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Biomedical subjects

R N Hauer

Publications and source records attributed to R N Hauer.

At least 37 records · Page 2Linked to original sources
PubMed1998

Electrocardiographic identification of abnormal ventricular depolarization and repolarization in patients with idiopathic ventricular fibrillation.

OBJECTIVES: We sought to gain more insight into the arrhythmogenic etiology of idiopathic ventricular fibrillation (VF) by assessing ventricular depolarization and repolarization properties by means of various electrocardiographic (ECG) techniques. BACKGROUND: Idiopathic VF occurs in the absence of demonstrable structural heart disease. Abnormalities in ventricular depolarization or repolarization have been related to increased vulnerability to VF in various cardiac disorders and are possibly also present in patients with idiopathic VF. METHODS: In 17 patients with a first episode of idiopathic VF, 62-lead body surface QRST integral maps, QT dispersion on the 12-lead ECG and XYZ-lead signal-averaged ECGs were computed. RESULTS: All subjects of a healthy control group had a normal dipolar QRST integral map. In patients with idiopathic VF, either a normal dipolar map (29%,), a dipolar map with an abnormally large negative area on the right side of the thorax (24%) or a nondipolar map (47%) were recorded. Only four patients (24%) had increased QT dispersion on the 12-lead ECG and late potentials could be recorded in 6 (38%) of 16 patients. During a median follow-up duration of 56 months (range 9 to 136), a recurrent arrhythmic event occurred in 7 patients (41%), all of whom had an abnormal QRST integral map. Five of these patients had late potentials, and three showed increased QT dispersion on the 12-lead ECG. CONCLUSIONS: In patients with idiopathic VF, ventricular areas of slow conduction, regionally delayed repolarization or dispersion in repolarization can be identified. Therefore, various electrophysiologic conditions, alone or in combination, may be responsible for the occurrence of idiopathic VF. Body surface QRST integral mapping may be a promising method to identify those patients who do not show a recurrent episode of VF.

Adult↗
PubMed1998

Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation.

AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.

Adult↗
PubMed1998

'Para' AV nodal re-entry tachycardias.

Aim AV node, para AV nodal, and parahisian areas are usually not clearly defined in the literature. Radiofrequency catheter ablation in these areas may be deleterious to normal AV conduction. The purpose of this contribution is to discuss the anatomy in these areas in relation to outcome an AV conduction disturbances after radiofrequency ablation. Guidelines for therapeutic management of AV nodal re-entry tachycardia and tachycardias with involvement of a parahisian pathway, will be discussed.

Atrioventricular Node↗
PubMed1997

Body-surface QRST integral mapping. Arrhythmogenic righ ventricular dysplasia versus idiopathic right ventricular tachycardia.

BACKGROUND: Ventricular tachycardia originating in the right ventricle may arise in the presence or absence of structural heart disease. The two main causes of right ventricular tachycardia are arrhythmogenic right ventricular dysplasia (ARVD) and idiopathic right ventricular tachycardia (IRVT) originating from the outflow tract. This study was carried out to determine whether body-surface QRST integral mapping can differentiate patients with ARVD from patients with IRVT. METHODS AND RESULTS: Body-surface QRST integral maps were obtained during sinus rhythm in 8 patients with ARVD, 8 patients with IRVT, and 27 healthy control subjects. QRST integral maps were analyzed both visually and mathematically. All control subjects had a normal dipolar QRST integral map. In all patients with ARVD, a specific dipolar QRST integral map with an abnormally large negative area covering the entire inferior and right anterior thorax was recorded. In 6 of 8 patients with IRVT, a normal map pattern was found, whereas the remaining 2 patients showed an abnormally large negative area on the right anterior thorax. CONCLUSIONS: Patients with ARVD display a specific abnormal QRST integral map that may be related to delayed repolarization in the structurally abnormal right ventricle. The majority of patients with IRVT demonstrate a normal QRST integral map. A slightly abnormal QRST integral map was noted in 2 of 8 patients with IRVT, which may be related to minor structural abnormalities, undetectable by the present routine diagnostic techniques. These preliminary results indicate that body-surface QRST integral mapping may become an important diagnostic tool to differentiate patients with ARVD from those with IRVT.

Adult↗
PubMed1997

Mitral valve prolapse and ventricular arrhythmias: observations in a patient with a 20-year history.

INTRODUCTION: Ventricular arrhythmias are a common feature in patients with mitral valve prolapse. In an attempt to determine the origin and underlying electrophysiologic mechanism, we describe a patient with ventricular fibrillation, exercise-induced ventricular tachycardia (VT), and, at the time of diagnosis, prolapse of the posterior mitral valve leaflet without mitral regurgitation. METHODS AND RESULTS: Treatment with beta-blockade and diphenylhydantoin prevented the occurrence of malignant ventricular arrhythmias for more than 17 years. Discontinuation of the therapy resulted in an immediate reappearance of the VT, which, despite the marked enlargement of the left ventricle (secondary to development of severe mitral valve regurgitation), had a strikingly similar morphology. For hemodynamic reasons, the patient was finally selected for valve replacement. Detailed pre-, peri-, and postoperative studies were performed, including administration of flunarizine, body surface mapping, construction of perioperative epicardial and endocardial maps, and studies of the excised muscles in vitro. CONCLUSIONS: Delayed afterdepolarization-induced triggered activity is the mechanism of VT in this mitral valve prolapse patient. The trigger is provided by isolated ventricular premature complexes elicited by a different electrophysiologic mechanism, possibly reentry, which is related to stretch and presumably to fibrosis of the papillary muscles.

Adult↗
PubMed1996

Can implantable cardioverter-defibrillator therapy reduce healthcare costs?

This article presents a comparison of the costs and the cost effectiveness of defibrillator implantation in a hypothetical scenario for the years 1996-2000, with recently reported actual data from the Dutch prospective study over the years 1989-1993. Recently, technological advances in pulse generator and leads have revolutionized implantable cardioverter-defibrillator (ICD) therapy. Major advances include (1) transvenous single lead positioning and (2) tremendously reduced size, combined with prolonged longevity of the pulse generator. Both have simplified implantation technique and provided for superior effectiveness and lower costs. This suggests that a more favorable cost-effectiveness is to be expected. The study group reported here consisted of patients successfully resuscitated after cardiac arrest due to malignant ventricular tachyarrhythmias in the chronic stage of myocardial infarction. During a mean follow-up of 27 months, starting on the day of therapeutic decision making, total costs and the cost-effectiveness ratio were estimated. Actual data from the prospective study in 1989-1993 are compared with a hypothetical scenario for 1996-2000. Mortality and costs for hospitalization per day, per procedure, and per device are taken from the prospective study and equalized for both scenarios. Transthoracic lead positioning and abdominal implantation of a Ventak P (CPI) defibrillator with +/- 3 years longevity were characteristic of the recently completed prospective study. The hypothetical future scenario uses the Ventak Mini-2 with assumed 5 years longevity, implanted pectorally and connected to a single transvenous lead. Implantation will be carried out in the catheterization laboratory and as first-choice treatment. Due to prolonged longevity of the device and shorter hospitalization, a cost reduction of US $11,530 per patient is expected. Total costs per patient in the 1989-1993 prospective study in the (1) conventional arm (drugs first choice), (2) early ICD arm (ICD first choice), and (3) early ICD arm in the 1996-2000 study (ICD first choice) are $63,032, $56,067, and $44,537, respectively. The corresponding cost-effectiveness ratios are $87, $64, and $51 per day alive, respectively. Thus, it appears that modem ICD technology will be associated with an increasing reduction in healthcare costs, at least in selected patients. This reduction is associated with a more favorable cost-effectiveness ratio.

Cost Control↗
PubMed1996

Cost-effectiveness of implantable defibrillator as first-choice therapy versus electrophysiologically guided, tiered strategy in postinfarct sudden death survivors. A randomized study.

BACKGROUND: Rising costs of health care, partly as a result of costly therapeutic innovations, are of concern to both the medical profession and healthcare authorities. The implantable cardioverter-defibrillator (ICD) is still not remunerated by Dutch healthcare insurers. The aim of this study was to evaluate the cost-effectiveness of early implantation of the ICD in postinfarct sudden death survivors. METHODS AND RESULTS: Sixty consecutive postinfarct survivors of cardiac arrest caused by ventricular tachycardia or fibrillation were randomly assigned either ICD as first choice (n = 29) or a tiered therapy starting with antiarrhythmic drugs and guided by electrophysiological (EP) testing (n = 31). Median follow-up was 729 days (range, 3 to 1675 days). Fifteen patients died, 4 in the early ICD group and 11 in the EP-guided strategy group (P = .07). For quantitative assessment, the cost-effectiveness ratio was calculated for both groups and expressed as median total costs per patient per day alive. Because effectiveness aspects other than mortality are not incorporated in this ratio, other factors related to quality of life were used as qualitative measures of cost-effectiveness. The cost-effectiveness ratios were $63 and $94 for the early ICD and EP-guided strategy groups, respectively, per patient per day alive. This amounts to a net cost-effectiveness of $11,315 per patient per year alive saved by early ICD implantation. Costs in the early ICD group were higher only during the first 3 months of follow-up, but as a result of the high proportion of therapy changes, including arrhythmia surgery and late ICD implantation, costs in the EP-guided strategy group became higher after that. Patients discharged with antiarrhythmic drugs as sole therapy had the lowest total costs. This subset, however, showed extremely high mortality, resulting in a poor cost-effectiveness ratio ($196 per day). Invasive therapies and hospitalization were the major contributors to costs. If quality-of-life measures are taken into account, the cost-effectiveness of early ICD implantation was even more favorable. Recurrent cardiac arrest and cardiac transplantation occurred in the EP-guided strategy group only, whereas exercise tolerance, total hospitalization duration, number of invasive procedures, and antiarrhythmic therapy changes were significantly in favor of early ICD implantation. CONCLUSIONS: In terms of cost-effectiveness, early ICD implantation is superior to the EP-guided therapeutic strategy in postinfarct sudden death survivors.

Anti-Arrhythmia Agents↗
PubMed1996

Effects of heating with radiofrequency power on myocardial impulse conduction: is radiofrequency ablation exclusively thermally mediated?

INTRODUCTION: Although it is generally accepted that radiofrequency (RF) ablation causes exclusively thermally mediated effects, it has never been proved. METHODS AND RESULTS: In a previous report, temperatures required to induce conduction block in superfused canine epicardial ventricular myocardium were identified by exposure to heated superfusate: 50.3 degrees +/- 1.1 degrees C and 53.6 degrees +/- 0.6 degree C for transient and permanent block, respectively. In the present study, heating was performed using RF power in an otherwise identical model. Nine preparations from four dogs were used. A 1-cm diameter electrode was placed beneath the center of each preparation for RF delivery. Incisions were made to create a conductive isthmus over the ablation electrode. Preparations were paced to one side of the isthmus and electrograms recorded from the center of the isthmus and to either side. Temperature was measured using a miniature thermocouple located just below the epicardial surface, adjacent to the recording electrode in the heated zone. RF was delivered for 30 seconds at 5-minute intervals with increments in power per episode causing increments in temperature of approximately 2 degrees C. Temperature during pulses at which transient block occurred was 50.7 degrees +/- 3.0 degrees C; temperature at 30 seconds of heating in pulses leading to permanent block was 58.0 degrees +/- 3.4 degrees C. CONCLUSION: These findings provide evidence suggesting that the electrophysiologic effects of RF ablation are exclusively thermally mediated and are otherwise unrelated to the dissipation of high-frequency current.

Animals↗
PubMed1995

Randomized study of implantable defibrillator as first-choice therapy versus conventional strategy in postinfarct sudden death survivors.

BACKGROUND: In retrospective studies of sudden cardiac death survivors, the implantable cardioverter-defibrillator (ICD) compares favorably with medical and surgical therapy. Thus, use of the conventional strategy of starting treatment with antiarrhythmic drugs (AD), at least in certain patient categories, may be questionable. The goal of this study was to analyze the effectiveness of ICD implantation as first-choice therapy versus the conventional therapeutic strategy of starting with AD. METHODS AND RESULTS: Sixty consecutive survivors of cardiac arrest caused by old myocardial infarction were randomly assigned early ICD implantation (n = 29) or conventional therapy (n = 31). Baseline characteristics were similar in the two groups. Therapy in each patient was always guided by ECG monitoring, exercise testing, and programmed electrical stimulation (PES). Primary end points (main outcome events, including death, recurrent cardiac arrest, and cardiac transplantation), number of invasive procedures and antiarrhythmic therapy changes, and duration of hospitalization were compared. Median follow-up was 24 months (mean, 27 months). In the early ICD group, 4 patients (14%) died, all of cardiac causes. In the conventional group, 20 patients failed AD and subsequently underwent map-guided ventricular tachycardia (VT) surgery (6 patients) or ICD implantation (14 patients). Of the 6 VT surgery patients, 1 died, 1 had cardiac transplantation, and 1 had an ICD implantation because of persistent inducibility despite the addition of AD. Of the 11 patients who remained on AD as sole therapy, 2 died in the hospital before they could be retested by PES, leaving 9, judged adequately protected by AD alone. Of those, 5 died, and 1 survived recurrent cardiac arrest followed by ICD implantation. In total, 16 conventionally treated patients ended up with late ICD implantation, 3 of whom died. Thus, total mortality in the conventional group was 11 patients (35%): 4 died suddenly, 5 died of heart failure, and 2 died of noncardiac causes. Comparison of the main outcome events in both strategies showed a significant difference in favor of early ICD implantation (hazard ratio, 0.27; 95% CI, 0.09 to 0.85; P = .02). In addition, the early ICD group underwent fewer invasive procedures (median, 1 versus 3; P < .0001), had less therapy changes (P < .0001), and spent fewer days in hospital (median, 34 versus 49; P = .02). CONCLUSIONS: These data suggest that ICD implantation as first choice is preferable to the conventional approach in survivors of cardiac arrest caused by old myocardial infarction. Conventionally treated patients are likely to end up with an ICD, and those who remain on AD as sole therapy have a high risk of death regardless of efficacy assessment, including PES.

Anti-Arrhythmia Agents↗
PubMed1995

Effects of heating on impulse propagation in superfused canine myocardium.

OBJECTIVES: The goal of the study was to quantify the response of myocardial impulse propagation to hyperthermia and identify the temperatures required for transient and permanent block in conduction. BACKGROUND: Although it is generally accepted that the effects of radiofrequency ablation are thermally mediated, the precise response of myocardial impulse conduction to heating remains to be quantified. METHODS: Twenty-three preparations of ventricular myocardium from 10 beagle dogs were superfused at 36.5 to 37.5 degrees C and paced at a cycle length of 600 ms. Heating was performed for 30 s at 5-min intervals by an independent flow of heated superfusate. A 16-electrode grid was used to record extracellular electrograms directly before each heating episode (control value) and at 10, 20 and 30 s. RESULTS: Between 38.5 and 45.4 degrees C, conduction velocity was higher than that at the directly preceding control value (p < 0.05), reaching a maximum of 114% between 41.5 and 42.5 degrees C. Above 45.4 degrees C, a gradual decrease occurred, with transient block (absence of impulse conduction for < or = 5 min) after heating to 49.5 to 51.5 degrees C. This was followed by tachycardia in 69% of all cases immediately after cessation of heating. Permanent block occurred after a significantly higher temperature of 51.7 to 54.4 degrees C had been reached. Pacing at sites allowing preferential conduction either parallel or perpendicular to fiber orientation caused no difference in reaction to heating. Repeated heating of some preparations to 47.0 to 50.5 degrees C revealed no cumulative effects on conduction velocity. CONCLUSIONS: Transient and permanent block in impulse conduction occurred at 49.5 to 51.5 degrees C and 51.7 to 54.4 degrees C, respectively, in superfused canine myocardium, the former frequently being followed directly by tachycardia. Reaction of conduction velocity to hyperthermia was independent of myocardial fiber orientation and number of preceding heating episodes. Results may contribute to a better understanding of electrophysiologic phenomena observed during radiofrequency ablation procedures.

Animals↗
PubMed1995

Myocardial temperature response during radiofrequency catheter ablation.

During radiofrequency catheter ablation, steady-state electrode-tissue interface temperatures are reached within 5 seconds. Within the myocardium, however, a much slower temperature rise has been observed in vitro with stabilization after approximately 2 minutes. The discrepancy suggests that tissue temperature rise time depends on distance from the ablation electrode and, thus, that temperature rise measured at the electrode-tissue interface does not correspond with temperature rise within the myocardium. In five beagles, closed-chest radiofrequency catheter ablation was performed in the vicinity of intramural thermocouples. Sequences of 60 seconds, 10- and 25-watt pulses were delivered in the unipolar mode via the 4-mm distal electrode of a 7 French steerable catheter. At all distances > 3 mm from the ablation electrode, the rate of myocardial temperature rise was low: relative rise after 5, 10, 20, and 30 seconds was 22%, 32%, 48%, and 63% of that achieved at 60 seconds, and even then steady-state temperatures had not yet been reached. Temperature rise was faster at sites closer to the ablation electrode. There was no difference in rate of rise between first and second pulses at the same site. A 6% higher myocardial temperature was reached with a second identical pulse at the same site. Tissue temperatures achieved with 25 watts were 2.4 times higher than with a preceding 10-watt pulse at the same ablation site.

Animals↗
PubMed1995

Is there space for surgery in the treatment of tachyarrhythmias?

Curative treatment of both supraventricular and ventricular tachyarrhythmias started with the introduction of surgical therapy. Surgical treatment modalities were often very successful and associated with low mortality and morbidity, especially in patients with various supraventricular tachyarrhythmias. However, results were acceptable in patients with ventricular tachyarrhythmias, with often a very complex and extended arrhythmogenic area associated with structural heart disease. Because of the development and proven effectiveness of catheter ablation and defibrillator implantation, the role of surgical therapy became limited. In the treatment of supraventricular arrhythmias, surgical therapy is an option after failure of catheter ablation. Since His-bundle catheter ablation is only a palliative treatment for atrial fibrillation, the potentially curative Maze operation may be an acceptable alternative. However, its potential against formation of intracavitary thrombi has not yet been proven. In the treatment of ventricular tachyarrhythmias, ischemia related polymorphic ventricular tachycardia and ventricular fibrillation can be treated very effectively by revascularization. Map-guided surgery is an appropriate treatment modality for patients with monomorphic ventricular tachycardia and an extended arrhythmogenic area. However, patients with very poor left ventricular function may have an unacceptable perioperative risk. In patients with congenital long QT syndrome who are refractory to beta blocking agents, left-sided sympathectomy is the most appropriate choice.

Humans↗
PubMed1995

Change in delay of atrioventricular conduction after radiofrequency catheter ablation for atrioventricular nodal re-entry tachycardia.

OBJECTIVE: To monitor atrioventricular conduction after radiofrequency ablation for atrioventricular nodal re-entry tachycardia. DESIGN: Measurement of PR interval from 12 lead surface electrocardiograms before; at 0, 24, 48, 72, and 96 hours; and at 1 and 6 months after radiofrequency ablation. PATIENTS: 40 consecutive patients with atrioventricular nodal re-entry tachycardia. The anterior approach was used in 23 patients, the posterior approach in 17. RESULTS: With the anterior approach the PR interval increased significantly and progressively until 48 hours after ablation (maximum 282 (SD 62.2) ms, before ablation 142 (29.5) ms; P < 0.0001). Up to 96 hours no further change was observed, but one month after ablation the PR interval had decreased to a value not significantly different from that 24 hours after the procedure (231 (51.2) ms). In one patient total atrioventricular block developed 24 hours after an uncomplicated procedure and a permanent pacemaker was implanted. With the posterior approach the PR interval increased slightly in the first 24 hours (156 (22.7) ms, before ablation 144 (21.2) ms P = 0.004), but it had returned to preablation values at 1 month. One patient developed second degree atrioventricular block during the first 24 hours after ablation, despite delivery of all radiofrequency pulses posterior to Koch's triangle at sites without His bundle deflection. PR intervals at 6 months did not differ significantly from the values at 1 month. CONCLUSION: After the anterior approach the progressive delay in atrioventricular conduction up to 48 hours after radiofrequency ablation for atrioventricular nodal re-entry tachycardia warrants continuous in hospital monitoring of patients for at least two days after the procedure.

Atrioventricular Node↗
PubMed1994

Value of body surface mapping in localizing the site of origin of ventricular tachycardia in patients with previous myocardial infarction.

OBJECTIVES: This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction. BACKGROUND: Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci. METHODS: Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping. RESULTS: Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias in patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction. CONCLUSIONS: This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG may be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

Body Surface Potential Mapping↗
PubMed1994

Atlas of paced body surface QRS integral maps for localization of the site of origin of postinfarction ventricular tachycardia.

Current mapping during radiofrequency (RF) catheter ablation of postinfarction ventricular tachycardia (VT) is based primarily on the use of single-site mapping techniques. Although such techniques are highly suitable for distinguishing the ultimate site where RF energy is delivered by enabling detailed localization of the exit site or critical component of the VT reentrant circuit, they are time-consuming and inefficient for initial rapid identification of the arrhythmogenic target area. This study features the design and preliminary clinical application of a new noninvasive method that is aimed at speeding up the initial phase of the VT mapping procedure. This method is based on the use of an atlas of 62-lead body surface QRS integral map patterns that was previously developed using left ventricular pace mapping in patients with remote anterior or inferior myocardial infarction. The atlas contains 18 and 22 different paced QRS integral map patterns obtained in patients with previous anterior or inferior myocardial infarction, respectively. Each specific QRS pattern in the atlas provides a unique infarct-specific spatial electrocardiographic representation of the onset of ectopic ventricular activation in a circumscribed endocardial segment of the left ventricle. Localization of the segment of VT origin is obtained by visually or mathematically comparing the QRS integral map recorded during VT with one of the two sets of paced QRS integral maps contained within the atlas with the purpose of selecting the best matching paced QRS integral map pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Surface Potential Mapping↗
PubMed1994

Bradycardia dependent QT prolongation and ventricular fibrillation following catheter ablation of the atrioventricular junction with radiofrequency energy.

Recurrent ventricular fibrillation was observed in a 67-year-old woman following catheter ablation of the AV junction using radiofrequency energy. This serious complication has been reported following direct current energy ablation of the AV junction, but not after using radiofrequency energy. This life-threatening arrhythmia seemed pause and bradycardia dependent. It was followed by QTc prolongation of the QRS escape rhythm 1 day after the procedure. Ventricular arrhythmias were suppressed by rapid ventricular pacing.

Aged↗