Carolyn Andrews

Lyme carditis: an important cause of reversible heart block.

Lyme disease is a tick-borne spirochetal infection, characterized by erythema chronicum migrans and an acute systemic illness. The disease is endemic in many parts of the north-eastern United States. Without treatment, late rheumatic, neurologic, and cardiac complications frequently occur. We report four serologically confirmed cases of Lyme carditis in previously healthy young men (mean age, 45 years) from endemic areas. Each presented with severe symptomatic atrioventricular block, three with episodes of prolonged ventricular asystole. Two had permanent pacemakers implanted (one was later removed), and another, very nearly did, before diagnosis. All four patients were treated with antibiotics, and in each case their rhythm returned to sinus, though one patient has Wenckebach second degree block with atrial pacing at 120 beats/min 16 months later. Carditis occurs in 4% to 10% of cases of Lyme disease and usually begins 3 to 6 weeks after the initial illness. It manifests as a transient myocarditis with varying degrees of atrioventricular block. The diagnosis is made primarily on clinical grounds and confirmed by serologic testing. Temporary cardiac pacing is frequently needed by patients who have severe heart block with hemodynamic instability. The evidence suggests that, in most cases, the block is at the level of the atrioventricular node. The block generally resolves completely with antibiotic treatment. Complete heart block rarely persists more than 1 week and the long-term prognosis appears to be excellent. Consideration and prompt recognition of this potentially lethal, but reversible, cause of heart block is crucial in order to avoid inappropriate permanent pacemaker implantation.

Surgical Removal of Infected Transvenous Pacemaker Leads

Infection, though uncommon, can be the most lethal of all potential complications following transvenous pacemaker implantation. Eradication of infection associated with pacemakers requires complete removal of all hardware, including inactive leads. Since 1972, 5,089 patients have had 8,508 pacemaker generators implanted at Montefiore Medical Center. There were 91 infections (1.06%); four of our patients required surgical removal. Nine additional patients were referred for surgical removal of infected transvenous pacemaker leads from other institutions. Surgical methods for removal included use of cardiopulmonary bypass or inflow occlusion. Surgery may be safely used in unstable or elderly patients and should not be reserved as a last resort. This article reviews our surgical experience removing infected pacemaker leads at Montefiore Medical Center.

Pacemaker Implantation in Children: A 21-Year Experience

Forty‐one children, 20 hoys and 21 girls, aged 11 days to 19 years (mean 9.9 years) at initial pacemaker implant, were followed 1 to 248 months (mean 90 months). Ten (mean age 8.2 years) were implanted between 1966 and 1972 (Group I), 14 (mean age 9.9 years) between 1973 and 1980 (Group 11) and 17 (mean age 10.9 years) from 1981 through April 1988 (Group 111). Arrhythmias were congenital complete heart block in 19, postoperative heart block in 15, acquired heart block in 3, sick sinus syndrome in 3, and bradycardia‐induced ventricular fibrillation in 1. Twenty‐eight of 41 children had a transvenous implant: 40% of Group I, 71% of Group 11 and 82% of Group III. Thirteen were cephalic, four subclavian and 11 jugular. Generator site was pectoral in 19, abdominal in 12, intrathoracic in one, and retromammary in nine of 12 girls aged 10 years or more at implant. In Groups 1,11 and 111, 5, 14 and 6 had VOO or WI units; 5, 0 and 8 dual chamber (VAT, VDD and DDD) pacemakers; 0, 0 and 1 AAI; and 0, 0 and 2 rate‐modulated (WIR) units at initial implant. The average interval between pacer‐related hospitalizations in Groups I, II and III was 20, 42, and 39 months. Complications included infection in six, hemothorax in one, and impending pacemaker erosion in one. Six patients died, one of pacer infection, four from primary cardiac disease, and one suddenly without apparent reason. Follow‐up continues in 31: 14 are employed full‐time, three are homemakers, eight are full‐time students, and six are active pre‐schoolers. Four women have had normal children. We conclude: (1) children with implanted pacemakers can have a normal lifestyle, with prognosis based on underlying cardiac disease; (2) elective epicardial electrodes are now rarely needed; (3) implantation via the cephalic vein is feasible and complication‐free; (4) retromammary implant is technically easy and cosmetic; (5) dual chamber and rate‐modulated pacemakers can be utilized effectively.(PACE, Vol. 11 November Part II 1988)

Effect of Varying Atrial Sensitivity, AV Interval, and Detection Algorithm on Automatic Mode Switching

Automatic mode switching (AMS) is absolutely dependent on atrial tachyarrhythmia detection. The effects of programming several features that could influence tachyarrhythmia detection were assessed in 18 patients (six women; mean age 64 years) with pacemakers having AMS capability. The atrial electrogram amplitude in sinus rhythm at implant (SR‐EGM), last measured atrial sensing threshold prior to tachycardia (A‐SENS), and atrial sensing threshold for effective AMS during atrial tachyarrhythmia (AMS‐SENS) were obtained. Additionally, ten patients had AV intervals increased from 60 to 200 ms, while seven patients had detection algorithms made more stringent from 5 beats at 150 beats/min to 11 beats at 200 beats/min to assess their effects on AMS efficacy. Results: Sensitivities: Mean SR‐EGM = 3.55 mV; mean A‐SENS = 2.06 mV; and mean AMS‐SENS = 1.46 mV. Fourteen patients developed atrial fibrillation and four atrial flutter. Thirteen of 14 patients who developed atrial fibrillation sensed adequately at ≥ 1.0 mV in normal sinus rhythm (NSR), but only six patients had effective AMS at these settings in atrial fibrillation. Three of four patients who developed atrial flutter had effective AMS at ≥ 2.0 mV. AV Interval: AMS was effective in eight of ten patients at AV intervals up to 200 ms. One patient lost AMS at an AV interval of 120 ms. Algorithm: In two of seven patients, AMS was not effective if the detection algorithm was more stringent than five beats at 150 beats/min. Conclusions: (1) In atrial fibrillation, effective AMS requires more sensitive atrial settings than in NSR: (2) AV intervals as short as 120 ms can interfere with AMS function; and (3) More stringent detection algorithms may be inappropriate for effective AMS function.

Pacemaker Infection with Mycobacterium Avium Complex

A 21 ‐year‐old, HIV negative, malnourished, homeless woman with congenital heart block had a pacemaker implanted at 7 years of age and multiple procedures thereafter. The most recent of these procedures was replacement of a pulse generator in the right pectoral region. Four months later she had fever, pain, and swelling over the implant site resulting from infection with mixed flora and Mycobacterium avium complex. The pacemaker system was removed fay thoracotomy via a median sternotomy and a new DDD pacemaker simultaneously implanted. She was treated with systemic antibiotics—isoniazid, rifampin, ethambutol—for 2 weeks. Six months later she was healthy, pacing well, and apparently free of infection, off all medications.

Clinical Predictors and Natural History of Atrial Fibrillation in Patients with DDD Pacemakers

GROSS, J., ET AL.: Clinical Predictors and Natural History of Atrial Fibrillation in Patients with DDD Pacemakers. Effective DDD pacing requires that patients remain free of atrial fibrillation (AF). Four hundred eighty‐nine consecutive patients undergoing initial transvenous DDD implants were reviewed to determine the incidence of postimplant AF in this population and to assess what factors, known at implant, predicted the later development of AF. The variables analyzed included age, sex, indication for implant (dominant SA or AV node disease), history of AF, atrial electrogram characteristics and pacing threshold, and the status of retrograde conduction. Forty‐eight patients (9.8%) developed AF a mean of 23 months postimplant, and 11 of these patients returned to sinus rhythm and were managed once again in DDD for significant periods. A prior history of AF and the presence of dominant sinoatrial disease were far more prevalent in the patients who developed AF (P < 0.001) though the vast majority of patients with these two independent risk factors remained in sinus rhythm through much or all of their follow‐up period. We conclude that the incidence of AF is not of a magnitude to preclude DDD pacing in the vast majority of patients in sinus rhythm at implant.

The Clinical Relevance of Electromyopotential Oversensing in Current Unipolar Devices

Electromyopotential Oversensing of unipolar pacemakers was first appreciated 20 years ago, but its prevalence in present day devices is less well defined. Thirty‐four pacemaker patients, only two with symptoms suggestive of Oversensing, were evaluated in unipolar settings to assess the frequency of provocation of oversensing in one or, if present, both pacing channels. The sensing threshold of each patient, whenever possible, was recorded as well. Results: atrial oversensing occurred in 11/18 patients (61%), all at sensitivities in the 0.4–1.0 mV range. Ventricular oversensing was noted in 13/33 patients (39%), with all but one programmed to settings of 1.25 mV or more sensitive (i.e. < 1.25 mV). Twenty six of 26 patients amenable to testing had ventricular sensing thresholds of at least 4.0 mV or more. Of the 15 patients amenable to atrial sensing threshold testing, 4 had a threshold of 1.0 mV or < 1.0 m V, 6 had thresholds between 1.0–2.0 mV, and 5 sensed at settings > 2.0 mV. Conclusion: electromyopotential oversensing remains a relevant issue in current day unipolar pacemakers. Most patients do not describe symptoms related to electromyopotential interference, yet such interference is frequently provoked. Over‐sensing is common at high sensitivities typically utilized for atrial sensing, but quite unusual at settings necessary for adequate ventricular sensing. Programming unipolar devices to unnecessarily high sensitivities should be avoided or serious consequences may result.

Treadmill Assessment of an Activity‐Modulated Pacemaker: The Importance of Individual Programming

Maximum benefit from a rate‐modulated pacemaker requires individualized programming of rate response settings. We tested an externally strapped activity‐sensing pacemaker (Activitrax ‐ Medtronic 8400) in eight healthy volunteers, to assess the pacing responses of the different rate response and activity threshold settings. Five males and three females, aged 20 to 70 years (mean 40), performed a total of 67 treadmill exercise tests, using a specijic protocol designed to assess the activity‐sensing unit. The external unit was compared to implanted units in four patients, to validate its accuracy. A reproducible sinus response to the treadmill protocol was observed, against which pacing responses were compared. The activity threshold determines the degree of activity required to elicit a pacing rate response, whereas the rate response setting determines the rate attained. Rates of 140 bpm were rarely achieved, despite vigorous exercise. The sensor responds rapidly to activity, not to physiologic demand; to increase in speed, not grade. Four patients performed repeated limited treadmill tests to determine their optimum program setting, with symptomatic status and the healthy volunteer sinus response as guides. These results, and those from the external Activitrax unit, suggest that LOW 6 and MEDIUM 6–10 settings will prove optimum for most patients.

Comparison of myopotential interference in unipolar-bipolar programmable DDD pacemakers.

Myopotontial interference (MPI) can inhibit or trigger single and dual chamber unipolar pacemakers while bipolar pacemakers are resistant. Twenty units of two different models of dual chamber pacemaker, each capable of being programmed to single chamber or dual chamber and unipolar or bipolar function were tested to provoke myopotential interference. No patient had evidence of myopotential interference at any sensitivity setting in the bipolar configuration either in atrium or in ventricle. All patients (20/20) interfered with pacemaker function at the highest atrial or ventricular sensitivity settings in the unipolar configuration. T wave sensing occurred at the 0.25 mV sensitivity setting in four patients in pacemaker model 925, in both bipolar and unipolar configurations. Tiventy‐five percent of patients had myopotential interference at the unipolar atrial sensing threshold and did not allow a setting which would reject myopotential interfercnce while providing satisfactory atrial sensing. Twenty percent (2/10) had myopotential caused ventricular inhibition at the least sensitive ventricular channel setting in model 240G so that myopotential interference could not be avoided in that unit no matter how large the electrogram.

“Pseudo-endless Loop” Tachycardia in an AV Universal (DDD) Pacemaker

A 3‐beat episode of ventricular arrhythmia was recorded in a patient with an AV universal (DDD) pacemaker. This arrhythmia mimicked “endless loop” tachycardia (ELT) because it appeared following a ventricular premature contraction (VPC), its rate approached the preset upper‐rate limit and the regular P waves disappeared during the episode. However, as retrograde conduction was absent ELT could not exist. The mechanism of this arrhythmia was based on a combination of interference by VPC of the regular sequence of this complexes produced by P wave and the pacemaker commitment to maintain an upper rate limit by prolongation of the programmed pacemaker AV delay.