Multifocal atrial tachycardia

Jump to: navigation, search
Multifocal atrial tachycardia
MAT 1.jpeg

WikiDoc Resources for Multifocal atrial tachycardia

Articles

Most recent articles on Multifocal atrial tachycardia

Most cited articles on Multifocal atrial tachycardia

Review articles on Multifocal atrial tachycardia

Articles on Multifocal atrial tachycardia in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Multifocal atrial tachycardia

Images of Multifocal atrial tachycardia

Photos of Multifocal atrial tachycardia

Podcasts & MP3s on Multifocal atrial tachycardia

Videos on Multifocal atrial tachycardia

Evidence Based Medicine

Cochrane Collaboration on Multifocal atrial tachycardia

Bandolier on Multifocal atrial tachycardia

TRIP on Multifocal atrial tachycardia

Clinical Trials

Ongoing Trials on Multifocal atrial tachycardia at Clinical Trials.gov

Trial results on Multifocal atrial tachycardia

Clinical Trials on Multifocal atrial tachycardia at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Multifocal atrial tachycardia

NICE Guidance on Multifocal atrial tachycardia

NHS PRODIGY Guidance

FDA on Multifocal atrial tachycardia

CDC on Multifocal atrial tachycardia

Books

Books on Multifocal atrial tachycardia

News

Multifocal atrial tachycardia in the news

Be alerted to news on Multifocal atrial tachycardia

News trends on Multifocal atrial tachycardia

Commentary

Blogs on Multifocal atrial tachycardia

Definitions

Definitions of Multifocal atrial tachycardia

Patient Resources / Community

Patient resources on Multifocal atrial tachycardia

Discussion groups on Multifocal atrial tachycardia

Patient Handouts on Multifocal atrial tachycardia

Directions to Hospitals Treating Multifocal atrial tachycardia

Risk calculators and risk factors for Multifocal atrial tachycardia

Healthcare Provider Resources

Symptoms of Multifocal atrial tachycardia

Causes & Risk Factors for Multifocal atrial tachycardia

Diagnostic studies for Multifocal atrial tachycardia

Treatment of Multifocal atrial tachycardia

Continuing Medical Education (CME)

CME Programs on Multifocal atrial tachycardia

International

Multifocal atrial tachycardia en Espanol

Multifocal atrial tachycardia en Francais

Business

Multifocal atrial tachycardia in the Marketplace

Patents on Multifocal atrial tachycardia

Experimental / Informatics

List of terms related to Multifocal atrial tachycardia

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

Synonyms and Keywords: MAT, Chaotic atrial tachycardia, Supraventricular tachycardia

Overview

Multifocal atrial tachycardia (MAT) is a cardiac arrhythmia which is specifically a type of supraventricular tachycardia with an irregular, rapid atrial rhythm arising from multiple ectopic foci within the atria with a heart rate exceeding 100 beats per minute. It is characterized by an organized atrial activity yielding three or more different non-sinus P wave morphologies in the same lead with variable or irregular PP, PR and RR intervals. There's an isoelectric baseline between P waves with the most P waves being conducted to the ventricles and some R waves being aberrantly conducted. This variability pattern makes MAT look irregular on the surface ECG, thus oftenly leading to misinterpretion as atrial fibrillation. It is typically seen in elderly patients with a variety of underlying comorbidities, the most common being chronic obstructive pulmonary disease (COPD) and congestive heart failure (CHF) and eventually it develops into atrial fibrillation. A rhythm with similar ECG characteristics but at a slow rate is referred to as multifocal atrial rhythm (MAR). The pathogenesis of MAT is not well understood and the patients are generally asymptomatic with mostly being hemodynamically stable. Typically, no treatment is required beyond treatment of underlying conditions in the majority of the MAT patients. However, it is very important to evaluate such patients as this arrhythmia is a poor prognostic sign in the setting of an acute illness.

Historical Perspective

Pathophysiology

Proposed theories suggesting the underlying mechanism of MAT
Theory Description
Theory of re-entry
Theory of abnormal automaticity
  • The main focus of the theory of abnormal automaticity is on an increase in the ability of atrial myocytes to spontaneously depolarize and thus triggering an action potential.
  • Many of the underlying conditions associated with MAT support this theory.
  • Pulmonary diseases such as COPD can cause any of the following pathological conditions known to be associated with an increase in 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.
Theory of triggered activity
  • 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.
Multifocal Atrial Tachycardia.

Causes

Following is a list of potential causes of multifocal atrial tachycardia:

Life Threatening Causes

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

Common Causes


Causes by Organ System

Cardiovascular Congestive heart failure, myocardial infarction,
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Aminophylline,, 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

  • MAT has been reported in >20% of the pediatric patients and up to 60% of the adult patients with coexisting pulmonary disease.
  • 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.[19]
  • rare multifocal atrial tachycardia in the neonate, initiated by a recent case in our clinic. The difficulties in prenatally diagnosing the disease by cardiotocography are as well discussed as the obstetric management.[20][21][22]
  • 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.[23]
  • The incidence of multifocal atrial tachycardia (MAT) is very low and accounts for less than 1% of supraventricular tachycardia in infants and children.[24]
  • Multifocal atrial tachycardia is a rare form of rhythm disturbance in infancy; it is difficult to treat but frequently resolves spontaneously within the first year of life.[25]

Natural history, Complications, and Prognosis

  • MAT is considered to be a relatively benign arrhythmia with likely good outcome if there is no severe underlying illness. It can be well controlled under appropriate drugs, and a long period of follow-up is suggested. If pharmacologic intervention is required, we suggest that amiodarone may be an excellent choice.[24]
  • 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).[26]
  • 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.[27][28]

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
  • 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.[29]
  • 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).
  • 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.[30]
  • 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.[2][26][31][32]

History and Symptoms

  • 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.

Physical Examination

  • 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.

Treatment

  • Combined flecainide and sotalol therapy for multifocal atrial tachycardia in cardio-facio-cutaneous syndrome.[33][31]
  • Successful treatment with Ibutilide is demonstrated. Treatment with a class III antiarrhythmic agent opposes the frequently accepted mechanism of triggered activity in causing this arrhythmia.[34]
  • 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.
  • MAT is best managed by an interprofessional 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.[26][35][36]
  • intramuscular and continuous intravenous magnesium sulphate regimens used in pre-eclampsia. Both routes of administration were successful in causing reversion to sinus rhythm but the intramuscular regimen, by attaining a higher and more sustained serum magnesium concentration, converted the arrhythmia to normal sinus rhythm in a shorter period of time (1-2 hours) than the intravenous regimen (4-8 hours).Intravenous magnesium sulfate is superior to amiodarone in the conversion of acute atrial tachyarrhythmias, while initial slowing of ventricular response rate in nonconverters appears equally efficacious with both agents.[37][38][39][36][40][41][42]
  • Parentral potassium, We believe that serum magnesium administered together with serum potassium stabilizes the ionic balance of atrial cells and thus prevents spontaneous ectopy.[38]

Prevention

Primary Prevention

  • Magnesium-sparing diuretics should be used in the treatment of patients with chronic obstructive pulmonary disease and congestive heart failure, which are both conditions associated with magnesium deficiency and MAT.[37]

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)[43][44]
  • 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[45]
  • 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)[46][47][48][49]
  • 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[50][51]
  • 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)[52][53]
  • 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[54][55]
  • 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)[56][57][58]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[59][60]
  • 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. Shine KI, Kastor JA, Yurchak PM (1968). "Multifocal atrial tachycardia. Clinical and electrocardiographic features in 32 patients". N Engl J Med. 279 (7): 344–9. doi:10.1056/NEJM196808152790703. PMID 5662166.
  2. 2.0 2.1 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.
  3. 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.
  4. Kastor JA (1990). "Multifocal atrial tachycardia". N Engl J Med. 322 (24): 1713–7. doi:10.1056/NEJM199006143222405. PMID 2188131.
  5. 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.
  6. Wang K, Goldfarb BL, Gobel FL, Richman HG (1977). "Multifocal atrial tachycardia". Arch Intern Med. 137 (2): 161–4. PMID 836113.
  7. McCord J, Borzak S (1998). "Multifocal atrial tachycardia". Chest. 113 (1): 203–9. doi:10.1378/chest.113.1.203. PMID 9440591.
  8. Serra Torres A, Ferriol Bergas J, García De La Villa Redondo B (2009). "[Multifocal atrial tachycardia]". Med Clin (Barc). 132 (3): 106–7. doi:10.1016/j.medcli.2008.09.015. PMID 19211063.
  9. Esser H, Kikis D, Trübestein G (1975). "[Proceedings: Multifocal atrial tachycardia]". MMW Munch Med Wochenschr. 117 (20): 837–8. PMID 805961.
  10. Kim LK, Lee CS, Jeun JG (2010). "Development of multifocal atrial tachycardia in a patient using aminophylline -A case report-". Korean J Anesthesiol. 59 Suppl: S77–81. doi:10.4097/kjae.2010.59.S.S77. PMC 3030063. PMID 21286467.
  11. Sessler CN, Cohen MD (1990). "Cardiac arrhythmias during theophylline toxicity. A prospective continuous electrocardiographic study". Chest. 98 (3): 672–8. doi:10.1378/chest.98.3.672. PMID 2394145.
  12. Poukkula A, Korhonen UR, Huikuri H, Linnaluoto M (1989). "Theophylline and salbutamol in combination in patients with obstructive pulmonary disease and concurrent heart disease: effect on cardiac arrhythmias". J Intern Med. 226 (4): 229–34. doi:10.1111/j.1365-2796.1989.tb01385.x. PMID 2681505.
  13. Sessler CN (1990). "Theophylline toxicity: clinical features of 116 consecutive cases". Am J Med. 88 (6): 567–76. doi:10.1016/0002-9343(90)90519-j. PMID 2189301.
  14. Bittar G, Friedman HS (1991). "The arrhythmogenicity of theophylline. A multivariate analysis of clinical determinants". Chest. 99 (6): 1415–20. doi:10.1378/chest.99.6.1415. PMID 2036824.
  15. Levine JH, Michael JR, Guarnieri T (1985). "Multifocal atrial tachycardia: a toxic effect of theophylline". Lancet. 1 (8419): 12–4. doi:10.1016/s0140-6736(85)90964-x. PMID 2856947.
  16. Sharma SN, Iyengar SS, Verma M (1993). "Multifocal atrial tachycardia: a complication of pneumomediastinum". J Assoc Physicians India. 41 (1): 50–1. PMID 8340335.
  17. Goudis CA, Konstantinidis AK, Ntalas IV, Korantzopoulos P (2015). "Electrocardiographic abnormalities and cardiac arrhythmias in chronic obstructive pulmonary disease". Int J Cardiol. 199: 264–73. doi:10.1016/j.ijcard.2015.06.096. PMID 26218181.
  18. Kothari SA, Apiyasawat S, Asad N, Spodick DH (2005). "Evidence supporting a new rate threshold for multifocal atrial tachycardia". Clin Cardiol. 28 (12): 561–3. doi:10.1002/clc.4960281205. PMC 6654295 Check |pmc= value (help). PMID 16405199.
  19. 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.
  20. Haenel AF, Olafsson A (1985). "[Multifocal atrial tachycardia in the newborn infant--obstetrical implications]". Z Geburtshilfe Perinatol. 189 (5): 228–31. PMID 4072318.
  21. Esterl D, Rösel HD (1987). "[Multifocal (chaotic) atrial tachycardia in a newborn infant]". Zentralbl Gynakol. 109 (14): 919–22. PMID 3660970.
  22. Bouziri A, Khaldi A, Hamdi A, Ben Massoud I, Borgi A, Menif K; et al. (2011). "Multifocal atrial tachycardia: an unusual cause of cardiogenic shock in a newborn". Tunis Med. 89 (1): 59–61. PMID 21267831.
  23. "StatPearls". 2020. PMID 29083603.
  24. 24.0 24.1 Hsieh MY, Lee PC, Hwang B, Meng CC (2006). "Multifocal atrial tachycardia in 2 children". J Chin Med Assoc. 69 (9): 439–43. doi:10.1016/S1726-4901(09)70288-6. PMID 17051756.
  25. Toussaint R, Hofstetter R, von Bernuth G (1984). "[Multifocal atrial tachycardia in infancy]". Klin Padiatr. 196 (2): 118–20. doi:10.1055/s-2007-1025591. PMID 6737948.
  26. 26.0 26.1 26.2 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.
  27. "StatPearls". 2020. PMID 30571060.
  28. Levin MD, Saitta SC, Gripp KW, Wenger TL, Ganesh J, Kalish JM; et al. (2018). "Nonreentrant atrial tachycardia occurs independently of hypertrophic cardiomyopathy in RASopathy patients". Am J Med Genet A. 176 (8): 1711–1722. doi:10.1002/ajmg.a.38854. PMC 6107379. PMID 30055033.
  29. van der Watt MJ, Aboo AA, Millar RN (1995). "A prospective study of electrical cardioversion for sustained tachycardias by emergency unit personnel". S Afr Med J. 85 (6): 508–11. PMID 7652630.
  30. 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.
  31. 31.0 31.1 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.
  32. 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.
  33. 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.
  34. Pierce WJ, McGroary K (2001). "Multifocal atrial tachycardia and Ibutilide". Am J Geriatr Cardiol. 10 (4): 193–5. doi:10.1111/j.1076-7460.2001.00016.x. PMID 11455238.
  35. Kantoch MJ, Gulamhusein SS, Sanatani S (2011). "Short- and long-term outcomes in children undergoing radiofrequency catheter ablation before their second birthday". Can J Cardiol. 27 (4): 523.e3–9. doi:10.1016/j.cjca.2010.12.043. PMID 21621374.
  36. 36.0 36.1 Ho KM (2008). "Intravenous magnesium for cardiac arrhythmias: jack of all trades". Magnes Res. 21 (1): 65–8. PMID 18557136.
  37. 37.0 37.1 Cohen L, Kitzes R, Shnaider H (1988). "Multifocal atrial tachycardia responsive to parenteral magnesium". Magnes Res. 1 (3–4): 239–42. PMID 3275209.
  38. 38.0 38.1 Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA (1985). "Magnesium and potassium therapy in multifocal atrial tachycardia". Am Heart J. 110 (4): 789–94. doi:10.1016/0002-8703(85)90458-2. PMID 4050650.
  39. Moran JL, Gallagher J, Peake SL, Cunningham DN, Salagaras M, Leppard P (1995). "Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: a prospective, randomized study". Crit Care Med. 23 (11): 1816–24. doi:10.1097/00003246-199511000-00005. PMID 7587256.
  40. Stühlinger HG, Kiss K, Smetana R (2000). "[Significance of magnesium in cardiac arrhythmias]". Wien Med Wochenschr. 150 (15–16): 330–4. PMID 11105328.
  41. Zehender M (1996). "[Magnesium as an anti-arrhythmic therapy principle in supraventricular and ventricular cardiac arrhythmias]". Z Kardiol. 85 Suppl 6: 135–45. PMID 9064958.
  42. Vester EG (1997). "[Clinico-electrophysiologic effects of magnesium, especially in supraventricular tachycardia]". Herz. 22 Suppl 1: 40–50. doi:10.1007/bf03042654. PMID 9333591.
  43. 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.
  44. 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.
  45. 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.
  46. 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.
  47. 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.
  48. "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  49. 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.
  50. 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.
  51. 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.
  52. 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.
  53. 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.
  54. 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.
  55. 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.
  56. 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.
  57. 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.
  58. 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.
  59. 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.
  60. Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

Additional resources



Linked-in.jpg