Multifocal atrial tachycardia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Mohsin, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3] Syed Hassan A. Kazmi BSc, MD [4]

Synonyms and keywords: MAT

Overview

Multifocal atrial tachycardia (MAT) or also called chaotic atrial tachycardia is a cardiac arrhythmia, specifically a type of supraventricular tachycardia (rate exceeding 100 beats per minute). This is characterized by 3 or more different P wave shapes  or contour, variable PP, PR and RR intervals. Most P waves are conducted to the ventricles but some are not. Some R  waves are aberrantly conducted.This variability makes it look irregular on the surface ECG and often misinterpreted as atrial fibrillation.

A rhythm with same the ECG characteristics but at a slow rate is called multifocal atrial rhythm (MAR).

It can be seen among elderly patients with COPD and CHF and eventually develop into atrial fibrillation. 

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.

Historical Perspective

  • Bradley et al reported the clinical course of MAT in infants and children in 2001.[1]

Pathophysiology

  • Possible mechanism for MAT has been suggested such as right atrial enlargement, hypercapnia, hypoxia, or adrenergic stimulation in pulmonary disease.3) The majority of MAT reports in pediatric patients have also reported not so low coexisting pulmonary disease (>20%) compared to the higher rate in adults (up to 60%). Unlike pulmonary physiology in adults, growth and development of bronchopulmonary system and pulmonary vessel continues for at least 2 years. It could be some role for the predominant infantile onset of MAT. Also, many of MAT have been detected in utero indicating that the immaturity and vulnerability of the atrium may also contribute to the infant-predominant age distribution of MAT.4) Therefore, immaturity of both the lungs and the heart might play a key role of infant-predominant age distribution and its favorable outcome in idiopathic infant cases.[2][3][4]
  • 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.
  • 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.

Causes

Multifocal atrial tachycardia usually results from an underlying medical condition such as COPD, chronic renal failure, pulmonary embolism, electrolyte imbalance, and many other conditions.

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.

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Congestive heart failure, myocardial infarction, valvular heart disease
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Aminophylline, isoproterenol, theophylline
Ear Nose Throat No underlying causes
Endocrine Diabetes mellitus
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic Postoperative complication
Infectious Disease Pneumonia, sepsis
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Lung cancer
Ophthalmologic No underlying causes
Overdose/Toxicity Aminophylline
Psychiatric No underlying causes
Pulmonary Chronic obstructive pulmonary disease, hypoxia, lung cancer, pneumonia, pulmonary embolism
Renal/Electrolyte Chronic renal failure, hypokalemia, hypomagnesemia
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous No underlying causes

Causes in Alphabetical Order

Epidemiology and Demographics

  • Although the prevalence of pulmonary disease in MAT has been well established in adult MAT patients, particularly those with pulmonary diseases including chronic obstructive pulmonary disease, it is relatively rare in the pediatric ages. Therefore, the clinical feature of MAT in children is not well known with several studies of small cases.[5]
  • 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.

Natural history, Complications, and Prognosis

  • Baek et al reported the clinical outcome of MAT and potential prognostic factors. Compared to the previous reports, this study has relatively large number of patients and composed of various etiologies despite of limitation of retrospective study from single tertiary center. Among 33 patients with identified MAT, 27 (82%) were infantile onset and 10 patients (30%) had fetal diagnosis. Incidental detection without significant clinical manifestation is rather high (27%). Comorbidities had a variety of SHD (42%) and lung disease (24%). Interestingly, syndromic diagnosis, including 3 with Costello syndrome and 2 with Noonan syndrome, and one suggestive of RASopathy were noted in infantile onset group. Among 27 patients with infant onset of MAT, 11 patients (41%) were included in the idiopathic group. Accompanying arrhythmias was revealed in 4 patients (2 atrioventricular reentrant tachycardia prior to MAT diagnosis; 2 catecholaminergic polymorphic ventricular tachycardia [CPVT] after MAT diagnosis). The arrhythmia control rate was higher in the infant group (85%) than in the non-infant group (67%), although this trend was not statistically significant. There was a significantly lower rate of unfavorable outcomes in the idiopathic infant group (n=11) than in the other groups (p=0.008). Considering the findings of previous studies, the mortality rate was significantly higher in patients with SHD than in patients without (21% vs. 5%, p=0.01). The idiopathic infant group had a significantly lower rate of unfavorable outcomes than did the others (0% vs. 47%, p=0.008).[6]

Diagnosis

Electrocardiography

  • There are P waves of varying morphology from at least three different foci
  • There is absence of one dominant atrial pacemaker
  • Variable PP intervals, RR intervals, and PR intervals
  • Atrial rate is above 100 beats per minute (bpm)
  • Can be mistaken for atrial fibrillation if the p waves are of low amplitude
  • High incidence in the elderly and in those with COPD
  • For the pediatric practitioners, 4 issues have arisen from above studies regarding MAT in children as follows: 1) how to detect early, 2) how to control, 3) how deep to investigate etiologies of MAT, and 4) how to predict another arrhythmia and outcome.
  • Firstly, early detection is very important to prevent worse outcome in infantile onset MAT. Tachycardia is usually first detected during the newborn period and incidental detection not based on clinical suspicion is rather high. Clinical suspicion of infantile onset of MAT is important for early detection. If tachycardia last long over several days without proper management, myocardial dysfunction can develop resulting in congestive heart failure. due to tachycardia-induced cardiomyopathy. So early detection and immediate proper management for tachyarrhythmias is necessary.
  • Secondly, complete control of MAT is not easily achievable with combination of multiple antiarrhythmic medications, even in high-dose combinations. A more realistic treatment goal is initially reducing the percentage of MAT and achieving ventricular rate control. Various drugs have been used for the purpose, including beta blocker, digoxin, and amiodarone, but there is no data to support the superiority of any one approach.
  • Thirdly, because of variety of etiology of MAT in children, delineation of etiology should be done to treat underlying problems and get better clinical outcome. Idiopathic infantile onset group shows a favorable outcome compared to the other groups including SHD and syndromic disease. RASopathy has been reported to be associated with high incidence of atrial arrhythmias.6),7) MAT in children should be checked the association of RASopathy and vice versa.[7]
  • Fourthly, further lethal arrhythmias could not be predicted not only by MAT but also by additional studies. Atrial premature beats, atrial fibrillation (AF), or atrial flutter are known to accompany MAT in both adults and pediatric patients.5),6),8) MAT may be an early manifestation of CPVT and also additional findings of atrioventricular nodal reentrant tachycardia. Phenotypical progression of MAT into CPVT and an association between the RyR2 mutation and AF and ectopic atrial tachycardia have reported.6),9) MAT in young children may be the initial manifestation of a potentially life-threatening arrhythmia of CPVT. Therefore, non-infantile form of MAT with structurally normal hearts might need aggressive evaluations and close follow-up.[1][6][8][9]

Treatment

  • Combined flecainide and sotalol therapy for multifocal atrial tachycardia in cardio-facio-cutaneous syndrome.[10][8]

Differentiating Multifocal Atrial Tachycardia From Other Disease

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[11][12]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[13]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[14][15][16][17]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R' in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[18][19]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[20][21]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[22][23]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[24][25][26]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[27][28]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

References

  1. ↑ 1.0 1.1 Bradley DJ, Fischbach PS, Law IH, Serwer GA, Dick M (2001). "The clinical course of multifocal atrial tachycardia in infants and children". J Am Coll Cardiol. 38 (2): 401–8. doi:10.1016/s0735-1097(01)01390-0. PMID 11499730.
  2. ↑ Huh J (2018). "Clinical Implication of Multifocal Atrial Tachycardia in Children for Pediatric Cardiologist". Korean Circ J. 48 (2): 173–175. doi:10.4070/kcj.2018.0037. PMC 5861009. PMID 29441751.
  3. ↑ Kastor JA (1990). "Multifocal atrial tachycardia". N Engl J Med. 322 (24): 1713–7. doi:10.1056/NEJM199006143222405. PMID 2188131.
  4. ↑ Pickoff AS, Singh S, Flinn CJ, McCormack J, Stolfi A, Gelband H (1985). "Atrial vulnerability in the immature canine heart". Am J Cardiol. 55 (11): 1402–6. doi:10.1016/0002-9149(85)90513-2. PMID 3993578.
  5. ↑ Lazaros G, Chrysohoou C, Oikonomou E, Tsiachris D, Mazaris S, Venieri E; et al. (2014). "The natural history of multifocal atrial rhythms in elderly outpatients: insights from the "Ikaria study"". Ann Noninvasive Electrocardiol. 19 (5): 483–9. doi:10.1111/anec.12165. PMID 24750225.
  6. ↑ 6.0 6.1 Baek SM, Chung H, Song MK, Bae EJ, Kim GB, Noh CI (2018). "The Complexity of Pediatric Multifocal Atrial Tachycardia and Its Prognostic Factors". Korean Circ J. 48 (2): 148–158. doi:10.4070/kcj.2017.0179. PMC 5861005. PMID 29441747.
  7. ↑ Lin AE, Alexander ME, Colan SD, Kerr B, Rauen KA, Noonan J; et al. (2011). "Clinical, pathological, and molecular analyses of cardiovascular abnormalities in Costello syndrome: a Ras/MAPK pathway syndrome". Am J Med Genet A. 155A (3): 486–507. doi:10.1002/ajmg.a.33857. PMID 21344638.
  8. ↑ 8.0 8.1 Fish FA, Mehta AV, Johns JA (1996). "Characteristics and management of chaotic atrial tachycardia of infancy". Am J Cardiol. 78 (9): 1052–5. doi:10.1016/s0002-9149(96)00536-x. PMID 8916490.
  9. ↑ Broendberg AK, Nielsen JC, Bjerre J, Pedersen LN, Kristensen J, Henriksen FL; et al. (2017). "Nationwide experience of catecholaminergic polymorphic ventricular tachycardia caused by RyR2 mutations". Heart. 103 (12): 901–909. doi:10.1136/heartjnl-2016-310509. PMID 28237968.
  10. ↑ Sakurai K, Takahashi K, Nakayashiro M (2018). "Combined flecainide and sotalol therapy for multifocal atrial tachycardia in cardio-facio-cutaneous syndrome". Pediatr Int. 60 (11): 1036–1037. doi:10.1111/ped.13695. PMID 30536490.
  11. ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  12. ↑ Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  13. ↑ Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  14. ↑ Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  15. ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  16. ↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  17. ↑ Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  18. ↑ Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  19. ↑ Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  20. ↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  21. ↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  22. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  23. ↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  24. ↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  25. ↑ Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  26. ↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  27. ↑ Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  28. ↑ Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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