Typical Electrocardiogram Pattern Research Articles

Evaluation of a new treadmill exercise protocol to unmask type 1 Brugada electrocardiographic pattern: can we improve diagnostic yield?

High precordial leads (HPL) on the resting electrocardiogram (ECG) are widely used to improve diagnostic detection of type 1 Brugada ECG pattern (Br1ECGp). A parasympathetic activation marks the initial recovery phase of treadmill stress testing (TET), and this can be useful for detecting the typical ECG pattern. Our study aimed to evaluate the role of a new HPL-treadmill exercise testing (TET) protocol in detecting Br1ECGp fluctuation compared to resting HPL-ECG. 74 out of 163 patients of a Brugada syndrome (BrS) Brazilian cohort (GenBra Registry) underwent exercise testing with HPL-TET protocol. Precordial leads were displayed in strategic positions in the right and left parasternal spaces. The step-by-step analysis included ECG classification (as presence or absence of Br1ECGp) in standard vs. HPL leads placement in the following sequences: resting phase, maximal exercise, and the passive recovery phase (including 'quick lay down'). For heart rate recovery (HRR) measurements and comparisons, a Student's t-test was applied. McNemar tests compared the detection of Br1ECGp. The significance level was defined as P < 0.05. Fifty-seven patients (57/74; 77%) were male, the mean age was 49.0 ± 14, 78.4% had spontaneous BrS, and the mean Shanghai score was 4.5. The HPL-TET protocol increased Br1ECGp detection by 32.4% against resting HPL-ECG (52.7% vs. 20.3%, P = 0.001) alone. Stress testing using HPL with the passive recovery phase in the supine position offers an opportunity to unmask the type 1 Br1ECGp, which could increase the diagnostic yield in this population.

Frontier and hotspot evolution in Brugada syndrome: A bibliometric analysis from 2002 to 2022.

Brugada syndrome (BrS) is a genetic disorder characterized by a typical electrocardiogram pattern and predisposition to arrhythmias and sudden cardiac death. Despite our considerably evolved understanding of BrS, no bibliometrics have been performed in this research field. We aimed to analyze and visualize the characteristics of the scientific outputs, topical evolutions, and research trends of BrS over the past 2 decades using bibliometric analysis. The literature associated with BrS was retrieved from the Science Citation Index Expanded of the Web of Science Core Collection database. Acquired data were then visually analyzed using CiteSpace and VOSviewer. 3042 qualifying records were included in the final analysis. The publication outputs increased over time. The United States was the leading country in the BrS research. The University of Amsterdam (Netherlands) was the most prolific and influential institution. Pedro Brugada, Arthur Wilde, and Charles Antzelevitch exerted notable publication impact and made the most significant contributions in the field of BrS. Heart Rhythm had the highest outputs and Circulation was the most influential journal. Bundle branch block, ST-segment elevation, mechanism, management, right precordial lead, and guideline were the keywords with the strongest citation burst. Research on BrS is prosperous. Keywords and co-citation analysis revealed that the mechanism, diagnosis, risk stratification, and management of BrS were the research hotspots. Besides, the underlying pathophysiology, novel therapies, and personalized risk assessment might be the emerging trends of future research.

409 Not all ST elevation are myocardial infarction: a lesson learned from ‘spiked helmet sign’

Abstract Aims ST segment elevation is an electrocardiogram (ECG) finding first of all suggestive of acute coronary syndrome (ACS). However, there are other causes of ST segment elevation that seem to not have any relationship with coronary artery disease (CAD). One of these is the so-called ‘Spiked Helmet Sign’ (SHS), an ECG pattern characterized by upslope of ST segment before R wave onset that is reported to be found in critical illness and is associated with negative outcomes. Methods and results A 14-years-old boy came comatose (Glasgow Coma Scale = 4) to the Emergency Room after being run over by a car. He was immediately intubated and mechanically ventilated. Baseline ECG was reported to be normal, showing an incomplete right bundle branch block and a slightly prolonged QTc interval. CT-scan showed subarachnoid haemorrhage and multiple skull fractures requiring decompressive craniectomy. During hospitalization the patient developed marked hypotension complicated by rise of inflammation indexes and 12 lead ECG revealed new-onset of diffuse ST-segment elevation with spike-and-dome appearance mainly in lateral precordial leads, while lead II and V2 didn’t show any ST-segment alteration. Transthoracic echocardiogram was reported to be normal. Due to critical conditions and low likelihood of CAD, angiography wasn’t performed. The clinical course was worsened by occurrence of hyperkalaemia, acute kidney injury, and multiple episodes of ventricular tachycardia evolving in pulselessness electrical activity which required advanced life support. The patient subsequently died due to multi-organ failure, without the possibility of escalation therapy due to his status. SHS is an emerging ECG sign that is reported to be associated with critical conditions (mechanical ventilation, sepsis, bowel perforation) and in the majority of cases it is not related to CAD. It usually occurs in inferior leads (especially in case of abdominal disease) and in precordial leads (pneumothorax, aortic dissection, mechanical ventilation). Our patient had features consistent with previous cases reported in literature and, even if he experienced several episodes of cardiac arrest and blood exams revealed elevated values of cardiac troponin, the typical ECG pattern and the normal echocardiogram suggest SHS instead of ACS, avoiding unnecessary percutaneous coronary intervention. As reported in literature, even if in our case the appearance of this sign was associated with poor prognosis. Conclusions SHS mainly occurs in critically ill patients and is associated with death and poor outcomes. The potential pathophysiological mechanisms are still unclear. It is important to promptly recognize this pattern and differentiate between other causes of ST-segment elevation to select the appropriate therapy according to the setting. This is the first case-report among Italian hospitals of SHS.

217 Why it is important to recognize Brugada syndrome in athletes: a case report

Abstract Aims The Brugada syndrome (Brs) is an inherited disorder associated with risk of ventricular fibrillation and sudden cardiac death in a structurally normal heart. The purpose of this case presentation was to spread awareness about this condition, highlight the importance of timely diagnosis and effective treatment of this channelopathy especially in asymptomatic young athletes at high risk of sudden cardiac death. Methods and results In this report, we discuss the case of a 47-year-old male. He was a tennis player who performed a visit to the sports doctor to have issued a certificate for competitive fitness. He had no familiar history of sudden death or syncope. The patient’s electrocardiogram (ECG) revealed J-point elevation and ST-segment elevation in the right precordial leads V1 and V2 positioned in the second, third, or fourth intercostal space, showing classic type II ‘saddleback’ morphology in V2 and BrS was suspected. Hence, the patient underwent Holter ECG monitoring with evidence of spontaneous type 1 Brugada pattern (‘coved’ morphology), as well as frequent ventricular ectopic beats with left branch block morphology. Indeed, a diagnosis of BrS was made. Antiarrhythmic prophylaxis therapy with hydroquinidine was initiated and the patient was suspended from competitive activity with a 3-month follow-up. Conclusions The BrS is a hereditary disease characterized by a typical ECG pattern potentially predisposing active individuals with no patent structural heart disease to ventricular arrhythmias (VA) and sudden cardiac death (SCD). Nowadays, it is difficult to discern the true burden of BrS due to the unknown real prevalence of asymptomatic patients and the dynamic variability of the ECG pattern in individuals. The purpose of this case presentation was to spread awareness about this condition, highlight the importance of timely diagnosis, and effective treatment of this channelopathy especially in asymptomatic young athletes at high risk of SCD. Indeed, exercise may potentially worsen the ECG abnormalities in BrS patients, resulting in higher peak J-point amplitudes during the vasovagal reaction of the recovery period, possibly leading to an increased risk of cardiac events. Moreover, the enhanced vagal tone in athletes could be both a BrS risk factor and an exercise effect. For this reason, athletic pre-participation screening is essential for minimizing the risk for SCD in athletes participating in either competitive or leisure sporting activities.

Brugada-like electrocardiogram pattern in a young man taking a proton-pump inhibitor

The Brugada syndrome (BrS) is an electrical heart disease with complex inheritance (some cases with SCN5A mutations), characterized by specific electrocardiogram (ECG) markers and high risk of associated lethal ventricular arrhythmias [1]. The ECG signature of BrS consists of right precordial ST-segment elevation (≥2 mm) followed by negative T waves [1]. It sometimes includes the findings of right bundle branch block (RBBB). In certain cases, the typical ECG pattern is present intermittently which creates a potential problem for reaching the diagnosis of BrS. Another problem in diagnosing BrS is the presence of so-called Brugada phenocopies (BrPs), i.e. an acquired Brugada-like ECG pattern that are visually identical and indistinguishable from true BrS [2]. This ECG pattern can be caused by other conditions including ischemia of the ventricular septum and/or right ventricle or by taking certain medications [2]. Proton-pump inhibitors (PPIs) are widely prescribed, often for prolonged use, and have been associated with electrolyte disturbances and cardiac arrhythmias [3,4]. We hereby present for the first time the case of a patient with an ECG suggestive of BrS while taking PPI; but no other medication known to cause BrS. The BrS ECG pattern disappeared a few months after stopping the medication.

Ventricular tachycardia originating from the septal papillary muscle of the right ventricle: electrocardiographic and electrophysiological characteristics.

Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) arising from papillary muscles of both ventricles have recently been described. There is a lack of data on VT originating from the right ventricular papillary (RV PAP) muscles. There have been no prior studies focused on the electrocardiogram (ECG) features and ablation of PVC/VT arising from the septal papillary muscle of the right ventricle. Among 155 consecutive patients with normal structural heart who underwent catheter ablation of PVC/VT, 8 patients with PVC/VT from the septal RV PAP muscle were identified. The site of origin of the arrhythmias was identified through activation/pace mapping and intracardiac echocardiography. All patients underwent radiofrequency ablation of the arrhythmia. Data on 8 consecutive patients (2 men, age 42 ± 13 years old) were collected. All patients had a preserved ejection fraction (60 ± 4%). Septal RV PAP arrhythmias had a left superior axis and negative concordance or late R-wave transition in precordial leads. PVCs were spontaneous in 5 cases, were induced by isoprotenerol in 2 cases and by isoproterenol plus phenylephrine in another one. PVCs were never induced with calcium bolus and only rarely with burst pacing. Adenosine never terminated VT or suppressed the VT/PVCs. Radiofrequency, fluoroscopic, and procedural time were, respectively, 10.3 ± 3, 36.4 ±11.3, and 76.3 ± 27.5 minutes. During a mean follow-up of 8 ± 4 months, mean PVC burden was reduced from 14 ± 3% preablation to 0.1 ± 0.2% postablation. PVCs and VT originating from septal RV papillary muscle could have a typical ECG pattern due to the site of the muscle involved. Radiofrequency ablation of this anatomic area is feasible and effective.

An unusual presentation of left anterior descending artery occlusion: significance of lead aVR and T-wave direction

Acute occlusion of the left anterior descending coronary artery (LAD) is frequently encountered in acute ST-elevation myocardial infarction. Early detection of the clinical entity by the presenting electrocardiogram (ECG) should result in immediate aggressive clinical management. Although the typical ECG pattern of LAD occlusion is ST elevation, also atypical presentations, like ST depression, may occur. We describe a case with an unusual ECG pattern that suggested acute anterior myocardial infarction due to LAD occlusion.

Characteristics of P wave in patients with sinus rhythm after maze operation.

Maze operation could alter P wave morphology in electrocardiogram (ECG), which might prevent exact diagnosis of the cardiac rhythm of patients. However, characteristics of P wave in patients with sinus rhythm after the operation have not been elucidated systematically. Consecutive patients who underwent the modified Cox Maze operation from January to December 2007 were enrolled. The standard 12-lead ECG and echocardiography were evaluated in patients who had sinus rhythm at 6 months after the operation. The average axis of P wave was 65±30 degrees. The average amplitude of P wave was less than 0.1 mV in all 12-leads, with highest amplitude in V1. The most common morphology of P wave was monophasic with positive polarity (49%), except aVR lead, which was different from those in patients with enlarged left atrium, characterized by large P-terminal force in the lead V1. There were no significant differences in P-wave characteristics and echocardiographic parameters between patients with LA activity (30.6%) versus without LA activity (69.4%) at 6 months after the operation. In conclusion, the morphology of P wave in patients after Maze operation shows loss of typical ECG pattern of P mitrale: P wave morphology is small in amplitude, monophasic and with positive polarity.

Heat stroke, an unusual trigger of Brugada electrocardiogram

A young male individual with diagnosis of heat stroke was admitted unconscious to hospital. Electrocardiogram (ECG) at admission demonstrated typical right bundle branch block and ST-segment elevation in V1 and V2 (coved morphology) diagnostic of Brugada syndrome. Maximal creatine kinase was 10,131 (IU/L); creatine kinase-MB, 15 (IU/L); troponin T, 0.039 ng/mL; and creatinine 1.6, mg/dL. Patient recovered from coma on day 6. Electrocardiogram normalized within the first 24 hours; no arrhythmias were documented. Echocardiogram before discharge was normal. Brugada ECG pattern can express intermittently, and challenge tests with a sodium channel blocker are often required for diagnosis. Ventricular arrhythmias and sudden death occur typically at night or during enhanced vagal activity. Fever has been related to polymorphic ventricular tachycardia particularly in children; nevertheless, prevalence is higher within males in their fourth to fifth decade. Mutations in SCN5A gene encoding a sodium channel can be found in up to 30% of cases. This sodium channel is sensitive to temperature changes. Sequencing of the gene failed to find any abnormality in our patient. A possible role of heat shock proteins in ion channels trafficking to cell membrane has been recently described. Despite diffuse ST-T deviations having been described in patients with heat stroke, localized right precordial leads ST elevation consistent with Brugada syndrome have not been reported. Recognition of typical ECG pattern is of importance because this syndrome is associated to an increased risk of sudden cardiac death.

Atrial Fibrillation and Pulmonary Embolism

Atrial fibrillation is a rare diagnosis in children and adolescents. We report a case of a 17-year-old previously healthy boy who presented to the emergency department with a 3-week history of shortness of breath, chest pain, and 1 episode of hemoptysis. Symptoms persisted despite a course of antibiotics and anti-inflammatory agents. The patient developed palpitations and was found to be in atrial fibrillation at the time of hospitalization. An extensive workup led to the diagnosis of pulmonary embolism. This case highlights the importance of evaluating for thromboembolic events in pediatric patients presenting with new-onset atrial fibrillation and typical electrocardiogram pattern of cor pulmonale with or without respiratory symptoms.

Brugada-like electrocardiogram pattern: how to stratify the risk for sudden cardiac death. Is sports activity contraindicated?

Brugada syndrome is associated with a considerable risk of sudden death in young and otherwise healthy adults. The syndrome is estimated to be responsible for at least 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts. The diagnosis of Brugada syndrome is based on peculiar electrocardiogram (ECG) abnormalities classified by the European Society of Cardiology in three types: type 1 (coved-type) is the diagnostic pattern; type 2 (saddle-back type); and type 3 are considered significant if there is a conversion to a type 1, spontaneously or during administration of class I A/C anti-arrhythmic drugs (flecainide, etc.). There is a general agreement about the high risk of sudden death in patients with previous cardiac arrest, for whom an implantable defibrillator (ICD) is recommended. In contrast, controversy exists on the correct clinical behaviour in individuals without a history of previous cardiac arrest. To stratify the risk in patients with type 1 pattern, three major factors have been suggested: typical ECG pattern in the basal state; a history of syncope; and inducible ventricular tachycardia/ventricular fibrillation during electrophysiological study (EPS). However, the indication and usefulness of an EPS is debatable. In patients with a type 2 or 3 pattern a pharmacological test is indicated in the presence of symptoms or of a familial history. With regard to sports eligibility, patients with a history of cardiac arrest should have an ICD and they can practise (low intensity) sport only after the implant of the device. Patients without documented cardiac arrest but at high risk (basal type 1 ECG pattern, syncope and/or positive EPS) should also have an ICD and they can practise (low intensity) sport only after the implant of the device. In patients at low risk (type 1 ECG pattern in the absence of symptoms, without family history and negative EPS) the behaviour regarding sport eligibility is not a matter of debate. In cases with type 2 or 3 pattern, in the absence of familial history and symptoms, a permissive behaviour should be assumed.

QT-interval prolongation inright precordial leads: an additional electrocardiographic hallmark of Brugada syndrome

ObjectivesThe aim of this study was to evaluate whether the occurrence of the Brugada Syndrome typical electrocardiogram (ECG) pattern (i.e., right bundle branch block, coved-type ST-segment elevation, and T-wave inversion in the right precordial leads) is characterized by a concomitant lengthening of QT intervals in the right precordial leads. BackgroundIt has been suggested that the typical ECG pattern of Brugada syndrome is due to a decreased net inward current during phase 1 of the action potential, which also leads to its prolongation in the right epicardium. MethodsThirty-two subjects (19 males) age 37 ± 15 years with a suspicious baseline ECG, or who were relatives of Brugada syndrome patients, underwent 12-lead ECG before and after the administration of flecainide. ResultsThe flecainide test was negative in 14 and positive in 18 subjects. After flecainide administration, the positive ECGs were characterized by a greater QT interval corrected for heart rate (QTc) prolongation in the right precordial leads than that in the negative ECGs (78.2 ± 35.5 ms vs. 22.0 ± 28.4 ms in V1and 107.1 ± 43.8 ms vs. 26.7 ± 30.1 ms in V2; p < 0.01), whereas there was no difference in the QTc prolongation in the left precordial leads (55.2 ± 25.3 ms vs. 35.1 ± 28.1 ms in V5and 53.1 ± 32.8 ms vs. 27.3 ± 22.4 ms in V6; p = NS). ConclusionsIn accordance with the electrophysiological background, the typical ECG pattern of Brugada syndrome is also characterized by a considerable prolongation of the QT interval in right precordial leads.

Electrocardiographic features of inherited diseases that predispose to the development of cardiac arrhythmias, long QT syndrome, arrhythmogenic right ventricular cardiomyopathy/dysplasia, and brugada syndrome

Analysis of the 12-lead electrocardiogram (ECG) provides important diagnostic and prognostic information in the long QT syndrome. The clinical diagnosis of long QT syndrome is determined by the presence of a QTc≥0.44 sec. A normal QTc does not exclude a family member from being a genetic carrier. The ECG patterns of depolarization, the ST segment and shape of the T-wave can provide important clues as to the affected gene, particularly in conjunction with clinical information as to the precipitating causes of syncope or cardiac events. In arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), the typical ECG pattern consists of T-wave inversion beyond lead V 1. Evidence of right ventricular parietal block is manifest by a QRS duration in V 1≥110 msec and a longer QRS duration in the right then left precordial leads. Evidence of slow fractionated conduction is present as epsilon waves. The signal averaged ECG may show exceedingly long and low late potentials. Information regarding the risk of sudden death may also be obtaioned from the ECG. The ECG changes alone or in combination can provide strong evidence for the diagnosis of ARVC/D and helps to differentiate ARVC/D from right ventricular outflow tract (RVOT) tachycardia. The typical pattern of the ECG in the Brugada syndrome is ST segment elevation in the right precordial leads. This abnormality can be dormant and elicited by administration of drugs that cause Na channel blockade, such as ajmaline or type 1a or 1C antiarrhythmic drugs. Individuals who do not have the Brugada ECG findings at baseline but have this pattern induced by antiarrhythmic drugs are also at risk for sudden death. Further risk stratification may be obtained in the asymptomatic patients if ventricular fibrillation is induced at electrophysiological study.

Optimal treatment after acute myocardial infarction in the elderly.

Elderly patients with acute myocardial infarction (AMI) more often have a previous history of cardiovascular disease than do younger patients. Furthermore, they less frequently present with typical symptoms and a typical electrocardiogram pattern. Whereas age is the most important predictor for mortality after AMI, the relationship between age and morbidity is more complex. Treatment of elderly patients with AMI is very similar to treatment of younger patients. However, the risk of intolerability to various drugs increases with age, and in many instances doses have to be adjusted. In many trials, the number of lives saved with various interventions seem, if anything, to be more numerous among the elderly. However, it should be remembered that experience with various treatments in the elderly (patients aged > 80 years) is limited. Whether experiences with people aged up to 80 years can be extrapolated to higher age groups is debatable. With increasing age, there is an increased frequency of other disabling diseases, as well as generalised atherosclerosis. It might very well be that even in the elderly it is possible to relieve symptoms and improve morbidity, even though the effects on the prognosis are likely to be less marked.