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Ventricular diverticula are saccule‐like structures formed by the protrusion of the ventricular myocardium from the endocardial surface towards the free wall. Most diverticula are muscular structures, and patients usually have no obvious clinical symptoms. However, diverticula may contribute to arrhythmogenesis due to localized myocardial structural disturbances. Right ventricular apical diverticulum (RVAD) is very rare, and we report a case of highly symptomatic accelerated idioventricular rhythm (AIVR) originating from the RVAD that underwent intracardiac echocardiography (ICE)–guided catheter ablation with no recurrence during follow‐up. [ABSTRACT FROM AUTHOR]

Introduction: We report a case of accelerated idioventricular rhythm (AIVR) identified by Emergency Medical Services (EMS) monitoring of an infant presenting with lethargy and respiratory distress. Accelerated idioventricular rhythms are rare ventricular rhythms originating from the His-Purkinje system or ventricular myocytes, consisting of >3 monomorphic beats with gradual onset and termination.1 An AIVR is usually well-tolerated and does not require treatment, though sustained arrythmia may induce syncope, and the rhythm has been seen in newborn infants with congenital heart diseases.1 Monitoring ill children with ECG can identify such dysrhythmias in the prehospital setting. Case Report: An 18-month-old male presented to their pediatrician with lethargy and respiratory distress, prompting activation of EMS. The patient was placed on a 4-lead ECG initially revealing monomorphic QRS complexes at a rate of 170 beats per minute (BPM). A 12-lead ECG was interpreted as sinus tachycardia by the paramedics who noted the QRS complexes were "getting taller and shorter" with a stable rapid heart rate. The clinician then noted a consistently wide tachycardia which spontaneously converted to a narrow complex tachycardia. The QRS pattern remained variable, with notation of variable R-wave height. After arrival to the emergency department, pediatric cardiology was consulted and interpreted the prehospital ECG findings as accelerated idioventricular rhythm. The patient experienced multiple occurrences of accelerated idioventricular rhythm during hospitalization without associated hypoxia or decreased perfusion. Discussion: Accelerated idioventricular rhythm is relatively rare entity without underlying cardiac disease and most cases are asymptomatic or benign. In the pediatric population, AIVR is generally related to congenital heart defects, cardiac tumors, and cardiomyopathies. In the prehospital setting, continuous ECG monitoring should be a part of care by Advanced Life Support personnel in children with altered mental status, respiratory distress, unexplained syncope, or suspected arrhythmias and 12 lead ECG should be considered if there is any abnormality noted. While this patient did not experience persisting morbidity from AIVR, the potentially hazardous rhythm would not have been recognized without the astute observation, clinical management and persistent follow up of the prehospital clinicians. [ABSTRACT FROM AUTHOR]

Background PTPN11 is ubiquitously expressed and has a variety of phenotypes even in a single heart. We examined LEOPARD syndrome (LS) in a patient with PTPN11 variants through pathological, electrophysiological, and anatomical studies. Case summary A 49-year-old man with no previous medical history was brought to our emergency department because of syncope. An electrocardiogram (ECG) revealed alternating bundle branch block, and echocardiography revealed hypertrophic cardiomyopathy-like morphology with systolic anterior motion of the posterior mitral valve. Atrioventricular block, left ventricular outflow tract (LVOT) obstruction, and ventricular tachycardia were considered the differential diagnoses; however, the treatment plan was difficult to determine. An electrophysiological study revealed the cause of the ECG abnormality to be accelerated idioventricular rhythm, and the programmed ventricular stimulation was negative. Genetic testing revealed LS with PTPN11 variant, which was speculated to be the cause of these various unique cardiac features. The cause of syncope was considered to be exacerbation of LVOT obstruction due to dehydration, and the patient was treated with oral beta-blockers. Implantable loop recorder observation for 1 year revealed no arrhythmia causing syncope, and an implantable cardioverter-defibrillator and pacemaker were deemed unnecessary for primary prevention of syncope. During 2.5 years of follow-up, the LVOT peak velocity fluctuated between 2.5 and 3.5 m/s, but the patient remained stable with no recurrent syncope. Conclusion We confirmed that LS is distinct from other cardiomyopathies using characterization, physiological, electrophysiological, and pathological examinations. Evidence supporting a specific treatment strategy for LS is limited, and understanding the pathogenesis may help establish effective treatment strategies. [ABSTRACT FROM AUTHOR]

In this case report, we describe a patient who presented with chronic symptoms and signs of uremia and persistent accelerated idioventricular rhythm (AIVR) on electrocardiogram. Findings from blood tests, echocardiography, renal ultrasound, and renal scan were suggestive of heart failure with reduced ejection fraction and chronic kidney disease, and attendance of daily hemodialysis sessions led to the restoration of sinus rhythm. Typically, AIVR has a favorable prognosis and, if necessary, medical intervention focuses on addressing the underlying responsible causes. Accumulation of uremic toxins has the potential to trigger the formation of AIVR and clearance of small solutes through conventional hemodialysis may contribute to sinus rhythm restoration. [ABSTRACT FROM AUTHOR]

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Abstract In this case report, we describe a patient who presented with chronic symptoms and signs of uremia and persistent accelerated idioventricular rhythm (AIVR) on electrocardiogram. Findings from blood tests, echocardiography, renal ultrasound, and renal scan were suggestive of heart failure with reduced ejection fraction and chronic kidney disease, and attendance of daily hemodialysis sessions led to the restoration of sinus rhythm. Typically, AIVR has a favorable prognosis and, if necessary, medical intervention focuses on addressing the underlying responsible causes. Accumulation of uremic toxins has the potential to trigger the formation of AIVR and clearance of small solutes through conventional hemodialysis may contribute to sinus rhythm restoration.

Abstract Background Accelerated idioventricular rhythm (AIVR) is a slow ventricular arrhythmia, commonly due to myocardial ischemia in coronary artery disease. It is a transitory rhythm that rarely causes hemodynamic instability or necessitates any specific therapy. Besides, the common predisposing factors for ventricular arrhythmias after open-heart surgery are hemodynamic instability, electrolyte imbalances, hypoxia, hypovolemia, myocardial ischemia and infarction, acute graft closure, reperfusion injury, and administration of inotropes and antiarrhythmic drugs. Here we report a case of AIVR after cardiac surgery, mostly due to hypothermia that to our knowledge, it is the first report. Case presentation We describe a 76-year-old man presenting with typical chest pain. Following routine investigations, the patient underwent coronary artery bypass grafting. Postoperatively, he was transferred to the intensive care unit with good hemodynamic status. However, about 3 h later, he developed rhythm disturbances, leading to hemodynamic instability without response to volume replacement or inotropic support. His rhythm was AIVR, although, at first glance, it resembled the left bundle branch block. Given his unstable hemodynamic status, he was emergently transferred to the operating room. Cardiopulmonary bypass (CPB) was resumed for hemodynamic support. After the patient was rewarmed to about 35 ºC, AIVR returned to normal. He was weaned from CPB successfully and with an uneventful hospital course. Conclusions Hypothermia is a potential cause of rhythm disturbance. Preventing the causes of arrhythmias, including hypothermia, is the best strategy.

Accelerated idioventricular rhythm (AIVR) originating from the right bundle branch (RBB) (RBB‐AIVR) is a rare ventricular arrhythmia. We delineated RBB and myocardial activation separately during RBB‐AIVR, which revealed the spatial relationship of the AIVR origin, preferential pathway, and breakout site. Radiofrequency ablation to the preferential pathway successfully eliminated this arrhythmia. [ABSTRACT FROM AUTHOR]

BackgroundExcessive electrocardiographic alarms contribute to "alarm fatigue," which can lead to patient harm. In a prior study, one-third of audible electrocardiographic alarms were for accelerated ventricular rhythm (AVR), and most of these alarms were false. It is uncertain whether true AVR alarms are clinically relevant.ObjectivesTo determine from bedside electrocardiographic monitoring data (1) how often true AVR alarms are acknowledged by clinicians, (2) whether such alarms are actionable, and (3) whether such alarms are associated with adverse outcomes ("code blue," death).MethodsSecondary analysis using data from a study conducted in an academic medical center involving 5 adult intensive care units with 77 beds. Electronic health records of 23 patients with 223 true alarms for AVR were examined.ResultsThe mean age of the patients was 62.9 years, and 61% were white and male. All 223 of the true alarms were configured at the warning level (ie, 2 continuous beeps), and 215 (96.4%) lasted less than 30 seconds. Only 1 alarm was acknowledged in the electronic health record. None of the alarms were clinically actionable or led to a code blue or death.ConclusionsTrue AVR alarms may contribute to alarm fatigue. Hospitals should reevaluate the need for close monitoring of AVR and consider configuring this alarm to an inaudible message setting to reduce the risk of patient harm due to alarm fatigue. Prospective studies involving larger patient samples and varied monitors are warranted.

The article discusses the case of an unresponsive patient with wide QRS complex rhythm on a 12-lead electrocardiogram. Topics discussed include the patient's history of myocardial infarction with coronary artery bypass graft surgery and an implantable cardioverter defibrillator (ICD), the ICD as the potential cause of the patient's unresponsive episode, and the management of the patient which includes undergoing percutaneous coronary intervention.

Abstract Accelerated idioventricular rhythm (AIVR) originating from the right bundle branch (RBB) (RBB‐AIVR) is a rare ventricular arrhythmia. We delineated RBB and myocardial activation separately during RBB‐AIVR, which revealed the spatial relationship of the AIVR origin, preferential pathway, and breakout site. Radiofrequency ablation to the preferential pathway successfully eliminated this arrhythmia.

Background: Accelerated idioventricular rhythm (AIVR) is a slow ventricular arrhythmia, commonly due to myocardial ischemia in coronary artery disease. It is a transitory rhythm that rarely causes hemodynamic instability or necessitates any specific therapy. Besides, the common predisposing factors for ventricular arrhythmias after open-heart surgery are hemodynamic instability, electrolyte imbalances, hypoxia, hypovolemia, myocardial ischemia and infarction, acute graft closure, reperfusion injury, and administration of inotropes and antiarrhythmic drugs. Here we report a case of AIVR after cardiac surgery, mostly due to hypothermia that to our knowledge, it is the first report. Case presentation: We describe a 76-year-old man presenting with typical chest pain. Following routine investigations, the patient underwent coronary artery bypass grafting. Postoperatively, he was transferred to the intensive care unit with good hemodynamic status. However, about 3 h later, he developed rhythm disturbances, leading to hemodynamic instability without response to volume replacement or inotropic support. His rhythm was AIVR, although, at first glance, it resembled the left bundle branch block. Given his unstable hemodynamic status, he was emergently transferred to the operating room. Cardiopulmonary bypass (CPB) was resumed for hemodynamic support. After the patient was rewarmed to about 35 ºC, AIVR returned to normal. He was weaned from CPB successfully and with an uneventful hospital course. Conclusions: Hypothermia is a potential cause of rhythm disturbance. Preventing the causes of arrhythmias, including hypothermia, is the best strategy. [ABSTRACT FROM AUTHOR]

Premature ventricular contractions with right bundle branch block morphology induced during left bundle branch (LBB) pacing (LBBP) lead implantation serve as a marker indicating that the lead is close to or has reached the LBB region. However, no reports to date have described accelerated idioventricular rhythm (AIVR) induced by LBBP lead deployment. We herein describe a patient who underwent LBBP for complete atrioventricular block. The patient's intrinsic escape rhythm was overtaken by AIVR induced immediately after LBBP lead deployment. AIVR is another marker indicating that the lead has reached the LBB region. [ABSTRACT FROM AUTHOR]

A patient with bradycardia and an idioventricular rhythm was observed. According to cardiologists, there is no reliable drug treatment for bradycardia with an idioventricular rhythm; instead, the sole treatment is a pacemaker. In the course of this case, it was shown that acupuncture can restore the heart rhythm from bradycardia to normocardia, and from idioventricular with third-degree atrioventricular node block and an average heart rate of 34 BPM, to normal sinus rhythm with a heart rate of 71 BPM. Additionally, at the end of the treatment, the patient's number of episodes of ventricular extrasystole decreased 36 times (3289 versus 91 episodes). These results show that research on this technique should be continued. [ABSTRACT FROM AUTHOR]

Sophisticated dual‐chamber atrioventricular and rate‐responsive pacing therapies, cardiac resynchronization therapy (CRT), detection and therapies for ventricular tachycardia and fibrillation (VT/VF) form some major components of multitask functions of current implantable cardioverter defibrillators (ICDs). Appropriate programming of these devices is necessary for them to perform all such tasks precisely. In this report, we describe a case of a patient with Chagas cardiomyopathy with marked cardiomegaly, scarred ventricles, prior epicardial and endocardial ablations and on antiarrhythmic pharmacotherapy for VT, who presented with symptomatic wide complex tachycardia at a slower rate than definition of VT, and in whom programming for detection and therapy for "slow" VT could not be performed due to default technological limitation of the CRT‐D. [ABSTRACT FROM AUTHOR]

Abstract Background Accelerated idioventricular rhythm (AIVR) is often transient, considered benign and requires no treatment. This observational study aims to investigate the clinical manifestations, treatment, and prognosis of frequent AIVR. Methods Twenty-seven patients (20 male; mean age 32.2 ± 17.0 years) diagnosed with frequent AIVR were enrolled in our study. Inclusion criteria were as follows: (1) at least three recordings of AIVR on 24-h Holter monitoring with an interval of over one month between each recording; and (2) resting ectopic ventricular rate between 50 to 110 bpm on ECG. Electrophysiological study (EPS) and catheter ablation were performed in patients with distinct indications. Results All 27 patients experienced palpitation or chest discomfort, and two had syncope or presyncope on exertion. Impaired left ventricular ejection fraction (LVEF) was identified in 5 patients, and LVEF was negatively correlated with AIVR burden (P

Some anesthetic agents or adjunct medications administered during general anesthesia can cause an accelerated idioventricular rhythm (AIVR), which is associated with higher vagal tone and lower sympathetic activity. We encountered AIVR induced by vagal response to injection-related pain following local anesthetic infiltration into the oral mucosa during general anesthesia. A 48-year-old woman underwent extraction of a residual tooth root from the left maxillary sinus under general anesthesia. Routine preoperative electrocardiogram (ECG) was otherwise normal. Eight milliliters of 1% lidocaine (80 mg) with 1:100,000 epinephrine (80 μg) was infiltrated around the left maxillary molars over 20 seconds using a 23-gauge needle and firm pressure. Widened QRS complexes consistent with AIVR were observed for ∼60 seconds, followed by an atrioventricular junctional rhythm and the return of normal sinus rhythm. A cardiology consultation and 12-lead ECG in the operating room produced no additional concerns, so the operation continued with no complications. AIVR was presumably caused by activation of the trigeminocardiac reflex triggered by intense pain following rapid local anesthetic infiltration with a large gauge needle and firm pressure. Administration of local anesthetic should be performed cautiously when using a large gauge needle and avoid excessive pressure. [ABSTRACT FROM AUTHOR]

Background: Accelerated idioventricular rhythm (AIVR) is often transient, considered benign and requires no treatment. This observational study aims to investigate the clinical manifestations, treatment, and prognosis of frequent AIVR.Methods: Twenty-seven patients (20 male; mean age 32.2 ± 17.0 years) diagnosed with frequent AIVR were enrolled in our study. Inclusion criteria were as follows: (1) at least three recordings of AIVR on 24-h Holter monitoring with an interval of over one month between each recording; and (2) resting ectopic ventricular rate between 50 to 110 bpm on ECG. Electrophysiological study (EPS) and catheter ablation were performed in patients with distinct indications.Results: All 27 patients experienced palpitation or chest discomfort, and two had syncope or presyncope on exertion. Impaired left ventricular ejection fraction (LVEF) was identified in 5 patients, and LVEF was negatively correlated with AIVR burden (P < 0.001). AIVR burden of over 73.8%/day could predict impaired LVEF with a sensitivity of 100% and specificity of 94.1%. Seventeen patients received EPS and ablation, five of whom had decreased LVEF. During a median follow-up of 60 (32, 84) months, LVEF of patients with impaired LV function returned to normal levels 6 months post-discharge, except one with dilated cardiomyopathy (DCM). Two patients died during follow-up. The DCM patient died due to late stage of heart failure, and another patient who refused ablation died of AIVR over-acceleration under fever.Conclusions: Frequent AIVR has unique clinical manifestations. AIVR patients with burden of over 70%, impaired LVEF, and/or symptoms of syncope or presyncope due to over-response to sympathetic tone should be considered for catheter ablation. [ABSTRACT FROM AUTHOR]

A 10-year-old female Labrador retriever was presented for evaluation and management of syncope. On presentation, idioventricular tachycardia (IT) was electrocardiographically evident but neither ventricular capture nor fusion complexes were recorded. Spontaneous termination of the IT resulted in prolonged ventricular asystole and revealed the underlying rhythm of third-degree atrioventricular block. The serum concentration of troponin-I was elevated, suggesting myocarditis, but this was not diagnostically confirmed. It is likely that overdrive suppression of subsidiary idioventricular pacemakers, and perhaps also disease of subsidiary ventricular pacemaker fibers, importantly contributed to the duration of asystole. [ABSTRACT FROM AUTHOR]

Background: Accelerated idioventricular rhythm (AIVR) is an uncommon and typically benign dysrhythmia with similarities to more malignant forms of ventricular tachycardia (VT). It is often seen in adults after myocardial infarctions, although it also arises in the newborn period, as well as in children with and without congenital heart disease.Case Report: We describe a presentation of AIVR in an otherwise healthy 13-year-old girl, discovered on arrival to the pediatric emergency department in the setting of post-tonsillectomy bleeding. The case reviews the diagnostic criteria of AIVR, associated symptoms, the pathophysiologic origin of AIVR, and potential treatment strategies. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Given its morphologic similarities to life-threatening forms of VT, AIVR can be misdiagnosed in the emergency department or primary care settings. With an understanding of the dysrhythmia's unique features, emergency physicians can avoid unnecessary interventions and provide the correct diagnosis, workup, and management of AIVR for pediatric patients. [ABSTRACT FROM AUTHOR]

Abstract Background Noonan syndrome is an autosomal dominant disorder secondary to RASopathies, which are caused by germ‐line mutations in genes encoding components of the RAS mitogen‐activated protein kinase pathway. RIT1 (OMIM *609591) was recently reported as a disease gene for Noonan syndrome. Methods and Results We present a patient with RIT1‐associated Noonan syndrome, who in addition to the congenital heart defect, had monocytosis, myeloproliferative disorder, and accelerated idioventricular rhythm that was associated with severe hemodynamic instability. Noonan syndrome was suspected given the severe pulmonary stenosis, persistent monocytosis, and “left‐shifted” complete blood counts without any evidence of an infectious process. Genetic testing revealed that the patient had a heterozygous c.221 C>G (pAla74Gly) mutation in the RIT1. Conclusion We report a case of neonatal Noonan syndrome associated with RIT1 mutation. The clinical suspicion for Noonan syndrome was based only on the congenital heart defect, persistent monocytosis, and myeloproliferative process as the child lacked all other hallmarks characteristics of Noonan syndrome. However, the patient had an unusually malignant ventricular dysrhythmia that lead to his demise. The case highlights the fact that despite its heterogeneous presentation, RIT1‐associated Noonan syndrome can be extremely severe with poor outcome.

Background: Noonan syndrome is an autosomal dominant disorder secondary to RASopathies, which are caused by germ‐line mutations in genes encoding components of the RAS mitogen‐activated protein kinase pathway. RIT1 (OMIM *609591) was recently reported as a disease gene for Noonan syndrome. Methods and Results: We present a patient with RIT1‐associated Noonan syndrome, who in addition to the congenital heart defect, had monocytosis, myeloproliferative disorder, and accelerated idioventricular rhythm that was associated with severe hemodynamic instability. Noonan syndrome was suspected given the severe pulmonary stenosis, persistent monocytosis, and "left‐shifted" complete blood counts without any evidence of an infectious process. Genetic testing revealed that the patient had a heterozygous c.221 C>G (pAla74Gly) mutation in the RIT1. Conclusion: We report a case of neonatal Noonan syndrome associated with RIT1 mutation. The clinical suspicion for Noonan syndrome was based only on the congenital heart defect, persistent monocytosis, and myeloproliferative process as the child lacked all other hallmarks characteristics of Noonan syndrome. However, the patient had an unusually malignant ventricular dysrhythmia that lead to his demise. The case highlights the fact that despite its heterogeneous presentation, RIT1‐associated Noonan syndrome can be extremely severe with poor outcome. [ABSTRACT FROM AUTHOR]

ECG of patients with Wolf Parkinson White (WPW) syndrome may simulate other entities such as myocardial infarction, ventricular premature complexes, ventricular bigeminy, accelerated idioventricular rhythm, intermittent bundle branch block or electrical alternans. On the other hand, the opposite can also occur where these other conditions may simulate WPW. We present the case of a young patient referred for WPW ablation showing an incessant accelerated idioventricular rhythm mimicking preexcitation. [ABSTRACT FROM AUTHOR]

Sotalol is a class III anti-arrhythmic agent with beta receptor blocking properties. Intravenous (IV) sotalol may be useful to treat refractory atrial and ventricular arrhythmias. A report on the efficacy and safety of IV sotalol in an infant on extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT), who developed refractory ventricular arrhythmias following surgery for congenital heart disease. A 10-day old infant with severe pulmonary valve stenosis underwent surgical pulmonary valvectomy and enlargement of the main pulmonary artery. Post-operatively, the patient developed hemodynamically significant accelerated idioventricular rhythm which was not responsive to a combination of amiodarone, lidocaine, and procainamide leading to 2 cardiac arrest events and placement on ECMO. The amiodarone infusion was uptitrated to 20 mcg/kg/min, but episodes of the hemodynamically compromising arrhythmia continued. Amiodarone was discontinued and IV sotalol was initiated at 42 mg/m2/day, divided to 3 doses, and administered every 8 h, which completely suppressed the arrhythmia. The initial sotalol dose was calculated based on a daily dose of 90 mg/m2 and reduced by an age-related factor as recommended by the FDA approved prescribing information. Subsequently, acute kidney injury requiring CRRT developed. The patient remained on IV sotalol for 3 weeks and then transitioned to oral sotalol. The oral dose was increased to 44 mg/m2/day (3.5 mg every 8 h) to account for the difference in bioavailability between the IV and oral formulations. Serial sotalol levels during IV and PO therapy remained therapeutic on ECMO and CRRT. The patient maintained normal sinus rhythm on sotalol without adverse events. IV sotalol in the setting of ECMO and CRRT was safe and effective in controlling refractory hemodynamically compromising accelerated idioventricular rhythm unresponsive to amiodarone. [ABSTRACT FROM AUTHOR]

Background: Accelerated idioventricular rhythm (AIVR) is a common arrhythmia observed in patients with ST segment elevation myocardial infarction (MI). It is not clear how much value AIVR has in predicting successful reperfusion, since there have been conflicting data regarding this in the past. Streptokinase (STK) even today is the commonest thrombolytic agent used in the public health care set-up in India.1 Most data for the use of STK are from the 1990s, which had showed that at best it is effective in only 50% of patients in restoring adequate flow.2 It is probable that with the current dual-antiplatelet loading dose regimen and other newer medications, this figure could be higher. Also, rescue angioplasty for failed thrombolysis is the standard of care now, unlike before. Hence, we need reliable non-invasive markers to judge successful reperfusion in the present era. While ST segment resolution is the standard marker for reperfusion used in thrombolytic trials, in several instances it is not definitive. An additional marker would thus be very useful, especially in such cases. Methods: This was a prospective observational study carried out at a public teaching hospital. 200 consecutive patients with a diagnosis of acute MI who were given STK within 12 h of index pain were included. The STK dose was 1.5 million units, infused over 30 min; the ECG was again recorded after 90 min of completion of the infusion. Continuous ECG monitoring for the first 24 h of ICCU stay was performed and AIVRs during this period were documented. Early AIVR was defined as that occurring within 2 h of completing the STK infusion. Echocardiography was performed 24 h after presentation. The time course of AIVR was studied vis-a-vis the outcome of thrombolysis. Results: AIVR was seen in 41% of the patients. Though AIVR was found to have low sensitivity (45%) and specificity (64%) as a predictor of successful thrombolysis, early AIVR was a reliable sign of successful thrombolysis (p

The aim of the work was to analyze 209 cases of accelerated idioventricular rhythms, after that we concluded with 4 types of an “interaction” of sinus node and ectopic pacemaker. The article is illustrated with 11 ECGs, among those rare phenomenon following the arrhythmia, and specifics of differential diagnosis.

Accelerated idioventricular rhythm is a ventricular rhythm consisting of three or more consequent mono- or polymorphic complexes. It might be registered in patients with structural heart diseases, rarer in completely normal heart, might be found in sportsmen and children. Idioventricular rhythm might be seen in myocardial infarction, in reperfusion and under medications influence.The article focuses on the literature data that led to identification of this important ventricular arrhythmia.

A neonate was seen for an evolving broad QRS complex rhythm initially captured at birth as intermittent escape beats on electrocardiogram. Continuous monitoring recorded features mimicking pre-excitation, but closer analysis revealed a regular broad QRS complex rhythm with isorhythmic atrioventricular dissociation, favouring a ventricular source. Treatment with flecainide and propranolol achieved successful control of the incessant arrhythmia with improvement in cardiac function on echocardiogram.

Objectives: As postnatal identification of accelerated idioventricular rhythm (AIVR) relies on specific electrocardiographic patterns, prenatal diagnosis of this condition is challenging and its true incidence is unknown. The objectives of this study were to evaluate the performance of prenatal ultrasonography in identifying intrauterine cardiocirculatory events linked to specific electrocardiographic signs of postnatal AIVR, including left or right ventricular origin, and to assess the prenatal prognosis of this arrhythmia.Methods: We reviewed Doppler tracings from the superior vena cava/ascending aorta (SVC/Ao), ductus venosus (DV), ductus arteriosus (DA) and aortic isthmus (AoI), as well as simultaneous M-mode recordings of septal and left ventricular wall motions of fetuses diagnosed with AIVR from January 2004 to December 2014.Results: Three cases of AIVR were identified among 27 912 fetuses. SVC/Ao Doppler flow recordings revealed atrioventricular dissociation (ventricular rates within 20% of atrial rates) in all three fetuses and episodes of isorhythmic atrioventricular dissociation in one, while M-mode confirmed normal left ventricular shortening fraction in all cases. Fusion beats were observed on AoI tracing in one fetus, while simultaneous recordings of AoI and DA revealed signs of right bundle branch block in one case and left bundle branch block in the other two. On DV Doppler recordings, retrograde a-waves in the presence of simultaneous atrial and ventricular contractions were observed in all three fetuses, leading to an increase in central venous pressure in all and hydrops fetalis in two cases without evidence of ventricular dysfunction.Conclusions: Echocardiographic criteria required for postnatal diagnosis of AIVR can be documented in utero using specific ultrasonographic approaches. During fetal life, AIVR may not be a benign entity. Hydrops fetalis is frequently associated with AIVR because of increase in central venous pressure related to simultaneous atrioventricular contractions; thus, the ultrasonographic investigation protocol of fetuses with unexplained hydrops fetalis should aim at ruling out AIVR and include Doppler flow recordings in SVC/Ao, DV, AoI, DA and umbilical vein. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Hypergravitational exposures during human centrifugation are known to provoke dysrhythmias, including sinus dysrhythmias/tachycardias, premature atrial/ventricular contractions, and even atrial fibrillations or flutter patterns. However, events are generally short-lived and resolve rapidly after cessation of acceleration. This case report describes a prolonged ectopic ventricular rhythm in response to high G exposure. CASE REPORT: A previously healthy 30-yr-old man voluntarily participated in centrifuge trials as a part of a larger study, experiencing a total of 7 centrifuge runs over 48 h. Day 1 consisted of two +GZ runs (peak +3.5 Gz, run 2) and two +GX runs (peak +6.0 Gx, run 4). Day 2 consisted of three runs approximating suborbital spaceflight profiles (combined +GX and +GZ). Hemodynamic data collected included blood pressure, heart rate, and continuous three-lead electrocardiogram. Following the final acceleration exposure of the last Day 2 run (peak+4.5 Gxand +4.0 Gz combined, resultant +6.0 G), during a period of idle resting centrifuge activity (resultant vector +1.4 G), the subject demonstrated a marked change in his three-lead electrocardiogram from normal sinus rhythm to a wide-complex ectopic ventricular rhythm at a rate of 91-95 bpm, consistent w ith an accelerated idioventricular rhythm (AIVR). This rhythm was sustained for 2 m, 24 s before reversion to normal sinus. The subject reported no adverse symptoms during this time. DISCUSSION: While prolonged, the dysrhythmia was asymptomatic and self-limited. AIVR is likely a physiological response to acceleration and can be managed conservatively. Vigilance is needed to ensure that AIVR is correctly distinguished from other, malignant rhythms to avoid inappropriate treatment and negative operational impacts. [ABSTRACT FROM AUTHOR]

A 33-year old female with a background of Eisenmenger syndrome secondary to multiple congenital muscular ventricular septal defects (VSD) was admitted with a recent history of frequent intermittent palpitations. It was noted that she had an independent accelerated idioventricular rhythm (AIVR), with rates varying between 85-110 bpm, which exhibited a repetitive grouped beating pattern. Although generally perceived as benign, in this case this rhythm was drug refractory, was associated with significant compromise to cardiac filling and output and progressed to haemodynamically intolerable sustained ventricular tachyarrhythmia. Successful ablation was performed at the inferior aspect of the residual VSD, from within the Purkinje network.

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.

Doppler interrogation of blood flow in the hepatic veins ( HVs) provides valuable information regarding a wide spectrum of pathological processes that affect the right heart. Systematic analysis of the direction, velocity, and phasicity of the HV waveforms allows one to distinguish normal from abnormal patterns and provides important diagnostic information. Abnormalities in heart rate, rhythm, and intracardiac conduction are commonly encountered during echocardiographic studies. Sinus bradycardia and tachycardia, bradyarrhythmias and tachyarrhythmias as well as atrioventricular conduction disturbances influence the flow pattern in the HVs and may pose a challenge to the correct interpretation of the HV Doppler. Alterations in HV flow that are induced by the electrical abnormalities may mimic right heart pathology. Awareness of these alterations allows one to avoid misinterpretation of the HV signal, helps diagnose the underlying rhythm or conduction abnormality, and permits assessment of the impact on right heart hemodynamics. [ABSTRACT FROM AUTHOR]

Atrioventricular valve regurgitation (AVVR) influences morbidity and mortality in the atrioventricular canal defect (AVC). Fetal cardiac structures are subject to hemodynamic changes, as well as growth and maturation during gestation, which may alter the degree of AVVR and affect prognosis. We sought to investigate the frequency of change in degree of AVVR documented by fetal echocardiography (echo) between different periods of gestational age. Subjects with AVC seen in the Fetal Heart Program between January 2008 and September 2010 were identified. Degree of AVVR was assessed by color Doppler imaging and categorized as Grade 0 (no AVVR), Grade 1 (hemodynamically insignificant AVVR = trivial or mild), and Grade 2 (hemodynamically important AVVR = ≥moderate). Levels of AVVR between periods were compared. Forty-three fetuses were analyzed. Overall, 60 % had no change, 14 % had a decrease, and 26 % had an increase in AVVR grade. Two fetuses progressed from Grade 0 or 1 to Grade 2, while one fetus decreased from Grade 2 to Grade 0. Trisomy 21 and heterotaxy syndrome were not risk factors for AVVR progression. Transitional and incomplete canal defects may be more susceptible to AVVR progression. Sixty percent of fetuses with AVC will not exhibit progression of AVVR between the second and third trimesters of gestation. In those who exhibit change, it is most often within a hemodynamically insignificant range between none and mild regurgitation (Grades 0 and 1). These findings have implications for the counseling, follow-up, and delivery plans of the fetus with AVC defect. [ABSTRACT FROM AUTHOR]