Typical ECG Research Articles

When to Perform Catheter Ablation in Asymptomatic Patients With a Wolff-Parkinson-White Electrocardiogram

What to do when a person without any cardiac complaint shows a Wolff-Parkinson-White (WPW) pattern on the ECG has been an important question for more than 2 decades. Recent articles by Pappone et al1–3 make it necessary to revisit that question. Epidemiological data indicate that 0.1% to 0.3% of the general population have ECG findings suggesting that during sinus rhythm, in addition to AV conduction over the AV node His pathway, there is also AV conduction over an accessory AV pathway (AP).4 This means that each year ≈4 new cases are found in a population of 100 000. It is also known that there is a 4-fold increase of this finding in family members of WPW patients.5 The WPW patient is often symptomatic because of cardiac arrhythmias. When arrhythmias are present, the disorder is called the WPW syndrome. The 2 most common types of arrhythmia in the WPW syndrome are (1) a circus movement tachycardia (CMT), also called an AV reentrant tachycardia, in which AV conduction goes by way of the normal AV conduction system and VA conduction over the AP and (2) atrial fibrillation (AF).6 AF can be a life-threatening arrhythmia in the WPW syndrome if the AV AP has a short anterograde refractory period (RP), allowing many atrial impulses to be conducted to the ventricle. That will result in very high ventricular rates with possible deterioration into ventricular fibrillation (VF) and sudden death.7,8 A CMT that in general is well tolerated by the patient when additional heart disease is absent may deteriorate into AF, and the ventricular rate and risk for VF will depend on the anterograde RP of the AP. Therefore, the most important question in the asymptomatic WPW patient in whom the typical ECG accidentally is recorded is whether he or …

Typical ECG Changes Unmasked by Ajmaline in a Patient with Brugada Syndrome and Left Bundle Branch Block

Brugada syndrome is a channelopathy associated with right bundle branch block and ST segment elevation in the right precordial leads. These electrocardiographic signs may not be apparent most of the time but can be unmasked by certain antiarrhythmic agents. Until now, all of the reports on this syndrome have focused on patients with no significant intraventricular conduction delay at baseline electrograms. In this report, we describe a patient with Brugada syndrome with left bundle branch block at baseline ECG. After intravenous ajmaline, the patient developed right bundle branch block and ST segment elevations in the right precordial leads.

Prevalence and Clinical Course of the Juveniles with Brugada‐Type ECG in Japanese Population

Although many studies on Brugada syndrome have been done, with many reports of genetic findings and clinical features, little evidence exists to support the role of this syndrome in sudden cardiac death in a juvenile population. We sought to determine the prevalence and clinical course in children exhibiting Brugada-type ECG in a community-based population. Our study population comprised 21,944 subjects (11,282 boys and 10,662 girls) who underwent ECG during their first-year elementary school health examinations between 1992 and 2001 in Izumi City, Osaka. Brugada-type ECG was defined as demonstrating ST-segment elevation (coved or saddle-back type, J wave amplitude > or =0.2 mV) in the right precordial leads. We also divided Brugada-type ECGs into three types according to a consensus report. Type 1: coved ST-segment elevation displaying high J wave amplitude followed by a negative T wave; Type 2: high take-off and gradually descending ST-segment elevation (remaining > or =1 mm) followed by a positive or biphasic T wave; and Type 3: ST-segment elevation of <1 mm of both types. Four subjects showed Brugada-type ECG (0.02%) (2 boys and 2 girls). Only one subject, a girl, met Type 1 criteria (0.005%). No history of structural heart disease was documented in these four subjects. During 6.8 +/- 1.0 years of follow-up, no episode of unexpected sudden death, syncopal attack, and fatal arrhythmia occurred. The prevalence of Brugada-type ECG in a juvenile population was extremely low. To investigate when the typical Brugada-type ECG might be manifested, it could be necessary to check ECGs after adolescence.

Ebstein's anomaly - review of a multifaceted congenital cardiac condition.

Ebstein's anomaly (EA) is a rare but fascinating congenital heart disorder accounting for <1% of all congenital heart defects. Since its description in 1866, dramatic advances in diagnosis and therapy have been made. In this review, we describe current diagnostic criteria and classification, natural history, clinical features, and prognosis, typical echocardiographic features and pathologic findings, and the spectrum of associated cardiac malformations including left heart anomalies associated with EA. Differences between Ebstein-like changes associated with congenitally corrected transposition and EA are described. The spectrum of typical ECG and conduction system changes, arrhythmias including accessory pathways and ectopic atrial tachycardias related to EA are also reviewed. Differential diagnosis of EA is discussed including tricuspid valve dysplasia and prolapse as well as arrhythmogenic right ventricular cardiomyopathy. The review describes management options in EA including catheter interventions, indication for operation and surgical options including tricuspid valve repair and replacement. Overall, EA is a complex congenital anomaly with a broad pathologic-anatomical and clinical spectrum and no two patients are alike. Therefore, precise knowledge of the different anatomic and hemodynamic variables, associated malformations and management options are essential. Management of EA patients is complex. Thus it is important that these patients are regularly seen by a cardiologist with expertise in congenital heart disease.

Ebstein's anomaly - review of a multifaceted congenital cardiac condition.

Ebstein's anomaly (EA) is a rare but fascinating congenital heart disorder accounting for <1% of all congenital heart defects. Since its description in 1866, dramatic advances in diagnosis and therapy have been made. In this review, we describe current diagnostic criteria and classification, natural history, clinical features, and prognosis, typical echocardiographic features and pathologic findings, and the spectrum of associated cardiac malformations including left heart anomalies associated with EA. Differences between Ebstein-like changes associated with congenitally corrected transposition and EA are described. The spectrum of typical ECG and conduction system changes, arrhythmias including accessory pathways and ectopic atrial tachycardias related to EA are also reviewed. Differential diagnosis of EA is discussed including tricuspid valve dysplasia and prolapse as well as arrhythmogenic right ventricular cardiomyopathy. The review describes management options in EA including catheter interventions, indication for operation and surgical options including tricuspid valve repair and replacement. Overall, EA is a complex congenital anomaly with a broad pathologic-anatomical and clinical spectrum and no two patients are alike. Therefore, precise knowledge of the different anatomic and hemodynamic variables, associated malformations and management options are essential. Management of EA patients is complex. Thus it is important that these patients are regularly seen by a cardiologist with expertise in congenital heart disease.

Mechanism of Brugada type ECG: Late repolarization in epicardium at right ventricular outflow tract

Mechanism of Brugada type ECG: Late repolarization in epicardium at right ventricular outflow tract

Umbilical vein catheterization under electrocardiogram guidance

In the neonate, umbilical venous catheters (UVC) are inserted and advanced blindly to a predetermined length from the umbilicus. The reported rates for UVC misplacement into the liver (and occasionally the spleen) range from 20 to 37%. Radiographs are routinely used to confirm the positioning of UVCs. This involves movement of often critically ill infants, as well as radiation exposure. This pilot study examines the potential value of confirming UVC placement in neonates using ECG. In critically ill neonates, a conductive Johans ECG adapter was connected to a UVC. A satisfactory tracing (lead II) was obtained (right arm lead connected to the adapter) when the UVC was filled with saline solution allowing the catheter tip to become a unipolar ECG electrode. The UVC was then advanced from the umbilicus until the tip reached the inferior vena cava (IVC) within the thoracic region, as demonstrated by appearance of normal sized QRS complexes with small P-waves. A small QRS indicated the catheter was below the diaphragm. The appearance of a tall positive P-wave indicated the tip was at the right atrium level. The UVC was then withdrawn until the P-wave size returned to normal. The final UVC position was later confirmed by X-ray. Eight neonates were studied. The figure shows typical ECG tracings when the UVC was placed in the liver, IVC, and right atrium, respectively. Three malpositioned catheters were detected (2 into liver and 1 into spleen). Based on these cases, the insertion of UVCs in neonates can be guided with ECG by observing sequential and characteristic alterations in P-waves and QRS complexes, thereby reducing the use of X-rays. In addition, this technique could prove to be beneficial in remote healthcare facilities where X-ray machines may not be readily available and quick intravenous access is required to transport sick neonates to major centers.

Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome

The purpose of this study was to compare the effect of intravenous flecainide and ajmaline with respect to their ability to induce or accentuate the typical ECG pattern of Brugada syndrome. Brugada syndrome is associated with a high incidence of sudden cardiac death. The typical ECG pattern of ST-segment elevation in the right precordial leads often is concealed, but it can be unmasked with sodium channel blockers such as flecainide and ajmaline. Little is known about the relative effectiveness of these provocative agents in unmasking Brugada syndrome. Intravenous pharmacologic challenge with flecainide and ajmaline was performed. Whole-cell patch clamp techniques were used to assess the relative potency of ajmaline and flecainide to inhibit the transient outward current (I(to)). A coved-type ST-segment elevation in the right precordial leads was induced or enhanced in 22 of 22 patients following ajmaline administration. Among the 22 patients, only 15 patients showed positive response to flecainide, resulting in a positive concordance of 68%. Both drugs produced equivalent changes in QRS and PQ intervals, suggesting similar effects on sodium channel current. Whole-cell patch clamp experiments revealed a reduction of the total charge provided by I(to) with an IC(50) of 216 and 15.2 microM for ajmaline and flecainide, respectively. Our data demonstrate disparate response of Brugada patients to flecainide and ajmaline, with a failure of flecainide in 7 of 22 cases (32%). Greater inhibition of I(to) by flecainide may render it less effective. These observations have important implication for identification of patients at risk for sudden death.

Short Atrioventricular Mahaim Fibers: Observations on Their Clinical, Electrocardiographic, and Electrophysiologic Profile

Short A-V manheim fiber. A short atrioventricular decrementally conducting accessory pathway is an uncommon variant of preexcitation. Available data from small series suggest that their decremental properties might not be caused by A-V nodal-like tissue. We compared clinical, electrocardiographic and electrophysiologic parameters in two groups of patients: 8 patients with a short A-V Mahaim pathway (Group A), and 33 patients with atriofascicular pathways (Group B). Radiofrequency catheter ablation was carried out guided by activation mapping at the annulus in Group A patients and targeting the "M" potential in Group B patients. After ablation of all associated rapidly conducting bypass tracts, 7 of the 8 Group A patients showed clear preexcitation. In only 1 of 8 patients the short A-V Mahaim fiber was actively engaged in a reentrant tachycardia circuit. During radiofrequency catheter ablation an automatic rhythm occurred in 4 of 8 patients. Intravenous adenosine caused conduction a block in the Mahaim fiber in 3 of the 5 patients tested. In group B, no patient showed clear preexcitation (P<00001) while 72% had a minimal preexcitation pattern. Twenty-nine of the 33 patients had a circus movement tachycardia with AV conduction over the atriofascicular fiber. During radiofrequency catheter ablation 30 of 33 patients showed accessory pathway automaticity. Adenosine caused transient block at the atriofascicular pathway in 11 (92%) of the 12 patients tested. While short decrementally conducting right-sided accessory pathways show a typical ECG pattern different from atriofascicular pathways, their electrophysiologic properties do not seem to be uniform. Those pathways can be successfully interrupted by catheter ablation.

ELECTROCARDIOGRAPHIC ASSESSMENT OF HYPERKALEMIA IN DOGS AND CATS

Objective: To demonstrate whether ECG changes induced by hyperkalemia correspond with previously described changes.Design: ProspectiveAnimals: Eighteen dogs and 22 cats with serum potassium levels &gt;5.5 mEq/L as the result of various disease processes.Procedure: Once hyperkalemia was documented, the following data were collected: ECG (n=40), total magnesium (mg/dl) (n=18), total calcium (mg/dl) (n=31), and venous blood gas (n=20). Animals were divided into 5 groups based on expected ECG's changes associated with hyperkalemia (mEq/L): Group 1‐ 5.5–6.5; Group 2‐ 6.6–7.0; Group 3‐ 7.1–8.5; Group 4‐ 8.6–10.0; Group 5‐ &gt;10.0. ECG's were interpreted to determine if the rate, rhythm and changes in the P‐QRS‐T complex were similar to those previously reported.Results: Twelve ECGs demonstrated changes previously described, while 28 did not: Group 1 (n=7)‐ 1/7; Group 2 (n=2)‐ 0/2; Group 3 (n=14)‐ 4/14; Group 4 (n=6)‐ 3/6; Group 5 (n=11)‐ 4/11. Many ECG abnormalities not previously described were also identified such as atrioventricular dissociation and ventricular tachyarrhythmias. Blood gas analysis revealed acidemia (19/20) with severe acidemia (pH&lt;7.2) in the majority (16/19). Hypocalcemia was documented (5/13) and most of these patents (4/5) were in Group 5. Hypermagnesemia was documented in the majority of patients (10/18), though not in one particular group.Clinical Implications: It is difficult to establish typical ECG changes in patients with hyperkalemia, which represents a departure from the historical description. Hypocalcemia may be involved with ECG changes and arrhythmias in Group 5. Hypermagnesemia causes electrocardiographic abnormalities similar to those described with hyperkalemia and therefore does not explain the results of this study. There likely are complex interactions with electrolytes and acid base abnormalities that affect ECG formation.

Electrocardiographic Diagnosis Of Critical Left Coronary Arterial System Stenosis

Coronary angiography is undoubtedly the gold standard diagnostic tool for coronary artery stenosis. However, if we could diagnose or highly suspect non-invasively critical and proximal stenotic lesions in the left coronary arterial system, this could salvage more myocardium and minimize the morbidity and mortality rate. There is no signal noninvasive variable indicating the culprit lesion in the coronary artery tree. However, in the emergency room we correctly suspected the presence of tight proximal stenosis in the left anterior descending artery just by following serial resting electrocardiogram done during chest pain and after relief of the pain. This was suggestive of Wellen's syndrome. In another patient presenting with chest pain and normal resting ECG an exercise treadmill test (ETT) was done. This test gave us a good clue for the presence of significant left main coronary artery stenosis and highlighted the significance of ST-elevation during ETT. Coronary angiogram supported our suggestion in the two cases. In view of the large area of the ventricle at risk, the recognition of such ECG patterns take on critical importance and provide important complementary information to that given by coronary angiogram and shorten the door-to-treat time. CASE REPORT NO. 1 & REVIEW A 55-year-old male Pakistani patient known to have hypertension and hyperlipidemia presented with typical anginal pain with no other symptoms. Electrocardiogram during chest pain showed sinus rhythm, normal axis, biphasic T-wave in V4-V5 minimal ST depression in V6. The pain was resolved then ECG was repeated and showed minimal ST elevation in V1 with inverted T wave in V2-V4, ST depression with inverted T in V5-V6 (fig. 1a,b). Figure 1 Figure 1 A & B: ECG on arrival to the emergency room with typical anginal pain and ECG 30 minutes after pain relief Half an hour later, chest pain recurred for a few minutes and then resolved. During the pain-free period, the ECG showed marked T-wave changes (fig.2a&b). Electrocardiographic Diagnosis Of Critical Left Coronary Arterial System Stenosis

P-319 Prevalence and prognosis of subjects with brugada type ECG pattern in finnish male population

P-319 Prevalence and prognosis of subjects with brugada type ECG pattern in finnish male population

P-319 Prevalence and prognosis of subjects with brugada type ecg pattern in finnish male population

P-319 Prevalence and prognosis of subjects with brugada type ecg pattern in finnish male population

The continuing story: The aetiology of Brugada syndrome: functional or structural basis?

In response to our consensus report on Brugada syndrome,1Dr Martini once again draws attention to the controversy as to whether the typical ECG pattern is based on structural or on functional alterations. Dr. Martini has raised this subject repeatedly in letters to the editors of various journals and the issue has been discussed at great length in previous responses.2,3Accordingly, our comments will be brief. The consensus report was meant to come to a uniform set of …

10.7 Heart rate variability trends in 90-minute period prior to onset of ventricular arrhythmias in ICD patients

�pattern in the V1 lead with the ST-segment elevation 0.2mV of a coved-type ECG was defined as “typical” Brugada-type ECG. Results: the Brugada-type ECG was found in 11 (10male) of 20387 children (0.054%, 95%CI: 0.022% to 0.086%). There was no child with typical Brugada-type ECG. The prevalence of Brugada-type ECG in male was significantly higher than that of female even in children (0.096% versus 0.010%, P=0.012), and was increased according to aging (first grader: 0.01%, fourth grader: 0.05%, seventh grader: 0.08%, tenth grader: 0.23%, p<0.008. ANOVA). Conclusions: the prevalence of Brugada-type ECG in Japanese children was much lower than that reported previously in adult population (0.7%) and was increased according to aging.

Surface electrocardiographic characteristics of right and left atrial flutter.

There is little information about the surface expression of non-cavotricuspid isthmus (CTI)-dependent right atrial (RA) or left atrial (LA) flutter circuits. We retrospectively evaluated 32 episodes (in 26 patients) of atypical RA and 22 episodes (in 21 patients) of LA flutter. The surface ECG of 13 patients with lower-loop reentry was similar to that of their pattern during counterclockwise (CCW) CTI atrial flutter (AFL), except for decreased amplitude of the terminal forces in the inferior leads. In 11 of 24 episodes characterized by high or multiple breaks over the crista, the ECG showed changes that depended on the initial activation sequence of the LA. In 7 of 8 episodes of upper-loop reentry, the ECG pattern completely mimicked that for clockwise (CW) CTI AFL. All 11 patients with an LA septal circuit showed a typical ECG pattern characterized by prominent forces in lead V1 with flat deflections in the other surface leads. Eleven patients with other LA circuits had a more variable pattern but showed decreased voltage in the inferior leads compared with that of a group with CCW-CTI AFL (1.6+/-1 vs 2.68+/-0.7 mV, respectively; P<0.05). The RA surface-ECG patterns different from those of CCW or CW-CTI could still be CTI dependent. In contrast, a typical CW-CTI surface pattern was always seen in patients with upper-loop reentry, which was non-CTI dependent. LA AFL circuits had either flat or low-amplitude forces in the inferior leads.

The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol.

The diagnostic ECG pattern in Brugada syndrome (BS) can transiently normalize and may be unmasked by sodium channel blockers such as ajmaline. Proarrhythmic effects of the drug have been well documented in the literature. A detailed protocol for the ajmaline challenge in Brugada syndrome has not yet been described. Therefore, we prospectively studied the risks of a standardized ajmaline test. During a period of 60 months, 158 patients underwent the ajmaline test in our institution. Ajmaline was given intravenously in fractions (10mg every two minutes) up to a target dose of 1mg/kg. In 37 patients (23%) the typical coved-type ECG pattern of BS was unmasked. During the test, symptomatic VT appeared in 2 patients (1.3%). In all other patients, the drug challenge did not induce VT if the target dose, QRS prolongation >30%, presence/appearance of the typical ECG, or the occurrence of premature ventricular ectopy were considered as end points of the test. A positive response to ajmaline was induced in 2 of 94 patients (2%) with a normal baseline ECG, who underwent evaluation solely for syncope of unknown origin. The ajmaline challenge using a protocol with fractionated drug administration is a safe method to diagnose BS. Because of the potential induction of VT, it should be performed under continuous medical surveillance with advanced life-support facilities. Due to the prognostic importance all patients with aborted sudden death or unexplained syncope without demonstrable structural heart disease and family members of affected individuals should presently undergo drug testing for unmasking BS.

The Brugada syndrome

Brugada syndrome describes the syndrome of sudden cardiac death in the setting of the following electrocardiographic findings: right bundle branch block pattern with ST-segment elevation in the right precordial leads. The right bundle branch block may be incomplete while the ST segment elevation is minimal. The electrocardiographic findings are not constant. Patients suspected of having Brugada syndrome should be promptly referred for electrophysiological testing and treatment. Rapid referral and placement of an implantable cardioverter defibrillator (ICD) is associated with an excellent prognosis, whereas failure to diagnose this condition is associated with a high risk for sudden death. Therefore, it is imperative that all emergency physicians be familiar with the typical ECG manifestations of Brugada syndrome. Three illustrative cases are presented with a review of the syndrome. (Am J Emerg Med 2003;21:146-151. Copyright 2003, Elsevier Science (USA). All rights reserved.)

Flecainide Test in Brugada Syndrome: A Reproducible but Risky Tool

The flecainide test is widely used in Brugada syndrome. However, its reproducibility and safety remain ill-defined. This study included 22 patients (18 men, mean age 34 years). Mutations in the SCN5A gene were found in eight patients. Two patients had aborted sudden cardiac death, 8 had syncope/presyncope, and 12 were asymptomatic. The ECG was diagnostic in 19 patients and suggestive in 3. At baseline, 21 of 22 patients underwent a flecainide test (2 mg/kg IV bolus over 10 minutes). In 21 of 21 patients the test was diagnostic or amplified the typical ECG pattern. At the end of drug infusion, sustained VT lasting 7-10 minutes developed in two patients. A second flecainide test was performed within 2 months in 20 patients. The test was not repeated in the two patients with prior development of VT. The flecainide test was diagnostic in 20 of 20 patients. Sustained VT occurred in one patient and recurrent VF in another. The reproducibility of the flecainide test was 100%. In 4 (18%) of 22 patients major VAs were documented after the end of flecainide infusion. VA occurred in 3 (43%) of 7 patients with, versus 1 (7%) 15 without SCN5A gene mutation (P < 0.05). No diagnostic ECG changes or arrhythmias developed in 25 control patients without structural heart disease who underwent the same study protocol. This study shows a high flecainide reproducibility, supporting its diagnostic value in Brugada syndrome. However, the occurrence of major VA, significantly higher in patients with documented SCN5A gene mutation, including in asymptomatic patients, mandates the performance under appropriate medical supervision. Whether a slower rate of drug infusion can lower the risk of VA induction, while maintaining the sensitivity of the test should be explored.

Proposed Diagnostic Criteria for the Brugada Syndrome

Asyndrome characterized by ST-segment elevation in right precordial leads (V1 to V3) that is unrelated to ischemia, electrolyte disturbances, or obvious structural heart disease was reported as early as 1953,1 but was first described as a distinct clinical entity associated with a high risk of sudden cardiac death in 1992.2–4⇓⇓ The Brugada syndrome is a familial disease that displays an autosomal dominant mode of transmission, with incomplete penetrance and an incidence ranging between 5 and 66 per 10 000. In regions of Southeast Asia where it is endemic, the clinical presentation of Brugada syndrome is distinguished by a male predominance (8:1 ratio of male:female) and the appearance of arrhythmic events at an average age of 40 years (range: 1 to 77 years).2,5⇓ Although a number of candidate genes are considered plausible, thus far the syndrome has been linked only to mutations in SCN5A , the gene encoding for the α subunit of the sodium channel.6 A number of ambiguities exist concerning the diagnosis of Brugada syndrome. The electrocardiographic signature of the syndrome is dynamic and often concealed, but can be unmasked by potent sodium channel blockers such as flecainide, ajmaline, and procainamide,7 although the specificity of this effect for uncovering patients at risk for sudden death has been an issue of concern. A recent report by Remme et al8 has shown that the number of idiopathic ventricular fibrillation patients diagnosed as having Brugada syndrome is a sensitive function of the diagnostic criteria applied. What are the proper diagnostic criteria for identifying Brugada syndrome? A definitive answer to this question has been out of reach and is the reason for the establishment of a special Arrhythmia Working Group of the European Society of Cardiology that met from August 31 to …