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)
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.
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.
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.
