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Precordial Leads (precordial + lead)

Distribution by Scientific Domains

Medical Sciences	100%

Kinds of Precordial Leads

right precordial lead

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]

Wide-QRS-Complex Tachycardia with a Negative Concordance Pattern in the Precordial Leads: Are the ECG Criteria Always Reliable?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2006
KOSTAS G. KAPPOS
We present a case of wide-complex tachycardia with negative concordance in the precordial leads and a qR pattern in V6, in a 42-year-old man with risk factors for coronary artery disease, in whom the electrocardiogram criteria were apparently fallible. This case highlights the key contribution of the electrophysiological study in rendering correct diagnosis. [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]

Enhanced Predictive Power of Quantitative TWA during Routine Exercise Testing in the Finnish Cardiovascular Study

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2009
MIKKO MINKKINEN B.M.S.
Introduction: We examined whether quantification of T-wave alternans (TWA) enhances this parameter's capacity to evaluate the risk for total and cardiovascular mortality and sudden cardiac death (SCD). Methods and Results: The Finnish Cardiovascular Study (FINCAVAS) enrolled consecutive patients (n = 2,119; 1,342 men and 777 women) with a clinically indicated exercise test with bicycle ergometer. TWA (time domain-modified moving average method) was analyzed from precordial leads, and the results were grouped in increments of 10 ,V. Hazard ratios (HR) for total and cardiovascular mortality and SCD were estimated for preexercise, routine exercise, and postexercise stages. Cox regression analysis was performed. During follow-up of 47.1 ± 12.9 months (mean ± standard deviation [SD]), 126 patients died: 62 were cardiovascular deaths, and 33 of these deaths were sudden. During preexercise, TWA , 20 ,V predicted the risk for total and cardiovascular mortality (maximum HR >4.4 at 60 ,V, P < 0.02 for both). During exercise, HRs of total and cardiovascular mortality were significant when TWA measured ,50 ,V, with 90 ,V TWA yielding maximum HRs for total and cardiovascular death of 3.1 (P = 0.03) and 6.4 (P = 0.002), respectively. During postexercise, TWA ,60 ,V indicated risk for total and cardiovascular mortality, with maximum HR of 3.4 at 70 ,V (P = 0.01) for cardiovascular mortality. SCD was strongly predicted by TWA levels ,60 ,V during exercise, with maximum HR of 4.6 at 60 ,V (P = 0.002), but was not predicted during pre- or postexercise. Conclusion: Quantification of TWA enhances its capacity for determination of the risk for total and cardiovascular mortality and SCD in low-risk populations. Its prognostic power is superior during exercise compared to preexercise or postexercise. [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

Wide-QRS-Complex Tachycardia with a Negative Concordance Pattern in the Precordial Leads: Are the ECG Criteria Always Reliable?

Is the Fascicle of Left Bundle Branch Involved in the Reentrant Circuit of Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2003
JEN-YUAN KUO
The exact reentrant circuit of the verapamil-sensitive idiopathic left VT with a RBBB configuration remains unclear. Furthermore, if the fascicle of left bundle branch is involved in the reentrant circuit has not been well studied. Forty-nine patients with verapamil-sensitive idiopathic left VT underwent electrophysiological study and RF catheter ablation. Group I included 11 patients (10 men, 1 woman; mean age 25 ± 8 years) with left anterior fascicular block (4 patients), or left posterior fascicular block (7 patients) during sinus rhythm. Group II included 38 patients (29 men, 9 women; mean age 35 ± 16 years) without fascicular block during sinus rhythm. Duration of QRS complex during sinus rhythm before RF catheter ablation in group I patients was significant longer than that of group II patients (104 ± 12 vs 95 ± 11 ms, respectively, P = 0.02). Duration of QRS complex during VT was similar between group I and group II patients (141 ± 13 vs 140 ± 14 ms, respectively, P = 0.78). Transitional zones of QRS complexes in the precordial leads during VT were similar between group I and group II patients. After ablation, the QRS duration did not prolong in group I or group II patients (104 ± 11 vs 95 ± 10 ms, P = 0.02); fascicular block did not occur in group II patients. Duration and transitional zone of QRS complex during VT were similar between the two groups, and new fascicular block did not occur after ablation. These findings suggest the fascicle of left bundle branch may be not involved in the antegrade limb of reentry circuit in idiopathic left VT. (PACE 2003; 26:1986,1992) [source]

Dispersion of QT Intervals: A Measure of Dispersion of Repolarization or Simply a Projection Effect?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2000
DIEGO DI BERNARDO
QT interval dispersion may provide little information about repolarization dispersion. Some clinical measurements demonstrate an association between high QT interval dispersion and high morbidity and mortality, but what is being measured is not clear. This study was designed to help resolve this dilemma. We compared the association between different clinical measures of QT interval dispersion and the ECG lead amplitudes derived from a heart vector model of repolarization with no repolarization dispersion whatsoever. We compared our clinical QT interval dispersion data obtained from 25 subjects without cardiac disease with similar data from published studies, and correlated these QT dispersion results with the distribution of lead amplitudes derived from the projection of the heart vector onto the body surface during repolarization. Published results were available for mean relative QT intervals and mean differences from the maximum QT interval. The leads were derived from Uijen and Dower lead vector data. Using the Uijen lead vector data, the correlation between measurements of dispersion and derived lead amplitudes ranged from 0.78 to 0.99 for limb leads, and using the Dower values ranged from 0.81 to 0.94 for the precordial leads. These results show a clear association between the measured QT interval dispersion and the variation in ECG lead amplitudes derived from a simple heart vector model of repolarization with no regional information. Therefore, measured QT dispersion is related mostly to a projection effect and is not a true measure of repolarization dispersion. Our existing interpretation of QT dispersion must be reexamined, and other measurements that provide true repolarization dispersion data investigated. [source]

Radiofrequency Catheter Ablation from the Left Sinus of Valsalva in a Patient with Idiopathic Ventricular Tachycardia

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2000
NAOHIKO TAKAHASHI
We report the case of a 54-year-old woman with idiopathic VT originating in the left ventricular outflow tract. She initially presented with palpitations and light-head-edness. The morphology of the PVCs exhibited an inferior axis and tall R waves were noted in all the precordial leads. Spontaneous PVCs were transiently terminated by an intravenous injection of adenosine triphosphate. Radiofrequency catheter ablation from the left sinus of Valsalva successfully abolished the PVCs and the VT. [source]

Circadian and Gender Effects on Repolarization in Healthy Adults: A Study Using Harmonic Regression Analysis

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2010
Kenneth A. Mayuga M.D.
Background: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT-dispersion and T-wave peak to T-wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization. Methods: Forty healthy adults (20 women), age 35,67 years old, with normal EKGs, echocardiograms, stress tests, and tilt-table tests were analyzed during a 27-hour hospital stay. EKGs were done at eight different time points. QT-intervals, QT-dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant. Results: The composite QT-interval was longer in women than in men (416 ± 17 msec vs 411 ± 20 msec, respectively, P = 0.006). The QT-dispersion among all leads was greater in men than women (37 ± 13 msec vs 30 ± 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT-dispersion had a significant circadian variation, primarily in men. In men, the maximum QT-dispersion occurred at 6 AM (45 ± 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads. Conclusions: A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT-dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed. Ann Noninvasive Electrocardiol 2010;15(1):3,10 [source]

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

Circadian Variation in QT Dispersion Determined from a 12-Lead Holter Recording: A Methodological Study of an Age- and Sex-Stratified Group of Healthy Subjects

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007
Stig Hansen M.D.
Background: QT dispersion is considered to reflect inhomogeneity of myocardial repolarization. Method: The circadian variation of QT interval dispersion was examined in 95 healthy subjects using 24-hour Holter monitoring. Three different methods of lead selection were applied: all 12 leads (QTdisp 12), only precordial leads (QTdisp 6), and the pair of leads selected at 3 a.m. in which the longest and shortest QT intervals were found in each individual subject (QTdisp 2). Results: A preliminary methodological study including measurements from every minute in 10 subjects revealed no significant circadian variation using mean values of QTdisp 12, QTdisp 6, or QTdisp 2 obtained every hour, every 2, or every 4 hours, except in QTdisp 6, which demonstrated a significant circadian variation (P < 0.01) in 1-hour measurements. Analysis of all 95 subjects using measurements obtained every 4 hours revealed a significant circadian variation in QTdisp 12 and QTdisp 6 (P < 0.0001), whereas no circadian variation was seen in QTdisp 2. A subdivision into 10-year age groups revealed that subjects at age >50 years had a significant circadian variation in QTdisp 12 and QTdisp 6, but not in QTdisp 2. Only in males a significant circadian variation was seen in QTdisp 12 (P < 0.0001), whereas QTdisp 6 demonstrated a circadian variation both in females (P < 0.001) and in males (P < 0.0001). Conclusions: Selection of leads is of crucial importance for repetitive measurements of QT dispersion. Circadian variation was detected in subjects over 50 years of age, when all 12 or only the 6 precordial leads were taken into account. [source]

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]

Acetylcholine- and ergonovine-induced coronary microvascular spasm reflected by increased coronary vascular resistance and myocardial lactate production

CLINICAL CARDIOLOGY, Issue 3 2000
Masashi Horimoto M.D.
Abstract Diagnosis of coronary microvascular spasm remains largely speculative because it has been mostly based on chest pain and electrocardiographic ST-segment shift with slow filling of contrast medium into the coronary artery. A patient with resting chest pain and normal coronary angiograms underwent provocative tests with intracoronary acetylcholine (ACh) and ergonovine. During the tests, coronary diameter and flow velocity in the left anterior descending (LAD) coronary artery were measured with quantitative coronary angiography and intracoronary Doppler guide wire, respectively. Vascular resistance of the LAD and lactate production were determined separately. With injections of 100 ,g of ACh and 20 ,g of ergonovine, chest pain occurred with ST-segment elevation in the precordial leads in the absence of epicardial coronary spasm. Coronary vascular resistance increased by 2.2- and 1.6-fold of the baseline value with ACh and ergonovine, respectively. Myocardial lactate production was noted during the ST-segment elevation. Coronary microvascular spasm was verified by the increment in coronary vascular resistance and myocardial lactate production with concomitant ST-segment elevation in the presence of normal coronary angiograms. [source]