Idioventricular Rhythm Research Articles

3rd-Degree Atrioventricular Block.

3rd-Degree Atrioventricular Block.

The Heart Awakens

<h3>Introduction</h3> Primary graft dysfunction (PGD) after orthotopic heart transplant (OHT) can be a challenging complication to manage. We present a 70 year-old male with severe PGD immediately after OHT that required mechanical circulatory support. <h3>Case Report</h3> The patient developed myocarditis at age 63 leading to dilated cardiomyopathy. By age 69, despite guideline-directed medical therapy, he required a HeartMate 3 ventricular assist device (VAD) as a bridge to transplant for progressive heart failure. He was discharged and listed for OHT. Five months later, he was admitted for ventricular tachycardia storm and his listing status was upgraded. After 3 days, a donor organ with mild left ventricular (LV) systolic dysfunction was accepted for OHT. Intra-operatively, the transplanted heart showed limited contractility, despite epicardial pacing (cross clamp time 237 minutes, warm ischemic time 60 minutes). Therefore, biventricular CentriMag VADs were implanted. Post-operative ECG showed a slow ventricular escape rhythm (Figure 1A). On post-operative day (POD) 5, due to left hemothorax, he returned to the operating room, where improved cardiac contractions were noted. Serial cardiac biopsies showed normal myocardium and no rejection (Figure 1B, 1D). Over the next 2 days, the heart regained contractility. ECG showed a junctional escape rhythm (Figure 1C). On POD 7, the transplanted heart showed recovery and the Centrimag VADs were explanted. By POD 12, he was weaned off vasoactive medications and transferred to the ward. Eventually, on POD 23, he was discharged home with a permanent pacemaker. <h3>Summary</h3> This case demonstrates severe PGD in the context of pre-existing mild donor LV dysfunction that was successfully managed by mechanical circulatory support as a bridge to recovery. A potential contributor to graft dysfunction may be myocyte stunning by antiarrhythmic medications infused pre-operatively for ventricular tachycardia storm. This case shows the utility of donor hearts with LV systolic dysfunction even in the presence of other risk factors for PGD.

Left Bundle Branch Pacing: Unexpected Resynchronization Effect of Anodal Capture.

Anodal capture can provide a resynchronization effect on biventricular pacing. However, evidence of such an effect remains unclear in left bundle branch pacing (LBBP). We report a patient with a baseline sinus rhythm with complete atrioventricular block and a ventricular escape rhythm with a right bundle branch (RBB) block QRS morphology and left axis deviation who received LBBP for cardiac resynchronization therapy (CRT), and its anodal capture stimulation (ANS) rendered a near-normal QRS morphology. The resolution of the RBB pattern during bipolar pacing in this patient resulted from a fusion of LBBP and right ventricular septal capture from ANS. In conclusion, CRT can be achieved during LBBP by ANS in patients who do not have retrograde RBB activation.

Seven day continuous ambulatory electrocardiographic telemetric study with pocket electrocardiographic recording device for detecting hydroxychloroquine induced arrhythmias.

Objective:The use of hydroxychloroquine (HCQ) for COVID-19 treatment and prophylaxis raised issues concerning its cardiac safety owing to the possibility of QT prolongation and arrhythmias. There was no study on long-term electrocardiographic telemetry monitoring of patients taking HCQ. We planned a continuous electrocardiographic Holter telemetry of these patients for 7 days.Material and Methods:Health care workers taking HCQ as pre exposure prophylaxis and patients on HCQ were monitored using seven day Holter electrocardiographic telemetry with continuous beat to beat analysis. Telemetry can instantly convey any arrhythmic event or significant QT prolongation to the medical faculty.Results:Twenty-five participants with a mean age of 42.4 ± 14.1 years were included in the study; 40% were females. Twenty percent of participants needed to stop HCQ. Four patients developed QT prolongation >500 ms and needed to stop HCQ, one patient had accelerated idioventricular rhythm and stopped treatment, and one had short episodes of atrial fibrillation. No malignant arrhythmia or ventricular arrhythmia, or torsade de pointis were noted. No episode of significant conduction disturbance and arrhythmic death was noted. Baseline mean QTc was 423.96 ± 32.18 ms, mean QTc corrected at 24 h was 438.93 ± 37.95, mean QTc was 451.879 ± 37.99 at 48 h, and change in baseline mean QTc to max QTc was 30.74 ± 21.75 ms at 48 h. All those who developed QTc prolongation >500 ms were greater than 50 years of age.Conclusion:Ambulatory telemetry ECG monitoring detects early QT prolongation, and stopping drugs prevents malignant arrhythmias. HCQ seems to have less risk of QT prolongation in young, healthy individuals.

Reperfusion Arrhythmia in Acute Myocardial Infarction: Clinical Implication and Management

Reperfusion is a critical component of myocardium survival in acute myocardial infarction to minimize infarct size and improve clinical prognosis. Reperfusion, on the other hand, may result in increased and accelerated myocardial injury, a condition known as reperfusion injury. Following reperfusion, several arrhythmias are observed, and it is called reperfusion arrhythmia. Reperfusion arrhythmia is one manifestation of reperfusion injury. Numerous modest studies have evaluated what reperfusion arrhythmias are defined. It is described as an arrhythmia that occurs immediately or within the first minutes after coronary blood flow is restored. Traditionally, Accelerated Idioventricular Rhythm (AIVR) has been seen as a reperfusion arrhythmia. However, reperfusion may reveal any arrhythmia (or none at all); conversely, AIVR may occur in the absence of reperfusion. Calcium excess within the cells is thought to be a significant factor in the development of reperfusion arrhythmias. This may affect the significant delay following depolarization and the regional heterogeneity of regional blood flow restoration inside the ischemic zone, resulting in reperfusion arrhythmia. In some studies, it was mentioned that these arrhythmias may be due to ongoing myocardial cell damage and ischemia. Arrhythmias associated with reperfusion require special attention since hemodynamics can deteriorate quickly. In this review, clinical significance and management of reperfusion arrhythmia, as well as its link with reperfusion injury will be discussed.

Drug-induced arrhythmia: Are we cautious enough?

Dear Editor, Many drugs, like antiarrhythmic agents, psychotropic medications, neurological drugs, and even antimicrobial agents, may trigger multiple types of arrhythmias.[1] Some arrhythmias may cause serious consequences, including death. We report a rare incident where psychotropic medications not only precipitated a life-threatening arrhythmia but also a stroke! A 64-year-old man with a history of bipolar disorder had no other comorbidity. He presented to the ER (emergency room) with hypotension and bradycardia. His GCS (Glasgow Coma Scale) score was 15/15 and had no neuro-deficit. We detected idioventricular rhythm, and a temporary pacemaker was implanted. His hypotension improved, and it stabilized him. We planned a permanent pacemaker the next morning. The family gave a history that he was on 400 mg of lithium and 400 mg of carbamazepine for more than a year. Considering their arrhythmogenic potential, they were withheld. (Blood lithium level was in the normal range.) The next morning we detected him to have right gaze deviation and left-sided complete hemiplegia (NIHSS of 17). He had established an infarct at the right frontal–temporal region with hemorrhagic conversion in the MRI (magnetic resonance imaging) brain [Figure 1a]. MRA (magnetic resonance angiography) brain revealed right M2 occlusion [Figure 1b]. Conservative stroke treatment along with rehabilitation was executed. TEE (transesophageal echocardiography) ruled out intracardiac clot and other cardiac pathology. Details of stroke workup were also not contributory. Since his sinus rhythm persisted even after removal of the temporary pacemaker, we canceled a permanent pacemaker implantation. We withdrew his offending drugs permanently. Henceforth, the cardiology team monitored the cardiac rhythm and until 2 years of follow-up, he had no further event. His Modified Rankin Scale (mRS), however, remained 5 (with no significant improvement).Figure 1: (a) Acute infarct with hemorrhagic conversion in the right frontal and temporal region. (b) Right M2 division of middle cerebra artery occludedThey associated junctional bradycardia with ischemic stroke, particularly in the absence of an identifiable retrograde P-wave.[2] He had the stroke just after his rhythm got converted to sinus rhythm from junctional bradycardia (like thromboembolism as happens in AF (atrial fibrillation) patients shortly after they get cardioverter).[3] Carbamazepine and lithium both can precipitate bradyarrhythmia.[45] Although we found his lithium level to be within range, there are reports where lithium has precipitated bradyarrhythmia even when the drug level was within therapeutic range.[5] The drugs might have had a synergistic action in our case causing precipitation of the bradyarrhythmia. Interesting learning points in our case are as follows: Arrhythmogenic drugs can precipitate stroke. While on these types of drugs, caregivers should monitor the heart rate and blood pressure regularly. Careful selection of drugs in psychiatric patients is important because they may have a synergistic action in causing arrhythmogenic insults. Before opting for a permanent pacemaker, careful history taking is important to isolate culprit drugs if any which might have precipitated arrhythmia. The status of the arrhythmia needs to be observed after their withdrawal before taking further action. In cardioversion, conversion to sinus rhythm may cause sudden dislodgement of clots from the heart, leading to systemic embolization. Similarly, the stoppage of the arrhythmogenic drugs may precipitate a similar event. So, we need to be more cautious during this time. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Acknowledgement We acknowledge the faith the patient and family kept on us during difficult times.

Clinical and functional characteristics of children with ventricular arrhythmias depending on the ectopic focus localization

Aim. To determine the prevalence of ventricular arrhythmias (VA) among children with cardiac arrhythmias and to assess the clinical, functional, and electrophysiological characteristics of VA, depending on the localization of the ectopic focus.Methods. The study included 260 children, 153 (58,8%) boys, the mean age of patients was 13.4±3.1years. Based on clinical and anamnestic data, ECG, Holter monitoring, echocardiography, dosed exercise test, invasive electrophysiological study (EPS), radiofrequency ablation (RFA) a comparative assessment of the clinical and functional features of the most frequently diagnosed localizations of the ectopic focus in children with VA was carried out according to the data of invasive EPS, RFA.Results. According to invasive EPI, the most frequent localization of VA in children is the right ventricle outflow tract (RVOT) - 144 (55%), less often - the Valsalva sinuses - 52 (20%) and the RV free wall - 47 (18%). In most cases (255 children, 98%) there was a focal arrhythmia (trigger activity). The localization of ectopia in the RV free wall is characterized by the predominance of single ventricular premature beats (VPB) or in combination with a paired VPB (78,7%) and polymorphism of ventricular complexes (30%). The peculiarity of ventricular tachycardia in this localization is its stable character (17,0%) and low heart rate in volleys (idioventricular rhythm) (12,8%). When the focus was localized in the RVOT, as well as when it was localized in the RV free wall, single VPB or in combination with paired VPB prevailed (84,7%), but polymorphism of ventricular complexes was less often observed (10,4%). Differences in myocardial contractility at the sinus rhythm in right ventricular arrhythmias were revealed. Thus, the ejection fraction at the localization of the lesion in the RV free wall was significantly lower than in the RVOT (63.4±5.5% and 65.8±5.9%, respectively; p&lt;0.01). Hemodynamic significance is characteristic for RV arrhythmias (21.3% and 16.0% of patients) and was practically not observed at the left-sided localization of the arrhythmogenic focus (3.8%; p&lt;0.01). VA in patients without structural heart disease, regardless of the localization of the arrhythmic focus in children, is asymptomatic and is detected, in most cases, within the framework of clinical examination 206 patients, 79.2%. The prevalence of syncope in children with idiopathic VA is 15.8% (41 patients), and in most cases, they are of vaso-vagal origin. In most children (178, 70%), idiopathic VA is dependent on the level of parasympathetic influences on the heart, disappearing or significantly decreasing during exercise, which is revealed during the stress test confirming the high role of autonomic influences on the regulation of heterotopic rhythm in children with VA.Conclusion. VA is a common arrhythmia in children. Depending on the localization of the arrhythmogenic focus, characteristic features of the structure and density of the heart, as well as differences in the contractile function of the myocardium on the sinus rhythm and on the ectopic complex were revealed.

124 Tiny but useful transportable remote monitoring device during SARS-CoV-2 pandemic

A 45-year-old woman, without cardiovascular risk factors and affected by chronic migraine, presented to the emergency department due to the onset of a typical chest pain. After performing an electrocardiogram she was promptly transported to the Cath lab, with the diagnosis of ST segment elevation myocardial infarction (STEMI), for urgent coronarography. A spontaneous dissection of the first obtuse marginal branch was detected which was treated with two drug eluting stents implantation. A day after the procedure, during a migraine crisis, at the continuous electrocardiographic monitoring it was registered a brief episode of complete atrioventricular block, which regressed spontaneously after a few minutes. For this reason, she underwent atropine test which resulted negative for AV conductance defects. No more episodes were recorded during the hospital stay, however it was decided to implant a loop recorder (Biotronik BIOMONITOR III) before the discharge. The patient received a remote monitoring device in order to allow a closer follow-up in course of the COVID-19-related lockdown, that caused a relevant reduction in the outpatients’ services. A few months later a sinusal pause of about 9 s was recorded with the emergence of an idioventricular rhythm at 25 b.p.m. When contacted by telephone the patient reported being hospitalized because of pulmonary complications of SARS-CoV-2 infection. She referred of being bedridden, without any cardiac monitor and of being asymptomatic for syncope. Thus, she was transferred to a Cardiology Unit dedicated to patients affected by SARS-CoV-2 disease, for further diagnostic investigations. This represents a case in which the remote monitoring technology resulted fundamental in the management of patients with implantable devices, in particular during COVID-19-related lockdown. However, it is at least as much important to encourage the patient to carry the transmitter with him, even in the case of unexpected events or hospitalizations, in order to gain access to all the information store in the CIED which might be useful to the diagnosis of the underlying disease. Biotronik has developed the smallest remote transmitter in commerce (CardioMessenger Smart) which is functional to this kind of use. Moreover, it has an automatic interrogation function which can send the alerts about the arrhythmic events quicker than the other brands and so it’s more practical in situations where the patient is hospitalized in non-cardiological units.

Potentially Life-threatening Arrhythmia Triggered by an Excessive Consumption of Dried Sweet Potato "Hoshi-Imo".

We herein report two cases of potentially life-threatening arrhythmia due to hyperkalemia triggered by the excessive consumption of “Hoshi-Imo” (dried sweet potato). Both patients with chronic renal disease on renin-angiotensin-aldosterone system inhibitors presented at the emergency room with non-specific symptoms. Electrocardiograms revealed potentially life-threatening arrhythmia due to hyperkalemia in both cases: sinus arrest with a ventricular escape rhythm, tall and peaked T waves; and a widened QRS complex in a nearly sine-wave configuration without discernible P wave. Both patients fully recovered after intensive care for hyperkalemia. Physicians should recognize the excessive consumption of “Hoshi-Imo” may lead to the development of life-threatening arrhythmia, especially in patients with risk factors for hyperkalemia.

Torsadogenic Potential of HCN Channel Blocker Ivabradine Assessed in the Rabbit Proarrhythmia Model.

Torsadogenic effects of ivabradine, an inhibitor of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, were assessed in an in vivo proarrhythmia model of acute atrioventricular block rabbit. Ivabradine at 0.01, 0.1, and 1 mg/kg was intravenously administered to isoflurane-anesthetized rabbits (n = 5) in the stable idioventricular rhythm. Ivabradine at 0.01 and 0.1 mg/kg hardly affected the atrial and ventricular automaticity, QT interval, or the monophasic action potential duration of the ventricle. Additionally administred ivabradine at 1 mg/kg decreased the atrial and ventricular rate significantly but increased the QT interval and duration of the monophasic action potential. Meanwhile, torsade de pointes arrhythmias were detected in 1 out of 5 animals and in 2 out of 5 animals after the administration of 0.1 and 1 mg/kg, respectively. Importantly, torsade de pointes arrhythmias could be observed only in 2 rabbits showing more potent suppressive effects on ventricular automaticity. These results suggest that the torsadogenic potential of ivabradine may become evident when its expected bradycardic action appears more excessively.

Effects of Cardiac Massage and β-Blocker Pretreatment on the Success Rate of Cardiopulmonary Resuscitation Assessed by the Canine Ischemia/Reperfusion-Induced Ventricular Fibrillation Model.

Effects of rapid electrical defibrillation and β-blockade on coronary ischemia/reperfusion-induced ventricular fibrillation (VF) during cardiopulmonary resuscitation (CPR) remain unknown.Methods and Results:After induction of VF by 30 min of ischemia followed by reperfusion, animals were treated with defibrillation alone (Group A, n=13), 2 min of open-chest cardiac massage followed by defibrillation (Group B, n=11), or the same therapy to Group B with propranolol (1 mg/kg, i.v.) treatment before ischemia/reperfusion (Group C, n=11). If return of spontaneous circulation (ROSC) was not attained, each therapy was repeated ≤3 times (Set-1). When ROSC was not obtained within Set-1, cardiac massage was applied to all animals followed by defibrillation, which was repeated ≤3 times (Set-2). ROSC after Set-1 was 8% in Group A, 82% in Group B and 82% in Group C, whereas that after Set-2 was 62% in Group A, 100% in Group B and 82% in Group C. Each animal with ROSC in Groups A (n=8) and B (n=11) showed sinus rhythm, whereas those in Group C (n=9) had sinus rhythm (n=5), atrial fibrillation (n=1), accelerated idioventricular rhythm (n=2) and atrioventricular block (n=1). Post ROSC heart rate and mean arterial pressure were significantly lower in Group C. Cardiac massage increased the likelihood of ROSC vs. rapid defibrillation, but β-blocker pretreatment may worsen hemodynamics and electrical stability after ROSC.

Clinical characteristics and therapeutic strategy of frequent accelerated idioventricular rhythm

BackgroundAccelerated 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.MethodsTwenty-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.ResultsAll 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.ConclusionsFrequent 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.

Atrial standstill in the newborn: a case report

Introduction. Persistent atrial standstill is a rare syndrome characterized by absence of mechanical and electrical atrial activity. The article presents a unique case of atrial standstill in the newborn patient with tachyarrhythmia.Brief description. The first manifestation of atrial standstill in the patient was heart failure (HF) manifestations and wide-complex tachycardia according to electrocardiography, which was identified as ventricular tachycardia. At the local outpatient clinic, the child was prescribed with antiarrhythmic therapy (AAT), which decreased heart rate. Three months later, a transesophageal electrophysiological study was carried out in our center in order to determine the arrhythmia origin. A multiform idioventricular rhythm with a heart rate of 46-119 beats per min was diagnosed, atrial pacing spike (A waves) was not recorded. Given bradyarrhythmia, hemodynamic abnormalities on echocardiography (significant atrial enlargement, decreased contractility), the patient, in order to prevent the risk of sudden cardiac death, underwent implantation of single chamber pacemaker in VVIR mode and bipolar ventricular lead. Anticoagulant therapy was prescribed. After 6-month follow-up, relief of HF symptoms and an increase in left ventricular contractile function was noted.Discussion. Timely diagnosis and implantation of pacemakers allowed avoiding AAT and minimizing the HF symptoms. Continuous ventricular pacing and anticoagulant therapy are important in HF prevention.

Idioventricular rhythm and shock after a honeybee sting

Idioventricular rhythm and shock after a honeybee sting

Ventricular arrhythmias in a patient with obstructive sleep apnea syndrome and its effective non-pharmaceutical treatment

Patients with obstructive sleep apnea syndrome (OSAS) are characterized by various cardiac arrhythmias during sleep. However, while the association between OSAS and atrial fibrillation is considered proven, the presence of a pathophysiological link between sleep apnea and ventricular arrhythmias remains a matter of debate.We present a case of a 51-year old man with arterial hypertension and type 2 diabetes who was referred for sleep assessment after being diagnosed with predominantly nocturnal cardiac arrhythmias. Overnight cardiorespiratory monitoring showed that the patient had a severe OSAS with an apnea-hypopnea index of 57 per hour and a minimal SpO2 during sleep of 73%. On the channel of electrocardiogram (ECG) frequent single monomorphic ventricular extrasystoles, eventually of the bigeminal type, and one short paroxysm of a wide-complex regular rhythm of 60 beats per minute (accelerated idioventricular rhythm) associated with prolonged apnea were identified. Continuous airway positive pressure (CPAP) therapy was started which was able to control for breathing disorders during sleep. At the follow-up 24-hours Holter ECG monitoring, the numbers of ventricular extrasystoles during sleep decreased 2-fold, without any idioventricular rhythm episodes.The clinical case clearly illustrates that in some patients with OSAS, first of all, in those with severe OSAS and comorbid cardiovascular disorders, breathing disorders during sleep can trigger ventricular arrhythmias. In such patients, CPAP therapy could both improves their quality of life and provide an indirect antiarrhythmic effect.

Expert consensus document on automated diagnosis of the electrocardiogram: The task force on automated diagnosis of the electrocardiogram in Japan. Part 1: Nomenclature for diagnosis and abnormal findings.

As these terms should accurately represent the abnormal findings and conditions as much as possible, we propose to unify these terms into terminologies that are not confusing and easy to understand for everyone.

Idioventricular tachycardia and unstable ventricular escape rhythm in a canine patient with third-degree atrioventricular block

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.

Severe Bradycardia Increases the Incidence and Severity of Torsade de Pointes Arrhythmias by Augmenting Preexistent Spatial Dispersion of Repolarization in the CAVB Dog Model.

IntroductionTorsade de pointes arrhythmias (TdP) in the chronic atrioventricular block (CAVB) dog model result from proarrhythmic factors, which trigger TdP and/or reinforce the arrhythmic substrate. This study investigated electrophysiological and arrhythmogenic consequences of severe bradycardia for TdP.MethodsDofetilide (25 μg/kg per 5 min) was administered to eight anesthetized, idioventricular rhythm (IVR) remodeled CAVB dogs in two serial experiments: once under 60 beats per minute (bpm), right ventricular apex paced (RVA60) conditions, once under more bradycardic IVR conditions. Recordings included surface electrocardiogram and short-term variability (STV) of repolarization from endocardial unipolar electrograms. TdP inducibility (three or more episodes within 10 min after start of dofetilide) and arrhythmic activity scores (AS) were established. Mapping experiments in 10 additional dogs determined the effect of lowering rate on STV and spatial dispersion of repolarization (SDR) in baseline.ResultsIVR-tested animals had longer baseline RR-interval (1,403 ± 271 ms) and repolarization intervals than RVA60 animals. Dofetilide increased STV similarly under both rhythm strategies. Nevertheless, TdP inducibility and AS were higher under IVR conditions (6/8 and 37 ± 27 vs. 1/8 and 8 ± 12 in RVA60, respectively, both p < 0.05). Mapping: Pacing from high (128 ± 10 bpm) to middle (88 ± 10 bpm) to experimental rate (61 ± 3 bpm) increased all electrophysiological parameters, including interventricular dispersion, due to steeper left ventricular restitution curves, and intraventricular SDR: maximal cubic dispersion from 60 ± 14 (high) to 69 ± 17 (middle) to 84 ± 22 ms (p < 0.05 vs. high and middle rate).ConclusionIn CAVB dogs, severe bradycardia increases the probability and severity of arrhythmic events by heterogeneously causing electrophysiological instability, which is mainly reflected in an increased spatial, and to a lesser extent temporal, dispersion of repolarization.

COVID-19-associated multisystem inflammatory syndrome in children presenting uniquely with sinus node dysfunction in the setting of shock

SARS-CoV-2, which causes the disease COVID-19, generally has a mild disease course in children. However, a severe post-infectious inflammatory process known as multisystem inflammatory syndrome in children has been observed in association with COVID-19. This inflammatory process is a result of an abnormal immune response with similar clinical features to Kawasaki disease. It is well established that multisystem inflammatory syndrome in children is associated with myocardial dysfunction, coronary artery dilation or aneurysms, and occasionally arrhythmias. The most common electrocardiographic abnormalities seen include premature atrial or ventricular ectopy, variable degrees of atrioventricular block, and QTc prolongation, and rarely, haemodynamically significant arrhythmias necessitating extracorporeal membrane oxygenation support. However, presentation with fever, hypotension, and relative bradycardia with a left axis idioventricular rhythm has not been previously reported. We present a case of a young adolescent with multisystem inflammatory syndrome in children with myocarditis and a profoundly inappropriate sinus node response to shock with complete resolution following intravenous immunoglobulin.

Accelerated Idioventricular Rhythm and Hypokalemia, Atypical Presentation in the Midst of a Pandemic

A 34-year-old female patient was referred to a private center from a rural population due to exertional dyspnea and palpitations for 15 days being previously asymptomatic, a surface electrocardiogram diagnoses sinus rhythm alternating with accelerated idioventricular rhythm with episodes of short-coupling intervals. When conducting a diagnostic investigation, hypokalemia and decreased serum magnesium were evidenced and, after correction of the water-electrolyte imbalance, the electrocardiographic disorders disappeared.