Giuliano Altamura

Do European GSM Mobile Cellular Phones Pose a Potential Risk to Pacemaker Patients

BARBARO, V., et al.: Do European GSM Mobile Cellular Phones Pose a Potential Risk to Pacemaker Patients? A series of in vivo trials were carried out in order to verify whether the electromagnetic field radiated by GSM (Groupe Systemes Mobiles) mobile cellular phones might affect implanted pacemakers. Two European GSM phones of 2‐watt power were tested and trials conducted on 101 pacemaker implanted outpatients attending day hospital for routine check‐up, who volunteered for trials. Forty‐three pacemaker models from 11 manufacturers were tested in all. When the sensing threshold of the pacemakers was set at a minimum and the antenna of the phone was in direct contact with the patients chest, interference was detected for 26 implanted pacemakers. Specifically, pulse inhibition in 10 of 101 cases, ventricular triggering in 9 of 46 DDD‐VDD pacemakers, and asynchronous pacing in 4 of 52 devices. Pulse inhibition was also observed combined with asynchronous pacing in 1 of 52 cases and with ventricular triggering in 2 of 46 cases. Minimum effect duration was ca. 3 seconds but in 6 cases effects continued as long as the interfering GSM signal was on. No permanent malfunctioning or changes in the programmed parameters were detected. Whenever interference was detected, trials were repeated to determine the maximum sensing threshold at which interference persisted (with the antenna in contact with the skin over the pacemaker). Then maximum distance between antenna and pacemaker at which interference occurred was determined at pacemaker maximum and minimum sensing threshold. Under our experimental conditions electromagnetic interference effects were detected at a maximum distance of 10 cm with the pacemaker programmed at its minimum sensing threshold. When the phone antenna was in direct contact with patients skin over the implant, electromagnetic interference effects occurred at maximum ventricular and atrial sensing thresholds of 4 mV and 2.5 mV, respectively.

Transthoracic DC Shock May Represent a Serious Hazard in Pacemaker Dependent Patients

External defibrillation is widely used for the termination of various atrial and ventricular tachyarrhythmias, including pacemaker patients. Our study was intended to evaluate the effects of DC shocks in 36 patients with unipolar pacemakers implanted in the right pectoral region (25 DDD, 10 VVI, 3 AAI). The shocks were delivered with paddles on the anterior surface of the thorax, as far as possible away from the pacemaker. The pacing output was programmed at 0.5 msec and 5 V (25 patients), 4 V (1 patient), and 2.5 V (10 patients). Transient loss of capture occurred in 18 patients (50%). These patients, compared with those without capture failure, received higher peak and cumulative shock energies, respectively, 216 ± 99 versus 123 ± 50 joules (P < 0.002) and 352 ± 62 versus 147 ± 98 joules (P < 0.004) and had a lower pacemaker pulse amplitude (4.0 ± 1.2 vs 4.6 ± 1.0 V, P = 0.11). Failure to capture lasted from 5 seconds to 30 minutes (mean 157 sec). In 15 patients the ventricular stimulation threshold was measured before and serially after cardioversion. A six‐fold threshold increase was observed 3 minutes after the shock (P < 0.004) with gradual recovery to nearly baseline values at 24 hours. Transient sensing failure occurred in 7 of the 17 patients in whom it could be evaluated (41%). Furthermore, three cases of shock induced pacemaker malfunctions were observed requiring replacement of the stimulator in two patients. In conclusion, the incidence of loss of capture in pacemaker patients subjected to electrical cardioversion/defibrillation is high. The phenomenon is due to an abrupt rise in stimulation threshold, caused by the electrical shock, and may represent a serious hazard in pacemaker dependent patients. The risk of pacing failure could be reduced by utilizing low shock energies when possible, and by programming the pacemaker at its maximal output before cardioversion.

Local Capture by Atrial Pacing in Spontaneous Chronic Atrial Fibrillation

BACKGROUND Atrial fibrillation (AF) is considered to be maintained by multiple reentrant circuits without or with a very short excitable gap. However, the possibility of local atrial capture has been shown recently in experimental AF or induced AF in humans. METHODS AND RESULTS This study was undertaken to evaluate the feasibility of atrial capture-suggestive of an excitable gap-in spontaneous chronic AF. Decremental pacing was performed in 47 right atrial sites in 14 patients with chronic AF, not taking antiarrhythmic drugs. A Franz catheter (for pacing and monophasic action potential recording) and a recording quadripolar catheter positioned about 10 mm apart were used. Local capture was achieved in 41 (87.2%) sites for a total of 100 captures. In 71 episodes the capture was lost within 15 seconds, while in the remaining 29, pacing was stopped after 15 seconds of stable capture. AF types immediately before capture were type 1 in 83 and type 2 in 17 episodes. Type 3 AF was never captured. Pacing cycle at capture was 175.7 +/- 20.9 ms. The baseline atrial interval (FF) was 185.4 +/- 24.5, significantly longer than the FF recorded during pacing immediately before capture (176.0 +/- 19.8 ms) (P < .02). CONCLUSIONS During spontaneous chronic AF in humans, (1) local capture by atrial pacing is possible up to at least 15 mm from the pacing site, (2) regional entrainment is possible during type 1 and type 2 AF but not type 3 AF, and (3) pacing before capture accelerates AF, probably by transient or local capture. These findings suggest that an excitable gap is present in chronic AF, therefore supporting the hypothesis that leading circle reentry is not the unique electrophysiological mechanism maintaining the arrhythmia.

Single shock endocavitary low energy intracardiac cardioversion of chronic atrial fibrillation.

Background.Discomfort related to low-energy internal cardioversion (LEIC) represents a real problem in patients (pts) with atrial fibrillation (AF). The aim of our study was to verify if a single shock could restore sinus rhythm (SR) with a lower discomfort for the pt.Methods. Thirty pts with chronic AF were randomized to receive a single 350 V shock (15 pts) or multiple shocks of increasing energy (15 pts). Three leads were positioned, respectively, in the coronary sinus and in the lateral right wall for shock delivery, and in the right ventricular apex for R wave synchronization. Truncated, biphasic shocks were used. In the first group a single 350 V shock was directly delivered and a second 400 V shock was given only if SR has not been restored. In the second group, beginning at 50 volts the voltage was increased in steps of 50 volts until SR restoration. No patient was sedated. After each shock the pts were asked to rate their discomfort on a scale of 1 to 5 (1 = not perceived, 5 = severe discomfort)Results. SR was restored in all the subjects. In group 1 SR was obtained in 12/15 (80%) pts with the first 350 V (8.1±0.8 joules) shock, while the remaining 3 patients required the second 400 V (10.2±10.3 joules) shock. In group 2 the mean atrial defibrillation threshold was 346.7±29.7 volts (8.0±1.5 joules). Then discomfort score was 2.5±0.6 in group 1 and 3.3±0.6 in group 2 (p < 0.01).Conclusions. A single shock of 350 V restores SR in the majority of pts with chronic AF; by use this new approach, LEIC is tolerated better than the multiple shocks step-up protocol.

Cardiovascular Effects of Omega-3 Free Fatty Acids.

Omega-3 fatty acids are essential substances for the development and function of human organism. They cannot be synthesized in humans, and consequently have to be acquired from food, almost exclusively from fish. Omega-3 fatty acids exert potent anti-inflammatory and anti-atherosclerotic actions by interfering with the metabolism of arachidonic acid, modifying lipid composition (mainly lowering triglycerides), improving hemodynamics and reducing cardiac hypertrophy. Recently, clinical and experimental studies demonstrated an anti-arrhythmic effect and a significant impact on survival after myocardial infarction (MI). It follows that omega-3 fatty acids have been widely accepted for clinical use in patients with dyslipidemia or with atherosclerotic disease and in survivors of acute MI. This review briefly explores the metabolic mechanisms and the clinical effects of this class of substances and considers their use in patients with cardiovascular disease.

Effects of Oral Propafenone Therapy on Chronic Myocardial Pacing Threshold

The effects of oral propofenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propa/enone dosage the threshold, measured at 2.5 V, rose from 0.14 ± 0.10 to 0.21 ± 0.16 msec (+ 55%) in the atrium (P < 0.0001) and from 0.10 ± 0.08 to 0.15 ± 0.09 msec (+ 63%) in the ventricle (P < 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 ± 0.10 to 0.17 ± 0.14 msec with the lower dose and to 0.27 ± 0.22 msec (+125%) with the higher dose (P < 0.0001) for both increments), With the 900 mg/day dose, a threshold increment ± 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QHS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.

Low Energy Intracardiac Cardioversion of Persistent Atrial Fibrillation

The aims of the study were to verify the efficacy and safety of low energy internal Cardioversion (LEIC) in patients with persistent at rial fibrillation (AF) and to identify the factors affecting the at rial defihrillation threshold (ADT). Forty‐nine patients with persistent (lasting ≥ 10 days) AF underwent LEIC. In each patient, two 6 Fr custom‐made catheters with large active surface areas were positioned in the coronary sinus (cathode) and the lateral right wall (anode), respectively, for shock delivery, and a tetrapolar lead was placed in the fight ventricular apex for R wave synchronization. Truncated, biphasic (3 ms+3 ms). exponential shocks were used, beginning at 50 V and increasing in steps of 50 V until sinus rhythm had been restored. Mild sedation (diazepam 5 mg IV) was administered to 12 patients. Sinus rhythm was restored in all the subjects with mean voltage and energy levels of 352.0 ± 80.3 V and 8.2 ± 3.4 J, respectively. The ADT in patients pretreated with amiodarone (6.4 ± 1.8 J) was lower than that of patients who had not received any antiarrhythmic drugs (9.2 ± 3.7) (P = 0.04). No ventricular arrhythmias were induced by any of the atrial shocks, and no other complications were observed. During a mean follow‐up of 162.9 ± 58.7 days, AF recurred in 21 (43%) patients; 71% of these occurred in the first week after Cardioversion. LEIC is effective in restoring sinus rhythm in patients with persistent AF. The technique seems to be safe and does not require general anesthesia or, in most cases, sedation. Patients pretreated with amiodarone have lower ADTs.

Indications for dual-chamber (DDD) pacing in implantable cardioverter-defibrillator patients.

New technologic development of implantable cardioverter-defibrillators (ICDs) keeps up with the exponential increase of their use for primary and secondary prevention of sudden cardiac death. The first-generation ICD with limited shock capability alone could be considered adequate in most cardiac arrest victims, but it was not suitable for sudden death prevention in all high-risk patients with cardiac disease. The second-generation ICD was comprised of hybrid pacemaker-defibrillator systems that provided on-demand ventricular antibradycardia pacing. The third-generation devices include additional functions, such as antitachycardia pacing for ventricular tachycardia (VT) reversion and low-energy ventricular cardioversion, in addition to ventricular defibrillation and single-chamber ventricular demand pacing. In the near future, advanced dual-chamber atrioventricular (AV) pacing and defibrillating systems will also be available. The dual chamber ICD will allow atrial inhibited/dual-chamber (AAI/DDD) rate-responsive pacing, simultaneous atrial and ventricular sensing to optimize the arrhythmia identification, and ICD shock delivery in the proper arrhythmia-related chamber. Clinical benefits of these devices compared with their cost and complexity will require careful evaluation.

Emergency Cardiac Pacing for Severe Bradycardia

ALTAMURA, G., ET AL.: Emergency Cardiac Pacing for Severe Bradycardia. Our study included the treatment of transcutaneous cardiac pacing (TCP) in 32 patients: (A) 19 patients were treated in the emergency area for complete symptomatic AV block before endocavitary pacing; (B) five patients were in asystole following DC shock or out‐of‐hospital cardiac arrest; and (C) eight patients were affected by bifascicular block undergoing emergency surgery and were treated in order to prevent complete AV block. Two transcutaneous stimulators were used. PaceAid‐CRC model 50/52 with 20‐msec pulse width; the electrodes were positioned on the V, ECG position and on the back. Results: in all but two patients, it was possible to obtain stable cardiac capture; in one patient arrived in hospital in asystole after prolonged cardiac arrest and in the other one was affected by complete AV block, TCP was ineffective. In groups A and B, TCP was maintained for a mean time of 15 minutes; in group C, TCP was tested in all patients, but performed in only one patient during surgery. Mean threshold was 81 mA. Stimulation was well tolerated in all but five patients. TCP is a reliable, noninvasive method that offers the possibility to initiate pacing within seconds and can be used by medical staff. In our opinion, it should be considered as the first choice emergency treatment of severe symptomatic bradycardia. In asystole, beneficial effects can be obtained only if TCP is performed early enough after the onset of arrhythmia.

Transcutaneous Cardiac Pacing for Termination of Tachyarrhythmias

ALTAMURA, G., ET AL.: Transcutaneous Cardiac Pacing for Termination of Tachyarrhythmias. Transcutaneous cardiac pacing (TCP) was used for interruption of tachyarrhythmias in 31 patients: 20 with ventricular tachycardia (VT); eight with atrioventricular reentrant tachycardia (AVRT) and three had atrioventricular nodal tachycardia (AVNT). The stimulators used (Pace Aid 50/52) allow pacing at programmable rates (50–160 ppm) and output (10–200 mA at 20‐msec pulse duration), when possible overdrive pacing was used. Short bursts of stimuli were delivered with increasing current intensity until interruption of the arrhythmia or to the maximum energy tolerated by the patient. VTs were interrupted in eight of the 20 patients: four of the six (67%) treated by overdrive pacing and four of the 14 (29%) were treated by underdrive pacing. Supraventricular tachycardias (SVT) were terminated in eight of the 11 patients: seven out of eight (88%) AVT, and one out of three AVNT (33%). We observed two cases of arrhythmia worsening: a VT acceleration and induction of ventricular fibrillation in a patient with AVNT. TCP was well tolerated by the majority of the patients. We conclude that TCP is an effective method for interruption of ventricular and supraventricular reentrant tachycardias, but the risk of arrhythmia worsening must be considered.