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Editor's note: This article is one in a series on electrocardiogram (ECG) interpretation. Nurses in all settings should know the basics, as medications and physiological changes can cause cardiac arrhythmias. Each article will start with a brief case scenario and an ECG strip and then take you step by step through analyzing the heart rhythm. To see all the articles in the series, go to http://links.lww.com/AJN/A207., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

It has long been known that the electrophysiological effects of many cardioactive drugs strongly depend on the rate dependent frequency. This was recognized first for class I antiarrhythmic agents: their V max suppressive effect was attenuated at long cycle lengths. Later many Ca 2+ channel blockers were also found to follow such kinetics. The explanation was provided by the modulated and the guarded receptor theories. Regarding the duration of cardiac action potentials (APD) an opposite frequency-dependence was observed, i.e. the drug-induced changes in APD were proportional with the cycle length of stimulation, therefore it was referred as "reverse rate-dependency". The beat-to-beat, or short term variability of APD (SV) has been recognized as an important proarrhythmic mechanism, its magnitude can be used as an arrhythmia predictor. SV is modulated by several cardioactive agents, however, these drugs modify also APD itself. In order to clear the drug-specific effects on SV from the concomitant unspecific APD-change related ones, the term of "relative variability" was introduced. Relative variability is increased by ion channel blockers that decrease the negative feedback control of APD (i.e. blockers of I Ca , I Kr and I Ks ) and also by elevation of cytosolic Ca 2+ . Cardiac arrhythmias are also often categorized according to the characteristic heart rate (tachy- and bradyarrhythmias). Tachycardia is proarrhythmic primarily due to the concomitant Ca 2+ overload causing delayed afterdepolarizations. Early afterdepolarizations (EADs) are complications of the bradycardic heart. What is common in the reverse rate-dependent nature of drug action on APD, increased SV and EAD incidence associated with bradycardia., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Fetal arrhythmias warrant sophisticated surveillance and management, especially for the high-risk pregnancies. Clinically, fetal arrhythmias can be categorized into 3 types: premature contractions, tachyarrhythmias, and bradyarrhythmias. Fetal arrhythmias include electrocardiography, cardiotocography, echocardiography and magnetocardiography. Oxygen saturation monitoring can be an effective way of fetal surveillance for congenital complete AV block or SVT during labor. Genetic surveillance of fetal arrhythmias may facilitate the understanding of the mechanisms of the arrhythmias and provide theoretical basis for diagnosis and treatment. For fetal benign arrhythmias, usually no treatment but a close follow-up is need, while persistant fetal arrhythmias with congestive heart dysfunction or hydrops fetalis, intrauterine or postnatal treatments are required. The prognoses of fetal arrhythmias depend on the type and severity of fetal arrhythmias and the associated fetal conditions. Responses of fetal arrhythmias to individual treatments and clinical schemes are heterogeneous, and the prognoses are poor particularly under such circumstances., (Copyright © 2018 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.)

The incidence of arrhythmias is the main cause of high mortality after myocardial infarction (AMI). The aim of the present study was to determine whether the rosmarinic acid (RA) could reduce the stretch-induced arrhythmias (SIAs) related to overexpression of NCX 1 after AMI. Adult male Sprague-Dawley rats were randomly allocated into six groups: Sham, MI (100 mg/kg of isoproterenol (Iso), subcutaneously, on two consecutive days), RA (30 mg/kg, orally, 14 days), and RA (10, 15 and 30 mg/kg, 14 days) + I. MI induction was performed on the 13th and 14th days of the study period. Forty-eight hours after the first injection of Iso, the parameters of hypertrophy, plasma levels of malondialdehyde (MDA) and lipid profile were evaluated. Using Langendorff apparatus, the isolated hearts were transiently stretched for 5 s with three different end-diastolic volumes (ΔV 1to3  = 0.05, 0.1 and 0.2 mL). Cardiac function parameters were measured for 30 s, and ventricular arrhythmias were recorded for 3 min after each stretch. Finally, the levels of cardiac troponin-I and NCX 1 mRNA expression were examined. The rats of MI group showed a significant increase in hypertrophy index, MDA, triglyceride and cholesterol (P < 0.001). Additionally, a marked impairment in cardiac parameters, an increase in the rates of SIA s and NCX 1 expression, and a decrease in troponin-I (P < 0.001) were observed. RA at three doses especially 15 mg/kg strongly improved almost all the mentioned factors (P < 0.001). Our results confirm that RA pretreatment could prevent hypertrophia, arrhythmia and cardiac dysfunction following AMI which is associated with inhibition of lipid peroxidation and overexpression of NCX 1 ., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Torsade de Pointes (TdP) is a lethal arrhythmia that is often drug-induced, thus there is an urgent need for development of models to test or predict the drug sensitivity of human cardiac tissue. Here, we present an in vitro TdP model using 3D cardiac tissue sheets (CTSs) that contain a mixture of human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes and non-myocytes. We simultaneously monitor the extracellular field potential (EFP) and the contractile movement of the CTSs. Upon treatment with IKr channel blockers, CTSs exhibit tachyarrhythmias with characteristics of TdP, including both a typical polymorphic EFP and meandering spiral wave re-entry. The TdP-like waveform is predominantly observed in CTSs with the cell mixture, indicating that cellular heterogeneity and the multi-layered 3D structure are both essential factors for reproducing TdP-like arrhythmias in vitro. This 3D model could provide the mechanistic detail underlying TdP generation and means for drug discovery and safety tests.

The atrioventricular junction has a central role in electrophysiology, responsible for reentrant and automatic forms of supraventricular tachycardia. During atrioventricular nodal reentry tachycardia, the circuit involves 2 electrophysiologically separate pathways located in the vicinity of the atrioventricular node. Atrioventricular reentry tachycardia is caused by the presence of an accessory pathway located almost anywhere along the atrioventricular groove; the macroreentrant circuit involves the atrioventricular node, the accessory pathway and necessarily portions of atria and ventricles. Junctional tachycardia is a rare form of nonparoxysmal supraventricular tachycardia, secondary to enhanced automaticity or triggered activity. By analyzing a 12-lead electrocardiogram during sinus rhythm and tachycardia, it is possible to accurately diagnose the specific type of supraventricular tachycardia., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Anabolic steroids used to improve muscular strength and performance in athletics. Its long-term consumption may induce cardiovascular adverse effects. We assessed the risk of ventricular arrhythmias in rats which subjected to chronic nandrolone plus high-intensity endurance exercise. Animals were grouped as; control (CTL), exercise (Ex): 8 weeks under exercise, vehicle group (Arach): received arachis oil, and Nan group: received nandrolone decanoate 5 mg/kg twice a week for 8 weeks, Arach+Ex group, and Nan+Ex. Finally, under anesthesia, arrhythmia was induced by infusion of 1.5 μg/0.1 mL/min of aconitine IV and ventricular arrhythmias were recorded for 15 min. Then, animals' hearts were excised and tissue samples were taken. Nandrolone plus exercise had no significant effect on blood pressure but decreased the heart rate (P<0.01) and increased the RR (P<0.01) and JT intervals (P<0.05) of electrocardiogram. Nandrolone+exercise significantly increased the ventricular fibrillation (VF) frequency and also decreased the VF latency (P<0.05 versus CTL group). Combination of exercise and nandrolone could not recover the decreasing effects of nandrolone on animals weight gain but, it enhanced the heart hypertrophy index (P<0.05). In addition, nandrolone increased the level of hydroxyproline (HYP) and malondialdehyde (MDA) but had not significant effect on glutathione peroxidase of heart. Exercise only prevented the effect of nandrolone on HYP. Nandrolone plus severe exercise increases the risk of VF that cannot be explained only by the changes in redox system. The intensification of cardiac hypertrophy and prolongation of JT interval may be a part of involved mechanisms., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Biological, physical, and social systems often display qualitative changes in dynamics. Developing early warning signals to predict the onset of these transitions is an important goal. The current work is motivated by transitions of cardiac rhythms, where the appearance of alternating features in the timing of cardiac events is often a precursor to the initiation of serious cardiac arrhythmias. We treat embryonic chick cardiac cells with a potassium channel blocker, which leads to the initiation of alternating rhythms. We associate this transition with a mathematical instability, called a period-doubling bifurcation, in a model of the cardiac cells. Period-doubling bifurcations have been linked to the onset of abnormal alternating cardiac rhythms, which have been implicated in cardiac arrhythmias such as T-wave alternans and various tachycardias. Theory predicts that in the neighborhood of the transition, the system's dynamics slow down, leading to noise amplification and the manifestation of oscillations in the autocorrelation function. Examining the aggregates' interbeat intervals, we observe the oscillations in the autocorrelation function and noise amplification preceding the bifurcation. We analyze plots--termed return maps--that relate the current interbeat interval with the following interbeat interval. Based on these plots, we develop a quantitative measure using the slope of the return map to assess how close the system is to the bifurcation. Furthermore, the slope of the return map and the lag-1 autocorrelation coefficient are equal. Our results suggest that the slope and the lag-1 autocorrelation coefficient represent quantitative measures to predict the onset of abnormal alternating cardiac rhythms.

Wide-complex tachycardia is a rare disease entity among patients presenting to the emergency department. However, due to its potential life-threatening nature, emergency clinicians must know how to assess and manage this condition. Wide-complex tachycardia encompasses a range of cardiac dysrhythmias, some of which can be difficult to distinguish and may require specific treatment approaches. This review summarizes the etiology and pathophysiology of wide-complex tachycardia, describes the differential diagnosis, and presents an evidence-based approach to identification of the different types of tachycardias through the use of a thorough history and physical examination, vagal maneuvers, electrocardiography, and adenosine. The treatment options and disposition for patients with various wide-complex tachycardias are also discussed, with attention to special circumstances and select controversial/contemporary topics.

Aims: Hypertension is a major risk factor for atrial fibrillation. We hypothesized that arterial hypertension would alter atrial myocyte calcium (Ca2+) handling and that these alterations would serve to trigger atrial tachyarrhythmias., Methods and Results: Left atria or left atrial (LA) myocytes were isolated from spontaneously hypertensive rats (SHR) or normotensive Wistar-Kyoto (WKY) controls. Early after the onset of hypertension, at 3 months of age, there were no differences in Ca2+ transients (CaTs) or expression and phosphorylation of Ca2+ handling proteins between SHR and WKY. At 7 months of age, when left ventricular (LV) hypertrophy had progressed and markers of fibrosis were increased in left atrium, CaTs (at 1 Hz stimulation) were still unchanged. Subcellular alterations in Ca2+ handling were observed, however, in SHR atrial myocytes including (i) reduced expression of the α1C subunit of and reduced Ca2+ influx through L-type Ca2+ channels, (ii) reduced expression of ryanodine receptors with increased phosphorylation at Ser2808, (iii) decreased activity of the Na+ / Ca2+ exchanger (at unaltered intracellular Na+ concentration), and (iv) increased SR Ca2+ load with reduced fractional release. These changes were associated with an increased propensity of SHR atrial myocytes to develop frequency-dependent, arrhythmogenic Ca2+ alternans., Conclusions: In SHR, hypertension induces early subcellular LA myocyte Ca2+ remodelling during compensated LV hypertrophy. In basal conditions, atrial myocyte CaTs are not changed. At increased stimulation frequency, however, SHR atrial myocytes become more prone to arrhythmogenic Ca2+ alternans, suggesting a link between hypertension, atrial Ca2+ homeostasis, and development of atrial tachyarrhythmias., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)

We present an 18-month boy with imipramine poisoning to illustrate the neuro-cardiac toxic effects of this potentially deadly poison in children. The toddler ingested an unknown amount of imipramine from a non-childproof bottle which clearly labelled that the drug must be kept out of reach from children. He developed neurologic and cardiac symptoms. Electrocardiography (ECG) showed tachycardia and widened QRS. He was immediately treated with bicarbonate infusion and made an uneventful recovery. This is the youngest and only reported case of symptomatic imipramine ingestion in our locality. Imipramine has been surpassed by newer antidepressants for the treatment of depression in the past decade. Literature is searched to review the mortality rate in young children. Intensive care neuro-cardiac support contributes to the favorable outcome. Despite clear labelling of the bottle, carelessness on the part of the adult and the use of non-childproof bottle are definite preventable factor to such potentially fatal ingestion.

T wave "memory" is a peculiar variety of cardiac remodeling caused by a transient change in the course of ventricular depolarization (due to ventricular pacing, rate-dependent intraventricular block, ventricular preexcitation or tachyarrhythmias with wide QRS complexes). It is usually manifested by inverted T waves that appears when normal ventricular activation is restored. This phenomenon is cumulative and occurs earlier if the ventricular myocardium has previously been exposed to the same conditioning stimuli. In this article the different conditions giving rise to "classical" T wave memory development are reviewed and also "another" type of T wave memory is described. It is also shown that cardiac memory may induce not only negative (pseudo-primary) T waves but also a reversal of primary and pseudoprimary T waves leading to "normalization" of ventricular repolarization. The knowledge of these dissimilar consequences of T wave memory is essential to assess the characteristics of ventricular repolarization.

True supernormality of excitability and conduction has been demonstrated in normal Purkinje fibers in in vitro studies. In the clinical setting, supernormality of conduction is manifested better than expected. This phenomenon is much more common than previously thought, particularly in the presence of certain clinical conditions. If a careful scanning of the cardiac cycle is performed on all patients with intermittent bundle branch block and second degree or advanced infranodal AV block, accessory pathways and mulfunctioning pacemakers, it is anticipated that a much larger amount of supernormal excitability and conduction will be unmasked.

Morphological ECG abnormalities occur in 5-12% healthy adults participating in early phase clinical trials. We retrospectively analyzed 16,472 12-lead ECGs recorded at multiple time points in 420 volunteers (282 males, 138 females; aged 18-76 years) randomized to receive placebo from 19 Phase I studies to see if some baseline ECG abnormalities may disappear or new abnormalities may appear during the study. One hundred forty-four (34.3%) subjects had abnormal baseline ECGs, of which 66 (44.8%) reverted to normal during follow-up. Of 276 (65.7%) subjects with normal baseline ECGs, 118 (42.8%) developed ECG abnormalities over the next 6 weeks. Common baseline abnormalities included sinus bradycardia, R wave transition abnormalities, right axis deviation, non-specific T wave changes and atrial premature complexes. On follow-up ECGs, prolonged QT interval, first-degree AV block, sinus bradycardia, short PR interval, and R wave transition abnormalities reverted to normal. Common new-onset abnormalities in subjects with normal baseline ECGs included sinus bradycardia, prolonged QT interval, non-specific T wave changes, R wave transition abnormalities, and sinus tachycardia. Thus, transient morphological ECG changes may occur in healthy volunteers possibly due to diurnal variation, effect of food, hormones, or autonomic changes. This should be considered when interpreting "treatment-emergent" ECG changes in clinical trials., (© 2014, The American College of Clinical Pharmacology.)

Cardiac arrhythmias comprise of a heterogeneous group of disorders which manifest in a wide range of clinical presentations. They can be associated with underlying cardiac disease and portend a grave prognosis, with some arrhythmias being rapidly fatal. Other arrhythmias, however are relatively benign and can be asymptomatic or may be a mere inconvenience for the patient. All primary care physicians can expect to encounter some forms of arrhythmias during the course of their practice. This review article provides a brief overview of the commonly seen tachyarrhythmias for the general practitioner and provides relevant updates on the recent developments in our understanding of their mechanisms and management., (Copyright © 2013 Elsevier Inc. All rights reserved.)

The diagnosis and management of prenatal tachyarrhythmias is well established; however, the postnatal course and outcomes are not. The purpose of our study was to review the natural history of patients with fetal tachycardia, determine the incidence of postnatal arrhythmias, and determine whether there are factors to predict which fetuses will develop postnatal arrhythmias. A retrospective chart review of patients with fetal tachyarrhythmias investigated at British Columbia Children's and Women's Hospitals between 1983 and 2010 was conducted. Sixty-nine mother-fetus pairs were eligible for the study. Fifty-two had fetal supraventricular tachycardia, and 17 had fetal atrial flutter. Conversion to sinus rhythm occurred prenatally in 52 % of patients. Postnatal arrhythmia occurred in two thirds of patients, with 82 % of those cases occurring within the first 48 h of life. Hydrops fetalis, female sex, and lack of conversion to sinus rhythm was predictive of postnatal arrhythmia (P = 0.01, P = 0.01, and P = 0.001, respectively). Conversion to sinus rhythm prenatally did not predict postnatal arrhythmia. Median duration of treatment was 9 months. Two postnatal deaths of unknown etiology occurred. Two thirds of all patients with prenatal tachycardia will develop postnatal arrhythmia. Prenatal factors that predict postnatal arrhythmia include hydrops, sex, and whether or not conversion to sinus rhythm occurred prenatally. The majority of patients with postnatal arrhythmia present within 48 h of life, which has clinical implications for monitoring. Postnatal outcome is generally very good with most patients being weaned off medication in 6-12 months.

I(Ks) blockade might be a promising way to treat tachyarrhythmia because of the accumulation of activated potassium channels. However, I(Ks) blockade during ischemia/reperfusion has not been investigated. Thus, the electrophysiological effects of two I(Ks) blockers, chromanol 293B (10 μm) and HMR 1556 (1 μm), were assessed in an in vitro model of border zone between normal and ischemic/reperfused right ventricular myocardium from guinea-pigs, and classic electrophysiological parameters and the incidence of arrhythmias were studied. HMR 1556 and chromanol 293B exhibited slight conventional class III effects on action potential duration in the normal zone (NZ) (APD(90) : -2 ± 5%, not significant (NS); +6 ± 3%, NS; and +5 ± 1%, P < 0.05, respectively, in control, HMR 1556, and chromanol 293B groups) but failed to oppose its decrease after 30 min of simulated ischemic superfusion (APD(90) : -52 ± 5%, P < 0.01; -64 ± 5%, P < 0.01; and -61 ± 3%, P < 0.01, respectively, in control, HMR 1556, and chromanol 293B groups), leading to repolarization dispersion between normal and ischemic zones. Chromanol 293B and HMR 1556 prolonged APD(90) during reperfusion, respectively, by +11 ± 1%, P < 0.01 and +25 ± 4%, P < 0.01 in the NZ and by +13 ± 3%, NS and +31 ± 2%, P < 0.01 in the simulated ischemic zone. Both compounds exhibited neutral arrhythmogenic effects during ischemia or reperfusion. Thus, I(Ks) blockade was neutral on the occurrence of ventricular arrhythmias during ischemia and reperfusion in guinea-pig ventricular tissue., (© 2011 The Authors Fundamental and Clinical Pharmacology © 2011 Société Française de Pharmacologie et de Thérapeutique.)

A potentially life-threatening arrhythmia appeared on the preinduction electrocardiogram of an asymptomatic young woman prior to spine surgery. The patient was evaluated by electrophysiology and had a rare accessory pathway, a Mahaim Fiber., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Sudden loss of consciousness can be caused by syncope or epileptic seizure, which therefore requires a diagnostic work-up including cardiological and neurological examinations. Thus, in clinical practice cooperation of these two medical specialties is common and of high relevance. Seizures may lead to cardiac arrhythmia or ictal asystole, and "sudden unexpected death in epilepsy" (SUDEP) is an important field of epilepsy research. Cardiac channelopathies such as long QT syndrome may be associated with seizures, suggesting a possible link between cardiac and cerebral channelopathy. We here review in detail cardiac effects due to epileptic seizures as well as possible pathogenetic correlations between cardiac and epileptic diseases., (© Georg Thieme Verlag KG Stuttgart · New York.)

1. It is currently unknown whether long-term voluntary exercise has enduring cardioprotective effects in animal models. 2. The present study was conducted in three groups of rats: (i) sedentary controls (n = 6); (ii) 24 h runners (n = 8; unlimited access to running wheels); and (iii) 2 h runners (n = 8; access to running wheels limited to 2 h daily). After termination of the 6 week exercise protocol, all rats were implanted with the telemetric electrocardiogram transmitters and were studied 1 week later. 3. Resting heart rate (HR) values in the control rats, 24 h runners and 2 h runners were 372 ± 7, 361 ± 9 and 298 ± 5 b.p.m., respectively (P < 0.05 for 2 h runners vs controls). The high-frequency spectral power in the control rats, 24 h runners and 2 h runners was 3.9 ± 0.2, 4.3 ± 0.3 and 5.3 ± 0.3 s², respectively (P < 0.05 for 2 h runners vs controls), whereas intrinsic HR was 383 ± 3, 377 ± 2 and 346 ± 3 b.p.m., respectively (P < 0.001 for 2 h runners vs controls). Restraint stress provoked tachycardia of similar magnitude in all groups. 4. After completion of telemetric studies, haemodynamic indices and susceptibility to cardiac arrhythmias were assessed in anaesthetized animals, there were no major between-group differences in HR, arterial pressure, contractility indices or sensitivity to β-adrenoceptor stimulation (dobutamine) or blockade (atenolol). The effective refractory period in the control rats, 24 h runners and 2 h runners was 49 ± 2, 55 ± 2 and 60 ± 4 ms, respectively (P = 0.054 for 2 h runners vs controls). A significantly higher dose of aconitine was required to provoke ventricular arrhythmias in the 24 h and 2 h running groups compared with controls (489 ± 76, 505 ± 88 and 173 ± 33 μg, respectively; P < 0.05). 5. We conclude that, in rats, long-term voluntary exercise has enduring cardioprotective effects mediated at the level of both the central nervous system and the heart., (© 2010 The Authors. Clinical and Experimental Pharmacology and Physiology © 2010 Blackwell Publishing Asia Pty Ltd.)

Studies with heart rate variability have revealed interictal autonomic alterations in patients with epilepsy. In addition, epilepsy is frequently associated with ictal tachycardia or bradycardia, which sometimes precedes the onset of seizures. Ictal tachycardia is sometimes associated with electrocardiography (ECG) morphologic changes and ictal bradycardia often progresses to asystole. Such cardiac manifestations of seizures have been hypothesized as possible causes for sudden unexplained death in epilepsy (SUPEP). The present review relates to interictal and ictal cardiac manifestations of epilepsy with focus on heart rate, heart rate variability, and ECG changes. Aspects of the supporting mechanisms are discussed and attention is drawn to the interaction between central and peripheral effects, interictal autonomic conditions, ictal autonomic discharges, and administration of antiepileptic drugs in shaping the ictal cardiac changes. Because these interactions are complex and not totally understood, closer surveillance of patients and more experimental work is necessary to elucidate the mechanistic support of autonomic and cardiac changes in epilepsy, and to design better strategies to avoid their undesirable effects. It is also suggested that some of these changes could be used as predictors or markers for the onset of seizures.

Objectives: Cardiac arrhythmias as a cause of syncope, collapse, or intermittent weakness can be challenging to diagnose. The purpose of this paper is to retrospectively review the diagnosis and outcome of 23 cases of syncope or collapse in dogs that had a Reveal Plus ILR recorder placed as part of the diagnostic evaluation., Animals, Materials and Methods: Medical records of 23 client-owned dogs that were presented for evaluation of syncope, collapse, or intermittent weakness were retrospectively reviewed., Results: Recurrent syncope occurred in 13/23 (57%) and a positive diagnosis of the cause of the event was made in 11/13 (48% of all dogs). Diagnoses included 6/11 with prolonged periods of sinus arrest with slow ventricular escape rate and one each of sub-optimal fixed heart rate by endocardial pacing, high grade second degree atrioventricular block, supraventricular tachycardia, normal ECG during multiple episodes, and high grade second degree atrioventricular block or sinus arrest., Conclusions: The Reveal Plus ILR device was successful in diagnosing a high percentage of cases of syncope or collapse in which signs recurred and implantation had a low complication rate. The Reveal Plus ILR device is a useful tool to diagnose the etiology of recurrent syncope, collapse, or intermittent weakness in the dog., (Copyright 2010 Elsevier B.V. All rights reserved.)

Background: Discomfort because of palpitation and tachycardia is a frequent phenomenon. Clinical practice for diagnosing tachycardia has a low sensitivity, and patients without a correct diagnosis are often not treated optimally., Material and Methods: Results from all 24-hour-ECGs taken at Telemark Hospital in the period 1.8.04-31.7.05 were reviewed. Indications and findings were retrieved from the hospital database. 252 of totally 614 ECGs were performed for the indications palpitation and tachycardia. 137 patients with an unclear diagnosis were offered a simple electrophysiologic examination with stimulation of the right atrium by a pacemaker electrode. 38 of these patients were included and underwent the examination. An additional 18 patients were referred to a simple electrophysiologic examination based on the same criteria., Results: 24-hour-ECG provided a diagnosis for 29 patients with palpitation and tachycardia. A simple electrophysiologic examination uncovered reentry tachycardia in nine patients and paroxystic atrial flutter in three patients. A total of 56 electrophysiologic examinations were performed, uncovering 12 cases of tachycardia suitable for ablation. Two patients had to undergo DC-conversion, no other complication was observed., Interpretation: A simplified electrophysiologic examination of this group of patients will uncover tachycardia suitable for ablation in approximately 20 % of the patients, and increase diagnostic yield of supraventricular tachycardia by 64 %.

To assess heart rate (HR) regulation in Machado-Joseph disease (MJD), we evaluated HR variability at rest and the initial HR response to standing suddenly in 13 MJD patients and 26 normal control subjects. A head-up tilt (HUT) test involving the monitoring of blood pressure, HR, and cerebral oxy/deoxyhemoglobin concentration was also performed in each participant. There was no significant difference in HR variability at rest between the two groups, but the transient HR rise just after standing suddenly in the MJD group was significantly less than that in the control group (p < 0.01). The HUT test, where each participant was gradually tilted upward, induced a significantly greater HR increase in the MJD group compared with the controls (p < 0.01), while there were no significant differences in the blood pressure and cerebral oxygenation changes between the two groups. In our MJD study, the transient HR rise just after standing suddenly was diminished, and HR markedly increased during sustained orthostatic stress.

Beta-adrenergic stimulation may increase heart rate and the potential for cardiac arrhythmias. The effect of inhaled long-acting beta2-agonists (LABAs) on these outcomes was evaluated in patients with chronic obstructive pulmonary disease (COPD) in 2 double-blind randomized clinical trials. The pretreatment arrhythmia occurrence frequency in these patients was also described. In this analysis, 24-hour Holter monitoring data were pooled from 2 identically designed Phase III trials. Patients were randomized to LABA treatment or placebo for 12 weeks: a) nebulized arformoterol 15 microg BID, b) 25 microg BID, or c) 50 microg QD; d) salmeterol metered dose inhaler 42 microg BID; or e) placebo. The 24-hour Holter monitoring was performed pretreatment and at Weeks 0 (first day of dosing), 6, and 12. We assessed the proportion of patients with each of 4 arrhythmias: atrial tachycardia, atrial fibrillation/flutter, and "nonsustained"; (4-10 beats) and "sustained"; (>10 beats) ventricular tachycardia. There were 5226 Holter recordings in 1429 treated patients. At baseline, there was a low frequency of occurrence of atrial fibrillation/flutter (0.1%), nonsustained ventricular tachycardia (3.1%), and >10 beat ventricular tachycardia (0.3%). Atrial tachycardia occurred frequently (41.8%). The proportion of patients with treatment-emergent atrial tachycardia ranged from 27% to 32% and was non-significantly higher, by approximately 2%-5% (p = 0.70), in the LABA groups compared with the placebo group. The rates of the other more serious arrhythmias did not increase with LABA treatment and were similar to placebo. All treatment groups (LABA and placebo) had consistent small decreases from baseline in mean 24-hour and maximum hourly heart rate. In conclusion, in this large cohort of COPD patients with no or stable cardiac comorbidities, a high proportion ( approximately 40%) of patients were observed to have atrial tachycardia before treatment, which increased by 2%-5% with LABA treatment. More serious arrhythmias were infrequent and did not increase with inhaled LABA therapy. LABA administration did not increase mean heart rate.

Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by alpha-adrenergic receptor blockade. In 30 anesthetized dogs, trains of five electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 atrial unipolar electrodes. Mediastinal nerve sites were identified that reproducibly initiated atrial arrhythmias. These sites were then restimulated following 1 h (time control, n = 6), or the intravenous administration of naftopidil (alpha(1)-adrenergic blocker: 0.2 mg/kg, n = 6), yohimbine (alpha(2)-adrenergic blocker: 1 mg/kg, n = 6) or both (n = 8). A ganglionic blocker (hexamethonium: 1 mg/kg) was tested in four dogs. Stimulation of mediastinal nerves sites consistently elicited atrial tachyarrhythmias. Repeat stimulation after 1 h in the time-control group exerted a 19% decrease of the sites still able to induce atrial tachyarrhythmias. Hexamethonium inactivated 78% of the previously active sites. Combined alpha-adrenoceptor blockade inactivated 72% of the previously active sites. Bradycardia responses induced by mediastinal nerve stimulation were blunted by hexamethonium, but not by alpha(1,2)-adrenergic blockade. Naftopidil or yohimbine alone eliminated atrial arrhythmia induction from 31% and 34% of the sites (similar to time control). We conclude that heterogeneous activation of the intrinsic cardiac nervous system results in atrial arrhythmias that involve intrinsic cardiac neuronal alpha-adrenoceptors. In contrast to the global suppression exerted by hexamethonium, we conclude that alpha-adrenoceptor blockade targets intrinsic cardiac local circuit neurons involved in arrhythmia formation and not the flow-through efferent projections of the cardiac nervous system.

Introduction: Rapid firing originating within pulmonary veins (PVs) initiates atrial fibrillation (AF). The following studies were performed to evaluate spontaneous PV firing in patients with AF to distinguish focal versus reentrant mechanisms., Methods: Intracardiac recordings were obtained in 18 patients demonstrating paroxysmal AF. Microelectrode (ME) recordings were obtained from superfused canine PV sleeves (N = 48)., Results: Spontaneous PV firing (566 +/- 16 bpm; 127 +/- 6 ms cycle length) giving rise to AF (52 episodes) was observed. Tachycardia-pause initiation was present in 132 of 200 episodes of rapid PV firing and 34 of 52 AF episodes. The pause cycle length preceding PV firing was 1,039 +/- 86 ms following tachycardia (420 +/- 40 ms cycle length). The remaining episodes were initiated following a 702 +/- 32 ms pause during sinus rhythm (588 +/- 63 ms). Spontaneous firing recorded with a multipolar mapping catheter did not detect electrical activity bridging the diastolic interval between the initial ectopic and preceding post-pause sinus beat. Tachycardia-pause initiated PV firing (138 +/- 7 ms coupling interval) in patients correlated with tachycardia-pause enhanced isometric force, early afterdepolarization (EAD) amplitude, and triggered firing within canine PVs. Rapid firing (1,172 +/- 134 bpm; 51 +/- 8 ms cycle length) following an abbreviated coupling interval (69 +/- 12 ms) was initiated in 13 of 18 canine PVs following tachycardia-pause pacing during norepinephrine + acetylcholine superfusion. Stimulation selectively activating local autonomic nerve terminals facilitated tachycardia-pause triggered firing in canine PVs (5 of 15 vs 0 of 15; P < 0.05)., Conclusions: The studies demonstrate (1) tachycardia-pause initiation of rapid, short-coupled PV firing in AF patients and (2) tachycardia-pause facilitation of isometric force, EAD formation, and autonomic-dependent triggered firing within canine PVs, suggestive of a common arrhythmia mechanism.

Objectives: The purpose of this study was to determine the patterns of autonomic nerve activity in congestive heart failure (CHF)., Background: The relationship between autonomic nerve activity and cardiac arrhythmias in CHF is unclear., Methods: We implanted radiotransmitters in 6 dogs for continuous (24/7) simultaneous monitoring of left stellate ganglion nerve activity (SGNA), vagal nerve activity (VNA), and electrocardiography before and after pacing-induced CHF., Results: Congestive heart failure increased both SGNA and VNA. The SGNA but not VNA manifested a circadian variation pattern. There was extensive sinus node fibrosis. We analyzed 2,263 episodes of prolonged (>3 s) sinus pauses (PSP) and 1,420 long (>10 s) episodes of paroxysmal atrial tachycardia (PAT). Most (95.3%) PSP episodes occurred at night, and 56% were preceded by a short burst of SGNA that induced transient sinus tachycardia. Long PAT episodes were typically (83%) induced by simultaneous SGNA and VNA discharge, followed by VNA withdrawal. Premature ventricular contractions and ventricular tachycardia were preceded by elevated SGNA., Conclusions: The reduction of sympathovagal balance at night in ambulatory dogs was due to reduced sympathetic discharge rather than a net increase of vagal discharge. The tachybrady syndrome in CHF might be triggered by an intermittent short burst of SGNA that resulted in tachycardia and sinus node suppression. Simultaneous sympathovagal discharge is a cause of long PAT episodes. These data indicate that there is an association between the specific patterns of autonomic nerve discharges and cardiac arrhythmia during CHF.

Background: The right atrium late after the Fontan procedure is characterized by multiple complex arrhythmia circuits. We performed simultaneous electroanatomic and noncontact mapping to assess the accuracy of both systems to identify scar and arrhythmia., Methods and Results: Mapping was performed in 26 patients aged 26.8+/-8.9 years, 18.7+/-4.4 years after Fontan surgery. The area and site of abnormal endocardium defined by electroanatomic mapping (bipolar contact electrogram <0.5 mV) were compared with those defined by noncontact mapping during sinus rhythm and by dynamic substrate mapping. Contact and reconstructed unipolar electrograms at a known distance from the multielectrode array, recorded by the noncontact system simultaneously at 452 endocardial sites, were compared for morphological cross correlation, timing difference, and amplitude. Mapping of arrhythmias was performed with both systems when possible. The median patient abnormal endocardium as defined by electroanatomic mapping covered 38.0% (range 16.7% to 97.8%) of the right atrial surface area, as opposed to 60.9% (range 21.3% to 98.5%) defined by noncontact mapping during sinus rhythm and 11.9% (range 0.4% to 67.3%) by dynamic substrate mapping. A significant decrease in electrogram cross correlation (P=0.003), timing (P=0.012), and amplitude (P=0.003) of reconstructed electrograms, but not of contact electrograms (P=0.742), was seen at endocardial sites >40 mm from the multielectrode array. Successful arrhythmia mapping by electroanatomic versus noncontact mapping was superior in 15 patients (58%), the same in 6 (23%), and inferior in 5 (19%; P=0.044)., Conclusions: Electroanatomic mapping is the superior modality for arrhythmia mapping late after the Fontan procedure. Noncontact mapping is limited by a significant reduction in reconstructed electrogram correlation, timing, and amplitude >40 mm from the multielectrode array and cannot accurately define areas of scar and low-voltage endocardium.

Congenital heart disease is associated with arrhythmias. Not only the congenital anatomic component but also the greater arrhythmogenic substrate related to surgical procedures is associated with the increased incidence of arrhythmias in these patients. In pediatric cardiology the study of these phenomena is becoming important and one factor associated with it is the longer follow up, which varies depending on the type of heart disease and arrhythmia. With the same impact, there are daily breakthroughs in diagnostic and treatment through pharmacological and interventional means. The incidence of arrhythmias in post-surgical patients with congenital heart disease is in constant increment, and this is related to the constant increment in the procedures, variety and frequency, as well as the long-term survival.

Unlabelled: Patients with surgical correction of congenital cardiopathies have a high incidence of macro-reentrant arrhythmias. In previous reports the incidence of atrial fibrillation or flutter is around 20% preoperatively and increases to 10% more after surgery. In Mustard and Senning procedures the incidence could be as high as 30%. The physiopathology of these arrhythmias is due to conduction block and heterogeneity of refractory periods due to scaring and fibrosis left by the surgical procedure. Radiofrequency ablation is a good treatment option in this patients, but with conventional approaches the percentage of success is lower and with higher recurrence. In our institution out of 39 patients with macro-reentrant atrial tachycardia, acute success was 77% in patients with isthmus dependent flutter and 44% if the Isthmus was not part of the circuit. Recurrence in both groups was 42%. New mappings systems like Localisa, CARTO an NavX, are useful to localize areas of scar and block, that produce multiple conduction channels that can participate in reentrant arrhythmias. Radiofrequency ablation of these channels is up to day the ideal approach for these patients., Conclusions: Arrhythmias in patients with congenital cardiopathies are frequent and complicate the evolutions of these patients. Radiofrequency ablation is the treatment of choice in centers with experience. The use of non fluoroscopic electroanatomic mapping systems is of great help in this setting.

The evolution of arrhythmologic technology introduced new therapeutic opportunities for cardiology patients. Competence, continuity of care, integration and collaboration between medical doctors and nurses allow a safe management of short and long term complications. A typical example of a new arrhythmic complication is the "electrical storm" or "arrhythmic warm up" in patients implanted with a cardioverter-defibrillator (ICD). The definition and epidemiology of the electrical storm stress the relevance of this clinical situation; its dramatic emergency involves several aspects of nursing care, clinical, prognostic, ethical and deontological. The definition and implementation of an integrated protocol for the treatment of this condition is described and ethical and unresolved questions are rised. One of these problems is the recommendation to offer the patient the opportunity to receive information about the option of inactivating the ICD.

Increased mechanical tension in the ischemic region during acute coronary occlusion might favor the occurrence of phase Ib ventricular arrhythmias. We aimed to investigate whether intracoronary administration of Gd(3+), a stretch-activated channel blocker, into the ischemic zone reduces the incidence of these arrhythmias. In thiopental-anesthetized, open-chest pigs, the left anterior descending coronary artery (LAD) was ligated for 45 or 48 min. Phosphate-free, HEPES-buffered saline bubbled with 100% N(2) was infused into the ischemic region for 4 min, starting 5 min (series A; n = 16) or 20 min (series B; n = 16) after coronary occlusion, at a rate doubling the baseline blood flow. Animals were blindly allocated to receive 40 muM Gd(3+) or only the buffer during the final 2 min of the infusion. There were no differences between groups with respect to hemodynamic variables, plasma K(+) levels, or size of the ischemic region. In neither series was the number of phase Ib premature ventricular beats reduced by Gd(3+) (46 +/- 20 in untreated vs. 91 +/- 37 in Gd(3+)-treated animals in series A and 19 +/- 7 vs. 22 +/- 13, respectively, in series B; both P = not significant). The occurrence of ventricular tachycardia or fibrillation was significantly associated with the magnitude of early ischemic expansion of the LAD region, as measured by ultrasonic crystals, but was also not prevented by Gd(3+). These results argue against a major role of stretch-activated channels inside the area at risk in the genesis of phase Ib ischemic ventricular arrhythmias.

Arrhythmic cardiomyopathies are due to ventricular dysfunction following prolonged or chronic tachycardia; the clinical pictures one of congestive heart failure, which is totally reversible after the treatment of tachycardia and the restoration of sinus rhythm. Since Whipple's first description of this model of heart failure, several teams have shown that ventricular or atrial pacing at rates exceeding 220 beats per minute produces a profound and largely reversible depression of ventricular function, and a constellation of neuroendocrine abnormalities and metabolic, electrophysiological and anatomic alterations of the myocardium. The associated heart failure generally starts to improve within days of achieving ventricular rhythm control, but clinical recovery may take several weeks or months. All forms of chronic tachycardia may induce heart failure, but the onset of cardiomyopathy depends more on the heart rate and the duration of the arrhythmia than on its type. The pathophysiological mechanisms are multiple and complex, and include abnormalities in the structure and function of cardiomyocytes and disturbances in excitation-contraction coupling. Treatment consists of restoring and maintaining sinus rhythm, or at least of controlling the ventricular rate. Because of its curative effect, selective radiofrequency ablation is the treatment of choice when the arrhythmogenic substrate is localized. Control of the ventricular rate by radiofrequency modification of atrioventricular conduction is the treatment of choice for chronic atrial fibrillation.

Background: We previously characterized a novel K+ current (IKH) with properties of constitutively active acetylcholine-related current in dog atrium. I(KH) is sensitive to tertiapin-Q (IC50 approximately 10 nmol/L), a highly selective Kir3 current blocker. This study assessed the role of IKH in atrial tachycardia (AT)-remodeled canine left atrium (LA) with the use of tertiapin-Q as a probe., Methods and Results: Dogs were subjected to 7 to 13 days of AT (400 bpm). Coronary-perfused LA preparations were studied intact or subjected to cardiomyocyte isolation. IKH was recorded with patch-clamp methods. AT pacing increased time-dependent hyperpolarization-activated current (IKH) at -110 mV from -1.8+/-0.3 (control) to -3.4+/-0.5 pA/pF (AT) and the 100-nmol/L tertiapin-sensitive component from -1.5+/-0.4 (control) to -3.3+/-0.6 pA/pF (AT). Prolonged atrial tachyarrhythmias could be induced with single extrastimuli in AT-remodeled, but not control, preparations, reflecting the atrial fibrillation-promoting effects of AT remodeling. In AT-remodeled preparations, tachyarrhythmia duration averaged 11.0+/-5.2 seconds, with a cycle length of 108+/-6 ms. Tertiapin-Q decreased tachyarrhythmia duration (to 0.6+/-0.1 second; P<0.001) and increased tachyarrhythmia cycle length (to 175+/-10 ms; P<0.001). Atrial action potential duration (APD) was increased 65+/-6% by tertiapin in AT-remodeled hearts versus 19+/-2% (P<0.001) in control. In 2 AT-remodeled preparations, tachyarrhythmia lasted uninterrupted for >20 minutes; tertiapin-Q slowed and then terminated arrhythmia in both. Tertiapin had no effect on left ventricular cardiomyocyte currents or APD., Conclusions: AT remodeling increases IKH, and a highly selective Kir3 current antagonist, tertiapin-Q, increases APD and suppresses atrial tachyarrhythmias in AT-remodeled preparations without affecting ventricular electrophysiology. Constitutive acetylcholine-related K+ current contributes to AT-remodeling effects in dogs and is a potentially interesting antiarrhythmic target.

There are many published papers focused on the topic of atrial electrical remodeling, which defined as the shortening and dispersion of effective refractory period (ERP) in patients with paroxysmal or persistent tachyarrhythmias or in animals with long-term rapid atrial pacing. Heart failure could produce the electrical remodeling of sinus node, manifesting the prolongation of corrected sinus node recovery time and sinus cycle length. It might be attributed to decreased hyperpolarization-activated cyclic nucleotide expression of sinus node. Rapid atrial pacing for only 10-15 min, simulating transient atrial tachyarrhythmias, alters sinus node function in human. Termination of atrial flutter by ablation induces reversible changes in sinus node function. After atrial fibrillation (AF) ablation, there was a significant improvement of sinus node function, with an increase in the mean heart rate, maximal heart rate and heart rate range significantly. Reverse electrical remodeling of the ERP occurs at different rates in different regions of the atrium. Previous experiments showed that electrical remodeling of atrial myocardium could be induced by autonomic nervous transmitters and suggested that autonomic nerve activity was an important factor to promote AF episodes. We postulated that electrical remodeling and reverse electrical remodeling are common features of the heart, including atrium, ventricle, sinus node, and conductive system. Inappropriate very rapid or slow electrical depolarization may cause electrical remodeling of the heart, but appropriate rates of electrical depolarization and cessation of rapid stimulation may contribute to the reverse electrical remodeling. So, we forward that a concept defined as cardiac electrical stunning, including electrical remodeling and reverse electrical remodeling, should be a common characteristic and mechanism of cardiac arrhythmias.

A 20-year-old active duty male presented with palpitations, tachycardia, and a nontender, diffusely enlarged thyroid. The differential diagnosis and appropriate management of this patient's symptoms and physical examination findings are reviewed. Various diagnostic modalities are highlighted and effective treatment strategies as well as their risks and benefits are discussed.