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" [21], 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 [22] 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 [23].

Harris [24] 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.

Mariot and Menendez [25] have introduced the currently accepted terminology: AIVR.

Dessertene [26] described for the first time the term "slow ventricular tachycardia"

Agustín Castellanos Jr [19] 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.

Rothfeld et al [27] showed for the first time the coexistence of paroxysmal ventricular tachycardia and "idioventricular rhythm" during an acute MI.

Rothfeld and Zucker [28], 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 [29].

Agustín Castellanos Jr et al [10] reported digitalis-induced AIVR for the first time in the literature. Scheinman et al [30] reported the efficacy of atropine to suppress AIVR during the acute MI. Basy and Scheinman [31] 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 [32] reported an AIVR from two different foci. They named it "double ectopic accelerated ventricular rhythm".

Hasin and Rogel [33] 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 [34], used the terminology "non-paroxysmal ventricular tachycardia".

Delise et al [15] reported the first case of AIVR associated with hypertrophic cardiomyopathy.

Bernard et al [1], described AIVR in a pediatric patient. They highlighted the usual benign course of this arrhythmia in this population.

Sclarovsky et al [35], showed a partial benefit of eliminating AIVR by treating a patient with Verapamil. The same year, Golderberg et al [36], 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 [9] described the association of AIVR with the use of cocaine.

Chiale et al [37], reported a case of slow automaticity in a young patient with no structural heart disease.

Martini et al [16] 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).

Tatu-Chitoiu [38], used the term "Non-paroxysmal ventricular tachycardia with isorhythmic atrioventricular dissociation" to described AIVR.

Nakawa et al [18], 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 [39], created the term "benevolent rhythm" to describe AIVR. This term has not convinced the cardiology community and currently is not been used.

Grimm et al [14] followed up a series of patients with AIVR with idiopathic dilated cardiomyopathy. The presence of the arrhythmia did not impact on long-term prognosis.

Marret et al [8] reported a case of AIVR associated with desflurane intoxication.

Dulac et al [4], reported the first case of AIVR in a pregnant woman in the antenatal period.

Bonnemeier et al [2], 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.

Tsai et al [13] reported the first case of AIVR in a post-resuscitated patient. The same year, Nasir et al [40], reported cases of AIVR in elite athletes. Again, the authors related the presence of the arrhythmia with autonomic dysfunction (hypervagotonia). Fuyita et al [7] reported a case of AIVR associated with intoxication with acotinine.

Hsu et al [41], reported the first case of AIVR associated with Buerger disease (also known as thromboangiitis obliterans) and MI. In the same year, Chhabra et al [6] reported a case of AIVR observed during inhalational induction with halothane in a child with congenital cataract. Osmancik et al [42], 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.