Indian Pacing Electrophysiol. J.
Indian Pacing Electrophysiol. J. 2010;
Accelerated Idioventricular Rhythm: History and Chronology of the Main Discoveries
Download PDF 687 KBAndres Ricardo Perez Riera MD1; Raimundo Barbosa Barros MD2; Francisco Daniel de Sousa MD2 Adrian Baranchuk MD, FACC3,
1ABC Medical Faculty. ABC Foundation. Santo Andre - Sao Paulo. Brazil
2Hospital de Messejana Dr. Carlos Alberto Studart Gomes, Fortaleza-Ceara-Brazil
3Kingston General Hospital, Queen's University, Kingston, Ontario, Canada.
Address for correspondence: Andres Ricardo Perez Riera MD, Sebastiao Afonso, 885CEP: 04417-000 - Jardim Miriam - Sao Paulo - Brazil. E-mail: riera/at/uol.com.br
Accelerated Idioventricular Rhythm (AIVR) is a ventricular rhythm consisting of three or more consecutive monomorphic beats, with gradual onset and gradual termination. It can rarely manifest in patients with completely normal hearts or with structural heart disease. It is usually seen during acute myocardial infarction reperfusion. This manuscript aims to review the history of the main discoveries that lead to the identification and comprehension of this fascinating arrhythmia.
Key words: Accelerated Idioventricular Rhythm; History and Chronology; Slow ventricular tachycardia
Introduction - Definitions
The so called "Accelerated Idioventricular Rhythm" (AIVR) is a ventricular rhythm (originating from the His, the Purkinje system or the working contractile ventricular cells) consisting of three or more consecutive monomorphic beats, with gradual onset. Less commonly, AIVR is polymorphic. The discharge rate of the ectopic focus is similar to the sinus rate (isorhythmic) between 50 and 120 bpm. The ectopic focus manifests when the sinus rate slows down (below the ectopic focus) or when the ectopic focus accelerates above the intrinsic rate by 30-40 beats per minute. When both discharge rates (sinus and ectopic focus) are similar, isorhythmic dissociation, fusion and capture beats can be seen.
AIVR is usually a benign and well-tolerated arrhythmia. Most of the cases will require no treatment and in rare situations such as sustained or incessant AIVR or when AV dissociation induces syncope, the risk of sudden death is higher, and the arrhythmia should be treated.
Different terminology was used to describe AIVR: Non paroxysmal ventricular tachycardia (VT), isorhythmic slow VT, and the curious benevolent tachycardia.
Non paroxysmal VT is currently a non accepted definition given the fact that AIVR is usually a ventricular rhythm at rate slower than 100 bpm, thus not meeting criteria to be called tachycardia.
AIVR - Clinical Scenarios
Rarely, AIVR can be detected in the youth and, in this subgroup, is usually benign  and requires no specific treatment.
AIVR occurs infrequently in patients without demonstrable heart disease and, in this case, it has a good prognosis. When AIVR presents in individuals with no structural heart disease, the mechanism involved is usually an increased vagal tone and decreased sympathetic tone , as observed in athletes. The acceleration of an independent focus during exercise strongly suggests that this ectopic focus is under autonomic influence, a phenomenon also seen during central nervous system (CNS) stimulation in dogs . A similar mechanism has also been described for pregnant women in the antenatal period .
AIVR is frequently observed during the reperfusion phase that follows an acute myocardial infarction (AMI) . It remains controversial whether or not, AIVR implies complete reperfusion of the culprit lesion or only some degree of reperfusion. AIVR has been also described associated with several drug intoxications such as halothane , aconitine , desflurane , cocaine , and digitalis [10-12]. Electrolyte imbalance has also been associated with AIVR in an experimental study . There are also case reports published on the association of AIVR with the post-resuscitation period  (as an initial resolving rhythm), in chronic ischemic and non ischemic dilated cardiomyopathy , and less frequently in cardiomyopathies such as hypertrophic cardiomyopathy , arrhythmogenic right ventricular dysplasia (ARVD) , and in newborn infants with different congenital heart diseases .
A typical example of AIVR in the setting of normal structural heart can be seen in Figure 1. In Figure 2, a case of AIVR in the context of a reperfused acute inferior MI can be seen.
Figure 1: This ECG belongs to a 23 year-old male patient, Caucasian, asymptomatic. No cardiovascular history. He practiced physical activities regularly. He has been treated with azitromicine for an upper airway infection. Both panels show sinus rhythm alternating with AIVR at approximately 60 bpm. Note fusion beats (F).
Figure 2: This ECG belongs to a 67 year-old woman, presenting to the ER with an acute inferior MI (superior panel). During the administration of thrombolytics, AIVR can be seen (inferior panel) at rate of 88 bpm. AIVR alternates with sinus captures (C) and fusion beats (F).
The main electrophysiological mechanism involved in AIVR is an abnormal calcium-dependent automatism (ectopic automaticity) that affect phase 4 of action potential (diastolic depolarization) . When AIVR is associated with digitalis intoxication, the main arrhythmogenic mechanism involved is trigger activity .
This manuscript aims to be a chronological historical review on the main findings that contributed to the understanding of this fascinating arrhythmia.
Chronology of discoveries
1925: Sir Thomas Lewis (December 26th, 1881, Cardiff, Gales - March 17th 1945) a pioneer of the British cardiology showed the first ECG trace of AIVR case in his book entitled "Mechanism and graphic registration of the heartbeat" , dedicated to Willem Einthoven. He failed to identify AIVR as an independent arrhythmia. This book is considered the first book on Electrocardiography, as highlighted by Prof. Schapiro  a well-recognized historian in electrocardiology and arrhythmias. Several years prior to the publication of his book, Sir Lewis reported in The Lancet (1909) an interesting article about the mechanisms of VT without mentioning its slower forms .
1950: Harris  was the first one to identify AIVR associated with ischemia and reperfusion in an experimental study. He observed this rhythm after clamping the right coronary artery. He identified the origin of this rhythm in the ventricles and described a similar heart rate than the sinus discharge. He also mentioned that this rhythm may overrate the sinus rate but also could be inhibited by increasing the sinus discharge.
1966: Mariot and Menendez  have introduced the currently accepted terminology: AIVR.
1967: Dessertene  described for the first time the term "slow ventricular tachycardia"
1969: Agustín Castellanos Jr  used the term "slow ventricular tachycardia" during an acute MI to describe a case of AIVR. Additionally, the authors explained the underlying electrophysiological mechanisms of AIVR.
1973: Rothfeld et al  showed for the first time the coexistence of paroxysmal ventricular tachycardia and "idioventricular rhythm" during an acute MI.
1974: Rothfeld and Zucker , were the first ones to describe the polymorphic form of AIVR. They named it "Multiform accelerated idioventricular rhythm". Sclarowski, 4 years later (1978), published 2 cases with polymorphic presentation in the Journal of Electrocardiology .
1975: Agustín Castellanos Jr et al  reported digitalis-induced AIVR for the first time in the literature. Scheinman et al  reported the efficacy of atropine to suppress AIVR during the acute MI. Basy and Scheinman  reported the sustained form of AIVR in an elderly patient suffering an inferior MI. The authors successfully treated the patient with IV Procainamide. The same year, Castellanos et al  reported an AIVR from two different foci. They named it "double ectopic accelerated ventricular rhythm".
1976: Hasin and Rogel  presented the currently accepted mechanism involved in AIVR. They postulated the involvement of the phase 4 slope of the action potential (ectopic automaticity) for the unstable form of AIVR that is frequently observed in acute MI. The same year, Doshchitsin and Merkulova from Russia , used the terminology "non-paroxysmal ventricular tachycardia".
1980: Delise et al  reported the first case of AIVR associated with hypertrophic cardiomyopathy.
1981: Bernard et al , described AIVR in a pediatric patient. They highlighted the usual benign course of this arrhythmia in this population.
1983: Sclarovsky et al , showed a partial benefit of eliminating AIVR by treating a patient with Verapamil. The same year, Golderberg et al , reported that the presence of AIVR during the acute phase of a MI treated with thrombolytic therapy, rather than a malignant sign, implies reperfusion of the culprit lesion. The sensitivity is low but the specificity is high (> 80%). Jonsson et al  described the association of AIVR with the use of cocaine.
1987: Chiale et al , reported a case of slow automaticity in a young patient with no structural heart disease.
1988: Martini et al  described the first case of AIVR originating in the infundibular region of the right ventricle in a patient with a concealed form of arrhythmogenic right ventricular dysplasia (ARVD).
1991: Tatu-Chiţoiu , used the term "Non-paroxysmal ventricular tachycardia with isorhythmic atrioventricular dissociation" to described AIVR.
1993: Nakawa et al , showed that AIVR had no impact in long-term prognosis in a large population of pediatric patients with congenital heart disease. The same year, Martinez-Lopez JI et al , created the term "benevolent rhythm" to describe AIVR. This term has not convinced the cardiology community and currently is not been used.
2000: Grimm et al  followed up a series of patients with AIVR with idiopathic dilated cardiomyopathy. The presence of the arrhythmia did not impact on long-term prognosis.
2002: Marret et al  reported a case of AIVR associated with desflurane intoxication.
2004: Dulac et al , reported the first case of AIVR in a pregnant woman in the antenatal period.
2005: Bonnemeier et al , determined that AIVR is not a specific marker of reperfusion during an acute MI treated with thrombolytics. The presence of AIVR could not distinguish between complete or incomplete reperfusion. They established a connection between AIVR and autonomic nervous system imbalance, AIVR being more frequently associated with increased parasympathetic tone and decreased sympathetic tone. The authors confirmed that the presence of AIVR did not affect the short or long-term prognosis.
2007: Tsai et al  reported the first case of AIVR in a post-resuscitated patient. The same year, Nasir et al , reported cases of AIVR in elite athletes. Again, the authors related the presence of the arrhythmia with autonomic dysfunction (hypervagotonia). Fuyita et al  reported a case of AIVR associated with intoxication with acotinine.
2008: Hsu et al , reported the first case of AIVR associated with Buerger disease (also known as thromboangiitis obliterans) and MI. In the same year, Chhabra et al  reported a case of AIVR observed during inhalational induction with halothane in a child with congenital cataract. Osmancik et al , confirmed that the value of AIVR alone as a criteria for reperfusion is low, but in addition to normalization of the ST-segment, the probability of successful reperfusion is higher.
This intriguing arrhythmia could manifest in several different clinical scenarios. There are benign forms in subjects with no structural heart disease in which case, it usually requires no intervention, but sometimes it can present as a more severe arrhythmia, requiring treatment. Since its initial identification by Harris, major advances have been done in the understanding on the underlying mechanisms involved in the genesis of this arrhythmia. Abnormal calcium-dependent automatism that affects the phase 4 slope of the action potential (ectopic automaticity) has been identified as the main electrophysiological mechanism involved in AIVR. Autonomic imbalance has also been identified as a trigger of this abnormal rhythm. More recent reports showed that the presence of AIVR does not constitute a specific marker of complete reperfusion during the acute phase of a myocardial infarction, but it could indicate that the responsible vessel is open. In this context, AIVR usually does not require specific treatment.
1. Bernard Y, Dambrine P, Ravault MC, et al. Accelerated idioventricular rhythm in children. Apropos of a case. Arch Mal Coeur Vaiss 1981; 74: 623-627.
2. Bonnemeier H, Ortak J, Wiegand UK, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann Noninvasive Electrocardiol 2005; 10: 179-187.
3. Comerford TJ, Propert DB. Accelerated idioventricular rhythm in patients without acute myocardial infarction. Angiology. 1979; 30: 768-775.
4. Dulac Y, Brosset P, Acar P, et al. Slow ventricular tachycardia presenting in the antenatal period. Arch Mal Coeur Vaiss 2004; 97: 564-566.
5. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: a marker of restoration of anterograde flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J 1983; 105: 26-32.
6. Chhabra A, Subramaniam R. Sudden appearance of idioventricular rhythm during inhalational induction with halothane in a child with congenital cataract. J Postgrad Med. 2008; 54: 337-339.
7. Fujita Y, Terui K, Fujita M, et al. Five cases of aconite poisoning: toxicokinetics of aconitines. J Anal Toxicol. 2007; 31: 132-137.
8. Marret E, Pruszkowski O, Deleuze A, et al. Accelerated idioventricular rhythm associated with desflurane administration. Anesth Analg 2002; 95: 319-321.
9. Jonsson S, O'Meara M, Young JB. Acute cocaine poisoning. Importance of treating seizures and acidosis. Am J Med. 1983; 75: 1061-1064.
10. Castellanos A, Azan L, Bierfield J, Myerburg RJ. Heart Lung. Digitalis-induced accelerated idioventricular rhythms: revisited. 1975; 4: 104-110.
11. Pellegrino L. Accelerated idioventricular rhythm (slow ventricular tachycardia) in patients with acute myocardial infarct and in patients with digitalis intoxication. Clinical and electrocardiographic study. Boll Soc Ital Cardiol. 1975; 20: 1785-1793.
12. Pellegrino LG. Accelerated idioventricular rhythm in patients with digitalic intoxication. Clinical and electrocardiographic study of two cases. Ital Cardiol. 1976; 6: 527-531.
13. Moroz VM, Lipnitskii TN. Study of pathogenesis of ventricular arrhythmia in experimental rats by separation of sinus and ventricular substitutional rhythms. Bull Exp Biol Med. 2006; 141: 400-403.
14. Tsai MS, Huang CH, Chen HR, et al. Postresuscitation accelerated idioventricular rhythm: a potential prognostic factor for out-of-hospital cardiac arrest survivors. Intensive Care Med 2007; 33: 1628-1632.
15. Grimm W, Hoffmann J, Menz V, et al. Significance of accelerated idioventricular rhythm in idiopathic dilated cardiomyopathy. Am J Cardiol 2000; 85: 899-904.
16. Delise P, D'Este D, Monico E, Millosevich P, Raviele A, Dainese F, Piccolo E. Accelerated idioventricular rhythm with isorhythmic A-V dissociation. An electrophysiological study. G Ital Cardiol 1980; 10:1588-1593.
17. Martini B, Nava A, Thiene G, et al. Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia. Br Heart J 1988; 59: 564-571.
18. Nakagawa M, Yoshihara T, Matsumura A, Fusaoka T, Hamaoka K. Accelerated idioventricular rhythm in three newborn infants with congenital heart disease. Chest 1993; 104: 322-323.
19. Castellanos A, Lemberg L, Arcebal AG. Mechanisms of slow ventricular tachycardias in acute myocardial infarction. Dis Chest 1969; 56: 470-476.
20. Holzmann M, Reutter FW. Accelerated idioventricular rhythm with second degree V.A. -block and reentry Z Kardiol. 1977; 66: 52-54.
21. Lewis T. Mechanism and graphic registration of the heartbeat. London: Shaw and Sons, 1925.
22. Shapiro E. The first textbook of electrocardiography. Thomas Lewis: Clinical Electrocardiography. J Am Coll Cardiol 1983; 1: 1160-1161.
23. Lewis T. Single and successive extrasystoles. Lancet 1909; 1; 382.
24. Harris AS. Delayed development of ventricular ectopic rhythms following experimental coronary occlusion. Circulation 1950; 1:1318-1328.
25. Marriott HJ, Menendez MM. A-V dissociation revisited. Prog Cardiovasc Dis 1966; 8: 522-538.
26. Dessertenne F. The ventricular electrical complex with prolonged slow phase. Sem Hop 1967; 43: 539-541.
27. Rothfeld EL, Zucker IR, Leff WA, Ritota MC. Coexisting paroxysmal ventricular tachycardia and idioventricular rhythm in acute myocardial infarction. J Electrocardiol. 1973; 6:149-152.
28. Rothfeld EL, Zucker IR. Multiform accelerated idioventricular rhythm. Angiology 1974; 25: 457-461.
29. Sclarovsky S, Strasberg B, Agmon J. Multiform accelerated idioventricular rhythm in acute myocardial infarction. J Electrocardiol 1978; 11: 197-200.
30. Scheinman MM, Thorburn D, Abbott JA. Use of atropine in patients with acute myocardial infarction and sinus bradycardia. Circulation 1975; 52: 627-633.
31. Basu D, Scheinman M. Sustained accelerated idioventricular rhythm. Am Heart J 1975; 89: 227-231.
32. Castellanos A, Sung RJ, Mayorga-Cortes A, Myerburg RJ. Double ectopic accelerated ventricular and nonaccelerated ventricular or supraventricular rhythms. Eur J Cardiol 1975; 3:153-156.
33. Hasin Y, Rogel S. Ventricular rhythms in acute myocardial infarction. Cardiology 1976; 61: 195-207.
34. Doshchitsin VL, Merkulova IN. Ventricular fibrillation and asystole precursors in myocardial infarct. Kardiologia. 1976; 16:19-22.
35. Sclarovsky S, Strasberg B, Fuchs J,et al. Multiform accelerated idioventricular rhythm in acute myocardial infarction: electrocardiographic characteristics and response to verapamil. Am J Cardiol 1983; 52: 43-47.
36. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: a marker of restoration of anterograde flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J 1983; 105:26-32.
37. Chiale PA, Sicouri SJ, Elizari MV, et al. Chronic idiopathic idioventricular tachycardia caused by slow response automaticity. Pacing Clin Electrophysiol 1987; 10: 1371-1377.
38. Tatu-Chiţoiu G. Non-paroxysmal ventricular tachycardia with isorhythmic atrioventricular dissociation. Rom J Intern Med1991; 29: 139-143.
39. Martinez-Lopez JI. ECG of the month. Benevolent rhythm. Escape impulses; escape rhythm. J La State Med Soc 1993; 145: 249-252.
40. Nasir JM, Durning SJ, Johnson RL, et al. Symptomatic hypervagotonia in a highly conditioned athlete. Clin J Sport Med 2007; 17: 70-71.
41. Hsu PC, Lin TH, Su HM, Voon WC, Lai WT, Sheu SH. Frequent accelerated idioventricular rhythm in a young male of Buerger's disease with acute myocardial infarction. Int J Cardiol 2008; 127:e64-66.
42. Osmancik PP, Stros P, Herman D. In-hospital arrhythmias in patients with acute myocardial infarction - the relation to the reperfusion strategy and their prognostic impact. Acute Card Care 2008; 10: 15-25.