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Coronavirus disease 2019 (COVID-19) is a global pandemic that is wreaking havoc on the health and economy of much of human civilization. Electrophysiologists have been impacted personally and professionally by this global catastrophe. In this joint article from representatives of the Heart Rhythm Society, the American College of Cardiology, and the American Heart Association, we identify the potential risks of exposure to patients, allied healthcare staff, industry representatives, and hospital administrators. We also describe the impact of COVID-19 on cardiac arrhythmias and methods of triage based on acuity and patient comorbidities. We provide guidance for managing invasive and noninvasive electrophysiology procedures, clinic visits, and cardiac device interrogations. In addition, we discuss resource conservation and the role of telemedicine in remote patient care along with management strategies for affected patients., (Copyright © 2020. Published by Elsevier Inc.)

We present the case of a patient who presented with worsening chest pain and tachycardia. We were able to monitor her remotely through her pacemaker. She had been started on the injectable medication teriparatide (Forteo) and since then she had an increase in her symptoms. She was found to have intermittent atrial tachycardia with 1:1 conduction and occasional atrioventricular block transiently, coinciding with her injection of teriparatide. This specific-associated arrhythmia has yet to be described., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Patients with syncope and organic heart disease remain a small but important subset of those patients who experience transient loss of consciousness. These patients require thoughtful and complete evaluation in an attempt to better understand the mechanism of syncope and its relationship to the underlying disease, and to diagnose and treat both properly. The goal is to reduce the risk of further syncope, to improve long-term outcomes with respect to arrhythmic and total mortality, and to improve patients' quality of life., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Inappropriate sinus tachycardia (IST) is a syndrome in which the sinus heart rate is inexplicably faster than expected and associated symptoms are present. The heart rate at rest, even in a supine position, can exceed 100 beats/min; minimal activity accelerates the rate rapidly and substantially. Patients with IST may require restriction from physical activity. Mechanisms responsible for IST are understood incompletely. It is important to distinguish IST from so-called appropriate sinus tachycardia and from postural orthostatic tachycardia syndrome, with which overlap may occur. Because the long-term outcome seems to be benign, treatment may be unnecessary or may be as simple as physical training. However, for patients with intolerable symptoms, therapeutic measures are warranted. Even at high doses, β-adrenergic blockers, the first-line therapy, often are ineffective; the same is true for most other medical therapies. In rare instances, catheter- or surgically- based right atrial or sinus node modification may be helpful, but even this is fraught with limited efficacy and potential complications. Overtreatment, in an attempt to reduce symptoms, can be difficult to avoid, but is discouraged., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Unexplained and potentially arrhythmic symptoms often lead to electrophysiology referral for evaluation. Implantable loop recorder (ILR) correlation of the symptom to the rhythm can secure a definitive arrhythmic diagnosis after a standard, yet nondiagnostic workup., Methods: This large single-center retrospective study sought to assess the role of ILR in the evaluation of potentially arrhythmic symptoms, both in terms of diagnosis of an arrhythmia as well as to rule out an arrhythmic cause. Clinical data, indications for ILR, interrogation reports, and further management strategies were collected in all 86 patients who received ILR from June 1999 to April 2008 at the University of Iowa Hospitals and Clinics. The indications for ILR were unexplained syncope (76%), palpitations (14%), and presyncope or dizziness (10%)., Results: During a mean follow-up period of 10 +/- 7 months, 53 patients (62%) had recurrent symptoms after ILR placement with the mean time to recurrence of 12 +/- 17 weeks. Of these, an arrhythmic diagnosis was established in 12 patients (14%). Forty-one patients (48%) did not have any arrhythmia during their symptoms. These patients were discharged from the electrophysiology clinic. Thirty-three patients (38%) did not have any symptoms following ILR placement. Out of these, device was explanted in 10 patients, while the rest are still being followed., Conclusions: In patients with potentially arrhythmic symptoms, ILR plays an important role not only in diagnosing an arrhythmia, but also to rule out an arrhythmic cause.

Background: The evaluation of syncope can be expensive, unfocussed, and unrevealing yet, failure to diagnose an arrhythmic cause of syncope is a major problem. We investigate the utility of noninvasive electrocardiographic evaluation (12-lead ECG and 24-hour ambulatory electrocardiographic recordings) to predict electrophysiology study results in patients with undiagnosed syncope., Methods: We evaluated 421 patients with undiagnosed syncope who had an electrocardiogram (ECG), an electrophysiology study, and 24-hour ambulatory monitoring. Noninvasive testing was used to predict electrophysiology testing outcomes. Multivariable logistic regression analysis adjusting for age, sex, presence of heart disease, and left ventricular ejection fraction (LVEF) was used to assess independent predictors for sinus node disease, atrioventricular node disease, and induction of ventricular tachyarrhythmias., Results: Patients were divided into four groups: group 1, abnormal ECG and ambulatory monitor; group 2, abnormal ECG only; group 3, abnormal ambulatory monitor; and group 4, normal ECG and ambulatory monitor. The likelihood of finding at least one abnormality during electrophysiologic testing among the four groups was highest in group 1 (82.2%) and lower in groups 2 and 3 (68.1% and 33.7%, respectively). In group 4, any electrophysiology study abnormality was low (9.1%). Odds ratios (OR) were 35.9 (P < 0.001), 17.8 (P < 0.001), and 3.5 (P = 0.064) for abnormal findings on electrophysiology study, respectively (first three groups vs the fourth one). ECG and ambulatory monitor results predicted results of electrophysiology testing., Conclusion: Abnormal ECG findings on noninvasive testing are well correlated with potential brady- or/and tachyarrhythmic causes of syncope, in electrophysiology study of patients with undiagnosed syncope.

Introduction: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported., Methods and Results: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia., Conclusion: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.

Most clinicians currently rely on patient history and specific electrocardiographic criteria to establish the diagnosis of arrhythmias. However, as illustrated by this case, the physical examination-especially auscultation of the first heart sound-can also provide useful diagnostic clues.

With the increasing flexibility allowed by implantable cardioverter defibrillators that use tiered therapy, it is important to match the therapy with the arrhythmia. In this article we present scatter diagram analysis, a new computationally efficient two-channel algorithm for distinguishing monomorphic ventricular tachycardia (VT) from polymorphic ventricular tachycardia and ventricular fibrillation (VF). Scatter diagram analysis plots the amplitude from one channel versus the amplitude from another channel on a graph with a 15 x 15 grid. The fraction (percentage) of the 225 grid blocks occupied by at least one sample point is then determined. We found that monomorphic VT traces nearly the same path in space and occupies a smaller percentage of the graph than a nonregular rhythm such as polymorphic VT or VF. Scatter diagram analysis was tested on 27 patients undergoing intraoperative implantable cardioverter defibrillator testing. Passages of 4.096 seconds were obtained from rate (bipolar epicardial) and morphology (patch) leads, and digitized at 125 Hz. Scatter diagram analysis distinguished 13 episodes of monomorphic VT (28.6% +/- 4.0%) from 27 episodes of polymorphic VT or VF (48.0% +/- 8.2%) with P < 0.0005. There was overlap in only one monomorphic VT episode and one polymorphic VT or VF episode.

During ventricular fibrillation (VF), electrograms from bipolar epicardial electrodes generally appear to have little organization or structure. We sought to identify any well defined organization or structure in these signals by determining if they could be modeled as an autoregressive stochastic process with a white noise excitation during the short time period (6.5-8 s) typically used by automatic implantable defibrillators. The autoregressive model is then used to synthesize VF signals using a white noise excitation with the same probability distribution function as the estimated excitation determined from the autoregressive model for that particular true VF episode. Both the original and ten synthesized VF signals for each patient are then compared using root mean square (rms) amplitude, the number of zero crossings per second, the amplitude distribution of the signals, the rate, and percent variation of rate. The results of examining the synthesized VF waveforms indicate that the rms amplitudes are similar to the true VF waveforms. While the synthesized VF signals had higher rate, more regular RR intervals, more zero crossings per second, and spent less time at baseline than the VF signal from which they were generated, these differences are generally not significant (p > or = 0.05). The use of such synthesized VF signals may allow more thorough testing of VF detection algorithms than is possible with the present limited libraries of human VF recordings.

Background: The electrical current and energy required to terminate ventricular tachyarrhythmias are known to vary by arrhythmia: Ventricular tachycardia (VT) is generally considered to require less energy than ventricular fibrillation (VF). The hypothesis of our study was that current requirements for transthoracic termination of VT are further determined by VT rate and QRS complex morphology., Methods and Results: We prospectively studied 203 patients who received a total of 569 shocks for VT or VF by following a current-based protocol. This protocol recommended shocks for VT beginning at 18 A (70 +/- 22 J) and shocks for VF beginning at 25 or 30 A (137 +/- 52 J or 221 +/- 70 J). The ventricular tachyarrhythmias were subclassified as monomorphic VT (MVT): uniform QRS complex morphology on surface electrocardiogram and heart rate greater than 100 beats per minute; polymorphic VT (PVT): nonuniform QRS complex morphology and heart rate less than or equal to 300 beats per minute; or VF: nonuniform QRS complex morphology and heart rate greater than 300 beats per minute. We found that shocks of 18 A and 25 A for terminating MVT had success rates of 69% and 82%, respectively, whereas such low-current shocks were less successful for PVT (33% at 18 A) and for VF (19% at 18 A, 53% at 25 A). High-current shocks of 35 A and 40 A were equally successful for the three ventricular tachyarrhythmias. Subdividing MVT revealed that slower MVT (heart rate less than 200 beats per minute) had a significantly better success rate with low-current shocks of 18 A and 25 A than did faster MVT (greater than 200 beats per minute) (89% versus 72% success, p less than 0.01). Bundle branch block morphology, QRS axis, and duration of ventricular tachyarrhythmia did not alter current requirements., Conclusions: Heart rate and electrocardiographic degree of organization of ventricular tachycardia are important determinants of transthoracic energy and current requirements for cardioversion and defibrillation. Transthoracic termination of MVT requires relatively low current or energy, but PVT behaves more like VF and requires higher electrical current or energy.

Background: A reliable, noninvasive procedure to determine the location of accessory atrioventricular connections in patients with Wolff-Parkinson-White syndrome would add an important diagnostic tool to the clinical armamentarium., Methods and Results: Body surface potential mapping (BSPM) using 180 electrodes in various-sized vests and displayed as a calibrated color map was used to determine the ventricular insertion site of the accessory atrioventricular (AV) connections in 34 patients with Wolff-Parkinson-White syndrome. Attempts were made to determine the 17 ventricular insertion sites described by Guiraudon et al. All 34 patients had an electrophysiologic study (EPS) at cardiac catheterization, and 18 had surgery so the ventricular insertion sites could be accurately located using EPS at surgery. A number of physiologic observations were also made with BSPM., Conclusions: The following conclusions were drawn: 1) BSPM using QRS analysis accurately predicts the ventricular insertion site of accessory AV connections in the presence of a delta wave in the electrocardiogram; 2) the ventricular insertion sites of accessory AV connections determined by BSPM and by EPS at surgery were identical or within one mapping site (1.5 cm or less) in all but four of 18 cases; three of the four exceptions had more than one accessory AV connection, and the other had a very broad ventricular insertion; 3) BSPM and EPS locations of the accessory AV connections correlated very well in the 34 cases despite the fact that BSPM determines the ventricular insertion site and EPS determines the atrial insertion site of the accessory AV connection; 4) as suggested by the three cases of multiple accessory AV connections, EPS and BSPM may be complementary since BSPM identified one pathway and EPS identified the other (in the case with a broad ventricular insertion, BSPM and EPS demonstrated different proportions of that insertion); 5) BSPM using ST-T analysis is very much less accurate in predicting the ventricular insertion site of accessory AV connections unless there is marked preexcitation; 6) standard electrocardiography using the Gallagher grid methodology (but with no attempt at stimulating maximal preexcitation) was not as accurate as QRS analysis of BSPM in predicting the ventricular insertion site of the accessory AV connection; however, exact comparison is hampered by the different number and size of the Gallagher and Guiraudon insertion sites; 7) BSPM using QRS analysis appears to be very accurate in predicting right ventricular versus left ventricular posteroseptal accessory AV connections; 8) typical epicardial right ventricular breakthrough, indicative of conduction via the specialized AV conduction system, occurs in all patients with left ventricular free wall accessory AV connections; 9) epicardial right ventricular breakthrough was not observed in cases with right ventricular free wall or anteroseptal accessory AV connections; 10) epicardial right ventricular breakthrough can occur in the presence of posteroseptal accessory AV connections, whether right or left ventricular; and 11) the delay in epicardial right ventricular breakthrough in cases with left ventricular insertion may provide a marker to estimate the degree of ventricular preexcitation.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

It is generally assumed that if a wide QRS complex tachycardia has the same morphology on the 12-lead electrocardiogram as during sinus rhythm, the tachycardia is supraventricular. The author presents unique electrocardiographic data on four patients with QRS complex morphologies that are nearly identical during ventricular tachycardia and during sinus rhythm. The QRS complex duration during sinus rhythm was 140-180 msec and was the same as that of the tachycardia. The QRS complex morphology on the electrocardiogram was a right bundle branch block, left axis in three patients and right bundle branch block, normal axis in one patient. The mean ventricular tachycardia cycle length was 345 msec. The diagnosis of ventricular tachycardia was established by electrophysiologic testing in two patients and by atrial electrograms demonstrating AV dissociation in two patients. Thus, if the 12-lead electrocardiogram morphology of a wide QRS complex tachycardia is similar to that during sinus rhythm, it does not necessarily imply that the tachycardia is supraventricular. Ventricular tachycardia can occur with the same QRS complex morphology as occurs during sinus rhythm.

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.

Prior data pertaining to transient entrainment and associated phenomena have been best explained by pacing capture of a reentrant circuit. On this basis, we hypothesized that rapid pacing from a single site of two different constant pacing rates could constantly capture an appropriately selected bipolar electrogram recording site from one direction with a constant stimulus-to-electrogram interval during pacing at one rate, yet be constantly captured from another direction with a different constant stimulus-to-electrogram interval when pacing at a different constant pacing rate. To test this hypothesis, we studied a group of patients, each with a representative tachycardia (ventricular tachycardia, circus-movement tachycardia involving an atrioventricular bypass pathway, atrial tachycardia, and atrial flutter). For each tachycardia, pacing was performed from a single site for at least two different constant rates faster than the spontaneous rate of the tachycardia. We observed in these patients that a local bipolar recording site was constantly captured from different directions at two different pacing rates without interrupting the tachycardia at pacing termination. The evidence that the same site was captured from a different direction at two different pacing rates was supported by demonstrating a change in conduction time to that site associated with a change in the bipolar electrogram morphology at that site when comparing pacing at each rate. The mean conduction time (stimulus-to-recording site electrogram interval) was 319 +/- 69 msec while pacing at a mean cycle length of 265 +/- 50 msec, yet only 81 +/- 38 msec while pacing at a second mean cycle length of 233 +/- 51 msec, a mean change in conduction time of 238 +/- 56 msec. Remarkably, the faster pacing rate resulted in a shorter conduction time. The fact that the same electrode recording site was activated from different directions without interruption of the spontaneous tachycardia at pacing termination is difficult to explain on any mechanistic basis other than reentry. Also, these changes in conduction time and electrogram morphology occurred in parallel with the demonstration of progressive fusion beats on the electrocardiogram, the latter being an established criterion for transient entrainment.(ABSTRACT TRUNCATED AT 400 WORDS)