7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Multifocal atrial tachycardia : Alfred Buxton, MD : Hugh Calkins, MD : Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Feb 21, 2022. INTRODUCTION Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety of clinical disorders [1]. In addition to a heart rate greater than 100 beats per minute (bpm), the characteristic electrocardiographic (ECG) feature is variability in P-wave morphology. Although this abnormality had been noted for many years during some types of atrial tachycardia, the term MAT became commonplace terminology in the late 1960s [2]. Patients with multiple P-wave morphologies but a normal heart rate (60 to 100 bpm) are considered to have a wandering atrial pacemaker, since the heart rate does not meet criteria for a tachycardia. (See 'Terminology' 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".) DEFINITION, PATHOGENESIS, AND PREVALENCE As with any tachycardia, the heart rate in MAT exceeds 100 bpm. To distinguish MAT from other tachyarrhythmias of atrial origin, there should be organized atrial activity yielding P waves with three or more different morphologies. (See 'Clinical manifestations and diagnosis' below.) https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 1/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate Terminology 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]. 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]. The tachycardic threshold for multifocal atrial tachycardia (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 COPD exacerbations and the diagnosis of MAT if a threshold of 90 bpm was used [7]. The definition of MAT also requires the presence of at least three distinct P-wave morphologies. Some patients have similar ECG findings with multiple P-wave morphologies but do not meet criteria for tachycardia. The arrhythmia is called a multifocal atrial rhythm or wandering atrial pacemaker if the rate is between 60 and 100 bpm. A distinction has been made between the two based on the clinical picture, with a wandering atrial pacemaker usually occurring in the asymptomatic or less ill individual [1]. 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 the identical ECG findings. There have only been a few invasive electrophysiologic investigations of MAT, but one study did show abnormal intraatrial, atrionodal, and atrioventricular (AV) nodal conduction in many individuals with MAT [5]. One case report demonstrated origin of multiform premature atrial complex (PACs; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) 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 normal, accelerated normal, or abnormal 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 MAT results from right atrial hypertension and distension, either from secondary pulmonary hypertension from advanced COPD or left ventricular dysfunction caused https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 2/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate by comorbid processes such as coronary heart disease, systemic hypertension, or aortic stenosis [11,12]. However, although frequently associated with exacerbations of pulmonary disease, MAT may occur in other circumstances, so atrial distension may not be a universal mechanism. Associated arrhythmias MAT (and wandering atrial pacemaker) is commonly accompanied by 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 [2,13]. In one report of 31 patients, for example, 55 percent developed atrial fibrillation or flutter [14]. Prevalence MAT is an uncommon but not rare arrhythmia. It has been estimated to occur in 0.05 to 0.32 percent of ECGs in general hospitals and in 0.37 percent of hospitalized patients [1,2]. The average age is approximately 70 years. These older adults are generally quite ill, with an in-hospital mortality rate of 40 to 60 percent due to pulmonary, cardiac, and other serious diseases. ASSOCIATED CLINICAL CONDITIONS Pulmonary disease MAT is associated with significant lung disease in roughly 60 percent of cases [1,15]. Furthermore, this arrhythmia has been identified in up to 20 percent of patients hospitalized for acute respiratory failure [16]. COPD 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, theophylline, or isoproterenol all may contribute to the enhanced ectopic atrial activity [2,9,17] (see "Arrhythmias in COPD"). MAT has also been identified in patients with coronavirus disease 2019 (COVID-19) [18]. In this setting, the presence of MAT was reported to not be associated with increased mortality [18]. (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 [2,13]. 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 https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 3/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate MAT) contribute to the progression and persistence of each other [12,19,20]. Illustrations of these relationships include: Severe pulmonary arterial hypertension has been associated with and may cause LV diastolic dysfunction [19,20]. (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 ( figure 1) 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 [21]. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion".) Drugs As noted above, isoproterenol, aminophylline, and theophylline can induce or exacerbate MAT, particularly in the presence of pulmonary disease [2,9,17]. By comparison, digitalis is generally not considered to be a cause of MAT, although some reports suggest that such an association may exist [2,3,13,14,22,23]. Chronic renal failure Approximately 15 percent of patients with MAT have chronic renal failure [3,22]. 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]. https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 4/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate 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'.) 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 [15]. Patients have an irregular heart rate greater than 100 bpm. The arrhythmia is usually recognized only 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 [15]. 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. 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 (including 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 https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 5/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate (COPD), 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 PACs or ventricular premature beats (VPBs) Atrial tachycardias (including atrial flutter) with variable AV conduction Atrial fibrillation MAT can usually be differentiated from both atrial flutter with variable AV conduction and sinus tachycardia with APBs/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'.) 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".) 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".) TREATMENT Most episodes of MAT do not precipitate hemodynamic compromise or symptoms. Thus, therapy in patients with MAT should be aimed at the inciting underlying disease [15,24,25]. 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 [2,9,17]. In many cases, MAT is precipitated by poor oxygenation and/or acid-base disturbances. https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 6/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate 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 [24]. 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 [21,26]. 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 [26]. 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".) Mild hypomagnesemia (serum magnesium 1.4 to 1.7 mg/dL) can be treated with 240 mg of elemental magnesium orally twice per day as magnesium oxide (400 mg twice daily) or a delayed release magnesium chloride preparation. Dose-dependent diarrhea occurs frequently. More significant hypomagnesemia (serum magnesium <1.4 mg/dL) can be treated with 1 gram (8 mEq) of magnesium sulfate given intravenously over 15 minutes, followed by a continuous infusion of 3 to 6 grams (24 to 48 mEq) over 24 hours, OR as repeated intermittent infusions, each consisting of 1 gram over one hour, for a total of 3 to 6 grams over 12 hours. Because magnesium distributes gradually to tissues, early serum levels can appear artificially high, and repletion may require several days of treatment. The dose should be reduced by approximately 50 percent with even mild renal insufficiency. Response to the initial dose may give an indication of whether the MAT will be responsive to magnesium therapy. (Conversion relationships: 1 mmol = 2 mEq = 24 mg of elemental magnesium.) Potassium repletion in the hypokalemic patient may also control MAT, with or without magnesium supplementation [21,27]. In an observational study of eight patients, the combined https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 7/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate use of magnesium and potassium was associated with conversion to sinus rhythm in seven [21]. Potassium depletion can be treated with potassium chloride given either orally (20 to 60 mEq per day in divided doses if >40 mEq) or intravenously (generally up to 10 mEq per hour, but occasionally at an initial rate of as much as 40 mEq per hour with severe hypokalemia with continuous echocardiogram monitoring). The patient's serum potassium should be carefully monitored to avoid hyperkalemia. Over the long-term, the cause of potassium loss should also be treated, (eg, the administration of a potassium-sparing diuretic to patients treated with loop or thiazide diuretics). (See "Clinical manifestations and treatment of hypokalemia in adults".) Pharmacologic therapy The use of antiarrhythmic drugs in the treatment of MAT has generally been disappointing [1,24]. Additionally, administration of antiarrhythmic agents to acutely ill patients with renal 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 [15,28]. 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 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 [1,29-32]. 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). https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 8/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate 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 [33-35]. Esmolol and acebutolol have also been used in small numbers of patients [36-38]. 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 [35]. We use the following protocol for intravenous (IV) metoprolol ( table 1) [34]. 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 [29,32]. 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 https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 9/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate 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 [28]. (See "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Secondary therapies' 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 [24]. Ineffective drugs include quinidine, procainamide, lidocaine, and phenytoin, among others [1]. Digitalis also appears to have little benefit [2,13]. Ibutilide has been used successfully to treat MAT in one older adult, but more experience with this drug is need [39]. 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 [13,24,40]. 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 [15]. 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. https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 10/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate Since most of the manifestations associated with MAT are due to the rapid ventricular rate, an alternative approach for rate control is 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 [41]. 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 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 electrocardiographic (ECG) feature in MAT is variability in P-wave morphology, with three or more distinct P-wave morphologies. (See 'Introduction' above.) Some patients have similar ECG findings with multiple P-wave morphologies but do not meet criteria for tachycardia. The arrhythmia is called a multifocal atrial rhythm or wandering atrial pacemaker if the rate is between 60 and 100 bpm. (See 'Terminology' above.) 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 https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 11/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate disease, particularly when associated with heart failure and/or underlying lung disease. (See 'Associated clinical conditions' above.) 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.) 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 (including 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 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.) 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.) 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. 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.) https://www.uptodate.com/contents/multifocal-atrial-tachycardia/print 12/20 7/5/23, 10:25 AM Multifocal atrial tachycardia - UpToDate 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.) Ablation of the atrioventricular (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. Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Kastor JA. Multifocal atrial tachycardia. 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