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.

Lymphotropic virions affect chemokine receptor-mediated neural signaling and apoptosis: implications for human immunodeficiency virus type 1-associated dementia.

Chemokine receptors pivotal for human immunodeficiency virus type 1 (HIV-1) infection in lymphocytes and macrophages (CCR3, CCR5, and CXCR4) are expressed on neural cells (microglia, astrocytes, and/or neurons). It is these cells which are damaged during progressive HIV-1 infection of the central nervous system. We theorize that viral coreceptors could effect neural cell damage during HIV-1-associated dementia (HAD) without simultaneously affecting viral replication. To these ends, we studied the ability of diverse viral strains to affect intracellular signaling and apoptosis of neurons, astrocytes, and monocyte-derived macrophages. Inhibition of cyclic AMP, activation of inositol 1,4,5-trisphosphate, and apoptosis were induced by diverse HIV-1 strains, principally in neurons. Virions from T-cell-tropic (T-tropic) strains (MN, IIIB, and Lai) produced the most significant alterations in signaling of neurons and astrocytes. The HIV-1 envelope glycoprotein, gp120, induced markedly less neural damage than purified virions. Macrophage-tropic (M-tropic) strains (ADA, JR-FL, Bal, MS-CSF, and DJV) produced the least neural damage, while 89.6, a dual-tropic HIV-1 strain, elicited intermediate neural cell damage. All T-tropic strain-mediated neuronal impairments were blocked by the CXCR4 antibody, 12G5. In contrast, the M-tropic strains were only partially blocked by 12G5. CXCR4-mediated neuronal apoptosis was confirmed in pure populations of rat cerebellar granule neurons and was blocked by HA1004, an inhibitor of calcium/calmodulin-dependent protein kinase II, protein kinase A, and protein kinase C. Taken together, these results suggest that progeny HIV-1 virions can influence neuronal signal transduction and apoptosis. This process occurs, in part, through CXCR4 and is independent of CD4 binding. T-tropic viruses that traffic in and out of the brain during progressive HIV-1 disease may play an important role in HAD neuropathogenesis.

Intracellular CXCR4 signaling, neuronal apoptosis and neuropathogenic mechanisms of HIV-1-associated dementia.

The mechanism(s) by which HIV-1 affects neural injury in HIV-1-associated dementia (HAD) remains unknown. To ascertain the role that cellular and viral macrophage products play in HAD neurotoxicity, we explored one potential route for neuronal demise, CXCR4. CXCR4, expressed on lymphocytes and neurons, is both a part of neural development and a co-receptor for HIV-1. Its ligand, stromal cell-derived factor-1alpha (SDF-1alpha), affects neuronal viability. GTP binding protein (G-protein) linked signaling after neuronal exposure to SDF-1alpha, virus-infected monocyte-derived macrophage (MDM) secretory products, and virus was determined. In both human and rat neurons, CXCR4 was expressed at high levels. SDF-1alpha/beta was detected predominantly in astrocytes and at low levels in MDM. SDF-1beta/beta was expressed in HAD brain tissue and upregulated in astrocytes exposed to virus infected and/or immune activated MDM conditioned media (fluids). HIV-1-infected MDM secretions, virus and SDF-1beta induced a G inhibitory (Gi) protein-linked decrease in cyclic AMP (cAMP) and increase inositol 1,4, 5-trisphosphate (IP3) and intracellular calcium. Such effects were partially blocked by antibodies to CXCR4 or removal of virus from MDM fluids. Changes in G-protein-coupled signaling correlated, but were not directly linked, to increased neuronal synaptic transmission, Caspase 3 activation and apoptosis. These data, taken together, suggest that CXCR4-mediated signal transduction may be a potential mechanism for neuronal dysfunction during HAD.

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.

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 cardioverter 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 felt 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-voltage output and the rate-sensing low-voltage input circuits of the implantable defibrillator.

Can the heart be chronically paced with electrodes on the pericardial surface?

During implantable defibrillator (ICD) operations, we measured acute and chronic transpericardial bipolar pacing thresholds through standard myocardial surface electrodes sewn on the pericardium for chronic ICD QRS rate-sensing use. We compared observations in 24 patients on day 0 with chronic measurements in seven patients at 27.4 +/- 12.1 (median 31.7) months. The leads were used only for QRS rate-sensing, not for pacing, during the time between acute and chronic measurements. Acute transpericardial pacing threshold at 0.5-msec stimulus duration on day 0 was 4.5 +/- 2.19 V (standard deviation), median 3.5 V, and at median time 964 days postimplantation was 3.8 +/- 2.07 V, median 3.5 V. Mean acute pacing current threshold was 3.7 +/- 1.90 mA, n = 23, and chronic was 2.7 +/- 1.79 mA, n = 6. Acute bipolar impedance was 1,209 +/- 383 ohms, median 1,138 ohms, and chronic was 1,550 +/- 358 ohms, median 1,410 ohms, n = 7. Acute bipolar QRS amplitude was 12.3 +/- 5.93 mV, median 12.1 mV, n = 24, and chronic was 13.5 +/- 8.5 mV, median 17.2 mV, n = 7. None of the changes between the acute and chronic states was statistically significant, with the exception of bipolar impedance (P = 0.054). We concluded that: (1) transpericardial pacing threshold did not increase with time; (2) initial and chronic pacing impedances were high and current low; (3) QRS amplitudes were highly satisfactory for defibrillator rate-sensing; and (4) this approach to ICD implantation left the surgically virgin heart unscarred to make future transplantation easier, and enhanced safety when previous cardiac operations had been done.

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. Intraoperative 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 technique, and the advantages and disadvantages of the four approaches as used by four surgeons in four different institutions.

Gross and microscopic changes associated with a nonthoracotomy implantable cardioverter defibrillator.

The pathology associated with an investigational transvenous defibrillating 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.

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 less than 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.

Inability of the signal-averaged electrocardiogram to determine risk of arrhythmia recurrence in patients with implantable cardioverter defibrillators.

Signal-averaged electrocardiography has been used to identify patients at risk for arrhythmic death after myocardial infarction. Since patients with implantable cardioverter defibrillators (ICDs) are at high risk for arrhythmic events, they should also be expected to have a high incidence of abnormal signal-averaged electrocardiograms (SAECGs). However, whether the SAECG can discriminate patients who will have arrhythmia recurrence and receive appropriate ICD shocks from those who will have no recurrence and no shocks is unknown. This study examines the usefulness of the SAECG to separate appropriate users from non-users of the ICD. Fifty patients with ICDs participated in this study. Those who received a shock preceded by symptoms, a shock without preceding symptoms but with electrocardiographic documentation of ventricular fibrillation or ventricular tachycardia, or a shock while asleep were classified as ICD users. All other patients were classified as nonusers. The SAECG was classified as normal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and if the total filtered QRS duration was less than 120 msec, the root-mean square voltage of the terminal 40 msec was greater than 25 muV, and the terminal low amplitude signal duration measured less than 38 msec. The SAECG was classified as abnormal if the QRS duration on the standard electrocardiogram was less than or equal to 110 msec and any one of these three criteria were outside the "normal range." The SAECG was classified as indeterminate if the QRS duration on the standard 12-lead electrocardiogram was greater than 110 msec. For the entire group of 50 patients, 8 (16%), 12 (24%), and 30 (60%) had normal, abnormal, and indeterminate SAECGs, respectively. Of the 22 ICD users, 1 (5%), 5 (23%), and 16 (73%) patients had normal, abnormal, and indeterminate SAECGs, respectively. Of the 28 ICD nonusers, 7 (25%), 7 (25%), and 14 (50%) patients had normal, abnormal, and indeterminate SAECGs, respectively. ICD users had lower left ventricular ejection fractions (P = 0.0002), a higher incidence of ventricular tachycardia (P = 0.04), prior exposure to a greater number of antiarrhythmic drugs (P = 0.04), and a lower likelihood for survival (P = 0.02) compared to the ICD nonusers. There was no statistically significant difference between the ICD users and nonusers as stratified by SAECG classification regardless of whether or not the interminate studies were included or excluded from the analysis.(ABSTRACT TRUNCATED AT 400 WORDS)

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 patient's 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-programmable 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 patient's subsequent rhythm remained stable atrial fibrillation with clinically successful control of both the ventricular rate and heart failure (NYHA class II) until the patient's 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.

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.

Failure of elective replacement indicator to predict end-of-life of the automatic implantable cardioverter-defibrillator.

A major limitation in the use of the automatic implantable cardioverter-defibrillator (AICD) is limited battery longevity and the absence of an accurate and precise end-of-life indicator. An elective replacement indicator, or ERI, was proposed by the manufacturer of the AICD in 1985. This ERI was evaluated in nine patients with AICDs. The ERI was exceeded at a mean of 10.9 +/- 3.0 months after implantation. Although 0.6 +/- 0.4 months of battery life were predicted to remain before battery failure, the devices were followed for 6.0 +/- 3.8 months (p = 0.002) during which time no device failed. Although 28.9 +/- 21.9 seconds of charging time were predicted to remain, 103.5 +/- 67.9 seconds were shown to be available by magnet charge time testing (p = 0.01). Thus, the ERI of the AICD, as originally proposed by its manufacturer, consistently underestimated both the predicted time to end-of-life as well as the cumulative charging time remaining before end-of-life for each AICD examined. We propose that this ERI not be used to predict end-of-life of the AICD. A "new" ERI has been recommended.

Cardiology office computer use: primer, pointers, pitfalls.

An office computer is a utility, like an automobile, with benefits and costs that are both direct and hidden and potential for disaster. For the cardiologist or cardiovascular surgeon, the increasing power and decreasing costs of computer hardware and the availability of software make use of an office computer system an increasingly attractive possibility. Management of office business functions is common; handling and scientific analysis of practice medical information are less common. The cardiologist can also access national medical information systems for literature searches and for interactive further education. Selection and testing of programs and the entire computer system before purchase of computer hardware will reduce the chances of disappointment or serious problems. Personnel pretraining and planning for office information flow and medical information security are necessary. Some cardiologists design their own office systems, buy hardware and software as needed, write programs for themselves and carry out the implementation themselves. For most cardiologists, the better course will be to take advantage of the professional experience of expert advisors. This article provides a starting point from which the practicing cardiologist can approach considering, specifying or implementing an office computer system for business functions and for scientific analysis of practice results.

Effects of various operations on the electrical activity of the human stomach recorded during the postoperative recovery period.

This study attempts to characterize any changes occurring in the human gastric control electrical rhythm (CER), following a variety of gastric surgical procedures. Pairs of electrodes were implanted in selected specific sites on the stomachs of 57 patients undergoing either antrectomy and vagotomy, proximal gastric vagotomy (PGV), vagotomy and drainage, gastric resection without vagotomy, or fundoplication. Five patients undergoing nongastric operations served as controls. After operation recordings were obtained with differential preamplifiers, an oscilloscope, and a dual-channel tape recorder. An electrical signal compatible with a CER was found almost always in the distal body or antrum, regardless of whether vagotomy was performed. In contrast, a CER was found only occasionally in the fundus, and was never found following PGV. Although there was a difference in the frequency of occurrence of fundic CER in patients with and without vagotomy, it was not statistically significant (p = 0.0668). Patients with prolonged postoperative convalescence because of gastric atony were compared with patients with normal postoperative courses regarding the presence or absence of CER in the gastric antrum or fundus. A statistically significant relationship between abnormal gastric motility and absence of CER was not established.