefit [2,14]. A case report suggests utility of ivabradine to treat MAT in an infant [41].

Ibutilide has been used successfully to treat MAT in one older adult, but more experience with this drug is needed [42]. Additionally, ibutilide should never be used in the presence of known or suspected hypokalemia or hypomagnesemia. (See "Therapeutic use of ibutilide".)

DC cardioversion — DC cardioversion has not proven effective in converting MAT into a sinus rhythm [14,26,43]. As such, we do not perform cardioversion for patients with symptomatic MAT that remains inadequately rate-controlled.

Radiofrequency ablation — Ablation of the AV node and the use of a permanent ventricular pacemaker is an option for patients with ongoing symptomatic MAT who do not respond to, or cannot tolerate, pharmacologic therapy. This procedure should rarely be required, because the vast majority of MAT episodes are brief and because the arrhythmia resolves with correction of the underlying abnormality [16]. To re-emphasize this, AV junction ablation resulting in creation of complete heart block necessitating permanent pacemaker implantation should not be performed for the purpose of making the ECG appear more normal. It should only be performed in order to improve cardiopulmonary function after proving that the arrhythmia is actually the cause of hemodynamic compromise.

Since most of the manifestations associated with MAT are due to the rapid ventricular rate, an alternative approach for rate control may be radiofrequency modification of the AV junction, similar to the approach taken for rate control in atrial fibrillation. Ablation to cure MAT is rarely indicated and not likely to be effective given the underlying diffuse atrial abnormalities. Early data concerning radiofrequency modification of the AV node were encouraging, but modification of AV transmission without producing complete heart block is unreliable and rarely long-lasting.

AV node modification with ablation was evaluated in one study of 13 patients with chronic obstructive lung disease and medically refractory MAT who underwent AV junctional modification [44]. This procedure resulted in adequate control of the ventricular response rate in 84 percent of patients, and the rate was reduced from an average of 145 to 89 bpm. One patient developed complete heart block, and one patient had recurrent symptomatic MAT, requiring a second procedure. After a six-month follow-up, all patients with successful modification had an improved quality of life, a reduction in symptoms, and an increase in left ventricular ejection fraction. (See "Atrial fibrillation: Atrioventricular node ablation".)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Supraventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●Definition of MAT – Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety of clinical disorders in adults, children, and infants. In addition to a heart rate >100 beats per minute (bpm), the characteristic ECG feature in MAT is variability in P-wave morphology, with three or more distinct P-wave morphologies (waveform 1).

●Clinical manifestations – In most cases, the clinical manifestations of MAT differ from those of other tachyarrhythmias in that symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia. Patients have an irregular heart rate greater than 100 bpm, usually identified only during the physical exam by the health care provider, and they rarely present with symptoms of palpitations, presyncope, or syncope as the sole manifestation of MAT. (See 'Clinical manifestations and diagnosis' above.)

●Associated clinical conditions – MAT is associated with significant lung disease in roughly 60 percent of cases and is identified in up to 20 percent of patients hospitalized for acute respiratory failure. MAT can also occur in the presence of coronary, valvular, hypertensive and other types of heart disease, particularly when associated with heart failure and/or underlying lung disease. (See 'Associated clinical conditions' above.)

●Diagnosis – The diagnosis of MAT can be suspected from the presence of an irregular rapid pulse and heartbeat on physical examination; however, the diagnosis cannot be confirmed without an ECG. A diagnosis of MAT requires the following be present on the ECG (waveform 1) (see 'Clinical manifestations and diagnosis' above):

•Discrete P waves with at least three different morphologies (excluding the normal sinus P wave)

•An atrial rate greater than 100 bpm

•P waves which are separated by isoelectric intervals

•P-P intervals, P-R duration, and R-R intervals which vary

●Differential diagnosis – The differential diagnosis for MAT includes sinus tachycardia with frequent premature atrial complexes (PACs) or ventricular beats (VPBs), atrial tachycardia (including atrial flutter) with variable atrioventricular (AV) conduction, atrial fibrillation, and wandering atrial pacemaker. (See 'Differential diagnosis' above.)

●Management – Most episodes of MAT do not precipitate hemodynamic compromise or limiting symptoms. Thus, therapy in patients with MAT should be aimed at the inciting underlying disease. (See 'Treatment' above.)

•Electrolyte repletion – Patients with MAT and associated hypokalemia or hypomagnesemia should undergo electrolyte repletion prior to the initiation of additional medical therapy for MAT. (See 'Magnesium and potassium repletion' above.)

•Pharmacologic therapy – Medical therapy for MAT is indicated only if MAT causes a sustained rapid ventricular response that causes or worsens myocardial ischemia, heart failure, peripheral perfusion, or oxygenation. Options for medical therapy for patients with symptomatic MAT requiring ventricular rate control include nondihydropyridine calcium channel blockers and beta blockers. (See 'Pharmacologic therapy' above.)

-For patients without heart failure or bronchospasm, we suggest initial therapy with a beta blocker, usually metoprolol, before calcium channel blockers (Grade 2C).

-Conversely, for patients with severe bronchospasm, we suggest initial therapy with a nondihydropyridine calcium channel blocker, usually verapamil, rather than a beta blocker (Grade 2C).

-Beta blockers may be used cautiously in some patients with heart failure. (See 'Pharmacologic therapy' above.)

•Treatments not used for MAT – Extensive literature has shown a lack of efficacy of numerous standard antiarrhythmic drugs (including quinidine, procainamide, lidocaine, phenytoin, and digoxin) as well as electrical cardioversion in treating MAT. (See 'Antiarrhythmic drugs' above and 'DC cardioversion' above.)

●Limited role of ablation – Ablation of the AV node and the use of a permanent ventricular pacemaker is rarely indicated and should be reserved for patients with ongoing symptomatic MAT who do not respond to or cannot tolerate pharmacologic therapy. (See 'Radiofrequency ablation' above.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.