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Right Precordial Leads (right + precordial_lead)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Transient ST Segment Elevation in Right Precordial Leads Induced by Psychotropic Drugs: Relationship to the Brugada Syndrome

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001
FREDERIC ROULEAU M.D.
Psychotropic Drugs and ST Segment Elevation. Transient ST segment elevation in right precordial leads with use of psychotropic drugs is reported in two cases of overdose and one case of therapeutic administration. Flecainide did not reproduce ST segment elevation. The relationship of these abnormalities to the Brugada syndrome and the electrophysiologic hypothesis are discussed. [source]

Sodium Channel Blockers Enhance the Temporal QT Interval Variability in the Right Precordial Leads in Brugada Syndrome

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2008
Tetsuzou Kanemori M.D.
Background: Temporal QT interval variability is associated with sudden cardiac death. The purpose of this study was to evaluate temporal QT interval variability in Brugada syndrome (BS). Methods: We measured QT and RR intervals in precordial leads (V1,V6) based on 12-beat resting ECG recordings from 16 BS patients (B group) with spontaneous ST elevation in right precordial leads (V1,V2) and from 10 patients with normal hearts (C group). We measured the response in B group before and after administration of pilsicainide (1 mg/kg). The standard deviation (QT-SD, RR-SD) of the time domain and total frequency power (QT-TP, RR-TP) were calculated for all precordial leads, and the latter was to analyze the frequency domain. Results: The right precordial leads in BS exhibited an additional and prominent ST elevation (coved-type) after pilsicainide administration. Both QT-SD and QT-TP values were significantly more increased in B, than in C (5.1 ± 1.2 vs 3.6 ± 0.2 and 23.4 ± 2.9 vs 12.3 ± 1.7 msec2, P < 0.01, respectively) and after pilsicainide administration in B. (5.1 ± 0.4 vs 3.9 ± 0.3, 25.8 ± 3.4 vs 16.3 ± 2.6 msec2, P < 0.01, respectively) However, QT-SD and QT-TP did not significantly change in any of other leads (V3,V6) and RR-SD and RR-TP were similar for both groups, as well as after intravenous pilsicainide administration in B. Conclusions: The temporal QT interval variability was identified in BS. Moreover, sodium channel blocker induced temporal fluctuation in QT interval and it may possibly provide a substrate for ventricular arrhythmia in BS patients. [source]

Electrophysiological Basis and Genetics of Brugada Syndrome

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005
AUGUSTUS O. GRANT M.B.Ch.B., Ph.D.
Brugada syndrome is a primary arrhythmic syndrome arising in the structurally normal heart. Any proposed mechanism should account for the major features of the syndrome: localization of the ST segment and T-wave changes to the right precordial leads, association of conduction slowing at several levels, precipitation or aggravation of the major ECG changes by sodium channel-blocking drugs and the occurrence of ventricular fibrillation. Heterogeneity of repolarization across the ventricle wall plays a major role. Any agency that shifts the net current gradient during phase I outward would exaggerate the normal heterogeneity of repolarization and result in the ST segment and T-wave changes characteristic of the syndrome. When the outward current shift is marked, premature repolarization may occur in epicardial zone and the resulting gradient may precipitate reentry. The syndrome is inherited as an autosomal dominant. However, 75% of clinically affected individuals are males. In 20% of cases, the syndrome is associated with mutations of the cardiac sodium channel gene SCN5A. The mutations result in a loss-of-function as a result of the synthesis of a non-functional protein, altered protein trafficking, or change in gating. Agencies that reduce the sodium current may precipitate the characteristic ECG changes, for example, sodium channel blockers and membrane depolarization by hyperkalemia. Sympathetic stimulation may reverse the ECG changes and reduce arrhythmia recurrence. By its nonspecific potassium channel blocking action, quinidine may also reduce arrhythmia recurrence. We still do not know the basis for defect in the majority of patients with Brugada syndrome. [source]

Transient ST Segment Elevation in Right Precordial Leads Induced by Psychotropic Drugs: Relationship to the Brugada Syndrome

Epsilon-Like Electrocardiographic Pattern in a Patient with Brugada Syndrome

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009
Ozcan Ozeke M.D.
Both Brugada syndrome (BrS) and arrhythmogenic right ventricle dysplasia/cardiomyopathy (ARVD/C) can cause repolarization abnormalities in right precordial leads and predispose to sudden cardiac death (SCD) due to ventricular arrhythmias. Although there is controversy over whether BrS is distinct from ARVD/C, it is believed that both are different clinical entities with respect to both the clinical presentation and the genetic predisposition. The coexistence of these two relatively rare clinical entities is also reported, but, some hypothesized that it is more possible that disease of the right ventricular muscle might accentuate the Brugada electrocardiographic pattern. In clinic practice, there may be cases where the dividing line is not so clear. We report a 33-year-old male presenting with recurrent syncope, who has a peculiar pattern of coved-type ST-segment elevation (ST-SE) with epsilon-like wave in right precordial leads. [source]

Sodium Channel Blockers Enhance the Temporal QT Interval Variability in the Right Precordial Leads in Brugada Syndrome

Brugada Syndrome: Current Clinical Aspects and Risk Stratification

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002
Ph.D., Takanori Ikeda M.D.
Brugada syndrome is a primary electrical disease of the heart that causes sudden cardiac death or life-threatening ventricular arrhythmias, especially in younger men. Genetic analysis supports that this syndrome is a cardiac ion channel disease. A typical electrocardiographic finding consists of a right bundle branch block pattern and ST-segment elevation in the right precordial leads. The higher intercostal space V1 to V3 lead electrocardiogram could be helpful in detecting Brugada patients. Although two types of the ST-segment elevation are present, the coved type is more relevant to the syndrome than the saddle-back type. These patterns can be present permanently or intermittently. Recent data suggest that the Brugada-type electrocardiogram is more prevalent than the manifest Brugada syndrome. Asymptomatic individuals have a much lower incidence of future cardiac events than the symptomatic patients. Although risk stratification for the Brugada syndrome is still incomplete, the inducibility of sustained ventricular arrhythmias has been proposed as a good outcome predictor in this syndrome. In noninvasive techniques, some clinical evidence supports that late potentials detected by signal-averaged electrocardiography are a useful index for identifying patients at risk. The available data recommend prophylactic implantation of an imptantabie cardioverter defibrillator to prevent sudden cardiac death. This review summarizes recent information of the syndrome by reviewing most of new clinical reports and speculates on its risk stratification. A.N.E. 2002;7(3):251,262 [source]

A Case of Brugada Syndrome Presenting With Incessant Polymorphic Ventricular Tachycardia

CLINICAL CARDIOLOGY, Issue 3 2010
Harn-Cherng Shiue MD
Brugada syndrome, an inherited arrhythmogenic cardiac disease, manifests with ST-segment changes in the right precordial leads, right bundle block pattern, and susceptibility to ventricular tachyarrhythmias and sudden death. The only established therapy for this disease is prevention of sudden death by implantation of a defibrillator. Herein we describe a case of a patient who presented with incessant ventricular tachycardia (VT) and syncope and who had a type 1 Brugada pattern on ECG. The patient was successfully treated with quinidine, after which the classically described type 2 and 3 patterns emerged. Copyright © 2009 Wiley Periodicals, Inc. [source]