Multifocal atrial tachycardia
| 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.[5]
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Aminophylline toxicity[6]
- Congestive heart failure
- Hypokalemia
- Hypoxia
- Myocardial infarction
- Pulmonary embolism
- Sepsis
Common Causes
- Chronic obstructive pulmonary disease
- Chronic renal failure
- Congestive heart failure
- Diabetes mellitus
- Hypokalemia
- Hypoxia
- Myocardial infarction
- Pneumonia
- Pulmonary embolism
- Sepsis
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.[7]
- 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.[8]
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).[9]
- 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.[10][11]
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.
- 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.[12]
- 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][9][13][14]
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.[15][13]
- 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.
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)[16][17] |
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| Atrial Flutter[18] |
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| Atrioventricular nodal reentry tachycardia (AVNRT)[19][20][21][22] |
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| Multifocal Atrial Tachycardia[23][24] |
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| Paroxysmal Supraventricular Tachycardia |
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| Premature Atrial Contractrions (PAC)[25][26] |
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| Wolff-Parkinson-White Syndrome[27][28] |
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| Ventricular Fibrillation (VF)[29][30][31] |
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| Ventricular Tachycardia[32][33] |
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References
- ↑ 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.
- ↑ 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.
- ↑ Kastor JA (1990). "Multifocal atrial tachycardia". N Engl J Med. 322 (24): 1713–7. doi:10.1056/NEJM199006143222405. PMID 2188131.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "StatPearls". 2020. PMID 29083603.
- ↑ 9.0 9.1 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.
- ↑ "StatPearls". 2020. PMID 30571060.
- ↑ 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.
- ↑ 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.
- ↑ 13.0 13.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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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