Restructuring Electrophysiology During the COVID-19 Pandemic: A Practical Guide From a New York City Hospital Network.

The coronavirus disease 2019 crisis is a global pandemic of a novel infectious disease with far-ranging public health implications. With regard to cardiac electrophysiology (EP) services, we discuss the "real-world" challenges and solutions that have been essential for efficient and successful (1) ramping down of standard clinical practice patterns and (2) pivoting of workflow processes to meet the demands of this pandemic. The aims of these recommendations are to outline: (1) essential practical steps to approaching procedures, as well as outpatient and inpatient care of EP patients, with relevant examples, (2) successful strategies to minimize exposure risk to patients and clinical staff while also balancing resource utilization, (3) challenges related to redeployment and restructuring of clinical and support staff, and (4) considerations regarding continued collaboration with clinical and administrative colleagues to implement these changes. While process changes will vary across practices and hospital systems, we believe that these experiences from 4 different EP sections in a large New York City hospital network currently based in the global epicenter of the coronavirus disease 2019 pandemic will prove useful for other EP practices adapting their own practices in preparation for local surges.

Acquired Long QT Syndrome and Electrophysiology of Torsade de Pointes.

Congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS remains the domain of cardiologists, cardiac electrophysiologists and specialised centres, the much more frequently acquired LQTS is the domain of physicians and other members of healthcare teams required to make therapeutic decisions. This paper reviews the electrophysiological mechanisms of acquired LQTS, its ECG characteristics, clinical presentation, and management. The paper concludes with a comprehensive review of the electrophysiological mechanisms of torsade de pointes.

Acquired long QT syndrome and torsade de pointes.

Since its initial description by Jervell and Lange-Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS continues to remain the domain of cardiologists, cardiac electrophysiologists, and specialized centers, the by far more frequent acquired drug-induced LQTS is the domain of all physicians and other members of the health care team who are required to make therapeutic decisions. This report will review the electrophysiological mechanisms of LQTS and torsade de pointes, electrocardiographic characteristics of acquired LQTS, its clinical presentation, management, and future directions in the field.

Sudden Cardiac Death in Ischemic Heart Disease: Pathophysiology and Risk Stratification.

Sudden cardiac death (SCD) accounts for approximately 360,000 deaths annually in the United States. Ischemic heart disease is the major cause of death in the general adult population. SCD can be due to arrhythmic or nonarrhythmic cardiac causes. Arrhythmic SCD may be caused by ventricular tachyarrhythmia or pulseless electrical activity/asystole. This article reviews the most recent pathophysiology and risk stratification strategies for SCD, emphasizing electrophysiologic surrogates of conduction disorder, dispersion of repolarization, and autonomic imbalance. Factors that modify arrhythmic death are addressed.

Congenital Long QT syndrome and torsade de pointes.

Since its initial description by Jervell and Lange-Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. A prolonged QT interval in the surface electrocardiogram is the sine qua non of the LQTS and is a surrogate measure of the ventricular action potential duration (APD). Congenital as well as acquired alterations in certain cardiac ion channels can affect their currents in such a way as to increase the APD and hence the QT interval. The inhomogeneous lengthening of the APD across the ventricular wall results in dispersion of APD. This together with the tendency of prolonged APD to be associated with oscillations at the plateau level, termed early afterdepolarizations (EADs), provides the substrate of ventricular tachyarrhythmia associated with LQTS, usually referred to as torsade de pointes (TdP) VT. This review will discuss the genetic, molecular, and phenotype characteristics of congenital LQTS as well as current management strategies and future directions in the field.

2017 ISHNE-HRS expert consensus statement on ambulatory ECG and external cardiac monitoring/telemetry.

Ambulatory ECG (AECG) is very commonly employed in a variety of clinical contexts to detect cardiac arrhythmias and/or arrhythmia patterns which are not readily obtained from the standard ECG. Accurate and timely characterization of arrhythmias is crucial to direct therapies that can have an important impact on diagnosis, prognosis or patient symptom status. The rhythm information derived from the large variety of AECG recording systems can often lead to appropriate and patient-specific medical and interventional management. The details in this document provide background and framework from which to apply AECG techniques in clinical practice, as well as clinical research.

2017 ISHNE-HRS expert consensus statement on ambulatory ECG and external cardiac monitoring/telemetry.

Ambulatory ECG (AECG) is very commonly employed in a variety of clinical contexts to detect cardiac arrhythmias and/or arrhythmia patterns which are not readily obtained from the standard ECG. Accurate and timely characterization of arrhythmias is crucial to direct therapies that can have an important impact on diagnosis, prognosis or patient symptom status. The rhythm information derived from the large variety of AECG recording systems can often lead to appropriate and patient-specific medical and interventional management. The details in this document provide background and framework from which to apply AECG techniques in clinical practice, as well as clinical research.

Cardiac Rhythm Device Threshold Testing Via Pulse Oxymetry.

Threshold testing of cardiac rhythm devices is essential to monitoring the proper functioning of such devices (1). However, the currently method of applying multiple ECG leads to the patient is burdensome and time consuming (2). We are presenting a completely new way to perform cardiac rhythm device threshold testing using pulse oximetry. Twenty patients, with varying cardiac rhythm devices and pacing modes, were enrolled and had their atrial and ventricular thresholds tested. A comparison was made between simultaneous threshold determinations via the standard EGM based method and the new pulse oximetry based method. 75% of the ventricular threshold tested and 58% of the atrial thresholds tested were the same with the two testing methods. The remainder of the tests (25% of ventricular threshold and 42% of the atrial threshold tests) varied by +0.25 V. This study shows that pulse oximetry based testing is an accurate, reliable, and easy way to perform cardiac rhythm device threshold testing and may complement traditional methods to perform such tests in the future.

Ambulatory electrocardiographic monitoring between artifacts and misinterpretation, management errors of commission and errors of omission.

BACKGROUND: The aim of the study is to contrast the role of conventional ambulatory electrocardiographic monitoring (AEM) artifacts with a less emphasized problem with potentially more serious implications, that is, the failure to recognize, and therefore misinterpret, a genuine arrhythmia episode in the AEM recording. METHODS: The study material included 500 Holter recordings and 500 recordings from the cardiac telemetry unit. RESULTS: Electrocardiographic (ECG) artifacts were more common in telemetry recordings (5.6%) compared to Holter recordings (4%) for a total of 4.8%. There were 35 examples of misinterpretation of AEM recordings (3.5%). These were significantly more common in telemetry recordings (2.6%) compared to Holter recordings (0.9%). The most common ECG artifacts were examples of pseudo ventricular tachyarrhythmia (VT). The majority of misinterpretation (26 of 35 examples) were fast supraventricular tachyarrhythmias with aberrant QRS (including six examples of atrial flutter with periods of 1:1 atrioventricular conduction) that were misdiagnosed as ventricular VT. Other examples were misinterpretation of arrhythmic episodes consistent with sick sinus syndrome, pacemaker malfunction, and long QT syndrome. Only 5 of 48 examples of AEM artifacts resulted in management errors of commission or errors of omission compared to all 35 examples of misinterpretation. CONCLUSIONS: Compared to conventional artifacts in AEM, misinterpretation of nonartifactual arrhythmic episodes consistently resulted in management errors. Misinterpretation was significantly more common with telemetry recordings compared to Holter ECG. This highlights the need for more appropriate training of the entire clinical team in charge of the management of the cardiac telemetry unit.

Electrolyte disorders and arrhythmogenesis.

Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mechanisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of electrolyte disorders. Potassium (K⁺) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most significant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and non cardiac drugs are known to suppress the HERG K⁺ channel and hence the I(K), and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricular tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia depends on serum K⁺ level. At 5.5-7.0 mmol/L K⁺, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K⁺, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca⁺⁺) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathyroidism, results in shortening of both intervals. Although magnesium is the second most abudent intracellular cation, the significance of magnesium disorders are controversial partly because of the frequent association of other electrolyte abnormalities. However, IV magnesium by blocking the L-type Ca(⁺⁺) current can successfully terminate TdP VT without affecting the prolonged QT interval. Finally, despite the frequency of sodium abnormalities, particularly hyponatremia, its EP effects are rarely clinically significant.

Improved activation time assignment of unipolar electrograms from ischemic canine epicardium.

AIMS: The present study attempts to develop an objective, statistically based set of criteria for activation time determination from unipolar electrograms (U-EGMs) using a standard of activation related to biophysical theory. METHODS: A high-resolution assembly of U-EGMs obtained from the epicardial surface of the canine postinfarction heart were analyzed in order to achieve the best prediction of local versus distant activation. An activation time standard (ATS) consisted of three properties: (1) propagation of activation, evidenced by a linear temporal shift of waveforms from closely spaced U-EGMs with little or no decay in amplitude; (2) cycle length-dependent changes of those propagating waveforms; and (3) evidence of electrotonic deflections, seen as nonpropagating potentials having decaying amplitude with distance. RESULTS: A number of U-EGM features were calculated and subjected to analysis by comparing their occurrence with the ATS. A discriminant function analysis incorporating multiple features (Voltage, -dV/dt and Ratio) of major U-EGM deflections improved prediction of activation time of complex fractionated EMGs from ischemic canine epicardium to 90%. CONCLUSION: A unique discriminant function based on sound biophysical principles markedly improved prediction of activation time of complex U-EGMs from ischemic canine epicardium. A computerized version of the algorithm could be developed to provide more accurate activation maps for both basic and clinical use.

A His bundle extrasystole can both induce and reverse 2:1 atrioventricular block.

An 84 year-old man with history of recurrent dizziness presented with first degree atrio-ventricular block (1° AVB) and periods of 2:1 AVB. An electrophysiological study revealed a predominant 1:1 AV conduction with markedly prolonged AH interval and frequent His bundle extrasystoles (H). A properly timed H could induce periods of 2:1 AV nodal block and 1:1 AV conduction could only resume following another properly timed H. Procainamide suppressed H. However, because of persistence of the patient symptoms, a permanent pacemaker was eventually inserted. The case illustrates a hitherto not described manifestation of H.

His bundle extrasystoles revisited: the great electrocardiographic masquerader.

A 74-year-old man with past history of near syncope presented with frequent periods of second-degree atrioventricular block (2° AVB). An electrophysiological study revealed prolonged atrial-His and His-ventricular (HV) intervals and frequent His bundle (H) extrasystoles. The latter manifested in the surface electrocardiogram as premature atrial, junctional, or ventricular beats, as well as 2° AVB that mimicked Wenckebach or Mobitz II block. Procainamide markedly suppressed H extrasystole. However, because of the presence of prolonged HV interval and history of presyncope, a permanent pacemaker was inserted. The case illustrates the varied manifestation of H extrasystole and presents guidelines for management.

Pathophysiology, risk stratification, and management of sudden cardiac death in coronary artery disease.

Management of sudden cardiac death (SCD) is undergoing radical change in direction. It is becoming increasingly appreciated that besides depressed left ventricular systolic function and the conventional risk stratification tools, new markers for plaque vulnerability, enhanced thrombogenesis, specific genetic alterations of the autonomic nervous system, cardiac sarcolemmal and contractile proteins, and familial clustering may better segregate patients with atherosclerotic coronary artery disease (CAD) who are at high risk of SCD from those who may suffer from nonfatal ischemic events. Better understanding of pathophysiologic processes such as post-myocardial infarction remodeling, the transition from compensated hypertrophy to heart failure, and the increased cardiovascular risk of CAD in the presence of diabetes or even a pre-diabetic state will help to improve both risk stratification and management. The rapidly developing fields of microchips technology, and proteomics may allow rapid and cost-effective mass screening of multiple risk factors for SCD. The ultimate goal is not only to change the current direction of management strategy of SCD away from increased ICD utilization, but to identify novel methods for risk stratification, risk modification, and prevention of SCD that could be applied to the general public at large.

Atrial flutter with spontaneous 1:1 atrioventricular conduction in adults: an uncommon but frequently missed cause for syncope/presyncope.

AIMS: To compare patients with atrial flutter (AFl) and 1:1 atrioventricular conduction (AVC) with patients with AFl and higher AVC. METHODS: The characteristics of 19 patients with AFl and 1:1 AVC (group A) were compared with those of 116 consecutive patients with AFl and 2:1 AVC or higher degree AV block (group B). RESULTS: Age, gender, and left ventricular function were similar in the two groups. In group A versus group B, more patients had no structural heart disease (42% vs 17%, P < 0.05) and syncope/presyncope (90% vs 12%, P < 0.05). The AFl cycle length (CL) in group A was longer than in group B (265 +/- 24 ms vs 241 +/- 26 ms, P < 0.01). The transition from AFl with 1:1 to 2:1 AVC or vice versa was associated with small but definite changes in AFl CL, which showed larger variations in response to sympathetic stimulation. In group A patients who were studied off drugs, the atrial-His interval was not different from group B, but maximal atrial pacing rate with 1:1 AVC was faster. In group A, five patients were misdiagnosed as ventricular tachyarrhythmias, and three with a defibrillator received inappropriate shocks. Four patients had ablation of AVC and six had ablation of AFl circuit. CONCLUSIONS: The main difference between groups A and B may be an inherent capacity of the AV node for faster conduction, especially in response to increased sympathetic tone. The latter affects not only AVC but also the AFl CL. One should be aware of the different presentations of AFl with 1:1 AVC to avoid misdiagnosis/mismanagement and to consider the diagnosis in patients with narrow or wide QRS tachycardia and rates above 220/min.

Prolonged transient atrial electrical silence following termination of chronic atrial tachyarrhythmias.

INTRODUCTION: Atrial standstill is a rare heterogeneous arrhythmia characterized by electrical and mechanical standstill and electrical inexcitability. A long-lasting progressive form is seen with cardiac and neuromuscular diseases, and a familial or idiopathic form may have a genetic basis. A transient form was described secondary to drug intoxication, electrolyte imbalance, cardiac inflammation, and ischemia. METHODS: We investigated three patients with long-standing atrial tachyarrhythmia (AT) (atrial flutter in two, and focal atrial tachycardia in one). All patients underwent a complete electrophysiological study with mapping of right and left atrial activity and radiofrequency ablation (RF Abl) of AT. RESULTS: Following RF Abl of AT, all three patients manifested transient atrial electrical silence in the absence of known reversible causes. Atrial electrical silence was observed when, following AT termination, an escape atrioventricular (AV) junctional rhythm (in two patients) and an escape VVI pacemaker rhythm (in one patient) showed transient ventriculo-atrial (VA) conduction block (up to 30 seconds). A dominant sinus rhythm was observed to return 30 minutes, 90 minutes, and 12 hours, respectively, in the three patients. Two patients received a dual chamber pacemaker and a decision was made not to upgrade the patient with VVI pacemaker. DISCUSSION AND CONCLUSIONS: The present report expands the spectrum of the syndrome of atrial standstill and raises interesting questions regarding possible electrophysiologic mechanism(s) of prolonged post overdrive atrial standstill. The report suggests that chronic overdrive of sinus and subsidiary atrial pacemakers may result in calcium overloading of cardiac cells, which is known to cause suppression of pacemaker activity as well as increased intracellular resistance. These mechanisms can possibly result in either prolonged suppression of sinus and atrial pacemaker activity and/or pacemaker exit block.

Cardiac resynchronization therapy: a review of proarrhythmic and antiarrhythmic mechanisms.

Available evidence supports the hypothesis that cardiac resynchronization therapy (CRT) results in favorable structural as well as electrical remodeling. Electrical remodeling seems to be related, to a large extent, to structural remodeling, usually referred to as reverse remodeling of left ventricular (LV) dysfunction. This can lead to amelioration of the arrhythmogenic substrate associated with depressed LV systolic function and heart failure. However, a direct electrophysiological effect due to favorable remodeling of repolarization with reduction of the dispersion of repolarization cannot be ruled out. On the other hand, in a small subgroup of patients, CRT could increase the dispersion of repolarization and induce malignant ventricular tachyarrhythmias. Clinical trials have consistently shown improved outcome with CRT-defibrillators (CRT-D) and more trials have demonstrated the benefits of the defibrillator in the population with depressed LV function. However, some physicians argue that implanting the less expensive and less complicated CRT-pacemaker (CRT-P) may be appropriate in certain groups of patients. Before this position is accepted, it is imperative that criteria for the selection of this group of patients with presumably low risk for sudden arrhythmic death as well as the proarrhythmic effect of CRT be clearly defined.

Electrophysiologic effects of carvedilol: is carvedilol an antiarrhythmic agent?

The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks beta(1)-, beta(2)-, and alpha(1)- adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its beta-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance.