Updated: May 11, 2009
Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than 100 beats per minute (bpm). Atrial activity is well organized, with at least 3 morphologically distinct P waves, irregular P-P intervals, and an isoelectric baseline between the P waves. Shine, Kastor and Yurchak first proposed this definition in 1968.1 Multifocal atrial tachycardia has previously been described by names such as chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT.
The mechanism of the arrhythmia has not been well defined. Delayed afterdepolarizations leading to triggered automaticity are postulated to result in the development of MAT. The evidence that implicates this mechanism is mainly indirect and points to intracellular calcium overload by various mechanisms (eg, catecholamine excess, phosphodiesterase inhibition, acidosis, hypoxemia). Electrolyte imbalances associated with severe underlying illnesses can further potentiate the development of this arrhythmia.
MAT is a relatively infrequent arrhythmia, with a prevalence rate of 0.05-0.32% in patients who are hospitalized. The condition is even less common in children and young adults.
Patients with MAT frequently have significant comorbidities, especially chronic obstructive pulmonary disease (COPD) and respiratory failure, and are often treated in ICUs. Consequently, a high mortality rate (ie, up to 45%) is associated with this arrhythmia, although it is not a direct consequence of the rhythm abnormality.
MAT is predominantly observed in males.
MAT is commonly observed in older patients. The average age of patients from 9 studies was 72 years.
The clinical profile of patients who develop this arrhythmia includes pulmonary, cardiac, metabolic, and endocrinopathic disorders.
Physical examination of the patient is typically related to findings associated with the underlying disease process and is not specific for MAT. The pulse is rapid and irregular2 , and the first heart sound may be variable. The physical examination is not typically sufficient to differentiate multifocal atrial tachycardia from atrial fibrillation.
Causes of MAT are mainly related to underlying illnesses.
Atrial Fibrillation
Atrial Flutter
Sinus tachycardia with frequent premature atrial contractions (PACs)
In patients who have persistent and recurrent episodes of MAT and problems with rate control, the AV node may be ablated using radiofrequency energy and a permanent pacemaker implanted.22
The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Calcium channel blockers are used as the first line of treatment. Antiarrhythmics are usually not indicated for treatment of MAT. Consider using antiarrhythmics when the arrhythmia is symptomatic and does not respond to correction or treatment of underlying diseases.
Diltiazem and verapamil have been used to control the ventricular rate.
During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
10-20 mg IV bolus, followed by 5-15 mg/h continuous infusion; alternatively, 120-360 mg PO divided tid/qid or qd in long-acting preparations
Not established
May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when administered with beta-blockers, may increase cardiac depression; cimetidine may increase diltiazem levels
Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, hypotension (<90 mm Hg systolic)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur
During depolarization, it inhibits the calcium ion from entering slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium. By interrupting reentry at AV node, verapamil can occasionally restore normal sinus rhythm.
0.075-0.15 mg/kg IV bolus over 5-10 min, followed by 0.005 mg/kg/min continuous infusion for 1 h; alternatively, 240-480 mg PO divided tid/qid
<2 years: Not established
>2 years: 0.075-0.15 mg/kg IV bolus over 2 min, followed by 0.005 mg/kg/min infusion
May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase verapamil levels; may increase theophylline levels
Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, hypotension (<90 mm Hg systolic)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver function periodically
These agents promote the conversion of arrhythmia to normal sinus rhythm.
Used IV or IM, found to significantly slow the ventricular rate and to convert patients to normal sinus rhythm.
2 g IV over 1 min followed by 2 g/h over 5 h continuous infusion; 1g IM q6h
25-50 mg/kg IV
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
A - Fetal risk not revealed in controlled studies in humans
Magnesium may alter cardiac conduction, leading to heart block in patients who are digitalized; monitor respiratory rate, deep tendon reflex, and renal function when electrolytes are administered parenterally; caution when administering magnesium dose because it may produce significant hypertension or asystole; in overdose, a 10-20 mL IV of 10% calcium gluconate solution can be administered as an antidote for clinically significant hypermagnesemia
The best means of prevention of MAT is prevention of respiratory failure plus careful monitoring of all electrolyte disorders, namely, hypokalemia, hypomagnesemia, and drug therapy (mainly digoxin toxicity).
Potential complications include development of tachycardia-induced cardiomyopathy if the arrhythmia is persistent. Other complications include those due to drug therapy used to treat the arrhythmia.
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MAT, chaotic atrial rhythm, chaotic atrial tachycardia, chaotic atrial mechanism, repetitive paroxysmal multifocal atrial tachycardia, intracellular calcium overload, catecholamine excess, phosphodiesterase inhibition, acidosis, hypoxemia, electrolyte imbalances associated with severe underlying illnesses, COPD, congestive heart failure, metabolic disorders, diabetes mellitus, hypokalemia, azotemia, postoperative infections, sepsis, pulmonary embolism, respiratory acidosis, coronary artery disease, valvular heart disease, hypomagnesemia, azotemia, multifocal atrial rhythm, multifocal atrial bradycardia, wandering atrial pacemaker
Neeraj Tandon, MB, BS, Chief, Cardiology Section, Associate Professor of Medicine, Medical Service, Overton Brooks Veterans Affairs Medical Center
Neeraj Tandon, MB, BS is a member of the following medical societies: American College of Cardiology and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Pratap Reddy, MD, Director, Electrophysiology Service, Professor, Department of Medicine, Section of Cardiology, Louisiana State University Health Sciences Center
Pratap Reddy, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.
Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of St Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa
Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Frank M Sheridan, MD, Cardiology, Providence Everett Medical Center
Frank M Sheridan, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.
Clinical guidelines
Expert consensus document on beta-adrenergic receptor blockers.
European Society of Cardiology - Medical Specialty Society. 2004 Aug. 22 pages. NGC:003854
Diagnosis and treatment of chest pain and acute coronary syndrome (ACS).
Institute for Clinical Systems Improvement - Private Nonprofit Organization. 2004 Nov (revised 2008 Oct). 69 pages. NGC:006889
Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young.
American Heart Association - Professional Association. 2004 Oct 26. 26 pages. NGC:003980
Clinical trials
Randomized Trial of Two Ablation Catheters in Paroxysmal Atrial Fibrillation
Pulmonary Vein (PV) -Isolation: Arrhythmogenic Vein(s) Versus All Veins
Routine Mini-Invasive Electrophysiology Study for Patients Feeling Tachycardia, With a Negative Holter ECG
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Multifocal Atrial Tachycardia
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Atrial Flutter
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