SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
BACKGROUND: Selection of antiarrhythmic therapy may be based on either suppression of spontaneous ventricular arrhythmias assessed by Holter monitoring or by suppression of inducible ventricular arrhythmias during electrophysiological study. This study examines the frequency and significance of concordance of these two approaches in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. METHODS AND RESULTS: Twenty-four-hour Holter monitoring was performed in patients randomized to the electrophysiology limb of the ESVEM study at the time of the first drug trial and at the time of an effective drug trial. Holter monitors were available in 65% (146/226) of patients at the time of the first drug trial and in 93% (100/108) of patients at the time of an electrophysiology study predicting drug efficacy. There were no clinical differences between patients who had and those who did not have a Holter monitor. At the time of the first drug trial, concordance of Holter and electrophysiological predictions of drug efficacy was observed in 46% of patients (both techniques predicted efficacy in 23%; neither predicted efficacy in 23%). Discordant results were observed in 54% (Holter suppression without electrophysiological suppression in 44%; electrophysiological suppression without Holter suppression in 10%). At the time of an electrophysiology study predicting drug efficacy, 68 of the 100 patients without inducible ventricular tachyarrhythmias also had suppression of spontaneous ventricular arrhythmias on the Holter recorded at the time of the electrophysiological study. Neither arrhythmia recurrence nor mortality was significantly different in patients with suppression of both inducible and spontaneous ventricular arrhythmias compared with those with only suppression of inducible arrhythmias. Comparison of patients with suppression of both inducible and spontaneous ventricular arrhythmias with the 188 patients in the Holter limb, in whom efficacy was predicted by Holter monitoring only, revealed no difference in outcome. CONCLUSIONS: In this population, (1) there is frequent discordance in prediction of drug efficacy and inefficacy between electrophysiological study and Holter monitoring; (2) a requirement to fulfill both Holter and electrophysiological efficacy criteria reduces the number of patients with an efficacy prediction; and (3) suppression of both spontaneous ventricular ectopy and inducible ventricular tachyarrhythmias does not identify a group with better outcome.
Explore the source record for details and available documents.
INTRODUCTION: Ivabradine is a heart rate-lowering agent that selectively inhibits the pacemaker current, I(f), in the sinoatrial node. The objective of this study was to evaluate the effects of a single intravenous administration of ivabradine on cardiac electrophysiological parameters in patients with normal baseline electrophysiology. The safety profile of ivabradine was also investigated. STUDY DESIGN: This was an open-label, single-dose, non-controlled study conducted at one centre. Patients received a single dose of ivabradine (0.2 mg/kg) intravenously as a slow bolus over 15 seconds. Electrophysiological investigations, after catheter ablation for cardiac dysrhythmia, were performed at baseline and 30 minutes and 1 hour after drug administration. Electrode catheters were introduced and advanced to the right atrium, the bundle of His and the right ventricular apex of the heart. Electrophysiological parameters assessed included heart rate, QT interval, corrected QT interval (QTc), PR interval, sinoatrial conduction time, sinus node recovery time, and right atrial and ventricle refractory periods. Changes in electrophysiological parameters over time were assessed using one-way analysis of variance. In the case of a significant time effect, the Newman-Keuls procedure was used for comparison. PATIENTS: A total of 14 patients, 12 male and 2 female, aged 18-75 years were included in the study. The arrhythmia requiring catheter ablation was atrioventricular (AV) excitation in seven patients, paroxysmal supraventricular tachycardia in five patients, atrial fibrillation and flutter in one patient, and cardiac dysrhythmia in one patient. All patients had normal electrophysiology at baseline. RESULTS: Mean heart rate decreased significantly with ivabradine by 12.9 beats/min at 30 minutes and 14.1 beats/min at 1 hour. The mean QT interval increased but QTc showed no significant change from baseline. The PR and QRS intervals were unchanged. The right atrial and right ventricle refractory periods showed no significant change from baseline. The measured QT interval and the sinus node recovery time were increased. There were no clinically relevant changes in any other major electrophysiological parameters. Ivabradine was well tolerated and no serious adverse events occurred. CONCLUSION: A single intravenous dose of ivabradine had a significant heart rate-lowering effect, observed at 30 minutes and 1 hour after administration. Ivabradine did not prolong QTc or modify conductivity and refractoriness of the atrium, AV node, His-Purkinje system and ventricles, or repolarisation duration. These results confirm the action of ivabradine as a specific heart rate-lowering agent.
In order to perform a technically adequate clinical electrophysiological procedure it is necessary to calibrate the stimulating and recording equipment. Published standards for the electroretinogram (ERG), electro-oculogram (EOG), visual evoked potential (VEP), and guidelines for the Pattern ERG (PERG) specify stimulus and recording parameters. Yet, most commercial instruments do not provide the means for calibration of these parameters. The goal of this document is to provide guidelines for proper calibration of stimulus and recording equipment. The need for such guidelines is clear on both clinical and scientific grounds. Stimulus and amplifier characteristics have substantial effects on the peak latency and amplitude measurements that are commonly used in clinical electrophysiology. Many review articles on clinical electrophysiology emphasize the need for establishing norms for each laboratory as a function of age and gender rather than relying on published norms. However, if stimulus and recording parameters are not calibrated periodically, then these norms may actually be misleading due to changes in stimulus or recording conditions induced by aging of equipment or inadvertent change in settings. This document is divided into two major sections. The first is concerned with calibration of the visual stimulus. It begins with background technical information on the physics of light and its measurement. This is followed by protocols for measurement of the luminous intensity of flash stimuli and the mean luminance, contrast, and visual angle of pattern stimuli. The second section is concerned with calibration of electrophysiologic recording systems. It begins with a description of the characteristics of bioelectrical signals and their measurement. This is followed by protocols for measurement of electrode impedance and amplifier calibration. Although this document was prepared as guidelines for clinical electrophysiological testing, it should be noted that the techniques described are more generally applicable to studies which are dependent upon accurate measurement of luminance or electrophysiological signals.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
PURPOSE: To analyze the value of electrophysiologic testing according to standards of the International Society for Clinical Electrophysiology of Vision (ISCEV) in infants less than 10 years of age. PATIENTS AND METHODS: In 64 infants less than 10 years, the results from of age electroretinograms (n = 47), visual evoked potentials (n = 30), or electro-oculograms (n = 1) were recorded. Twenty-nine infants were less than 6 years of age, and 17 infants were less than 3 years of age. Indications for examination were unexplained visual loss in 54 infants and familial hereditary retinal dystrophies in ten infants. Sedation with chloral hydrate was performed in seven children. RESULTS: In 40/64 infants (62%), the results of electrophysiologic examination were pathologic. In 29 infants visual loss was due to retinochoroidal dystrophies, and in 11 infants it was due to disturbances in the optic pathway. In 7/64, infants the suspected retinochoroidal dystrophy could be excluded. Therefore electrophysiologic testing was diagnostically accurate in 47/64 (73%) of cases. CONCLUSION: Electrophysiologic testing according to TSCEV standards can be reliably performed in infants less than 10 years of age. When the indication for electrophysiologic testing is made following meticulous ophthalmologic examination, diagnostic accuracy is given in at least 73% of cases.
BACKGROUND: Invasive electrophysiologic study and noninvasive Holter monitoring (in conjunction with exercise testing) have both been used to evaluate the efficacy of antiarrhythmic drugs in patients with sustained ventricular tachycardia and in survivors of cardiac arrest. We directly compared these two approaches to the prediction of drug efficacy. METHODS: A total of 486 patients who had documented ventricular tachyarrhythmias that were inducible during electrophysiologic study and 10 or more premature ventricular complexes per hour during Holter monitoring were randomly assigned to undergo serial testing of antiarrhythmic-drug efficacy by electrophysiologic study or Holter monitoring. The patients received up to six drugs in random order until one was predicted to be effective either in suppressing inducible arrhythmia (in the electrophysiologic-study group) or in suppressing premature ventricular complexes (in the Holter-monitoring group). The patients were then followed for recurrences of arrhythmia or death. RESULTS: In the electrophysiologic-study group, 108 of 242 patients (45 percent) received a prediction of efficacy, as compared with 188 of 244 patients (77 percent) in the Holter-monitoring group (P < 0.001). Over a six-year follow-up period, there were 150 recurrences of arrhythmia and 46 deaths among the 296 patients receiving drugs predicted to be effective. Thirty-four of the deaths were from arrhythmic causes, and eight were from cardiac causes. There was no significant difference between the two study groups in the actuarial probabilities of these events. The risk of a recurrence of arrhythmia was significantly lower in patients who received sotalol than in those who received other antiarrhythmic drugs, and the risk was lower in those who had not previously failed to respond to antiarrhythmic drugs than in those who had. CONCLUSIONS: Although Holter monitoring led to predictions of antiarrhythmic-drug efficacy more often than did electrophysiologic study in patients with sustained ventricular tachyarrhythmias, there was no significant difference in the success of drug therapy as selected by the two methods.
Training in clinical cardiac electrophysiology should take place in an Accreditation Council for Graduate Medical Education accredited cardiology program, and the electrophysiology training program itself should be accredited by the Council. Each trainee must be eligible for board certification in Internal Medicine and either eligible for certification in Cardiovascular Diseases or in a program leading to eligibility. Training faculty should be certified in clinical cardiac electrophysiology or demonstrate equivalent credentials. At least two training faculty members are preferred. The faculty must be dedicated to teaching, active in performing or promoting research and must spend a substantial portion of their time in research, teaching and practice of clinical electrophysiology. A curriculum of training should be established. Faculty experts in the related basic sciences should be available and involved in teaching. The institution should have a fully equipped clinical electrophysiology laboratory and complete noninvasive capabilities. A close working relation with a cardiac surgery faculty member skilled in surgical treatment of arrhythmias is required. Training in application of pharmacologic and all current nonpharmacologic therapies, in the outpatient and inpatient setting, is necessary. The clinical exposure must include all facets of arrhythmia diagnosis and treatment and must be quantitatively sufficient to allow the trainee to develop proficiency. The period of training should not be less than one year in addition to the period of cardiology fellowship required by the ABIM for board eligibility. A continuous period of training is preferred.
BACKGROUND: The number of data acquired in electrophysiology and the need for immediate analysis and interpretation justified the use of computerized signal acquisition and -analysis. Since such techniques are well known and established in computerized perimetry, the user of EOG, ERG, and VEP will profit from such an approach. METHOD: A computer program for signal acquisition and -analysis of clinical electrophysiology is described. The software is written in BASIC for IBM compatible PC/XT/AT computers. The program supports all electrophysiological examinations (EOG, ERG, VEP). It contains a subroutine for automated EOG recording and -analysis, allows measurements of amplitude and latency of standardized Ganzfeld-ERG and pattern-ERG. Options for recording and analysis of further stimuli are prepared. The possibility of determination of area under the curve is implemented. In the VEP subroutine evaluation of amplitude, latency, area under the curve, and Fast-Fourier-Transformation--necessary for steady-state-VEP--is installed. CONCLUSION: The program demonstrates that with the now available low cost Personal Computer technology it is possible to build up individual software systems for clinical electrophysiology supporting and optimizing all recording, analysing, and administrative procedures.
This article is the second part of a three article series reviewing computer simulation models of the heart, in particular of cardiac electrophysiology. The previous section of the review discussed the methodological principles of the construction and application of computer models. This article overviews the development of mathematical and computer modeling studies applied to cardiology. The models are classified according to the physiological processes that were simulated; this article distinguishes models oriented to cardiac mechanics, hemodynamics, and electrophysiology. The electrophysiology models are discussed in more detail and the review classifies them into four main categories: models of cellular processes, models of tissue behavior, models of the ventricular electric field, and models of macroconduction disturbances. In each category, the historical development of the models and their key achievements are described.
The long-term outcome of 241 survivors of out of hospital ventricular fibrillation who underwent programmed electrical stimulation was evaluated. Patients were categorized according to the rhythm induced at baseline drug-free electrophysiologic testing. Ventricular fibrillation was induced in 39 patients (16%) (Group 1), sustained ventricular tachycardia in 66 patients (27%) (Group 2) and nonsustained ventricular tachycardia in 34 patients (14%) (Group 3); 102 patients (42%) (Group 4) did not have an arrhythmia inducible at baseline electrophysiologic testing. Antiarrhythmic drugs were administered over the long term to 92% of patients in Group 2, 91% of patients in Group 1 and 47% of patients in Group 4. At a mean follow-up time of 30 +/- 15 months, recurrent sudden cardiac death or nonfatal ventricular fibrillation occurred in 11 (28%) of 39 patients with inducible ventricular fibrillation (Group 1), 14 (21%) of 66 patients with inducible sustained ventricular tachycardia (Group 2), 4 (12%) of 34 patients with inducible nonsustained ventricular tachycardia (Group 3) and 16 (16%) of 102 patients without inducible arrhythmias (Group 4). Actuarial analysis revealed a 2 year cumulative arrhythmia-free survival rate of 65% for patients in Group 2, 71% for patients in Group 1, 79% for patients in Group 3 and 81% for patients in Group 4 (p = 0.02). Actuarial survival of patients with inducible sustained ventricular tachycardia or ventricular fibrillation suppressed by electrophysiologically guided drug therapy was not significantly different from that in patients whose arrhythmia was not suppressed. Multivariate regression analysis revealed that only the presence of congestive heart failure was an independent predictor of outcome in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated the clinical features, surface ECG findings, associated with congenital heart disease (CHD), and status at follow-up in 103 children who underwent intracardiac electrophysiologic evaluation of supraventricular tachycardia (SVT). Age at catheterization ranged from 2 days to 17 years (mean 4.2 years). Diagnosis of the mechanism was based upon standard electrophysiologic techniques. Of the 103 patients, 37 had reentry without a bypass tract (10 sinoatrial node, two atrial muscle, and 25 atrioventricular node); 51 had reentry with a bypass tract (28 manifest Wolff-Parkinson-White [WPW], 18 unidirectional retrograde accessory pathway [URAP], an five Lown-Ganong-Levine); and 15 had an ectopic focus (11 atrial, four junctional). Distinguishing features among the common types are depicted in Table III. We conclude that in children the various mechanisms of SVT (1) are likely to be found in different clinical situations, (2) have a different potential for surgical cure, and (3) have a different prognosis for long-term treatment. Since curative surgery was theoretically possible in 57% of our patients (WPW, concealed WPW, atrial, and junctional ectopic), we recommend electrophysiologic study in any patient who has had frequent recurrences of SVT for longer than 1 year and who requires drugs in addition to digoxin for treatment.
Because of the known higher incidence of cardiac arrhythmia in aged patients we tried to define the underlying arrhythmogenic substrate by quantifying those electrophysiological alterations in aged rabbit hearts, which are commonly believed to be arrhythmogenic, relating them to histological findings in the same hearts. This is the first investigation that analyses the effect of ageing on the epicardial excitation spreading. Isolated hearts from young (ten weeks) and old (1.5-2 years) white New Zealand rabbits were perfused according to the Langendorff-technique, submitted to epicardial potential mapping for 60 min and investigated histologically. Electrophysiological data in aged hearts showed a) a higher variability of the activation pattern, b) an increased dispersion of the epicardial potential duration; c) a prolongation of the AV-conduction time and of the duration of the epicardial activation signal, which was fractionated in aged hearts. Histological findings showed extensive incorporation of fat cells and connective tissue in ventricular and AV-node tissues, which may explain the prolonged conduction time, and a marked hypertrophy of the ventricular myocytes. The observed high dispersion, the broadened and fractionated epicardial activation signal and the enhanced variability of the activation patterns may be due to the observed long strands of collageneous tissue separating ventricular muscle fibres in aged hearts. These changes help to explain the enhanced susceptibility to arrhythmogenic stimuli with age.
Regular atrial tachycardias classically are classified into flutter or tachycardia, depending on the rate and presence of a stable baseline on the ECG. However, current understanding of electrophysiology atrial tachycardias makes this classification obsolete, because it does not correlate with mechanisms. The proposed classification is based on electrophysiologic mechanisms, defined by mapping and entrainment. Radiofrequency ablation of a critical focus or isthmus can afford proof. Focal tachycardias are characterized by radial spread of activation and endocardial activation not covering the whole cycle. Ablation of the focus of origin interrupts the tachycardia. The mechanism of focal firing is difficult to ascertain by clinical methods. Macroreentrant tachycardias are characterized by circular patterns of activation that cover the whole cycle. Fusion can be shown during entrainment on the ECG or by multiple endocardial recordings. Ablation of a critical isthmus interrupts the tachycardia. Macroreentry can occur around normal structures (terminal crest, eustachian ridge) or around atrial lesions. The anatomic bases of these tachycardias must be defined, to guide appropriate treatment. Atrial flutter is a mere description of continuous undulation on the ECG, and only some strictly defined typical flutter patterns correlate with right atrial macroreentry bounded by the tricuspid valve, terminal crest, and caval vein orifices. This classification should be considered open, as some classically described tachycardias, such as reentrant sinus tachycardia, inappropriate sinus tachycardia, and type II atrial flutter, cannot be classified accurately. Furthermore, the possibility of fibrillatory conduction makes the limits with atrial fibrillation still ill defined.
INTRODUCTION: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias. METHODS AND RESULTS: We conducted a cohort study of all patients with myocardial infarction (MI) undergoing EP studies at our institution. Of 344 consecutive patients, 181 had previously documented spontaneous sustained ventricular arrhythmias, 61 had suspected ventricular arrhythmias, and 102 had neither. Ventricular flutter was induced in 65 (19%) of the patients. Left ventricular ejection fraction was highest among patients with inducible VF (35 +/- 13), lowest for patients with inducible sustained monomorphic ventricular tachycardia (SMVT; 27 +/- 9), and intermediate for patients with inducible ventricular flutter (30 +/- 10). Similarly, the coupling intervals needed to induce the arrhythmia were shortest for VF (200 +/- 28 msec), intermediate for ventricular flutter (209 +/- 27 msec), and longest for SMVT (230 +/- 35 msec). During 5 +/- 8 years of follow-up, the risk for ventricular tachycardia/VF was high for patients with SMVT and ventricular flutter and low for patients with inducible VF and noninducible patients (46%, 34%, 17%, and 14%, P < 0.005). CONCLUSION: Patients with inducible ventricular flutter appear to be "intermediate" between patients with inducible VF and patients with SMVT in terms of clinical and electrophysiologic correlates. However, the prognostic value of inducible ventricular flutter is comparable to that of SMVT.
The aim of this study was to determine whether the different morphological classes of pyramidal neurons in layers 2/3 and 5 of rat visual cortex (Larkman and Mason, 1990) have particular electrophysiological properties. Neurons in in vitro slices of rat visual cortex were impaled with glass micropipettes containing horseradish peroxidase (HRP) and studied using current-clamp techniques prior to pressure injection of HRP into the neurons. On morphological grounds, cells stained in layer 2/3 were placed into a single class whereas layer 5 cells were divided into 2 classes. Cells in one of these classes had thick apical dendrites which arborized in layer 1, whereas the apical dendrites of cells in the other class were thinner and did not reach layer 1 (Larkman and Mason, 1990). Despite variation between individual cells of a single class, significant differences were found in the time constants, current/voltage relations, and repetitive firing behaviors of the 3 classes. Burst firing responses to injected current pulses were confined to the layer 5 cells with thick apical dendrites. These results add to those from other areas of the brain demonstrating that the electrophysiological properties of pyramidal neurons are heterogeneous. Furthermore, we have shown that distinctive intrinsic membrane properties of pyramidal neurons in visual cortex are correlated with different morphologies.