Electrocardiographic Appearance Research Articles

Impact of hypokalemia on Brugada syndrome: case report unveiling mechanisms beyond QT interval prolongation.

Brugada syndrome (BrS) is associated with an increased risk of sudden death caused by ventricular arrhythmias. The characteristic electrocardiographic appearance of ST-segment elevation of more than 2mm with coved-type morphology in more than 1 right precordial lead is seen. Hypokalemia is known to unmask the Brugada type-1 pattern, but its exact role and mechanisms in this context are not well understood. We report a case of first-time diagnosis of BrS in a 51-year-old man with hypokalemia 2.8mmol/L. Despite the normalization of potassium levels with potassium chloride (KCL), the Brugada type-1 pattern persisted on ECG. Interestingly, the corrected QT interval was shorter during hypokalemia (QTc 390ms) compared to when potassium levels were normal (QTc 432ms). This case highlights that hypokalemia can unmask the Brugada type-1 electrocardiographic pattern, but does not alter it once unmasked. The observed shorter QT interval during hypokalemia challenges the assumption that QT prolongation is the sole mechanism by which hypokalemia influences Brugada syndrome. This underscores the need for further research into additional mechanisms by which hypokalemia might trigger ventricular arrhythmias in Brugada syndrome.

Multifocal Atrial Tachycardia Transitioning to Atrial Fibrillation in an Octogenarian

Abstract Multifocal atrial tachycardia (MAT) is an arrhythmia frequently seen in the elderly whose prevalence increases with aging. These arrhythmias may eventually lead to more chaotic arrhythmias such as atrial fibrillation (AF) and flutter. MAT is frequently mistaken for AF in electrocardiogram (ECG). The importance of differentiating MAT from AF is that the former requires no anticoagulation and, therefore, avoids the risks associated with their administration. It is also important to realize that the elderly have multiple conditions such as senile tremors and Parkinson’s disease which may cause mechanical movement artifacts in resting ECGs mimicking cardiac arrhythmias leading to incorrect interpretation of ECGs. Educating physicians about the electrocardiographic appearance of atrial dysrhythmias and the recognition of the confounding artifacts can prevent unnecessary use of treatment which could potentially cause adverse effects in the patient.

1101 AN UNUSUAL CASE OF PHRENIC NERVE STIMULATION IN A PATIENT WITH SINGLE CHAMBER IMPLANTABLE CARDIOVERTER DEFIBRILLATOR

Abstract Background Phrenic nerve stimulation is a well-recognized complication related to cardiac implantable electronic devices, in particular with left ventricular coronary sinus pacing leads for cardiac resynchronization therapy. Case presentation We report an unusual case of symptomatic phrenic nerve stimulation due to inadvertent placement of a right ventricular defibrillation lead in coronary sinus posterior branch in a patient with heart failure with reduced ejection fraction with a recently implanted single-chamber cardioverter defibrillator. Discussion Phrenic nerve stimulation is a relatively common complication of left ventricular pacing. Inadvertent placement of a right ventricular lead in a coronary sinus branch is a rare but possible cause of phrenic nerve stimulation. Careful evaluation of intraprocedural fluoroscopic and electrocardiographic appearance of pacing and defibrillation leads during implantation may prevent inadvertent placement of a right ventricular lead in the coronary sinus.

Takotsubo Syndrome

Abstract Takotsubo syndrome occurs in 1-2% of patients admitted in the emergency department with suspicion of ST-segment elevation myocardial infarction (STEMI), over 90% being postmenopause women. Psycho-emotional or physical stress is the main trigger that causes the release of catecholamines, with an important role in the pathophysiology of Takotsubo cardiomyopathy. In most cases, supportive and symptomatic treatment is sufficient, with a dynamic follow-up of the left ventricular (LV) function. Usually, a complete recovery occurs in 3-4 weeks. We are presenting the case of a 67-year-old patient with a severe angina attack which occuredafter a major psycho-emotional stress, with an electrocardiographic appearance of an anterior STEMI and echocardiographic apical ballooning, both compatible with Takotsubo syndrome. Coronary angiography showed a muscle bridge with a systolic compression of 75% on the anterior descending artery (ADA). The evolution was marked by the occurrence of cardiogenic shock remitted under treatment, with complete recovery of LV systolic function. The particularity of the case resides in an acute coronary syndrome (ACS) after a psycho-emotional stress associated with a muscular bridge, as well as the appearance of the cardiogenic shock.

The electrocardiographic interpretation of ventricular pacing suppression algorithms in the pacemaker

Algorithms designed to reduce the right ventricular (RV) pacing burden are widely available in modern dual-chamber implantable pacing devices. These algorithms allow the atrioventricular delay for sensed ventricular events to be longer than for ventricular paced events. However, since these features are unique to pacemaker manufacturers, they often produce unfamiliar electrocardiographic (ECG) appearances that suggest pacemaker dysfunction. We describe a Vp suppression algorithm used in Biotronik dual-chamber pacemakers and implantable cardioverter-defibrillator devices.

Histologic comparison in two Doberman pinschers with a dilated cardiomyopathy phenotype

Idiopathic dilated cardiomyopathy (DCM) is a common acquired cardiac disease in large breed dogs with a high prevalence in Doberman pinschers. It is characterized histologically by attenuated wavy fibers and fatty infiltration with degeneration. The phenotypic appearance of DCM includes ventricular dilation with systolic dysfunction and ventricular arrhythmias. These changes can be caused by other etiologies, including infectious, toxic, metabolic, and nutritional deficiencies. Chagas disease is the result of an infection with the protozoal parasite, Trypanosoma cruzi, transmitted by an insect vector. Histopathology of the myocardium is characterized by inflammation, fibrosis, and pseudocysts containing T. cruzi amastigotes. Differentiating idiopathic DCM from infectious myocarditis can be challenging when the clinical presentation and diagnostic test results are similar in affected dogs. We present thoracic radiographs, echocardiography, and post-mortem histopathology images obtained from two Doberman pinschers with similar signalment, clinical presentation, and electrocardiographic and echocardiographic appearance but with different appearing radiographs and different etiologies for their heart disease, one with idiopathic DCM and one with myocarditis attributed to Chagas disease, to highlight the value of considering alternative etiologies for DCM to guide additional clinical evaluation and owner counseling.

Electrocardiographic interpretation of pacemaker algorithms enabling minimal ventricular pacing

Cardiac pacing from the apex of the right ventricle has been shown to result in left ventricular dysfunction, atrial fibrillation, and increased mortality. To counter these effects, one of the strategies developed is avoidance of ventricular pacing when not necessary, using programmable algorithms to minimize ventricular pacing. Seven algorithms are available from 5 manufacturers. Four of the manufacturers have mode conversion algorithms that pace AAI(R) but, in the presence of failed atrioventricular (AV) conduction, demonstrate algorithm-offset and convert to DDD(R) with ventricular pacing. Three manufacturers do not have mode conversion but rather AV extension to encourage AV conduction. Each of these algorithms has a unique design and, when ventricular pacing is present, will regularly schedule conduction testing to encourage AV conduction and hence algorithm-onset. All of these algorithms seem to violate the rule of AV conduction by allowing the AV delay for sensed ventricular events to be longer than for ventricular paced events. The result is frequently bizarre electrocardiographic (ECG) appearances that often are unique to the company's algorithm but also suggest pacemaker malfunction. This review highlights and illustrates the features of these algorithms as they appear on ECG, and discusses other situations that result in unintended ventricular pacing.

Electrocardiographic appearance of aortic stenosis before and after aortic valve replacement.

So far, the specific appearance of QRS complex, ST-segment, and T wave was observed in aortic stenosis (AS). S-wave dynamic change in leads V1 -V3 was not reported in AS. In a single-center, prospective study, we included a total number of 1.175 patients who underwent surgical aortic valve replacement (AVR). We conducted 3-year gathering of patients with symptomatic and asymptomatic severe AS, and separated them by hemodynamic stability into groups A and B, through EFLV (of more or less than 50%), AVA (of more or less than 0.9cm2 ), PG (between 55 and 75mm Hg or over 75mm Hg), and end-diastolic LV dimension (of more or less than 56mm). We evaluated the impact of S-wave magnitude in right precordial leads before and after AVR in all patients. We followed S-wave changes in electrocardiogram altogether with hemodynamic measurements derived from echocardiography. Analysis of echocardiographic parameters, measured in patients before surgery, did not show statistical significance between asymptomatic and symptomatic group. The statistical significance was observed in the change in S-wave magnitude in the right precordial leads in both subsets of patients before AVR. We found statistically significant predictive value of S-wave magnitude in leads V2 -V3 for dependent variables PG and end-diastolic LV dimension. S-wave changes in right precordial leads can predict increase in PG and critical narrowing of AVA, suggestive of timely referral for AVR.

Wolff-Parkinson-White syndrome: lessons learnt and lessons remaining.

The Wolff-Parkinson-White pattern refers to the electrocardiographic appearance in sinus rhythm, wherein an accessory atrioventricular pathway abbreviates the P-R interval and causes a slurring of the QRS upslope - the "delta wave". It may be asymptomatic or it may be associated with orthodromic reciprocating tachycardia; however, rarely, even in children, it is associated with sudden death due to ventricular fibrillation resulting from a rapid response by the accessory pathway to atrial fibrillation, which itself seems to result from orthodromic reciprocating tachycardia. Historically, patients at risk for sudden death were characterised by the presence of symptoms and a shortest pre- excited R-R interval during induced atrial fibrillation <250 ms. Owing to the relatively high prevalence of asymptomatic Wolff-Parkinson-White pattern and availability of catheter ablation, there has been a need to identify risk among asymptomatic patients. Recent guidelines recommend invasive evaluation for such patients where pre-excitation clearly does not disappear during exercise testing. This strategy has a high negative predictive value only. The accuracy of this approach is under continued investigation, especially in light of other considerations: Patients having intermittent pre-excitation, once thought to be at minimal risk may not be, and the role of isoproterenol in risk assessment.

Cardiac Arrest and Resuscitation

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.

Case Scenario

The long QT syndrome (LQTS) is characterized by prolonged ventricular repolarization, the electrocardiographic appearance of long QT intervals, an atypical polymorphic ventricular tachycardia known as torsades de pointes (TdP), and an increased risk for sudden cardiac death. Patients with LQTS can suffer severe cardiac events resulting in syncope, seizures, and sudden cardiac death during times of physical and emotional stress and when exposed to certain pharmacological agents. The perioperative management of patients with LQTS has been reviewed1,2; however, the individual risk posed by exposure to perioperative and anesthetic medications and interventions has not been quantified by prospective studies.

Introduction to the Series on Computational Approaches to Cardiac Arrhythmias

Of all the cardiac arrhythmias seen in clinical practice, atrial fibrillation (AF) and ventricular tachycardia/fibrillation (VT/VF) are among the leading causes of morbidity and mortality in the developed world. AF is the most common sustained arrhythmia and is associated with an increased risk of stroke, heart failure, dementia, and death.1–3 In developed nations overall prevalence of AF is 0.9% and the number of people affected is projected to more than double over the next 2 decades.3,4 VT/VF is the most important immediate cause of sudden cardiac death (SCD). Incidence of SCD is estimated to be 4 to 5 million cases per year worldwide.5,6 Thus arrhythmias and SCD are among the most significant manifestations of cardiovascular diseases worldwide, but their underlying mechanisms remain elusive. Arrhythmogenic substrates may be established by ischemia, infarction, heart failure and genetic mutations, all of which may cause inflammation, extracellular matrix remodeling, interstitial fibrosis, fatty infiltration, and changes in the 3-dimensional cellular architecture of the working myocardium.7,8 Over the last 17 years, the study of the molecular genetic basis of monogenic cardiac rhythm disorders, together with characterization of functional expression and biophysical properties of mutant channels from patients with inheritable ion channel diseases, has significantly advanced our understanding of the molecular basis of cardiac arrhythmias.9 Yet, this clearly has not been sufficient. Despite such advances, predictable prevention of AF or VF is currently not possible and the development of effective antiarrhythmic pharmacological agents has been extremely difficult. Not all questions related to arrhythmia mechanisms are directly answerable by reductionist experiments such as DNA sequencing or patch clamping. There is a hierarchy of questions whose levels are determined by the generality of the answers sought. Thus the question of what a mutation in an ion …

Case Scenario

The long QT syndrome (LQTS) is characterized by prolonged ventricular repolarization, the electrocardiographic appearance of long QT intervals, an atypical polymorphic ventricular tachycardia known as torsades de pointes (TdP), and an increased risk for sudden cardiac death. Patients with LQTS can suffer severe cardiac events resulting in syncope, seizures, and sudden cardiac death during times of physical and emotional stress and when exposed to certain pharmacological agents. The perioperative management of patients with LQTS has been reviewed1,2; however, the individual risk posed by exposure to perioperative and anesthetic medications and interventions has not been quantified by prospective studies.

Cardiac Resuscitation

Over 1,000 people suffer sudden cardiac death every day in the United States. About half occur in the hospital, the remainder occurring in the home, outpatient medical environments, or public spaces. The ultimate goal of cardiac resuscitation is survival with full neurologic recovery. Interventions that have the greatest potential to provide this outcome are often those interventions that can be performed by trained laypersons. Delay in the initiation of compressions in a cardiac arrest is one of the leading predictors of mortality. This chapter deliberately opens with a discussion of one of the most vital, yet relatively under-appreciated aspects of cardiac resuscitation—teamwork. Following an overview of cardiac arrest, the chapter covers epidemiology and recognition of cardiac arrest, then activation of the emergency response system. Chest compressions, defibrillation and airway management are discussed, then end-tidal CO2, vascular access, rhythm analysis during cardiac arrest, and drugs used during cardiac resuscitation. The chapter concludes with a look at postresuscitation care, special considerations in cardiac arrest, and future directions. Figures include the foundations of cardiac resuscitation, a management algorithm for the initial treatment of cardiac arrest, coronary perfusion pressure as a function of time, an impedance threshold device incorporated into a bag-valve mask, a colorimetric CO2 detector, four basic phases of a capnogram, sample capnographs, a battery-powered intraosseous drill, electrocardiogram readouts of ventricular arrhythmias, a sonogram of large pericardial effusion, and electrocardiographic appearance of varying degrees of hyperkalemia. Tables summarize recommendations from the American Heart Association, the components of optimal and suboptimal chest compressions, and underlying causes of nonshockable rhythms and their management. This chapter contains 11 highly rendered figures, 3 tables, 138 references, 5 MCQs.

A Neonate with Long QT Syndrome, Refractory Ventricular Arrhythmias, and Lidocaine Toxicity

Long QT syndrome is characterized by electrocardiographic appearance of long QT intervals and propensity to polymorphic ventricular tachycardia. Aggressive anticipatory clinical management is required for a good outcome, especially in the symptomatic neonate. We present a neonate with a compound mutation with refractory ventricular tachycardia that necessitated multimodal pharmacotherapy with lidocaine, esmolol, and amiodarone along with ventricular pacing. Despite normal serum lidocaine levels, complex pharmacokinetic interactions resulted in presumed neurotoxicity due to lidocaine. This report discusses the implications and challenges of management of a neonate with compound long mutations.

Atypical Electrocardiographic Features of Cavotricuspid Isthmus‐Dependent Atrial Flutter Occurring during Left Atrial Fibrillation Ablation

Patients who have undergone percutaneous catheter ablation for atrial fibrillation (AF) may develop cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL), which can occur either spontaneously during left atrial (LA) ablation for AF or by induction from sinus rhythm during the procedure. The electrocardiographic (ECG) characteristics of CTI-dependent AFL occurring during LA ablation have not been described. The purpose of this study was to describe the ECG features of CTI-dependent AFL occurring during percutaneous LA catheter ablation for AF. Of 223 patients presenting for first AF ablation at our institution between May 2004 and February 2008, 20 patients (9%) developed CTI-dependent AFL during LA ablation for AF. CTI-dependent AFL developed spontaneously in 4 patients (20%) and was induced in 16 patients (80%). Among these 20 patients, 3 (15%) had typical ECG patterns and 17 (85%) had atypical ECG patterns. Flutter waves in the inferior leads were biphasic in 10 patients (50%), downward in 3 patients (15%), positive in 3 patients (15%), and not fitting the above classifications in 4 patients (20%). There was no statistically significant association between AFL pattern and LA size, left ventricular ejection fraction, total ablation time, duration of prior AF, or type of prior AF. A majority of patients with CTI-dependent AFL occurring during LA ablation have atypical ECG patterns. Biphasic flutter waves in the inferior leads are common ECG features, occurring in one-half of patients. Right atrial CTI-dependent AFL should be suspected even if the ECG appearance is atypical.

Biexcitability and Early Afterdepolarization-Mediated Cardiac Arrhythmias

Under normal conditions in ventricular tissue, both planar wave propagation and spiral wave reentry are mediated by Na current (INa)-mediated depolarization. Under diseased conditions in which repolarization reserve is reduced, however, secondary depolarizations can occur in the plateau or repolarizing phase of the action potential (AP) due to reactivation of the L-type calcium current (ICa,L), known as early afterdepolarizations (EADs). Under these conditions, we observed a novel behavior in which both INa-mediated spiral wave reentry and ICa,L-mediated spiral wave reentry coexisted in the same homogeneous tissue. INa-mediated spiral waves were similar to those observed under normal condition, with high rotation frequency (∼10 Hz) and nearly full repolarization between beats. ICa,L-mediated spiral waves, however, rotated much slower (2-3 Hz) with membrane voltage remaining above −40 mV, at which INa is inactivated. We call this novel property of an excitable medium biexcitability. In heterogeneous tissue with transmural AP gradients, pause-induced EADs initiated ICa,L-mediated rotors from the M-cell region. The resulting arrhythmia was characterized by co-existing ICa,L- and INa-mediated wavefronts, with a frequency and electrocardiographic appearance resembling Torsades de Pointes. The arrhythmia either terminated spontaneously or degenerated to ventricular fibrillation. We propose biexcitability as a novel mechanism of Torsades de Pointes in long QT syndromes.

A cardiac magnetic resonance imaging study of electrocardiographic Q waves in type 2 diabetes: The Fremantle Diabetes Study

To investigate the evolution and significance of Q waves in type 2 diabetes, we studied 36 patients of mean (±S.D.) age 69.9 ± 7.1 years from the longitudinal observational Fremantle Diabetes Study (FDS). All had (i) neither history/symptoms of coronary heart disease (CHD) nor pathological Q waves at FDS recruitment between 1993 and 1996, (ii) five consecutive annual assessments by FDS close-out in 2001, and (iii) contrast-enhanced cardiac magnetic resonance imaging in 2005. At this latter assessment, there were (i) 9 with no history of CHD or Q waves during follow-up (Group 1), (ii) 13 with Q waves on ≥1 electrocardiogram but no CHD history/symptoms (Group 2), and (iii) 14 with CHD history/symptoms irrespective of electrocardiographic status (Group 3). Of 20 episodes of new Q waves in 17 Group 2 or Group 3 patients during FDS follow-up, 17 (85%) resolved within 2 years. A myocardial infarction (MI) was detected by CMR in three patients (8.3%; one subendocardial in Groups 1 and 3, one non-full-thickness in Group 3) but these did not correlate with electrocardiographic appearances. Q waves may have unreliable pathological significance in type 2 diabetes, including as a marker of silent MI.

Parkinson’s tremor mimicking ventricular tachycardia

We report the case of an elderly lady with Parkinson's tremor whose electrocardiographic (ECG) appearance simulated ventricular tachycardia. As a result she underwent unnecessary clinical intervention. We also highlight the difficulty in correctly identifying a tremor-induced ECG artefact with regard to Parkinson's disease, due to the diverse range of possible clinical scenarios presented by patients with this condition.

An Unusual Accessory Pathway: Anteroseptal to Ventricular Outflow Region Connection

Accessory pathways are typically located along the left or right atrioventricular junction. Distinct ventricular pre-excitation patterns determined by surface electrocardiography can provide reasonable pathway localization prior to invasive mapping and catheter ablation. We report an accessory pathway producing an unusual electrocardiographic appearance suggestive of ventricular outflow region pre-excitation. Pacing maneuvers and standard intracardiac recordings confirmed an atrial insertion immediately adjacent to the atrioventricular (AV) node and supported a ventricular insertion at the outflow tract region well away from the AV junction. The elimination of pathway conduction was achieved with radiofrequency (RF) energy at the atrial insertion after successful ice mapping excluded AV block at the target site. This is the second such pathway observed at our institution over a 20-year period.