Biomedical subjects
Publications and source records attributed to A Waleffe.
Arrhythmogenic right ventricular dysplasia is an unfrequent disease that associates ventricular tachycardia with left bundle branch block morphology and right ventricular fibro-fatty degeneration. The etiology, pathogenesis, criteria for diagnosis and treatment are discussed.
Tachycardias arise from an arrhythmogenic substrate triggered by a random factor (generally an extrasystole) and modulated by the autonomic nervous system. The three components are interactive, but their intensity and conjunction vary continuously. During the last decade, major achievements have been made to clarify definition and classification of data reported in the literature, helping our understanding of the mechanisms of ventricular arrhythmias. Nowadays, the pathophysiology of cardiac arrhythmias is well-known at the cellular and molecular ion channel activity. The progress of epidemiology and molecular genetics have allowed a better knowledge of the genotype-phenotype correlation in young patients presenting syncopes due to torsades de pointes or polymorphic ventricular tachychardia episodes which may degenerate into ventricular fibrillation and cause sudden death. The data of numerous large prospective randomised studies have led to more rational treatments with the progressive withdrawal of class I antiarrhythmics and their replacement by betablocking agents. The surgical approach of ventricular tachycardia has been overcome by the automatic implantable defibrillator and in some well-defined clinical situations, catheter ablation is used.
Paroxysmal atrial fibrillation is one of the most common disorders of cardiac rhythm. It is often a step toward permanent arhythmia, specially if associated with cardiac disease. The management objectives of intermittent arhythmia may be different, as maintenance of sinus rhythm. However, risks of stroke and thrombo-embolism are similar to those for sustained atrial fibrillation and must be carefully assessed. In this article we review the epidemiology, pathophysiology, clinical aspects and current guidelines for treatment and management of paroxysmal atrial fibrillation.
Syncope remains a clinical challenge. Accurate history taking, physical examination and EKG are mainstays of the diagnosis work up. The most important parameter for prognosis and requiring aggressive management is a structural heart disease. Patient without cardiopathy presenting multiple episodes may be candidate for tilt testing and loop EKG recorder.
The Brugada syndrome, a genetically transmitted disease according to an autosomal mode with a variable penetrance, is responsible for sudden death secondary to polymorphic ventricular tachycardia. The diagnosis is based on a typical electrocardiographical paturn that combines a right bundle branch block with ST elevation in the right precordial leads. In high risk patients, the automatic implantable defibrillator has the unique capability to protect against the occurrence of ventricular arrhythmias.
After reviewing the historical background, the morphology and physiopathology of left ventricular aneurysms, the authors review the physiology, the technical aspects, and the current surgical indications of aneurysmectomy, with a particular emphasis on the concept of endoventriculoplasty of Jatène & Dor.
During the past 15 years, the efficacy of antiarrhythmic drugs has been investigated for reducing sudden cardiac death in patients at high risk of arrhythmia. Whereas the benefits of beta-blocker therapy are well established, a reduction in mortality with other antiarrhythmic drugs remains unproved and in some cases, there is evidence of increased mortality with class I and some class III agents. At the same time, the development of the automatic implantable cardioverter-defibrillator has been one of the spectacular achievements in cardiology. It has altered the therapeutic landscape for patients with symptomatic ventricular tachycardia or cardiac arrest. In these patients, the automatic implantable defibrillator is clearly first line therapy, as recognized by the international scientific cardiac societies guidelines.
For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.
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To question the possible proarrhythmic effects of cardiomyoplasty (CMP), six adult goats were submitted to rhythmic and electrophysiological (EP) study 15 days before and 8 months after a posteroanterior clockwise CMP procedure using Medtronic Cardiomyostimulator (CMS) (SP1005) and electrodes (SP5528) and completion of a progressive stimulation protocol. Pre and postoperative screening included a surface ECG, 24-hour Holter monitoring, high amplitude and filtered QRS averaging, and invasive EP study performed in the postoperative period with the CMS "ON" and "OFF." One-hour Holter recording with desynchronization of the CMS was obtained. Comparison of pre and postoperative ECG and rhythmic data showed no significant difference. High amplitude QRS averaging did not evidence meeting the usual criteria of late potentials. EP values were stable in both conditions and the aggressive EP program did not show evidence of increased susceptibility to arrhythmias. Asynchronous cardiomyostimulation did not induce arrhythmias. Our data strongly suggest that provided meticulous surgical technique is used, CMP does not significantly interfere with the electrical characteristics of the normal goat heart. The procedure, despite the disturbances it provokes, does not seem to be arrhythmogenic. The function of the CMS was always appropriate, even under stressful EP conditions.
UNLABELLED: The rate modulation of Relay 294-03 is individually adjusted during a 3-minute calibration test corresponding to the collection of moderate acceleration signals (MAL), which are related to a programmable moderate pacing rate (PR). Those rate/acceleration values form a calibration point in the flat part of the rate response curve (RRC). To help in a more clinically oriented analysis of this feature, the stimulator was first calibrated while strapped on a volunteer who remained seated (low MAL), walked (medium MAL), or jogged (high MAL). The device was then mechanically submitted to three calibrated to and fro movements corresponding to the sensitivity spectrum of the sensor. Each movement was repeated ten times to test the influence of the slope (1-10). RESULTS: (1) One-way ANOVA significant effect of the MAL recorded during the calibration test on subsequent rate modulation (P = 0.0001); (2) The sensor amplifier gain was inversely related to the MAL: high MAL induced lower amplifier gain and lower PR for identical accelerations; (3) Lower amplifier gain allowed to discriminate highest acceleration magnitudes before reaching an overflow of the sensor; (4) The maximum achievable PR increased not only with the programmed slope, but also with decreasing MAL (P = 0.0055): a low MAL shifts to the left calibration point located on the part of the RRC and makes the last steep part of the RRC start earlier, thus leading to higher maximum achievable PR. In conclusion the calibration procedure is crucial not only in defining a moderate acceleration intensity but also in determining the sensor amplifier gain and the maximum achievable PR.
Ninety-three patients, who underwent DC shock ablation were reviewed over a mean follow-up period of 54 months (range 3 to 84 months). These patients (46 male and 47 female, mean age: 58 years) had failed an average of 3 drugs, and the duration of symptoms was more than 2 years. Paroxysmal atrial fibrillation or flutter was treated in 75 patients (80.6%); the remainder had supraventricular tachycardia or reciprocating tachycardia using an accessory pathway. One shock of 200 J was effective in producing third degree AV block in 40 patients (43%), while 2 or more shocks were used in another 53 patients (57%). Chronic complete heart block (CHB) was obtained in 85 patients (91%), modification of conduction was seen in 2 patients (2.1%), and failure to achieve an improvement in 6 patients (6.4). All the patients of the last group had received more than 4 shocks (200 to 400 J). However no significant difference between the amplitude of atrial and His electrograms could be shown between the CHB patients and those in whom conduction persisted. Over a mean follow-up of 54 months, 66 patients (72%) with successful ablation during the first 48 hours after the procedure remained in CHB. In 18 patients AV conduction resumed but they were all asymptomatic: 10 patients (10.8%) without antiarrhythmic therapy and 8 patients (8.6%) with medication. In conclusion, ablation of the AV junction is effective in more than 82% of patients. Most of the time long-term success can be predicted within 48 hours. However, due to the invasive character of DC shocks, this technique has been supplanted by the less aggressive radiofrequency method.
Of 150 consecutive patients with sustained monomorphic ventricular tachycardia (VT) (n = 116) or ventricular fibrillation (VF) (n = 34) late after acute myocardial infarction, 17 had reproduction of their sustained monomorphic VT during exercise testing. Data from these patients (group I) were compared with data from patients without exercise-induced VT (group II). No statistical difference was found between groups I and II with relation to age, sex, number of vessels with greater than 70% stenosis, left ventricular ejection fraction, number of previous myocardial infarctions, inducibility during programmed stimulation and total mortality during follow-up. In group I, only 1 patient (6%) developed ST depression during exercise compared with 47 patients (35%) in group II (p less than 0.01). After a 34-month mean follow-up, 6 patients in group I (35%) and 18 patients in group II (13%) died suddenly (p = 0.02). It is concluded that sustained monomorphic VT is reproduced during exercise in only 11% of patients with spontaneous late sustained monomorphic VT or VF. Electrocardiographic findings do not support ischemia as a triggering mechanism of exercise-induced sustained monomorphic VT. Patients with exercise-induced sustained monomorphic VT have a high incidence of sudden death.
The usefulness of sensor data storage for rate response simulation was evaluated using a new dual chamber rate modulated pacemaker sensitive to acceleration forces (Relay 294-03 [Intermedics Inc.]). The pacemaker can store the sensor output during routine exercise and those values can be used to simulate rate profiles for other rate response settings. The predictive value of this feature was evaluated in three studies (mechanical, external pacemaker, and implanted pacemaker). In the first study, the pacemaker was submitted to three runs of eight different mechanical calibrated to-and-fro movements. In the second study, nine external pacemakers were strapped on healthy volunteers who performed three jogging tests. Finally, the predictive value of the simulation was studied in five implanted patients during three successive walking tests. In each study, the pacemaker was submitted three times to the same activity. The responsiveness was successively set to 5, 1, and 10, and the pacemaker outputs were continuously recorded on a Holter monitor. At the end of the first run, rate profile simulations for slopes 1 and 10 were performed; slope 5 rate response was simulated after the second run. A regression analysis was used to establish the correlation between predicted and achieved pacing rates for each study. The coefficients of correlation between predicted and measured pacing rates for the mechanical, external, and clinical studies were 0.999, 0.985, and 0.823, respectively. The corresponding slopes of regression lines were 1.005, 0.971, and 0.935. Calculated rate profile has a high predictive value and could be used to optimize rate responsive settings without serial exercise testings.
UNLABELLED: A sensor driven algorithm limiting ventricular pacing rate during supraventricular tachycardia (SVT) is included in a dual chamber rate modulated pacemaker sensitive to acceleration forces (Relay, 294-03, Intermedics Inc.). According to the intensity of concomitant exercise, the ventricular pacing rate is limited either to the programmed maximum pacing rate (MPR) or to an interim lower limit, called "conditional ventricular tracking limit" (CVTL). The MPR prevails over the CVTL when the sensor calculated pacing rate exceeds the minimal rate by more than 20 beats/min. The purpose of the study is to determine the clinical safety and efficacy of this algorithm in patients with intermittent SVT. METHOD: A Relay was implanted in four patients with a bradycardia/tachycardia syndrome and in four patients with complete atrioventricular block (CAVB). All had episodes of paroxysmal atrial tachycardia. The units were programmed in DDDR: rate responsive parameters were adjusted by simulating the rate response during three levels of exercise to let the MPR override the CVTL only during strenuous exercise. Holter monitors and exercise testings were performed at 3-month follow-up. RESULTS: In seven patients, Holter recordings showed supraventricular arrhythmias at rest with a ventricular pacing rate limited to the CVTL. Appropriate rate increases during exercise testings were also demonstrated. Three devices had to be reprogrammed in DDIR (one patient suffering from nearly permanent atrial flutter and two patients not tolerating the CVTL pacing rate at rest). CONCLUSION: The CVTL algorithm is effective in protecting against high ventricular pacing rates during supraventricular arrhythmias. It allows the selection of the DDDR mode even with a high MPR in patients with intermittent SVT.
UNLABELLED: The characteristics of the sensor and rate adaptive algorithm included in a new dual chamber rate responsive pacemaker (Relay 294-03, Intermedics, Inc.) were studied by submitting the device to calibrated to-and-fro movements of specific frequencies and peak accelerations by means of a mechanical arm connected to a speed adapter. Atrial pacing rate was continuously recorded on a Holter monitor. The influences of the frequency, the magnitude, and the axis of the acceleration forces as well as the reproducibility of the rate response were evaluated. RESULTS: (1) The sensor was sensitive to frequencies ranging from 0.5 to 7 Hz with a peak sensitivity at 3 Hz; (2) the pacing rate was not affected during movements at frequencies > 6 Hz, commonly presented as nonactivity related signals (car, bus transportation, drilling....); (3) the pacing rate increased as a function of the acceleration magnitude up to 0.5 G (0.3 G for 3 Hz), then remained constant. This level of acceleration usually corresponds to high degrees of activity; (4) rate response was maximum when acceleration was directed in the anteroposterior direction; (5) reproducibility of the rate response was excellent (R2: 0.999; slope of the regression line: 0.999). CONCLUSION: Relay 294-03 is a low frequency signal sensing rate modulated pacemaker using an accelerometer sensitive to motion, mainly in the anteroposterior direction.