Accelerated idioventricular rhythm as a manifestation of chronic renocardiac syndrome: A case report.

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.

18-Month-Old with Lethargy and Accelerated Idioventricular Rhythm in Prehospital Setting: A Case Report.

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.

Intracardiac echocardiography-guided catheter ablation of highly symptomatic accelerated idioventricular rhythm originating from the right ventricular apical diverticulum.

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.

Presumed primary cardiac mast cell tumor, pericardial effusion, and arrhythmia in a dog.

A 13-year-old female spayed border collie cross presented for pericardial effusion, arrhythmia, and a suspected cardiac mass. Echocardiogram revealed severe thickening and hypokinesis of the interventricular septum with a heterogenous, cavitated myocardium, concerning for neoplasia. Electrocardiogram revealed predominantly accelerated idioventricular rhythm with frequent periods of nonsustained ventricular tachycardia. Occasional prolonged PR intervals terminating in an aberrantly conducted QRS complex were present. These beats were postulated to represent either first-degree atrioventricular block with aberrant QRS conduction or atrioventricular dissociation. Cytology of the pericardial effusion revealed atypical, suspected neoplastic, mast cells. The patient was euthanized, and postmortem examination confirmed full-thickness infiltration of the interventricular septum by a mast cell tumor, with metastasis to the tracheobronchial lymph node and spleen. Given the anatomic location of the mass, the observed atrioventricular nodal conduction delay may represent neoplastic infiltration of the atrioventricular node. Neoplastic infiltration of the ventricle was suspected to cause the accelerated idioventricular rhythm and ventricular tachycardia. To the authors' knowledge, this is the first reported case of a primary cardiac mast cell tumor causing arrhythmia and pericardial effusion in a dog.

Hypothermia-induced accelerated idioventricular rhythm after cardiac surgery; a case report.

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.

Frequent accelerated idioventricular rhythm in an otherwise healthy child: a case report and review of literature.

BACKGROUND: Accelerated idioventricular rhythm (AIVR) is a wide QRS complex dysrhythmia that, as far as pediatric population is concerned, occurs mostly in children with underlying systemic or heart disease. Its clinical course is thought to be typically benign in otherwise healthy children and treatment to be completely needless. Existing guidelines/recommendations are based entirely on cases that had low daily burden of AIVR, and those referring to treatment itself are very unspecific. Pharmacologic therapy has been mostly unsuccessful and catheter ablation as a way of treatment has been only sporadically reported. This article is a case report with a literature review that aims to practically separate the age groups into newborn and older children and to emphasize the different clinical outcomes of children with occasional and frequent AIVR. There are only a few cases so far describing undesirable outcomes of this condition, and most of these patients had high daily burden of AIVR. To be more specific, among 38 healthy children older than 1 year reported in total, 6 had undesirable outcomes, short-term in terms of developing malignant arrhythmia or long-term in terms of developing cardiomyopathy/heart failure. CASE PRESENTATION: An 11-year-old boy had been referred to our center for a workup of incidentally discovered wide-complex arrhythmia. He was asymptomatic, with no underlying cardiac or systemic diseases. Continuous heart rate monitoring detected AIVR during most time of monitoring. In 24-h Holter-ECG, wide QRS complexes accounted for 73%. With parental consent, we conducted an electrophysiological study accompanied by radiofrequent ablation of ectopic focus, which lead to an instantaneous sinus rhythm that continued during the entire follow-up. CONCLUSION: AIVR is a rare dysrhythmia in the pediatric population, typically considered benign. Nevertheless, more than a few cases evidence its harmful potential, short-term in terms of developing malignant arrhythmia or long-term in terms of developing cardiomyopathy. Gathering more knowledge and experience along with conducting further studies is essential for the enhancement of understanding this condition, and selecting potentially vulnerable patients as well as their treatment.

New-Onset Accelerated Idioventricular Rhythm During Dental Rehabilitation.

Accelerated idioventricular rhythm has been documented in several cases involving the induction of general anesthesia; however, it has not previously been known to occur during reversal of neuromuscular blockade with neostigmine and glycopyrrolate. The current understanding of the pathophysiology of accelerated idioventricular rhythm involves enhanced automaticity of ventricular myocardium in the setting of increased vagal tone suppressing sinoatrial node pace making. We present the case of an 8-year-old boy who developed accelerated idioventricular rhythm during dental rehabilitation. In this case, accelerated idioventricular rhythm developed immediately upon reversal of neuromuscular blockade with neostigmine and glycopyrrolate and recurred intermittently during his recovery in the postanesthesia care unit. This was a benign occurrence in our patient who remained asymptomatic and hemodynamically stable, and his arrhythmia eventually subsided without intervention after several hours of telemetry. This case suggests that reversal of neuromuscular blockade with neostigmine and glycopyrrolate may induce accelerated idioventricular rhythm in certain patients without known cardiovascular disease.

Accelerated idioventricular rhythm in a healthy newborn: frightening but non-threatening.

Accelerated idioventricular rhythm is a rare but benign form of ventricular tachycardia which might be challenging to differentiate from other more worrisome forms. We present the case of a healthy newborn diagnosed with an accelerated idioventricular rhythm which is spontaneously terminated without the need for medical therapy.

Accelerated Idioventricular Rhythm Following Intraoral Local Anesthetic Injection During General Anesthesia.

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.

Clinical characteristics and therapeutic strategy of frequent accelerated idioventricular rhythm.

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.

Accelerated Idioventricular Rhythm: A Rare Case of Wide-Complex Dysrhythmia in a Teenager.

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.

The clinical impact of untreated slow ventricular tachycardia in patients carrying implantable cardiac defibrillators.

INTRODUCTION: The clinical impact of slow ventricular tachycardia (VT), occurring in patients carrying implantable cardiac defibrillators (ICD), is still under debate. METHODS AND RESULTS: From the UMBRELLA registry (multicenter, observational, and prospective study on patients with ICD), 659 episodes of slow VT were observed in 97 patients. Untreated slow VT (n = 93) had longer duration (23.7 min, CI95%: 10-39), compared with episodes treated effectively by anti-tachycardia pacing (ATP; n = 527; 0.32 min, IC95%: 0.22-0, 48) or shock (n = 39; 1 min, CI95%: 0.8-1.2). Despite of longer duration, the time to the first contact with the medical services was similar to those episodes treated by ATP (50 days [CI95%: 45-55] vs. 41 days [CI95%: 39-44]). However, both were significantly longer than the time observed in episodes treated with shock (10 days, CI95%: 6-15). This tendency was maintained with successive interrogations of the device (2nd and 3rd). There were no significant differences in mortality during follow-up (48 ± 16 months), neither other adverse outcomes, between patients who presented untreated slow TV and those who did not (log-rank p = 0.28). In a Cox regression analysis, the variable "presenting untreated episodes of slow VT" was not able to predict mortality. However, being in sinus rhythm (vs. atrial fibrillation, OR: 0.31, p = 0.009), narrower QRS (OR: 1.036, p = 0.037) and diabetes (OR 4.673, p = 0.049) appropriately predict survival. CONCLUSIONS: Untreated slow VT does not significantly worsen patient prognosis. Our results support the limitation of therapies to ATP only, thus avoiding therapies that have been associated with increased risk of morbidity and mortality.

Incessant accelerated idioventricular rhythm mimicking preexcitation.

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.

Diagnosis of slow ventricular tachycardia by cardiac resynchronization devices utilizing a desynchronization detection algorithm.

Some cardiac resynchronization therapy (CRT) devices equipped with left ventricular (LV) sensing can develop a specific desynchronization rhythm. Contemporary BIOTRONIK devices are designed with an algorithm called "CRT pacing interrupt" exclusively designed to record the occurrence of the specific form of desynchronization. We report six patients in whom the CRT pacing interrupt function permitted the diagnosis of slow ventricular tachycardia (VT). Slow VT was defined as slower than the programmed VT intervention rates. Although the CRT pacing interrupt function is not designed to detect slow VT, certain episodes of the CRT pacing interrupt function were falsely interpreted by the device as a desynchronization arrhythmia, and the recordings then provided data consistent with the presence of slow VT. The CRT pacing interrupt algorithm permitted a diagnosis of slow VT irrespective of the relationship of LV upper rate interval and cycle length of slow VT.

Accelerated idioventricular rhythm resulting in torsades de pointes and cardiac arrest in a child: successfully cryoablated in left'coronary cusp.

Known as a benign arrhythmia and normally requiring no specific treatment, accelerated idioventricular rhythm can rarely degenerate to a life-threatening arrhythmia. Here, we present a child with left coronary cusp-originating accelerated idioventricular rhythm, degenerating into torsades de pointes and resulting in cardiac arrest, which was ablated with a cryocatheter. An 11-year-old boy, followed due to asymptomatic accelerated idioventricular rhythm before, was referred to our department because he had experienced an aborted cardiac arrest during sleep. He had been resuscitated for 5 minutes. Twenty-four-hour Holter-ECG revealed incessant accelerated idioventricular rhythm, consisting up to 90% of the whole record and two torsades de pointes attacks, triggered by accelerated idioventricular rhythm-induced "R on T" phenomenon, and resulting in syncope and cardiac arrest. Transthoracic echocardiography revealed no structural cardiac defect but mild left ventricular systolic dysfunction with an ejection fraction of 45% and shortening fraction 23%. An electrophysiologic study was conducted, and accelerated idioventricular rhythm focus was mapped to left aortic coronary cusp. A cryocatheter with an 8-mm tip was preferred for successful ablation of the accelerated idioventricular rhythm focus, due to close neighbourhood to coronary ostium. The patient was discharged in 3 days without any premature ventricular contractions or accelerated idioventricular rhythm and with normalised cardiac functions. After 9 months on follow-up, he was still asymptomatic, without any premature ventricular contractions or accelerated idioventricular rhythm and with normal cardiac functions. Although the clinical course of accelerated idioventricular rhythm is known as benign, accelerated idioventricular rhythm can rarely degenerate to a life-threatening arrhythmia. In such cases, electrophysiologic study and catheter ablation are a good option in such cases with accelerated idioventricular rhythm for an ultimate cure.