Richard B. Shepard

Combined automatic implantable cardioverter-defibrillator and pacemaker systems: Implantation techniques and follow-up

The automatic implantable cardioverter-defibrillator (AICD) effectively prevents death due to ventricular tachycardia or ventricular fibrillation. Some patients who need an AICD also require cardiac pacing to treat symptomatic bradycardia, bradycardia after defibrillation, or to provide a rate floor to reduce the frequency of bradycardia-related ventricular arrhythmias. Some patients also can benefit from antitachycardia pacing. A mapping technique to implant a pacemaker and AICD sensing leads is presented. For patients with a pacemaker who later need an AICD, the left ventricle is mapped with use of the AICD rate-sensing electrodes to identify a site at which the minimal pacemaker stimulus and maximal ventricular electrogram amplitudes are recorded. An external cardioverter-defibrillator that has amplifiers similar to those in the AICD is used to monitor the rate-sensing electrogram. For patients with an implanted AICD, pacemaker implantation is undertaken by mapping the right ventricle with the pacemaker lead while the AICD is in standby mode; the AICD beep monitor is then used to determine a site where pacemaker stimulus detection by the AICD does not occur. Eight patients underwent implantation of a combined AICD-pacemaker system (four ventricular antitachycardia pacemakers, three ventricular demand pacemakers and one atrial demand pacemaker). Neither inhibition of AICD arrhythmia detection nor double counting occurred. Satisfactory AICD-pacemaker function was shown in all patients postoperatively, and no pacemaker malfunction was observed. Thus, with currently available technology, a combined AICD-pacemaker system can be implanted with satisfactory function of both devices and without adverse device-device interactions.

Pacemaker interference by magnetic fields at power line frequencies

Human exposure to external 50/60-Hz electric and magnetic fields induces electric fields within the body. These induced fields can cause interference with implanted pacemakers. In the case of exposure to magnetic fields, the pacemaker leads are subject to induced electromotive forces, with current return paths being provided by the conducting body tissues. Modern computing resources used in conjunction with millimeter-scale human body conductivity models make numerical modeling a viable technique for examining any such interference. In this paper, an existing well-verified scalar-potential finite-difference frequency-domain code is modified to handle thin conducting wires embedded in the body. The effects of each wire can be included numerically by a simple modification to the existing code. Results are computed for two pacemaker lead insertion paths, terminating at either atrial or ventricular electrodes in the heart. Computations are performed for three orthogonal 60-Hz magnetic field orientations. Comparison with simplified estimates from Faradays law applied directly to extracorporeal loops representing unipolar leads underscores problems associated with this simplified approach. Numerically estimated electromagnetic interference (EMI) levels under the worst case scenarios are about 40 /spl mu/T for atrial electrodes, and 140 /spl mu/T for ventricular electrodes. These methods could also be applied to studying EMI with other implanted devices such as cardiac defibrillators.

Pacemaker interference and low-frequency electric induction in humans by external fields and electrodes

The possibility of interference by low-frequency external electric fields with cardiac pacemakers is a matter of practical concern. For pragmatic reasons, experimental investigations into such interference have used contact electrode current sources. However, the applicability to the external electric field problem remains unclear. The recent development of anatomically based electromagnetic models of the human body, together with progress in computational electromagnetics, enable the use of numerical modeling to quantify the relationship between external field and contact electrode excitation. This paper presents a comparison between the computed fields induced in a 3.6-mm-resolution conductivity model of the human body by an external electric field and by several electrode source configurations involving the feet and either the head or shoulders. The application to cardiac pacemaker interference is also indicated.

Pacing threshold spikes months and years after implant.

To determine patterns of variation in chronic pacing thresholds, we made 4,942 threshold measurements in 257 patients with 312 leads, at times from implant to 295 months (median 17 months) including 1,053 determinations in 46 children < 12 years old. Motivation was late sudden death in two single‐ventricle pacemaker‐dependent children with multiple possible death causes. At stimulus duration 0.5 ± 0.04 msec, mean of the thresholds, measured 1 month or more after implant, was 1.3 ± 0.66 volts (V) for endocardial electrodes and 2.8 ± 1.39 V for epicardially applied electrodes. Highest mean thresholds were in the 6 to 12‐year‐old age group. In 34 leads studied at implant, again within a month and for at least three years thereafter, time of maximum threshold occurred after one month in 59%, independent of lead type or patient age. Of 107 leads with five or more measurements after 3 months use, gradual increase in threshold continued after 3 months in 24%. An additional 21% had at least one threshold that exceeded the post‐three‐months individual patient lead mean by three standard deviations. Most striking was the occurrence of transient several‐volt increases and decreases in threshold as late as 8 years after lead implantation in at least three children. These temporary changes were detected initially transtelephonically by the vario method of threshold measurement. They occurred during minor illnesses such as summer colds, yet similar illnesses also occurred without threshold elevation. We suggest further study of pacing threshold variations in highly pacemaker‐dependent children whose cardiac anatomy makes use of epicardial electrodes necessary.

Failure of One Conductor in a Nonthoracotomy Implantable Defibrillator Lead Causing Inappropriate Sensing and Potentially Ineffective Shock Delivery

We describe how a single defect in a new model transvenous lead for an implantable curdiuverter defibrillator can result in malfunction of the sensing and defibrillation circuits. The patient had received shocks during atrial fibrillation without premonitory symptoms. At least one shock was delivered and not fell by the patient. In addition, late in the course, a shock was delivered during atrial fibrillation documented to be with a slow ventricular response. In the transvenous lead, a distal spring functions as the anode for rate sensing and the cathode for defibrillation. The wire from this spring bifurcates near the proximal end of the catheter. One wire from the bifurcation leads to the positive (anode) rate‐sensing socket of the pulse generator, and the other wire leads to the negative (cathode) high voltage output socket of the defibrillator for defibrillation and cardioversion. After the inappropriate and unperceived shocks were documented, intraoperative and postoperative electrical testing indicated that intermittent discontinuity of the distal spring system within the proximal yoke of the catheter caused faulty sensing and potentially unreliable defibrillation. This dual malfunction was possible because the distal spring of the lead functions in the high‐voitage output and the rate‐sensing iow‐vollage input circuits of the implantable defibrillator.

Gross and Microscopic Changes Associated with a Nonthoracotomy Implantable Cardioverter Defibrillator

The pathology associated with an invesrigational transvenous defibriliating and sensing lead is described. The lead system had delivered a total of 865 J from the time of implantation to the time of patient death from a noncardiac cause 7 months after implantation and 1 month after his last defibrillator shock. There was mild, superficial fibrous thickening on the endothelial surface of the superior vena cava adjacent to the proximal spring electrode, which did not extend into the vessel wall. The distal portion of endocardial lead was embedded in the interventricular septum near the apex of the right ventricle, surrounded by fibrous thickening, and partially covered by endocardial tissue. Microscopically, there was a thick bed of fibrous connective tissue surrounding the lead with extensive interstitial fibrous connective tissue radiating into the adjacent myocardium. Since this pattern is different from the more generalized fibrotic scarring produced by myocardial infarction, we speculate that the mechanism for the observed interstitial fibrosis is replacement fibrosis following acute myocyte injury that resulted from prior defibrillator shocks and possibly from the trauma produced by the lead compressing adjacent myocardium during systole. Potential effects on device efficacy of these fibrotic changes at the bioelectric interface include their representing a new arrhythmia substrate, the possibility that fibrosis could increase both defibrillation and pacing thresholds, and that the inflammatory reaction may cause deterioration of intracardiac electrograms and interfere with sensing and tachycardia recognition.

Chronic Rapid Atrial Pacing to Maintain Atrial Fibrillation: Use to Permit Control of Ventricular Rate in Order to Treat Tachycardia Induced Cardiomyopathy

LR was a patient, followed over a 16‐year period, who presented with an atrial tachycardia which was initially intermittent, but became incessant. Neither the atrial tachycardia nor the associated rapid ventricular response rate could be treated successfully with available drug therapy, resulting in a dilated cardiomyopathy and New York Heart Association (NYHA) class III‐IV congestive heart failure. Acute induction of atrial fibrillation with rapid atrial pacing demonstrated that the associated ventricular rate could be satisfactorily slowed with digitalis therapy. Initially, short bursts from an implanted, radiofrequency controlled, patient activated pacemaker programmed to a rate of 600 bpm and connected to a permanent endocardial atrial J lead successfully interrupted the tachycardia and precipitated atrial fibrillation. Over a period of 3 months, this therapy changed the patients heart failure to NYHA class II status. Subsequently, precipitation of atrial fibrillation with this technique failed, resulting in return to NYHA class III‐IV congestive heart failure. Therefore, a custom‐designed, high rate, rate‐programmabie pacemaker was implanted to pace the atria rapidly and continuously to maintain atrial fibrillation. A pacing rate of 375 bpm plus digoxin slowed the ventricular rate to 70–80 bpm, with stabilization of the congestive heart failure to NYHA class II. The pacemaker generator was replaced 6 months later, and after another 5 months, pacing was discontinued. The patients subsequent rhythm remained stable atrial fibrillation with clinically successful control of both the ventricular rate and heart failure (NYHA class II) until the patients death 72 months later. This unique case demonstrates another form of chronic therapy which, in selected cases, can be used for the long term control of rapid ventricular response rates to supraventricular arrhythmia.

Simultaneous Use of an Implanted Defibrillator and Ventricular Assist Device

A left ventricular assist device was placed as a bridge to cardiac transplantation in a 51-year-old man with cardiogenic shock. Placement of the left ventricular assist device occurred 5 years after implantation of an implantable cardioverter/defibrillator. The implantable cardioverter/defibrillator discharged appropriately during ventricular assist device support to terminate episodes of sustained ventricular tachycardia without causing malfunction of the ventricular assist device.

Automatic Implantable Cardioverter Defibrillator: Surgical Approaches for Implantation

Surgical approaches for implantation of the automatic cardioverter defibrillator are sternotomy, left thoracotomy, subxiphoid, and subcostal. Although any one of these may be combined with insertion of one or more of the electrodes transvenously, surgical entry into the chest is required for every noninvestigational defibrillator implantation operation. The approaches differ in exposure provided for selecting electrode sites and for handling untoward events, in amount and location of tissue that must be divided or dissected, and in average time required. The operation is an electrical one. Its purpose is to obtain reliable rhythm sensing so that defibrillation or cardioversion shocks will occur only when necessary, and to obtain low enough defibrillation thresholds for shocks of 30 joules or less to have a 10‐joule defibrillation safety margin. Many of the patients have had previous cardiac operations. They usually have low or very low ejection fractions. lntraoperative electrophysiological testing with often multiple defibrillation episodes is required. The choice of approach varies with the state of the patient, the institutional experience, and the surgeon. This article describes techniques, and the advantages and disadvantages of the four approaches as used by four surgeons in four different institutions.

Effects of partitioning operations on the electrical activity of the human stomach

Abstract To identify the effects that various gastric partitioning procedures have on the electrical activity of the stomach, pairs of bipolar Teflon-coated electrode wires were placed in selected sites of the stomach of 18 patients. Recordings from the proximal gastric fundus above the staple line, from the distal fundus below the staple line, and from the distal gastric antrum were obtained using differential preamplifiers, an oscilloscope, and a dual-channel tape recorder. Oscilloscopic displays were photographed and the electrical signals were recorded for subsequent analysis. The total number of readings at each recording site were: proximal fundus, 79; distal fundus, 59; and antrum, 96. Control electrical rhythm (CER) was found in all the 96 antral recordings. The mean period was 21.6 ± 0.22 sec (SEM). The frequency was 2.8 ± 0.03/min. Only in 4 of the 138 recordings from the gastric fundus, could a low-amplitude CER be identified. Although partitioning of the stomach by stapling produces some degree of crushing injury to the gastric wall, no abnormalities of the CER were noted in the antrum, supporting the concept that the gastric pacemaker of the slow-wave electrical activity (CER) in the human stomach is located below the gastric fundus. Furthermore, in contrast to cardiac muscle, localized mechanical injury to the gastric wall did not result in ectopic foci of electrical activity.