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Biomedical subjects

M S Stanton

Publications and source records attributed to M S Stanton.

At least 37 records · Page 2Linked to original sources

Importance of pacemaker noise reversion as a potential mechanism of pacemaker-ICD interactions.

Numerous types of interactions between pacemakers and implantable cardioverter defibrillators (ICDs) have been described. Pacemaker outputs preventing appropriate detection of ventricular tachycardia or ventricular fibrillation by the ICD is one of the more serious. Asynchronous pacemaker activity during ventricular arrhythmias may be caused by either nonsensing of the arrhythmia or by noise reversion, which is an algorithm that causes the pacemaker to switch to asynchronous pacing when repetitive sensing at a high rate occurs. We analyzed the mechanisms underlying asynchronous pacemaker activity in ventricular arrhythmias using pacemaker telemetry during the arrhythmia. Thirty-nine induced arrhythmias from 26 different procedures in 19 patients with both pacemakers and ICDs were analyzed. Of the 39 arrhythmias, asynchronous pacemaker activity occurred in 16. The underlying mechanism was nonsensing in 4 episodes and noise reversion in 12 episodes. Clinically significant interference with detection arose on three occasions. Conditions favoring the occurrence of noise reversion include specific pacemaker models, arrhythmia cycle lengths in the range causing noise reversion of the individual pacemaker model, long noise sampling periods, and VVI pacing mode. Noise reversion can be diagnosed by telemetering the pacemaker marker channel during ventricular arrhythmias as a part of routine pacemaker-ICD interaction evaluation. It can be prevented or minimized by programming short ventricular refractory periods or using pacemakers with short retriggerable refractory periods.

Bradycardia↗

Randomized prospective pilot study of long-term dual-site atrial pacing for prevention of atrial fibrillation.

OBJECTIVE: To determine whether dual-site atrial pacing is feasible, safe, and effective. DESIGN: We undertook a randomized prospective single-blind crossover study. MATERIAL AND METHODS: Nine patients with at least two episodes per month of symptomatic paroxysmal atrial fibrillation participated in a randomized crossover study involving three separate 3-month blocks of single-site atrial pacing, dual-site atrial pacing, and control (support-only) pacing. RESULTS: Dual-site atrial pacing resulted in shorter P wave duration (81 +/- 14 ms) than did single-site pacing (111 +/- 12 ms) or control sinus rhythm (123 +/- 9 ms) (P<0.0001) and in fewer premature atrial complexes on Holter monitoring (P = 0.06). The arrhythmia-free interval was longer with dual-site pacing (67 +/- 17 days) than with single-site (62 +/- 30 days) or support-only (49 +/- 34 days) pacing (P = 0.10). This pilot study was not statistically powered to detect a difference between pacing modes. CONCLUSION: (1) Dual-site atrial pacing is feasible and safe; (2) it shortens the P wave duration and tends to decrease premature atrial complexes on Holter monitoring; (3) any atrial pacing tends to prolong the arrhythmia-free interval; and (4) this pilot study enrolled too few patients to determine whether a significant difference in pacing modes exists and supports the need for a larger study.

Adult↗

Thoracotomy elevates the defibrillation threshold and modifies the defibrillation dose-response curve.

INTRODUCTION: Despite innovations in nonthoracotomy defibrillation systems, thoracotomies are still required in some clinical settings and are utilized in many animal-based research protocols. The effect of a thoracotomy on defibrillation energy, however, has not been well characterized. METHODS AND RESULTS: Ten dogs in the immediate testing group underwent defibrillation testing immediately following a thoracotomy; another ten dogs in the delayed testing group were given 48 to 72 hours of recovery before defibrillation testing. A right ventricular endocardial coil to cutaneous thoracic patch biphasic system was used. At the time of defibrillation testing, the immediate testing group had a faster mean heart rate (144.7 +/- 30.2 vs 105.8 +/- 17.5 beats/min, P < 0.01), higher mean pulmonary artery pressures (systolic: 18.14 +/- 9.48 vs 11.28 +/- 6.46 mmHg, P = 0.1; diastolic: 6.59 +/- 2.88 vs 3.89 +/- 1.75 mmHg, P < 0.05), and higher mean defibrillation shock impedance (89.0 +/- 11.6 vs 70.9 +/- 7.3 omega, P < 0.002) than the delayed group. The mean ED50 (energy with a 50% success rate) was significantly higher in the immediate group than in the delayed group (26.9 +/- 14.9 vs 14.2 +/- 6.9 J, P < 0.05), and the slopes of the dose-response curves were significantly different (P = 0.03). CONCLUSION: In a right ventricular endocardial to cutaneous patch system, thoracotomy significantly and transiently increased the defibrillation threshold and modified the defibrillation dose-response curve.

Animals↗

Effects of slow pathway ablation on fast pathway function in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: This study investigated whether fast pathway conduction properties are altered by slow pathway ablation in patients with AV nodal reentrant tachycardia. METHODS AND RESULTS: Forty consecutive patients who underwent successful ablation of the slow pathway were prospective subjects for the study. Isoproterenol was used to enhance conduction and to differentiate interactive mechanisms. Potential electrotonic interactions were assessed by comparing patients with and those without residual dual AV node physiology after slow pathway ablation. Paired and unpaired t-tests were used when appropriate P < 0.05 was considered statistically significant. In the entire study population, heart rates were not significantly different before and after slow pathway ablation (RR = 770 +/- 114 msec before and 745 +/- 99 msec after, P = 0.07). Anterograde fast pathway conduction properties were unchanged after slow pathway ablation (effective refractory period, 348 +/- 84 msec before and 336 +/- 86 msec after, P = 0.13; shortest 1:1 conduction, 410 +/- 93 msec before and 400 +/- 82 msec after, P = 0.39). Retrograde fast pathway characteristics also were similar before and after ablation. Neither anterograde nor retrograde fast pathway conduction properties during isoproterenol infusion were changed by slow pathway ablation. When the study population was further divided into patients with (n = 13) or without (n = 27) residual dual AV node physiology, no significant change was detected in fast pathway function in either group after slow pathway ablation. CONCLUSIONS: Fast pathway conduction characteristics were not affected by slow pathway ablation. In patients with AV nodal reentrant tachycardia, observations suggest that fast and slow pathways are functionally distinct.

Adolescent↗

Adenosine: potential modulator for vasovagal syncope.

OBJECTIVES: This study examined the hypothesis that adenosine could provoke a vasovagal response in susceptible patients. Mechanisms of the vasovagal response were further explored by studying the adenosine-mediated reactions. BACKGROUND: Increased sympathetic activity is frequently observed before vasovagal syncope. Recent studies have demonstrated that adenosine, in addition to its direct bradycardiac and vasodilatory effects, can increase sympathetic discharge by activating cardiovascular afferent nerves. METHODS: The effects of adenosine and head-up tilt-table testing with or without isoproterenol were prospectively evaluated in 85 patients examined for syncope after negative results of electrophysiologic testing (51 men and 34 women, mean [+/- SD] age 61 +/- 17 years). Adenosine bolus injections of 6 mg and 12 mg were sequentially administered to patients in the upright position. The same protocol was implemented in 14 normal control subjects (7 men and 7 women, mean [+/- SD] age 38 +/- 10 years). RESULTS: Transient hypertension or tachycardia was observed in 57 (67%) and 20 (24%) patients after administration of 6 mg and 12 mg of adenosine, respectively, during the immediate phase (first 15 s), suggesting direct sympathetic activation. Hypotension and reflex tachycardia were observed in all patients during the delayed phase (15 to 60 s after adenosine injection), suggesting baroreceptor unloading. A vasovagal response was induced in 22 (26%) and 29 (34%) patients after adenosine administration and during tilt-table testing. Inducibility of a vasovagal response by these two methods was comparable (p = 0.12). Of the control subjects, one (7%) had a vasovagal response after adenosine administration and one (7%) had a positive response during tilt-table testing. CONCLUSIONS: These observations support the idea that adenosine is an endogenous modulator of the cardiac excitatory afferent nerves. Sympathetic activation by adenosine can be direct (i.e., cardiac excitatory afferent nerves) and indirect (i.e., vasodilation and reflex sympathetic activation). Adenosine could be an important modulator in triggering a vasovagal response in susceptible patients during examination for syncope.

Adenosine↗

Electromagnetic interference from welding and motors on implantable cardioverter-defibrillators as tested in the electrically hostile work site.

OBJECTIVES: This study was designed to determine the susceptibility of an implanted cardioverter-defibrillator to electromagnetic interference in an electrically hostile work site environment, with the ultimate goal of allowing the patient to return to work. BACKGROUND: Normal operation of an implanted cardioverter-defibrillator depends on reliable sensing of the heart's electrical activity. Consequently, there is concern that external electromagnetic interference from external sources in the work place, especially welding equipment or motor-generator systems, may be sensed and produce inappropriate shocks or abnormal reed switch operation, temporarily suspending detection of ventricular tachycardia or ventricular fibrillation. METHODS: The effects of electromagnetic interference on the operation of one type of implantable cardioverter-defibrillator (Medtronic models 7217 and 7219) was measured by using internal event counter monitoring in 10 patients operating arc welders at up to 900 A or working near 200-hp motors and 1 patient close to a locomotive starter drawing up to 400 A. RESULTS: The electromagnetic interference produced two sources of potential interference on the sensing circuit or reed switch operation, respectively: 1) electrical fields with measured frequencies up to 50 MHz produced by the high currents during welding electrode activation, and 2) magnetic fields produced by the current in the welding electrode and cable. The defibrillator sensitivity was programmed to the highest (most sensitive) value: 0.15 mV (model 7219) or 0.3 mV (model 7217). The ventricular tachycardia and ventricular fibrillation therapies were temporarily turned off but the detection circuits left on. CONCLUSIONS: None of the implanted defibrillators tested were affected by oversensing of the electric field as verified by telemetry from the detection circuits. The magnetic field from 225-A welding current produced a flux density of 1.2 G; this density was not adequate to close the reed switch, which requires approximately 10 G. Our testing at the work site revealed no electrical interference with this type of defibrillator. Patients were allowed to return to work. The following precautions should be observed by the patient: 1) maintain a minimal distance of 2 ft (61 cm) from the welding arc and cables or large motors, 2) do not exceed tested currents with the welding equipment, 3) wear insulated gloves while operating electrical equipment, 4) verify that electrical equipment is properly grounded, and 5) stop welding and leave the work area immediately if a therapy is delivered or a feeling of lightheadedness is experienced.

Defibrillators, Implantable↗

Effect of failed defibrillation shocks on electrogram amplitude in a nonintegrated transvenous defibrillation lead system.

Concern has been raised regarding the ability of a nonthoracotomy integrated lead system to redetect ventricular fibrillation following failed defibrillation shocks due to diminution in postshock intracardiac electrogram amplitude. Whether such a problem could occur with other lead systems is not known, leading to uncertainty regarding a potential ongoing risk of sudden cardiac death in some patients despite implantable cardioverter-defibrillator therapy. To investigate this problem, we measured the amplitude of 10 consecutive ventricular fibrillation endocardial electrograms immediately before and immediately after failed defibrillation shocks in 15 patients at the time of implantation of a nonintegrated, transvenous, pace/sense/defibrillation lead. Overall, mean electrogram amplitude decreased 21%, from 10.7 +/- 4.6 mV before to 8.5 +/- 4.9 mV immediately after failed defibrillation shocks. The change in electrogram amplitude postshock was directly related to shock energy (r = 0.85, p < 0.0005), but shock waveform had no differential effect. Electrogram amplitude could also increase after failed shocks, particularly following those of low energy. No failures to redetect ventricular fibrillation were found. Thus, intracardiac electrogram amplitude is reduced following failed defibrillation shocks in this nonintegrated lead system, but by an amount less than that previously reported for some integrated lead systems. Our findings reveal that failed low energy defibrillation shocks are likely to result in less diminution in postshock intracardiac electrogram amplitude than high energy shocks, and that the postshock amplitude may even increase after some failed shocks.

Aged↗

Termination and acceleration of ventricular tachycardia with autodecremental pacing, burst pacing, and cardioversion in patients with an implantable cardioverter defibrillator. Multicenter PCD Investigator Group.

This multicenter study reports the outcome of ventricular tachycardia (VT) therapy (conversion or acceleration) and the relationship to initial tachycardia cycle length and other clinical variables using an implantable device with the capability of autodecremental or burst pacing, cardioversion, and defibrillation. The device was implanted in 444 patients (mean age 58 +/- 15 years) with 1,240 episodes of VT induced with noninvasive programming and reported in a multicenter database. Only the first sequence attempted for conversion by pacing or cardioversion was assessed, and cardioversion energies were 0.2-5 J. Autodecremental pacing was used to treat 700 induced episodes of VT during titration of pacing therapies (57% converted and 12% accelerated), burst pacing to treat 357 episodes (49% converted under 11% accelerated), and cardioversion to treat 183 episodes (82% converted and 4% accelerated). Cardioversion was the most effective treatment and had the lowest acceleration rate. Shorter VT cycle lengths were more likely to accelerate with burst pacing and longer VT cycle lengths to convert with both burst and autodecremental pacing. Patients with higher ejection fractions were more likely to convert with autodecremental and burst pacing. Use of cardioversion, higher ejection fraction, absence of unrepaired aneurysm, longer VT cycle lengths, coronary artery disease, and use of autodecremental pacing predicted conversion. Lower ejection fraction and VT cycle lengths < or = 300 msec predicted tachycardia acceleration.

Adult↗

Unmasking of retrograde conduction by isoproterenol in a concealed accessory pathway.

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635-700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285-315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.

Bundle-Branch Block↗

Transtelephonic monitoring and transmission of stored arrhythmia detection and therapy data from an implantable cardioverter defibrillator.

A new transtelephonic monitoring device designed for use with implantable cardioverter defibrillators (ICDs) was evaluated. It is capable of interrogating ICDs and transmitting the following data via telephone: programmed parameters (e.g., ventricular tachycardia [VT] and ventricular fibrillation [VF] detection, therapies), number of VT and VF episodes, identification of successful therapies, the 20 cycle lengths preceding the last episode detected, the 10 cycle lengths after the last delivered therapy, battery voltage, and real-time transmission of the patient's rhythm. Eighteen patients (mean age 64 +/- 17 years; 15 males) were implanted with an ICD and epicardial lead system. The patients who did not live near the primary hospital were provided with this transmitter and instructed to transmit monthly and whenever presyncope, syncope, or a shock were experienced. Five hundred ten episodes of spontaneous arrhythmia (495 VT, 15 VF) were detected in 14 of 18 patients in a 24-month period and the success of each therapy (antitachycardia pacing, cardioversion 0.4-34 J, defibrillation 34 J) was analyzed. The number of therapies delivered and their success (%) in terminating the arrhythmia were: 380 ramp/86%, 116 burst/84%, 119 cardioversion/57%, and 15 defibrillations/100%. Sixty-three (42%) of the 152 transmissions indicated an arrhythmia. Twenty-five (16%) of the 152 were transmitted because of symptoms. Sixteen (9.7%) of 165 VT episodes could not be terminated by the full set of programmed VT therapies. Analysis of the pre- and post-episode intervals along with the patient's transmitted rhythm indicated that sinus tachycardia or atrial fibrillation were likely responsible for these episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗

The pacer-cardioverter-defibrillator: function and clinical experience.

Pacer-Cardioverter-Defibrillator. This article reviews the function of the pacer-cardioverter-defibrillator (PCD). Detection of ventricular arrhythmias occurs in two programmable zones, with onset and stability modifiers available to diminish overdetection of sinus tachycardia and atrial fibrillation, respectively. The sensing circuitry utilizes an auto-adjusting sensitivity with exponential decay to allow detection of low-amplitude ventricular fibrillation electrograms without T wave oversensing. Treatment can be accomplished by tiered therapy with two types of antitachycardia pacing, cardioversion and defibrillation. Cardioversion and defibrillation shocks are programmable between single pathway when two leads are used and simultaneous or sequential shock delivery when a three-lead system is used. A telemetered marker channel and electrogram aid in assessing device function during implantation and follow-up. Previously published literature is cited to expand on various aspects of PCD function and programming.

Cardiac Pacing, Artificial↗

Narrow QRS complex tachycardias.

Regular narrow QRS complex tachycardias are a common problem encountered by general internists or family practitioners. Although such tachycardias often occur in patients with a normal heart and seldom represent life-threatening conditions, they may cause bothersome symptoms. The key to approaching the diagnosis of these arrhythmias is identifying atrial activity (P waves) on the surface electrocardiogram and classifying the tachycardia as long RP or short RP. On the basis of that information, a differential diagnosis can be generated, logical therapy can be delivered for termination of the tachycardia, and a plan can be developed to prevent recurrence. Because intravenously administered adenosine alleviates 90% of the episodes of supraventricular tachycardias and has minimal side effects, it has become the drug of choice for termination of most types of narrow QRS complex tachycardias.

Humans↗

Propafenone-induced peripheral neuropathy.

Propafenone hydrochloride, a class IC antiarrhythmic drug, is used in the treatment of ventricular and supraventricular arrhythmias. Herein we describe a patient with episodic jabbing and crushing pain in his hands and feet, aching in his forearms, and hyperesthesias of his extremities. He had been taking propafenone for 1 year because of ventricular arrhythmias. Results of a nerve conduction velocity test were abnormal. Electron microscopic findings on a sural nerve biopsy specimen represented distal small fiber neuropathy. Findings on a thermoregulatory sweat test and on autonomic tests were abnormal, compatible with a distal small fiber neuropathy. To our knowledge, peripheral neuropathy has not previously been reported to occur with use of propafenone. In this patient, propafenone seemed to be responsible for the development of peripheral neuropathy, which resolved after use of the drug had been discontinued.

Adult↗

Operation for ventricular tachyarrhythmias: refining current treatment strategies.

For many patients with ventricular tachyarrhythmias, the optimal choice of palliative or curative therapies is not yet well established. To refine optimal current treatment strategies, baseline patient characteristics were studied in relation to likelihood of successful outcome in 240 consecutive patients undergoing operation for treatment of ventricular tachyarrhythmias from 1981 to 1991. Indications for operation were sudden cardiac death or inducible ventricular tachyarrhythmias refractory to medical therapy (or both). Treatment was directed endocardial procedures in 77 patients (32%), other cardiac procedures in 57 patients (24%) (coronary artery bypass grafting in 94% and valve procedure in 14%, either with [35%] or without [65%] concomitant implantable cardioverter-defibrillator), and implantable cardioverter-defibrillator alone in 106 patients (44%). Overall 30-day operative mortality was 5% (70% confidence interval, 4%-7%) and 2-year survival was 74% (70% confidence interval, 71%-77%). Overall 2-year freedom from sudden cardiac death was 97% (70% confidence interval, 96%-98%) and was similar (p = not significant) for all treatment modalities. For each treatment modality, multivariate analysis identified independent risk factors for operative mortality and 2-year tachyarrhythmia recurrence, advanced angina and congestive heart failure New York Heart Association classes, and overall mortality. To characterize better the use and benefit of coronary artery bypass grafting, risk factors related to outcome also were identified for patients stratified according to absence (44 patients) or presence (119 patients) of coronary artery disease excluding patients treated by directed endocardial procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗