Unipolar cardioverter/defibrillator systems implanted under local anaesthesia--a further step to feasibility and safety.
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Publications and source records attributed to P Weismüller.
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In a female patient with paroxysmal AV nodal reentrant tachycardias the electrophysiological study revealed three AV nodal pathways. During atrial extrastimulation a sudden AH interval prolongation of more than 50 ms ("break" phenomenon) was observed twice at one basic cycle length. During ventricular extrastimulation a sudden prolongation of the AH interval of the anterograde AV nodal conduction of the induced echo beats was recorded. Three AV nodal pathways were thus present. The atypical form of AV nodal reentrant tachycardia was induced, showing a varying cycle length (290-340 ms). After radiofrequency catheter ablation of the fast conducting beta-pathway, another tachycardia was initiated, now showing a constant cycle length, using the two remaining, more slowly conducting alpha-pathways. One of these was eliminated in another ablation procedure.
Sinus node dysfunction (SND) is a rare cause of bradycardia in children without structural heart disease. The clinical and diagnostic findings in 4 children with this condition are described. Two of them presented with symptoms, in one arrhythmias had been noted before birth, and a routine physical examination had revealed bradycardia in another. Age at onset of either clinical symptoms or bradycardia ranged from 0 to 11 1/2 years. Routine and 24-h-electrocardiograms showed atrioventricular junctional rhythms with minimal rates of 25/min and episodes of asystole with a maximal duration of 10.3 s. Other electrocardiographic abnormalities such as first degree atrioventricular block, ventricular extrasystoles or tachycardia were common findings. Electrophysiological studies were performed in 3 cases and confirmed the diagnosis of SND. A permanent pacemaker was inserted in 2 children; medical treatment did not have any long-term effect. During a follow-up period of 5 to 13 years there were no complications. In summary, SND in childhood can be assessed by Holter monitoring with high reliability. Electrophysiological studies are not necessary and of limited value. Therapeutic policies and prognostic statements are difficult to establish due to the small number of cases so far described. Permanent cardiac pacing, however, is unavoidable in symptomatic children.
In view of the reported high risks resulting from the implantation of a cardioverter (ICD) and our own experience, we retrospectively evaluated the patients who received an ICD at our institution, so as to predict factors that could lead to a high peri-operative risk. The patients were divided into three groups according to their diagnoses and the surgical procedure. Group I: 10 patients with non-ischaemic cardiomyopathy, age 53.9 +/- 14.0 years, ejection fraction (EF) 33.1 +/- 11.8; group II:13 patients with coronary artery disease (CAD), diffuse arteriosclerosis, age 60.0 +/- 6.8 years, EF 31.4 +/- 9.1%; group III:12 patients, age 61.9 +/- 9.4 years, EF 41.2 +/- 8.6, CAD, concomitant bypass grafting. In cases of cardiomyopathy, cardiac complications (30%) were reversible by adequate drug therapy. However, five patients in group II (38.5%) died from cardiac complications, mainly frequent arrhythmias and subsequent pump failure. In group III no peri-operative complications occurred. Therefore the high mortality (overall 13.2%) in our series was exclusively due to patients suffering from severe CAD and unsuitable for revascularization. Considering the high risk after ICD placement, primary heart transplantation might be the better procedure in younger patients with end-stage CAD.
The aim of this study was to assess variability of ventricular late potentials (VLP) in patients with and without inducible ventricular tachycardia (VT), and the effects of antiarrhythmic drugs on VLP variability in the high-resolution electrocardiogram (HRECG). In 27 patients 90 s of unaveraged HRECGs were analysed before and 2 h after oral administration of 200 mg disopyramide, 400 mg mexiletine, 300 mg propafenone and 160 mg DL-sotalol. The duration of the QRS (QRSD) and the duration of the terminal low amplitude signal (LASD) was measured from each beat. Beat-to-beat variability was defined as standard deviation of the differences between consecutive beats. Patients with inducible sustained VT (n = 9) showed higher LASD variability than patients without inducible VT (12.3 vs 9.3 ms.beat-1, P < 0.01). Patients with VLP (n = 17), as defined by the signal averaged ECG, also had higher QRSD and LASD variability (11.8 vs 9.5 ms.beat-1, P < 0.05; 11.5 vs 8.2 ms.beat-1, P < 0.01, respectively) compared to those without VLP. All class I drugs lengthened QRSD and LASD in terms of the absolute values, but only propafenone increased QRSD and LASD variability (9.7 to 12.0 ms.beat-1, P < 0.01; 8.9 to 11.9 ms.beat-1, P < 0.01, respectively). In patients with inducible VT, sotalol decrease LASD variability from 14.3 to 9.3 ms.beat-1 (P < 0.05). We conclude that beat-to-beat VLP variability is increased in patients at a high risk of malignant arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: It is well known that patients with coronary heart disease and ventricular tachycardia show a high incidence of arrhythmogenic complications and sudden cardiac death. The best predictor of spontaneous ventricular tachycardia and sudden death in these patients is programmed ventricular stimulation, but this invasive method is limited to specialized institutions. The purpose of our study was to assess the predictive value of Holter monitoring, late potentials and heart rate variability as markers for these high-risk patients. We investigated 20 patients (18 m, 2 f, age range 31-79 years) with coronary artery disease documented angiographically (6 patients with single vessel disease (vd), nine patients with 2 vd, five patients with 3 vd) and previous myocardial infarction. Each patient underwent 24-h ambulatory monitoring with analysis of rhythm of heart rate variability (24-h spectral and non-spectral analysis) and a signal-averaged ECG with late potential measurement. In all patients, sustained ventricular tachycardia was inducible during programmed ventricular stimulation. Late potentials were recorded in 12 out of the 20 patients (60%). Ventricular arrhythmias of Lown classes IVa, IVb or V were recorded in 12 patients. Analysis of heart rate variability compared to 20 age- and sex-matched healthy controls revealed a loss of parasympathic activity and increased sympathic activity in 16 of the 20 patients (80%). CONCLUSION: in this study, heart rate variability was the most sensitive method with which to recognize patients at a high risk of arrhythmogenic complications. Evaluation of the above parameters in large controlled clinical trials may help predict arrhythmogenic complications and sudden cardiac death.
The purpose of this study was to detect ventricular late fields recorded by a biomagnetic multichannel system in patients with ventricular late potential and to determine the site of these ventricular late fields non-invasively in three dimensions. Biomagnetic signals of sinus beats during a 5-min acquisition period simultaneously recorded by a 37-channel system Krenikon were averaged in all channels. Ventricular late fields were determined in each channel according to the algorithm of Simson for ECG data. For the localization process, baseline correction from the averaged non-filtered signals was performed at the end of the QRS complex under visual control. The single current dipole model within the homogeneous half-space was applied. Eight patients post myocardial infarction with ventricular late potentials (four with recurrent sustained ventricular tachycardia) and four healthy individuals were examined. In the normal subjects, no ventricular late fields were detected. However, ventricular late fields were found in all patients, and were localized in six patients within the border zone of myocardial infarction. In the four patients with ventricular tachycardia, a spatial coincidence of the site of origin of ventricular late fields and the site of origin of ventricular tachycardia determined by catheter mapping was found in two. It is concluded that magnetocardiography is able to detect ventricular late fields and can be used to determine their site of origin.
Arrhythmogenic substrate diagnosis has been achieved by electrophysiological studies and best localized by successful radiofrequency ablation. Pre-invasive localization procedures have been based on surface ECGs and more recently on biomagnetism, but in addition to these electric and magnetic signals a mechanical signal may be utilized: the initial site of contraction may be detected by phase analysis during radionuclide ventriculography. Generation of three-dimensional data set of phases is achieved by incorporating the new emission tomography technique. The performance of this modified phase analysis has been investigated for the detection of the normal contraction pattern during sinus rhythm, the arrhythmogenic substrate of the WPW syndrome and ventricular tachycardia, and further, to define the limitations of the method in experimental studies on pigs. In 30 out of 44 patients with normal sinus rhythm and no ventricular lesion, a characteristic phase pattern was found. Physiologically, the initial site of contraction appeared to be paraseptal and in the anterior wall of the right ventricle close to the apex. In 13 patients with WPW syndrome and in seven with ventricular tachycardia, the phase data were compared to the electrophysiological study. In 14 of 20 there was a complete match, in 3 of 20 a mechanical focus was found in the area adjacent to the electric focus. From experimental pig studies with simulated stimulation, a spatial precision of at least 20 mm was found at a pre-excitation of 20 ms.(ABSTRACT TRUNCATED AT 250 WORDS)
The Long QT syndrome (LQTS) is a relatively rare disorder. It has a major clinical impact as affected individuals are prone to syncope and sudden arrhythmogenic cardiac death. The LQTS comprises three groups of patients. The Jervell-Lange-Nielsen syndrome is characterized by an autosomal recessive pattern of inheritance and congenital neural deafness. The Romano-Ward syndrome shows an autosomal dominant pattern of inheritance and normal hearing. Patients with the sporadic form of LQTS have no evidence of familial transmission and have normal hearing. Imbalance of sympathetic cardiac innervation with predominance of the left stellate ganglion and an intrinsic myocardial defect leading to early afterdepolarization are the two pathogenetic mechanisms of LQTS discussed today. More recently a genetic basis for the Romano-Ward LQTS has been reported. The genetic linkage to the Harvey ras-1 gene provides the basis for a new hypothesis that an impairment of guanine nucleotide binding proteins is responsible for symptoms observed in LQTS. This paper discusses the genetic basis, pathology and pathophysiology of LQTS and tries to unify the different theories.
Magnetocardiography (MCG) allows one to noninvasively localize cardiac electrical activity in three dimensions. It was the purpose of this study to obtain information about the spatial variations of signal-averaged ventricular late magnetic fields recorded by a biomagnetic multichannel system. Biomagnetic signals of 170-600 heart cycles obtained by the 37-channel system KRENIKON (Siemens Medical Engineering Group) were simultaneously averaged in all channels. The absolute values of the filtered signals (digital, bidirectional, four-pole butterworth, bandpass filter [3-dB range, 40-250 Hz]) were calculated in each channel. The noise level was determined within the TP segment. The onset of the terminal low amplitude signals (TLAS) was defined when the signals became lower than 1/23 of Rmax of the QRS complex for the channel with the largest filtered QRS complex after filtering. The TLAS ended when the signal was lower than twice the standard deviation (2 sigma) above the mean noise level. Ventricular late fields were defined as present when the TLAS had a duration of more than 39 msec. In this study, five patients with ventricular late potentials (four with sustained ventricular tachycardia) and three healthy individuals were examined. Ventricular late fields were detected in the patient group in 2-15 MCG channels with a mean length of 49.6 msec (43-60 msec). The spatial distribution of the ventricular late fields was consistently found to exhibit maximum duration in a certain area. In the normal subjects no ventricular late fields were detected. Thus, MCG is able to detect ventricular late fields and their spatial variations. In addition to the information obtained by signal averaging from the surface ECG, averaging of biomagnetic signals with a multichannel device can reveal spatial inhomogeneity of delayed myocardial excitation.
A new tomographic technique combined with phase analysis was used to detect premature and ectopic ventricular contraction patterns in 15 patients with Wolff-Parkinson-White syndrome and during ventricular tachycardia in seven patients. Data generated by gated single-photon emission computed tomography (SPECT) were analysed by backprojection of the Fourier coefficients, double-angulation, and integration to thick slices containing the ventricles, thus allowing visualisation of the contraction patterns in three perpendicular views. The results were compared with those of catheter mapping. In nine patients with Wolff-Parkinson-White syndrome the site of initial contraction detected was identical with the site of the accessory pathway found by catheter mapping. The sites of origin of the ventricular tachycardias determined by catheter mapping were within 3 cm of the sites detected by the new technique. This new technique seems to be a promising non-invasive method for localising ectopic ventricular activity that will considerably shorten the time required for subsequent invasive procedures.
Electrical activity can be localized by magnetocardiography (MCG) non-invasively. In this study a 37-SQUID (Super Conducting Quantum Interference Device) sensor multi-channel system (KRENIKON) was used to assess the potential of magnetocardiography to localize accessory pathways with a multichannel system. Seven WPW patients were studied by means of magnetocardiography. Prior to the MCG recordings, the site of the accessory pathway had been determined in all patients by invasive catheter mapping. MR images of the heart were used for anatomical correlation. The magnetocardiographic localization of the accessory pathway corresponded with catheter mapping within 2.1 cm on average (total range: 0-5 cm). This is thus, a promising new method for non-invasive localization of accessory pathways in WPW patients.
The non-invasive measurement of the extremely weak magnetic fields generated by heart and brain is motivated by the possibility of obtaining quantitative diagnostic information about electric function. Magnetic signals (MCG, MEG) are significantly less influenced by body tissue than the corresponding electric signals (ECG, EEG). Measurement of biomagnetic signals is performed by superconducting sensors, consisting of pickup coils and SQUIDs (superconducting quantum interference device) operating in liquid Helium. For clinical investigations a biomagnetic multi-channel system (KRENIKONR) has been designed. It uses a flat array of 37 magnetic field sensors and is operated inside a shielded room. Evaluation of biomagnetic signals by use of simple source and body models and in combination with anatomical data from 3D MR- or CT-images yields sequences of locations of electrical function with a spatial resolution of some millimeters and a time resolution better than one millisecond. More than three years of clinical studies have demonstrated the value of the method primarily in cases with localized functional pathologies. In cardiology this is pathologies of the cardiac conductive pathway, ectopies, and arrhythmias. Validation has been performed by catheter stimulation in volunteers, and by catheter mapping and nuclear medical methods in patients. Extension of modelling and evaluation to cases with distributed activity, e.g. ventricular excitation, is under investigation.
For the determination of the defibrillation threshold, the induction of ventricular fibrillation is mandatory. However, in severely damaged hearts it is sometimes difficult to induce ventricular fibrillation by rapid stimulation or alternating current. Only rapid nonclinical ventricular tachycardias may result, and their cardioversion threshold may be different from the defibrillation threshold. Therefore, it was the purpose of this study to test the potential of direct current (DC) application to rapidly induce ventricular fibrillation in patients with an implanted cardioverter defibrillator. The defibrillation threshold had to be determined in 13 patients (9 with coronary heart disease, 4 with dilative cardiomyopathy, ejection fraction 35%) during and 2 weeks after the implantation of a cardioverter defibrillator. DC was applied 37 times by a commercially available 9-V DC battery via a bipolar catheter for about 3 seconds. Ventricular fibrillation was induced 23 times (62%) and rapid nonclinical ventricular tachycardias were induced six times (16%). In one patient clinical ventricular tachycardia was observed. In seven instances (19%) sinus rhythm remained. In 12 of the 13 patients, ventricular fibrillation could be induced by DC. Thus, the induction of ventricular fibrillation by DC application may serve as an additional tool to induce ventricular fibrillation, determining the defibrillation threshold in implantable cardioverter defibrillator patients.
Since catheter or surgical techniques for ablating the arrhythmogenic substrate in patients with SVT due to accessory pathways or those with VT are now available, exact localization of the substrate is mandatory. We report preliminary results of two new non-invasive techniques for localizing either the site of earliest ventricular contraction using ISPECT, or the site of initial ventricular depolarization by magnetocardiography (MCG) in WPW syndrome and in VT patients. Thirteen patients with WPW syndrome and 8 patients with sustained VTs were studied with ISPECT. In 9/13, comparative catheter mapping data were available. Two patients had two Kent bundles. 13/15 Kent bundles could be localized by ISPECT. In 5/9 patients the area of Kent bundle insertion was identical with ISPECT and catheter mapping, in 3 correlation was fair, and in 2 patients with 2 Kent bundles ISPECT failed to localize their insertion. In 3/8 patients with VT catheter mapping could not be performed for hemodynamic reasons. In 2/5 patients the area of VT focus was identical with both methods, in one patient it was adjacent to each other, and in 2/5 patients a larger anatomic distance of the focus was found with both methods. In 3/7 patients with WPW the MCG showed the site of Kent bundle insertion, which was identical to that seen by catheter mapping. In one patient the area was adjacent, and in 3 more distant from the site determined by catheter mapping. In 1/2 patients with 2 Kent bundles, one of these could be detected by MCG. In 1/3 patients with VT, the site of VT focus was identical with both methods, but in the remaining two a distance of 3-4 cm was observed between the area seen with MCG and that with catheter mapping. In 4 further VT patients with stable and uniform ventricular late potentials, ventricular late magnetic activity was found with different QRS lengths within the single MCG channels. From our results we conclude that both ISPECT and MCG seem to become very promising non-invasive techniques for localizing ectopic ventricular depolarization in WPW syndrome and VT patients. However, these methods have to be refined, improved and validated by further systematical studies.
This study was set up to discover how a subendocardial application of ethanol administered via a catheter would affect an animal model. A 7 F bipolar catheter with a lumen, through which a 2 mm needle was inserted, was placed in the left ventricle of 11 pigs. Altogether, 33 subendocardial injections into the left ventricular myocardium were performed under fluoroscopic control using a mixture of 0.5-1.5 ml ethanol and 0.5-1 ml iopamidol as contrast medium. The mixtures were injected into the apical, lateral and septal walls of the left ventricle. After 25 days, the hearts were removed and the lesions examined pathologically. The calculated volume of the lesions was about 60 mm3, the area in projection to the endocardium about 35 mm2, the depth relative to the endocardium about 1.5 mm and the maximum diameter about 8 mm. Perforation of the myocardial wall by pericardial injection occurred twice without further complications. Subendocardial application of concentrated ethanol by catheter caused a controlled local necrosis. This technique may become a new approach with which to treat ventricular tachycardia by chemical ablation.
It was our purpose to assess the clinical relevance of noninvasive magnetocardiographic localization of accessory pathways. Nine patients with Wolff-Parkinson-White (WPW) syndrome were studied. For all of them the site of the accessory pathway was known from invasive catheter mapping. A 37-SQUID (superconducting quantum interference device) sensor multichannel system (KRENIKON) was used, allowing synchronous registration with all channels. The site of the electrophysiological activity at the beginning of the delta wave was determined. Magnetic resonance images of the heart were obtained to correlate the biomagnetically localized activity with the anatomy. Magnetocardiographic localization of the bypass tract corresponded with catheter mapping with a spatial difference of 0-5 cm, 1.8 cm on the average, compared to the results obtained by catheter mapping. Thus, magnetocardiography is a promising new method for noninvasive localization of accessory pathways in WPW patients. This may streamline further invasive procedures.
An atypical presentation of purulent pericarditis caused by Staphylococcus aureus is described. A bacterial etiology was initially not taken into consideration because the clinical course was torpid and afebrile. Therefore, the appropriate treatment was delayed. The patient recovered after percutaneous pericardial drainage of his purulent pericardial effusion and antimicrobial therapy. The importance of a high index of suspicion of a bacterial cause in patients with pericardial effusion of unexplained etiology is emphasized.