Multifocal Atrial Tachycardia (MAT)

Article Author:
Adam Custer
Article Editor:
Sarah Lappin
Updated:
6/3/2019 1:18:47 PM
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Multifocal Atrial Tachycardia (MAT)

Introduction

Multifocal atrial tachycardia (MAT) is a supraventricular tachycardia with a rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria. This arrhythmia is characterized by a heart rate of greater than 100 beats per minute with organized atrial activity yielding three or more different non-sinus P-wave morphologies in the same lead. There are irregular PP intervals and an isoelectric baseline between P waves (Figure 1). This condition is typically seen in elderly patients with a variety of underlying conditions, the most common of which is a chronic obstructive pulmonary disease (COPD). While the pathogenesis is not well understood, it is generally asymptomatic, and most patients are hemodynamically stable. For the majority of patients, no treatment is required beyond treatment of underlying conditions. However, evaluation is important as this arrhythmia is a poor prognostic sign in the setting of acute illness.[1][2][3]

Etiology

Multifocal atrial tachycardia is most often seen in association with an underlying medical condition, most commonly COPD. This arrhythmia is associated with significant lung disease in 60% of cases and has been found in 20% of patients with acute respiratory failure and 17% of patients hospitalized with COPD. It has also been associated with conditions such as coronary artery disease, congestive heart failure, diabetes, chronic renal failure, major surgery, electrolyte abnormalities including hypokalemia and hypomagnesemia, and use of medications such as aminophylline, theophylline, and isoproterenol.[4][5][6][7]

Epidemiology

Multifocal atrial tachycardia is a relatively uncommon arrhythmia seen in 0.05% to 0.32% of electrocardiograms in general hospital admissions. The average age of patients is approximately 70 years.

Pathophysiology

The pathogenesis of multifocal atrial tachycardia is not well understood. The multiple discrete p wave morphologies with variable PR intervals suggest atrial pacemaker activity originating from multiple ectopic foci within the atria. Thus, each unique P wave corresponds to a different site of atrial origin. Several theories have been proposed, including re-entry, abnormal automaticity, and triggered activity, but no theory has yet been demonstrated conclusively.[8][9][10]

The theory of re-entry centers upon the idea that automaticity foci with different exit pathways or electrical circuits with abnormal intra-atrial conduction could produce tachycardia with several discrete P wave morphologies. However, the role of reentrant pathways has yet to be elucidated. Studies with programmed electrical stimulation, which can both trigger and terminate reentrant rhythms, have not been found to affect or reproduce multifocal atrial tachycardia. However, one electrophysiological study of patients with multifocal atrial tachycardia did find abnormal intra-atrial, atrionodal, and atrioventricular nodal conduction pathways.

The theory of abnormal automaticity focuses on an increase in the ability of atrial myocytes to spontaneously depolarize and trigger an action potential. This theory is supported by many of the underlying conditions associated with this arrhythmia. Pulmonary diseases, like COPD, can result in hypoxia, hypercapnia, acidosis, and increased adrenergic stimulation, all of which are known to increase automaticity. Furthermore, pulmonary hypertension associated with pulmonary diseases can result in right atrial enlargement and right atrial hypertension, which can also increase automaticity. Similarly, the ventricular dysfunction seen in coronary artery disease and congestive heart failure can result in atrial enlargement and atrial hypertension that can also increase automaticity. The electrolyte abnormalities and medications associated with this arrhythmia, are also known to increase automaticity. However, given all the above information the role of abnormal automaticity in multifocal atrial tachycardia has not yet been fully understood.

The theory of triggered activity involves spontaneous action potentials generated from afterdepolarizations due to myocardial cell membrane instability. According to this theory, a normal stimulus, such as an action potential generated by the sinoatrial node, gives rise to afterdepolarizations due to changes in membrane potential that can achieve threshold and “trigger” spontaneous action potentials. It is proposed that intracellular calcium overload may lead to afterdepolarization which can result in triggered activity. This theory also has yet to be elucidated, however, the effectiveness of calcium channel blockers, such as verapamil, which may act to reduce the intracellular calcium overload, supports this theory.

History and Physical

Multifocal atrial tachycardia is most often asymptomatic. However, patients typically have symptoms related to their underlying condition. Therefore, this arrhythmia is often found incidentally on the routine electrocardiogram. Studies show most people do not report palpitations or symptoms of syncope or pre-syncope. Once a diagnosis is made, a thorough history should be obtained with a focus on commonly associated conditions including cardiac and pulmonary diseases. On physical exam, most patients will have an elevated heart rate and an irregularly irregular rhythm. Most patients are hemodynamically stable, however, due to the association with underlying conditions, it is sensible to conduct a general assessment for signs of cardiopulmonary disease, especially since this arrhythmia can trigger decompensation of underlying cardiac and pulmonary disease.

Evaluation

Multifocal atrial tachycardia should be suspected in patients with tachycardia and irregularly irregular rhythm. Given its association with underlying medical conditions, it should also be suspected in patients with cardiac and pulmonary disease. Diagnosis is not clinical, but is made with electrocardiogram and can be made using the following diagnostic criteria. The electrocardiogram should show an atrial rate of greater than 100 beats per minute (although some suggest using a threshold of 90 beats per minute) with three or more discrete P wave morphologies in the same lead, not including that originating from the sinoatrial node. Furthermore, there should be irregular PP intervals, and the baseline should be isoelectric between P waves. Other findings that are commonly seen, but are not diagnostic include irregular PR and RR intervals. Variation in PR intervals has not been included in the diagnostic criteria because the PR interval varies with the length of the preceding RP interval.[11]

A diagnosis of multifocal atrial tachycardia does not typically warrant any additional workup, other than workup required for any underlying conditions. However, if the arrhythmia persists despite treatment of underlying medical conditions it may be worth checking a complete blood count and serum chemistry for signs of infection, anemia, or electrolyte abnormalities such as hypokalemia and hypomagnesemia. 

Other diagnoses that may present with similar findings on electrocardiogram that should be included in the differential diagnosis include sinus tachycardia with frequent premature atrial contractions (this would have regular PP intervals), atrial flutter with variable AV node conduction (this would have regular PP intervals and flutter waves), atrial fibrillation (this would not have discrete P-wave morphologies), and wandering atrial pacemaker which would have a heart rate less than 100 beats per minute).

Treatment / Management

The treatment of multifocal atrial tachycardia should focus on treating underlying medical conditions. Most episodes of multifocal atrial tachycardia resolve with treatment of underlying conditions. Specific treatment is indicated if the patient develops symptomatic decompensation of their underlying cardiac or pulmonary disease or in the rare setting of persistent symptomatic arrhythmia despite adequate treatment of underlying conditions. If treatment is indicated, therapy should begin with first correcting underlying electrolyte abnormalities with repletion of potassium or magnesium. Studies have shown magnesium suppresses ectopic atrial activity and can be beneficial even if magnesium levels are within the normal range. Once electrolyte abnormalities have been corrected, possible treatment options include non-dihydropyridine calcium channel blockers, beta-blockers, and atrioventricular (AV) node ablation. Studies have found no role for antiarrhythmic agents, cardioversion, or anticoagulation.

In the absence of underlying pulmonary disease, the first line agent is beta blockers. Beta blockers act to suppress ectopic foci by reducing sympathetic stimulation and decreasing conduction through the atrioventricular node, thereby slowing the ventricular response.  Studies have found an average decrease in heart rate of 51 beats per minute and 79% of patients reverted to sinus rhythm.  Most patients did not need beta-blocker therapy long term as studies found long-term therapy was needed in only 25% of patients.  Caution should be used in patients with an underlying pulmonary disease such as COPD and patients with decompensated heart failure due to the increased risk for bronchospasms and decreased cardiac output.  Furthermore, beta-blockers should be avoided in patients with atrioventricular blocks unless a pacemaker has been implanted.

In the presence of underlying pulmonary disease, the first line agent is non-dihydropyridine calcium channel blocker such as verapamil or diltiazem. These agents act to suppress atrial rate and decrease conduction through the atrioventricular node, thereby slowing the ventricular rate.  Studies have found an average reduction in the ventricular rate of 31 beats per minute and 43% of patients reverted to sinus rhythm. Caution should be used in patients with preexisting heart failure or hypotension due to negative inotropic effects and peripheral vasodilation.  Similarly, calcium channel blockers should also be avoided in patients with atrioventricular blocks unless a pacemaker has been implanted.

In select cases of refractory multifocal atrial tachycardia, AV node ablation has been performed. Studies have found an average reduction in the ventricular rate of 56 beats per minute with adequate control of ventricular response in 84% of patients.  However, AV node ablation creates a complete heart block and requires placement of a permanent pacemaker. 

Pearls and Other Issues

While most patients with multifocal atrial tachycardia are hemodynamically stable, it is a poor prognostic sign in the setting of an acute illness. Studies have shown a 60% in-hospital mortality and mean survival of just over one year.

Enhancing Healthcare Team Outcomes

MAT is best managed by a multidisciplinary team, including cardiology nurses. In general, MAT is benign and usually resolved if the offending agent or disease is managed.  Therapies that have not been found to have a role in the treatment of multifocal atrial tachycardia include antiarrhythmics, cardioversion, or anticoagulation. Studies have found most cases of multifocal atrial tachycardia will resolve without specific antiarrhythmic therapy. Antiarrhythmics such as quinidine, procainamide, lidocaine, and phenytoin have yet to be proven successful. Furthermore, digitalis has also not been shown to have any benefit. Cardioversion has not been shown to be effective in converting to sinus rhythm and should not be used in the treatment of multifocal atrial tachycardia. While one study found 55% of patients with multifocal atrial tachycardia developed atrial fibrillation or atrial flutter, current guidelines do not support the use of anticoagulation.[12][13][14]


References

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