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Biomedical subjects

B Waldecker

Publications and source records attributed to B Waldecker.

At least 19 recordsLinked to original sources
PubMed1997

Inappropriate management of self-terminating ventricular arrhythmias by implantable cardioverter defibrillators despite a specific reconfirmation algorithm: a report of two cases.

Algorithms that attempt to reconfirm the presence of an arrhythmia prior to definite treatment have been implemented in ICDs to prevent inappropriate shock therapy due to self-terminating ventricular arrhythmias. Nevertheless, in two patients, clinically inappropriate shocks were delivered after spontaneous conversion of the arrhythmia despite the use of a specific reconfirmation algorithm. Reconfirmation criteria were met due to a premature ventricular complex causing a short cycle in the first patient and a long postextrasystolic pause in the second patient. To avoid inappropriate shock therapy due to self-terminating ventricular arrhythmias, further improvement of detection algorithms is required.

Algorithms↗
PubMed1996

Specific cardiological evaluation after focal cerebral ischemia.

Purpose of this study was to define a subgroup of TIA/stroke patients who should be examined by transthoracal and transesophageal echocardiography or Holter-electrocardiography to identify those with cardiogenic brain embolism reliably; 300 consecutive patients with acute focal brain ischemia underwent a standardized diagnostic protocol for the evaluation of the etiology including, clinical examination by a cardiologist and routine electrocardiography, Holter-electrocardiography, transthoracal and transesophageal echocardiography. 188 patients had a potential cardiac source of embolism. In particular echocardiography was diagnostic in 163 patients, and Holter-electrocardiography 10; 159 of these 188 patients (84.6%) had competitive etiologies, predominantly large vessel atherosclerosis. In 136 patients cardiogenic brain embolism was assumed as quite definite or possible. To identify these patients reliably, transthoracal and transesophageal echocardiography would have been necessary in 89% of the entire group of patients (all with clinically cardiological abnormalities, pathological routine ECG, without vascular risk factors, or no atherosclerosis in duplex sonography), and Holter-electrocardiography in 54%.

Cerebral Infarction↗
PubMed1995

Electrophysiological effects of flecainide on anisotropic conduction and reentry in infarcted canine hearts.

BACKGROUND: The class IC antiarrhythmic drug flecainide has been shown to be ineffective for the treatment of ventricular arrhythmias in some patients who have had a prior myocardial infarction and sometimes even provoke arrhythmias (proarrhythmic effect). Since some ventricular tachycardias may be caused by anisotropic reentry, we determined the effects of flecainide on this mechanism for reentry in infarcted canine hearts in order to determine possible causes for its clinical effects. METHODS AND RESULTS: The effects of flecainide were determined on ventricular tachycardia induced by programmed electrical stimulation in dogs with healing myocardial infarction 4 days after coronary artery occlusion. Activation in the reentrant circuits causing tachycardia was mapped with a 196-channel computerized mapping system. We found that flecainide converted inducible unsustained ventricular tachycardia to inducible sustained ventricular tachycardia by modifying conduction in the reentrant circuit. In general, by slowing conduction, the reentrant wave front did not block after flecainide, leading to perpetuation of reentrant excitation. When sustained ventricular tachycardia could be induced before the drug, flecainide prolonged the coupling interval of premature impulses necessary to induce tachycardia by lengthening the line of block and slowing conduction around it. Flecainide also slowed the rate of the tachycardia but did not terminate it. The anisotropic reentrant circuits were modified so that the central common pathway of "figure-of-eight" circuits was narrowed and lengthened due to extension of the lines of block that bounded the pathways. Extension of the lines of block resulted from depression of conduction in the direction transverse to the long axis of the myocardial fiber bundles caused by flecainide. Flecainide also slowed conduction in the longitudinal direction in part of the circuits. The depressant effects of flecainide on both longitudinal and transverse anisotropic conduction were quantified by pacing from the center of the electrode array and it was found, contrary to predictions, that transverse conduction was depressed as much as longitudinal conduction. CONCLUSIONS: Flecainide slows conduction in both the longitudinal and transverse direction relative to the orientation of the myocardial fibers. This enables sustained reentry to occur more easily. Flecainide does not cause conduction block in crucial regions of reentrant circuits (central common pathway) and therefore does not prevent reentrant tachycardia in healing infarcts.

Animals↗
PubMed1994

[Heart rhythm after conversion of ventricular tachyarrhythmia by internal shock delivery].

The purpose of this retrospective study is the analysis of dysrhythmias following internal cardioversion/defibrillation of ventricular tachycardia (VT) or fibrillation (VF) and to discuss their relevance to the therapy with automatic implantable devices. Therefore, 304 internal conversions of VT/VF during and/or after implantation of automatic defibrillators were evaluated in 51 patients. Significant post-shock arrhythmias (bradycardia, atrial fibrillation, non-sustained VT of > or = 10 cycles) were absent after 89% of internal shocks. Pauses of > 2 s were observed in 2/9 patients without VVI-back-up pacing. The heart rate was > or = 50 bpm in 10/51 patients. Atrial fibrillation occurred in 7 patients. Non-sustained, mostly polymorphic VT consisting of > or = 10 cycles followed 18/304 (6%) internal shocks in 13 patients. The VT rate was > or = 200/min in 17/18 episodes and triggered an inadequate shock once. The incidence of non-sustained VT post-shock was unrelated to shock energy, type, and duration of the converted arrhythmia. In conclusion, automatic implantable devices should provide back-up pacing. Tachycardic rhythms can mislead automatic interpretation of the effect of internal shocks.

Adult↗
PubMed1993

In-hospital experience with multiprogrammable implantable antitachycardia/antifibrillation devices.

Multiprogrammable, automatic internal defibrillators with (n = 45) and without (n = 15) antitachycardia pacing features were implanted in 60 consecutive patients with refractory, malignant ventricular tachycardia (VT) (n = 42) or fibrillation (VF) (n = 18). Left ventricular (LV) ejection fraction was reduced to 39% +/- 12% as a result of structural heart disease in 56 patients. The complexity of the systems caused no additional risks to the surgical procedure or postoperative management. VT/VF detection parameters were individually adjusted to the arrhythmia type (detection cycle length 323 +/- 40 ms in patients with VF vs 405 +/- 40 ms for VT patients, P < 0.05) and incidence (longer detection periods if frequent nonsustained VT was also present). Shock energy was reduced in patients with VT as compared to VF (11J vs 24J, P < 0.05). Antitachycardia pacing was activated in 19/28 (68%) patients with well tolerated VT. Signal, telemetry, as detected by the device, combined with programmability allowed the device to be checked for correct decisions (these were inappropriate in four patients in three of whom corrections were non-invasive) prior to discharge. In conclusion, in the automatic tachyarrhythmia control devices we studied, programmability and flexibility appeared to be clinically safe and useful. Prolonged observation periods are required, however, to evaluate the true clinical safety and persistent efficacy of device programmability and flexibility.

Algorithms↗
PubMed1993

Effects of overdrive stimulation on functional reentrant circuits causing ventricular tachycardia in the canine heart: mechanisms for resumption or alteration of tachycardia.

INTRODUCTION: The purpose of the experiments described in this article was to investigate the effects of overdrive stimulation on functional anisotropic reentrant circuits causing ventricular tachycardia in infarcted canine ventricles. We determined how overdrive stimuli affect reentrant circuits to alter characteristics of the tachycardia. METHODS AND RESULTS: Activation patterns were determined by mapping excitation with a 192 bipolar electrode array. We found that overdrive stimuli could activate the circuits with the same pattern as the reentrant wavefront and that after overdrive stopped either the last or the next to last stimulated wavefront continued propagating through the circuit as a new reentrant impulse and tachycardia continued. When the circuit was not altered after overdrive, the exit route that the stimulated wavefront took from the circuit to activate the rest of the ventricles was also not altered and the tachycardia after overdrive had the same cycle length and QRS morphology as prior to overdrive. In some experiments, however, the overdrive stimuli did not follow the original reentrant pathway but led to the formation of a different circuit with a different exit route to the ventricles. As a result, after overdrive stimulation tachycardia had a different QRS morphology and cycle length than prior to stimulation. When the new circuit after overdrive was small and the revolution time of the reentrant impulse around the circuit was short, fibrillation occurred. CONCLUSION: Functional reentrant circuits can either be maintained or altered after a period of overdrive stimulation. The results explain many of the effects that have been seen during overdrive stimulation of clinical ventricular tachycardia.

Animals↗
PubMed1993

Overdrive stimulation of functional reentrant circuits causing ventricular tachycardia in the infarcted canine heart. Resetting and entrainment.

BACKGROUND: Clinical electrophysiology studies have used, for the most part, models of anatomic reentrant circuits to explain entrainment of ventricular tachycardia. Our studies use activation maps to directly determine mechanisms of entrainment of functional circuits that cause tachycardia. METHODS AND RESULTS: Electrograms were recorded from 192 sites on reentrant circuits in the epicardial border zone of canine myocardial infarcts during sustained ventricular tachycardia. Overdrive stimulation from different sites and at different cycle lengths was investigated. The reentrant circuits were shown to be functional, yet stimulated impulses could enter and repetitively reset the circuits (entrainment), demonstrating the presence of an excitable gap. Entrainment could occur from different stimulation sites with the stimulated impulses from each site activating the circuit with a different pattern. Entrainment, however, did not occur when the stimulated wave fronts obliterated the lines of functional block in the circuit. Fusion on the ECG occurred during entrainment when the stimulated impulses activated the ventricles concurrently with a previous stimulated impulse leaving the reentrant circuit at a different site. The first postpacing QRS was captured but not fused because it was caused by the last stimulated impulse emerging from the circuit. The first postpacing cycle length on the ECG was either equal to or longer than the overdrive cycle length depending on whether there was a fusion QRS during overdrive. The first postpacing cycle length at sites in the reentrant circuit equaled the pacing cycle length. At an appropriately short overdrive cycle length, stimulated impulses blocked in the circuit to terminate reentry. CONCLUSIONS: Functional reentrant circuits causing ventricular tachycardia can be reset and entrained. Activation maps directly show the mechanisms.

Animals↗
PubMed1991

Reverse use-dependent effects of sotalol demonstrated by recording monophasic action potentials of the right ventricle.

In 22 patients referred for electrophysiologic study, monophasic action potentials (MAP) were recorded from the right ventricular aspect of the ventricular septum. The duration of MAP at 90% (MAP90) and 30% (MAP30) repolarization was measured in sinus rhythm, at a constant atrial paced cycle length of 600 ms for 3 minutes and at constant ventricular paced cycle lengths of 600, 500, 400 and 300 ms for 20 beats. Programmed ventricular stimulation from the apex of the right ventricle was performed at a basic drive cycle length of 400 ms and MAP90 and MAP30 of premature beats was determined. Changes of MAP duration were assessed 20 minutes after administration of intravenous sotalol 1.5 mg/kg. Sotalol significantly increased MAP90 and MAP30 in sinus rhythm. This was independent from sinus cycle length prolongation as evidenced by a significant prolongation of MAP90 and MAP30 with constant atrial pacing after sotalol. With slow ventricular stimulation frequencies and with long coupling intervals at programmed ventricular stimulation, sotalol significantly prolonged MAP90 and MAP30; with high stimulation frequencies and at short coupling intervals the action potential-prolonging effect of sotalol was diminished, indicating a reverse use-dependent effect of sotalol on repolarization of the right ventricle in humans.

Action Potentials↗
PubMed1991

[Combined anti-bradycardia/anti-tachycardia pacemaker-cardioverter-defibrillator systems in patients with recurrent ventricular tachyarrhythmias].

In 41 patients with recurrent sustained ventricular tachycardia and/or ventricular fibrillation an integrated pacemaker-defibrillator-system (PCD, Medtronic, model 7216 A or 7217 B) was implanted. In 21 out of 24 (88%) patients a new transvenous implantation technique in combination with a subcutaneous patch electrode was used. The implanted devices comprise antibradycardiac pacemaker functions, two different forms of antitachycardiac pacemaker functions (ramp and burst pacing), and internal cardioversion or defibrillation capabilities. During a mean follow-up of 8 months 147 episodes of ventricular tachycardia were detected, 131 of them were terminated successfully by antitachycardiac pacing; in 13 episodes internal cardioversion was applied to revert ventricular tachycardia. Twenty-seven episodes of ventricular fibrillation or rapid ventricular tachycardia (greater than 200/min) were detected and successfully terminated by internal defibrillation. In six patients with intermittent rapid atrial fibrillation, change of antiarrhythmic therapy was required to avoid activation of the device. The new integrated pacemaker-defibrillator systems improve therapy in patients with life-threatening tachyarrhythmias by reducing the number of internal cardioversions/defibrillations; the non-thoracotomy approach reduces the post operative risk.

Adult↗
PubMed1990

Electrophysiologic effects of bepridil in patients with refractory ventricular tachycardia assessed by programmed electrical stimulation.

The effect of intravenous bepridil, a new calcium antagonist with class I and III properties, was tested in 21 patients with sustained ventricular tachyarrhythmias refractory to a mean of five antiarrhythmic agents as assessed by programmed right ventricular stimulation. At control electrophysiologic study without antiarrhythmic agents, sustained monomorphic ventricular tachycardia (VT) was initiated in 20 patients and ventricular fibrillation (VF) was initiated in one patient. After 3 mg/kg of bepridil was administered, VT was still inducible in 19 patients (3 patients had self-terminating VT); the other 2 patients had no inducible VT after bepridil. Bepridil prolonged significantly the QTc interval, the effective refractory period, and the cycle length of induced ventricular tachycardia. Two patients with no inducible VT after intravenous bepridil were placed on oral bepridil (300 mg/day). One patient died suddenly and one patient died of progressive heart failure. The results seem to indicate that the efficacy of bepridil in patients with refractory ventricular tachycardia is limited.

Aged↗
PubMed1990

[Predictive value of programmed electrostimulation in patients with spontaneous idiopathic ventricular tachycardia].

In contrast to patients with organic heart disease, there are only few data available on the incidence and type of inducible arrhythmias during programmed electrical stimulation (PES) in patients with spontaneous ventricular tachycardia (VT) but without evidence of underlying heart disease. Additionally, no consensus has been achieved in these patients on the most appropriate stimulation protocol required to reproduce the clinical arrhythmia. In a prospective study we analyzed in 40 patients without idiopathic VT, incidence and type of inducible VT, as well as the mode of initiation during a right ventricular PES protocol with 1-2 (part I) and three extrastimuli (part II). Twelve patients had spontaneous sustained monomorphic VT (group A), 28 patients were studied with spontaneous non-sustained VT (group B). During PES, a non-sustained polymorphic VT was induced in 3/12 patients (group A, 25%) and in 10/28 patients (group B, 36%); a non-sustained monomorphic VT was induced in 5/12 patients (group A, 41%) and in 4/28 patients (group B, 14%). In all 7/12 patients (59%) of group A with inducible sustained monomorphic VT, the arrhythmia was initiated with 1-2 extrastimuli. In group B, only 2/28 patients (7%) were induced to a sustained monomorphic VT. When the clinical arrhythmia was exercise-related, 5/6 patients (83%) in group A and 7/13 patients (54%) in group B were induced to a VT, while 2/6 patients (33%) in group A and 1/13 (8%) patients in group B were induced to a sustained monomorphic VT. Isoprenaline was not effective to increase the incidence of sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Conversion of sustained into nonsustained ventricular tachycardia during therapy assessment by programmed ventricular stimulation: criterion for a positive drug effect?

Serial electropharmacologic testing using up to 11 different antiarrhythmic drugs was performed in 130 consecutive patients (107 men, 23 women, ages 56 +/- 12) with inducible sustained ventricular tachycardia (VT). After 4 +/- 2.3 drug tests, complete suppression of VT inducibility (defined as less than 6 consecutive beats, mean 1.4 +/- 1.6) was achieved in 86 patients (66%), whereas in 44 patients (34%) nonsustained VTs (greater than or equal to 6 consecutive beats, less than 30 seconds in duration) were still inducible. There was no statistical difference between both groups regarding age, sex, underlying heart disease, ejection fraction or entry arrhythmia. After a mean follow-up period of 19 +/- 17 months, 24 patients (18%) had died, 8 (6%) suddenly. Eight patients (6%) experienced recurrent sustained VT. Symptomatic recurrences (sudden death or VT) occurred in 10 (11%) and 6 patients (13%, difference not significant), respectively. Probability of arrhythmia-free survival was comparable for patients with 0 to 5, 6 to 10, 11 to 15 and 16 to 32 inducible ventricular complexes with discharge medication. The negative predictive value of electropharmacologic drug testing was about 89%, irrespective of the maximal number of inducible complexes used for the definition of a negative test result. It is therefore concluded that conversion of sustained into nonsustained VT during therapy assessment by programmed ventricular stimulation indicates a positive drug effect.

Anti-Arrhythmia Agents↗
PubMed1989

[Continuous ventricular tachyarrhythmia in patients without detectable organic heart disease: clinical and electrophysiologic findings].

In 22 of 335 consecutive patients (6.6%) referred for evaluation and treatment of sustained ventricular tachyarrhythmias, hemodynamic and angiographic findings revealed no structural heart disease. Entry arrhythmia was ventricular fibrillation in 10 patients and sustained ventricular tachycardia in 12 patients. A subgroup of four young patients presented with slow recurrent (during 51 +/- 43 months) sustained ventricular tachycardias that were reproducibly terminated by intravenous application of verapamil. Programmed ventricular stimulation replicated the clinical arrhythmia in nine patients (75%) with ventricular tachycardia. In five patients (50%) with ventricular fibrillation no sustained ventricular arrhythmia could be induced, and only with three extrastimuli in four of the remaining five patients. On hospital discharge, 14 patients received type III antiarrhythmic agents, five patients received type I agents, and one patient received verapamil. Two patients were discharged without medical therapy. During the following 24 +/- 9 months, four patients had recurrent sustained ventricular tachycardia. No patient died suddenly during follow-up. We conclude that about 6% of all patients with ventricular tachyarrhythmias have apparently normal hearts. These idiopathic tachyarrhythmias seem to have a benign course, at least when treated. Slow, verapamil-sensitive tachycardias of young people may represent a unique entity.

Adolescent↗
PubMed1989

[Long-term results of pacemaker therapy in hypersensitive carotid sinus syndrome].

131 patients received permanent pacemakers to treat their hypersensitive carotis sinus syndrome (HCSS). Prior to implantation, HCSS was diagnosed whenever spontaneous episodes of faintness or dizziness (n = 25) or syncope (n = 106) coincided with an abnormal response to carotis sinus massage (asystole greater than 3 s). 123 patients were followed for 48 +/- 27 months after implantation to assess the value of pacemaker therapy. 77% of all patients were free of initial symptoms. 90% of patients with syncope prior to pacemaker therapy were free of recurrence. Therefore, permanent pacing appears to be the treatment of choice for these patients. Since carotis sinus massage produced high-degree AV-block in at least 33% of patients, ventricular (rather than exclusive atrial) pacing seems to be mandatory. However, syncope did recur in 10% despite normal pacemaker function. The etiology of these recurrences remained unclear in almost all patients. As opposed to patients with syncope, cardiac pacing prevented symptoms in only 26% of patients with faintness or dizziness without full syncope. In these patients primary and sole pacemaker therapy does not appear to be appropriate.

Aged↗
PubMed1987

Programmed electrical stimulation in healed myocardial infarction using a standardized ventricular stimulation protocol.

The diagnostic accuracy of programmed electrical stimulation was prospectively assessed in 111 patients with myocardial infarction (MI) with or without a history of spontaneous ventricular arrhythmias. In 29 patients neither ventricular tachycardia (VT) nor episodes of 10 premature ventricular depolarizations per hour was documented. Fifty patients had documented nonsustained VT and 32 had sustained monomorphic VT. One and 2 extrastimuli (twice diastolic threshold, 2 ms in duration) were given during sinus rhythm and ventricular pacing at 100, 120 and 140 beats/min in the right ventricular apex (part I). When this protocol failed to induce a sustained monomorphic VT, a third extrastimulus was introduced (part II). Repetitive ventricular responses were induced in all patients, and in 15 (14%) polymorphic ventricular arrhythmias requiring DC shock were induced. Incidence of initiation of sustained monomorphic VT and polymorphic ventricular arrhythmias requiring DC shock was related to the clinical arrhythmia and the stimulation protocol. In patients with documented sustained monomorphic VT, a third extrastimulus only increased the incidence of sustained monomorphic VT (68% to 94%), whereas in patients with documented nonsustained VT and without VT the incidence of both polymorphic and monomorphic arrhythmias increased by 7 to 12%. Sustained monomorphic VTs induced in patients without such a history were faster (p less than 0.01), depended on site of MI (p less than 0.05) and were more often preceded by nonsustained polymorphic VT (p less than 0.01) than in patients with documented sustained monomorphic VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗