Dopamine and beta-band oscillations differentially link to striatal value and motor control.

Parkinson's disease is characterized by decreased dopamine and increased beta-band oscillatory activity accompanying debilitating motor and mood impairments. Coordinate dopamine-beta opposition is considered a normative rule for basal ganglia function. We report a breakdown of this rule. We developed multimodal systems allowing the first simultaneous, chronic recordings of dopamine release and beta-band activity in the striatum of nonhuman primates during behavioral performance. Dopamine and beta signals were anticorrelated over seconds-long time frames, in agreement with the posited rule, but at finer time scales, we identified conditions in which these signals were modulated with the same polarity. These measurements demonstrated that task-elicited beta suppressions preceded dopamine peaks and that relative dopamine-beta timing and polarity depended on reward value, performance history, movement, and striatal domain. These findings establish a new view of coordinate dopamine and beta signaling operations, critical to guide novel strategies for diagnosing and treating Parkinson's disease and related neurodegenerative disorders.

Do battery depletion indicators reliably predict the need for pulse generator replacement?

The aim of this study was to test the validity of battery depletion indicators to forecast end of service (EOS) in dual chamber pulse generators (PG). Two additional approaches for prediction of EOS were evaluated as well: the real-time telemetry of cell impedance and a battery stress test (BST) that used a transitory increase in pacing rate. The study population consisted of 119 patients with Intermedics dual chamber PG models Cosmos II and Relay, in which cell impedance had exceeded 2.5 k omega. The patients were followed in 6-month intervals. If the interrogation of the PG or the BST prompted the appearance of the intensified follow-up indicator (IFI), the next follow-up was scheduled within 2 months. PG replacement was performed on physician's discretion or immediately on appearance of the elective replacement indicator (ERI), regardless of the method of ERI provocation. During a period of 2 years/and 9 months, 33 patients underwent PG replacement. Out of 21 patients with positive ERI indicators, only 5 had positive warning indicators of approaching battery depletion in the preceding follow-up (IFI during BST, n = 4; ERI during BST n = 1). The majority of patients (n = 16, 76%) revealed ERI without prior activation of IFI, neither spontaneous nor during the BST. Four of these 16 ERI-positive patients had cell impedance values far below the ERI limits of the manufacturer. Based on battery depletion indicators, an exact prediction of EOS of dual chamber pacemakers is not possible. Measuring battery impedance allows for a statistical estimation of remaining service life but it may be misleading in the individual case. A BST that is based on a temporary increase of pacing rate is invalid in forecasting battery depletion. As activation of the ERI can trigger an abrupt change to the VVI backup mode, pacemaker dependent patients with low programmed basic pacing rates may be hemodynamically compromised by an unexpected activation of ERI. Close monitoring intervals and PG replacement before appearance of the ERI is recommended in those patients.

Safety and efficiency of pulse charge multiplication for chronic ventricular output programming.

Fifty-one patients with Intermedics pacemakers and different chronic (> or = 12 months) ventricular lead models were investigated. Ventricular charge thresholds (microC) were measured telemetrically at 1.0, 2.0, 2.5, and 3.5 V, respectively. Then pulse duration was increased until charge per pulse (microC) was twice the threshold value in patients not being pacemaker dependent (n = 39) and three times the threshold in pacemaker dependent patients (n = 12), thus giving a 2:1 or 3:1 safety factor in terms of charge ("safety charge"). At safety charge settings, the battery current was measured telemetrically for all four pulse amplitudes (PA) in VVI mode at 70 beats/min. For safety purposes, only pulse amplitudes were considered that fulfilled two conditions: (1) pulse duration threshold (PDT) < or = 0.30 ms at PA and (2) PDT < or = 1.00 ms at a pulse amplitude of (PA-0.5 V). The combination of pulse amplitude and pulse duration that yielded the safety charge at the lowest battery current was defined as optimized ventricular output (Copt). It was found at 1.0 V in 27 patients and at 2.0 V in 24 patients. The safety pulse duration (SPD) that yielded a 2:1 safety charge in patients who were not pacemaker dependent was 0.32 +/- 0.12 ms for both, 1.0 V (n = 23) and 2.0 V (n = 16), respectively. In pacemaker dependent patients, the SPD for the 3:1 safety charge was 0.61 +/- 0.25 ms (at 1.0 V, n = 4) and 0.47 +/- 0.11 ms (at 2.0 V, n = 8), respectively. The safety factor for conversion of PDT into SPD was 3.15 (range 3.00-3.38) for pacemaker dependent patients and 2.04 (range 2.00-2.43) for patients who were not pacemaker dependent, respectively. Charge thresholds measured at study entrance, after 24 hours, and again after 6 months showed a median variation of 14% and a maximum individual variation of 55%. On day 0 and 180, 24-hour Holter recordings were obtained from all patients and revealed constant ventricular capture at output settings Copt. When the output was changed from a fixed setting (2.5 V at 0.50 ms) to Copt, the battery current decreased by 17.5% (P < 0.0001). In conclusion, pacing thresholds in patients with chronic ventricular leads are stable enough to permit programming battery-saving low output settings, if pacemakers are followed on a regular basis. Titration of a 2:1 safety charge (a 3:1 safety charge in pacemaker dependent patients) by prolongation of pulse duration is safe, provided that pulse amplitude is chosen carefully. Using this approach, current consumption can significantly be reduced without jeopardizing patient's life.

AV conduction with atrial rate adaptive pacing in the bradycardia tachycardia syndrome.

AV conduction with atrial rate adaptive pacing (AAIR) during exercise was investigated in 43 patients (28 men, 15 female, mean age 68 +/- 7 years) who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome (BTS). Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval < or = 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest (R) with maximum AAI pacing rate (Fmax) achieved below the Wenckebach point (SQ-R-Fmax). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol, and AAI pacing rate was increased stepwise by programming load-adapted increments. Seven patients showed intrinsic rhythm during exercise. In those 36 patients who were atrially paced throughout ergometry (E), SQ was measured with 70 beats/min on the lowest CAEP stage (SQ-E-70) and with Fmax at maximum work load (SQ-E-Fmax). During exercise, no second-degree AV block was observed, but 28 of 36 patients (78%) showed a nonphysiological increase of the SQ interval, and the average SQ-E-Fmax was significantly longer than SQ-E-70 (250 +/- 31 versus 228 +/- 32 ms, P < 0.01). There was only a weak correlation between SQ-R-Fmax and SQ-E-Fmax (r = 0.35824, P < 0.05). When Fmax obtained during exercise was kept during recovery, 14 patients (39%) developed a second-degree AV block between 15 and 240 seconds after ergometry, 8 patients within 90 seconds. Patients who had exhibited a P on T wave in the ECG with Fmax at the end of exercise (11 of 36 patients) were reevaluated by Doppler echocardiography. Using the same exercise protocol and identical, load-adapted rate increments, only 3 of 11 patients showed premature mitral valve closure. It is concluded that patients paced and medicated for BTS are prone to a nonphysiological prolongation of AV conduction with AAIR pacing during and after exercise. As this risk can hardly be predicted by rapid atrial pacing at rest, the pacing system should be dual chamber in this subset of patients. This especially applies to the patients in whom mechanical AV timing is affected by the conduction delay.

Five-year follow-up of a bipolar steroid-eluting ventricular pacing lead.

Steroid-eluting pacing leads are known to attenuate the threshold peaking early after implantation. Long-term performance, however, is not yet settled. The lead design tested in this prospective study combines a 5.8-mm2 tip of microporous platinum-iridium with elution of 1.0 mg of dexamethasone sodium phosphate and tines for passive fixation (model 5024, Medtronic Inc.). In 50 patients (mean age 69 +/- 10 years), the electrode was implanted in the right ventricular apex. Follow-up was performed on days 0, 2, 5, 10, 28, 90, 180 and every 6 months thereafter for 5-years postimplant. At each visit, pacing thresholds were determined as pulse duration (ms) at 1.0 V and as the minimum charge (microC) delivered for capture. Lead impedance (omega) was telemetered at 2.5 V-0.50 ms, and sensing thresholds (mV) were measured in triplicate using the automatic sensing threshold algorithm of the pacemaker implanted (model 294-03, Intermedics Inc.). On the day of implantation, mean values were 0.10 +/- 0.03 ms, 0.12 +/- 0.03 microC, 758 +/- 131 omega, and 13.1 +/- 1.8 mV, respectively. Beyond 1-year postimplant, pacing thresholds did not vary significantly. Sensing thresholds and lead impedance values were stable during long-term follow-up. Five years after implantation, mean values were 0.23 +/- 0.11 ms, 0.24 +/- 0.07 microC, 670 +/- 139 omega, and 11.6 +/- 3.1 mV for pulse width and charge threshold, lead impedance, and sensing threshold, respectively, and all leads captured at 1.0 V with the longest pulse duration available (1.50 ms). It is concluded that the bipolar steroid-eluting tined ventricular lead showed stable stimulation thresholds, lead impedance values, and sensing thresholds for 5 years after implantation.

Influence of right ventricular stimulation site on left ventricular function in atrial synchronous ventricular pacing.

OBJECTIVES: The study investigates the correlation between left ventricular function and QRS duration obtained by alternate right ventricular pacing sites. BACKGROUND: 1. Right ventricular apical pacing is associated with alterations of left ventricular contraction sequence. 2. A stimulation producing narrow QRS complexes is supposed to provide for better left ventricular contraction patterns. METHODS: Fourteen patients with third degree AV block received one ventricular pacing lead in apical position. The alternate lead was attached to that site on the septum that produced the smallest QRS complex as measured from the earliest to the last deflection in any of the orthogonal Frank leads (xyz). During atrial synchronous ventricular pacing, the AV delay was optimized individually and for each stimulation site using mitral valve doppler or impedance cardiography. By radionuclide ventriculography, the phase distribution histogram of left ventricular contraction was evaluated as area under the curve (AuC); systolic function was determined as ejection fraction (EF) and as absolute ejected counts (EC) in random order. The difference (delta) in QRS duration between apical and septal stimulation (deltaxyz) was correlated with the difference in phase distribution (deltaAuC) and ejection parameters (deltaEF, deltaEC). RESULTS: QRS duration was shorter with septal than with apical pacing in 9 out of 14 patients (64%); it was longer in 4 (29%), and no difference was seen in 1 patient. There was a significant positive correlation between the change in QRS duration (deltaxvz) and phase distribution (deltaAuC: r = 0.66393, p = 0.010) and a significant negative correlation to systolic function (deltaEF: r = 0.70931, p = 0.004; deltaEC: r = 0.74368, p = 0.002). CONCLUSIONS: In atrial synchronous right ventricular pacing, if the AV delay is adapted individually, decreased QRS duration obtained by alternate pacing sites is significantly correlated with homogenization of left ventricular contraction and with increased systolic function in acute tests.

Telemetry guided pacemaker programming: impact of output amplitude and the use of low threshold leads on projected pacemaker longevity.

In a prospective study, a low threshold screw-in electrode (Medtronic 5078, group I, n = 9) was compared to a conventional active fixation lead (Biotronik Y60BP, group II, n = 9) to investigate whether lower pacing thresholds really translate into longer projected service life of the pacemaker. The leads were implanted in the atrium and were connected to a dual chamber pacing system which included the same ventricular lead (Medtronic 5024) and the same pulse generator model (Intermedics 294-03) in both groups. Eighteen months after implantation, atrial and ventricular pacing thresholds were measured as the charge delivered per pulse [microC] at 0.5, 1.0, 1.5, 2.0, and 3.5 V, respectively. For chronic output programming in both channels, patients capturing at 0.5 V were set to 1.0 V, those capturing at 1.5 V were permanently programmed to 2.0 V with the double of the charge threshold as the safety margin for pacing ("safety charge"). A combination of atrial and ventricular output settings was optimal, if it resulted in minimum battery current drain (microA] as measured by pacemaker telemetry. In both groups, current consumption [microA] decreased significantly as output amplitude was decreased, exhibiting its lowest value at 1.0 V in either channel. All ventricular leads could be programmed to the optimum output amplitude of 1.0 V in groups 1 and 2. As the 2:1 "safety charge" values were almost identical, the ventricular channel essential contributes the same amount to the battery drain of the pacing system in both groups. In the atrium, all patients of group 1 could be programmed to the optimum output amplitude of 1.0 V with an average pulse duration of 0.42 +/- 0.15 ms. In group 2, however, all patients had to be programmed to 2.0 V with a mean pulse width of 0.52 +/- 0.15 ms. With the atrial and ventricular output being optimized, the average battery drain of the whole pacing system was 12.19 +/- 0.63 microA in group 1 versus 14.42 +/- 0.32 microA in group 2 (P < 0.001). As patients were chronically programmed to these output settings, this difference translates into a clinically relevant gain in projected pacemaker longevity of 17 months or 18.3% (121 +/- 4 vs. 104 +/- 2 months; P < 0.001). Thus, programming a 2:1 safety margin in terms of charge and optimizing the output parameters by real-time telemetry of the battery current is a useful approach to reduce battery current drain. Making the most of modern lead technology with a different performance in only one channel of an otherwise identical DDD pacing system translates into a significant prolongation of projected pacemaker service life which is of great importance with the increasing awareness of health care expenditures. The gain in projected longevity is mainly due to the option of reducing the output amplitude which is still significantly beneficial well below the nominal voltage of the power source.

Neutrophil adhesion and activation during systemic thrombolysis in acute myocardial infarction.

In a pilot study, alterations of polymorphonuclear neutrophil function during systemic thrombolysis in acute myocardial infarction have been investigated in humans. The following parameters of neutrophil function were measured before and at 15 and 45 minutes after initiation of systemic thrombolysis with a recombinant tissue-type plasminogen activator in 20 patients with acute myocardial infarction: (1) neutrophil adhesion and (2) neutrophil activation. During systemic thrombolysis a significant decrease was observed in neutrophil adhesion (5.5+/-6.4 to 3.2+/-3.3; p<0.05), in phagocyting neutrophil activation (39+/-18 to 25+/-14%; p<0.05), and in resting neutrophil activation (9+/-7 to 3+/-4%; p<0.05). Successful reperfusion coincided with a significantly higher reduction of phagocyting neutrophil activation (40+/-14 to 20+/-12% vs. 39+/-24 to 26+/-19% in unsuccessful reperfusion; p<0.05), and of neutrophil adhesion (6.2+/-5.7 to 2.7+/-3.0 vs. 4.1+/-3.8 to 3.5+/-4.0 in unsuccessful reperfusion; p<0.05) during thrombolysis. Systemic thrombolysis in acute myocardial infarction is accompanied by a reduction in neutrophil adhesion and activation dependent on thrombolytic success.

[Effect of programmed safety margin on function time of modern dual chamber pacemakers]. / Einfluss der programmierten Sicherheitsmarge auf die Funktionszeit moderner Zweikammer-Schrittmacher.

In 55 consecutive patients with the same dual chamber pacemaker (Relay, Intermedics) and different pacing leads, the influence of different safety margins for pacing on battery current was investigated. 2.8 +/- 0.9 years after implantation, atrial and ventricular pulse-width thresholds (tRS) (ms) were determined at 0.5, 1.0, and 2.0 V, and the charge delivered at threshold was telemetered. If tRS was < 1.50 ms at 0.5 V, an amplitude of 1.0 V was programmed in the atrium and the ventricule; if tRS was < 1.50 ms at 1.0 V, then an amplitude of 2.0 V was chosen. Two times the charge threshold (2 x QRS), two times the voltage threshold (2 x URS), and three times the pulse-width threshold (3 x tRS) were programmed as the safety margins for pacing. With every safety margin, battery current (IBat) (microA) was averaged from 5 telemetric readings in D00 mode with 70 bpm. IBat was significantly lower with 2 x QRS as compared with 2 x URS (13.43 +/- 1.0 vs. 14.20 +/- 1.2 microA, p < 0.01) and as compared with 3 x tRS (13.99 +/- 1.2 microA, p < 0.05). Pacemaker longevity derived from these current data was significantly longer with 2 x QRS (112 +/- 8 months) as compared with 2 x URS (106 +/- 9, p < 0.01) and as compared with 3 x tRS (108 +/- 8, p < 0.05). If current consumption is compared intraindividually in dependance on the programmed amplitude, battery current is significantly lower at 1.0 V as compared with 2.0 V resulting in a mean reduction of 0.63 microA (-4.9%, p < 0.05) and an average gain in longevity of 5 months. This applies to every safety margin tested. Differences in battery current caused by the safety margins will translate into a greater gain in longevity in future pacemaker models with reduced internal current consumption.

Whipple's disease with aortic regurgitation requiring aortic valve replacement.

Cardiac involvement in Whipple's disease is well established. However, clinical consequences beside antibiotic therapy have rarely been reported. Our observation of a middle-aged man with increasing dyspnea, fatigue, chest pain, and dizziness leading to admission to a cardiology department demonstrates that cardiac symptoms may represent the main symptoms in patients with Whipple's disease. The diagnosis was not made prior to upper endoscopy, performed because of diarrhea, and revealed Whipple's agent now classified as Tropheryma whippelii, which is a PAS-positive rod-shaped bacterium in the macrophages of the intestinal lamina propria. The aortic valve was replaced after the intestinal symptoms were resolved by antibiotic treatment reducing the number of infectious agents in the duodenal mucosa. Histological analysis of the aortic valve demonstrated the presence of PAS-positive rod shaped material as the most likely cause of aortic insufficiency. Five months after valve replacement, the patient had completely recovered from intestinal and cardiac symptoms. Still under antibiotic treatment 16 months later, no more PAS-positive macrophages were detectable in the intestinal mucosa.

A fractally coated, 1.3 mm2 high impedance pacing electrode.

Minimizing the geometric surface area of pacing electrodes increases impedance and reduces the current drain during stimulation, provided that voltage (pulse-width) thresholds remain unchanged. This may be feasible by coating the electrode surface to increase the capacity of the electrode tissue interface and to diminish polarization. Ten unipolar, tined leads with a surface area of 1.3 mm2 and a "fractal" coating of iridium (Biotronik SD-V137) were implanted in the ventricle, and electrogram amplitude (unfiltered), slew-rate, pacing threshold (0.5 ms), and impedance (2.5 V; 0.5 ms) were measured by the 5311 PSA (Medtronic). On days 0. 2. 5. 10, 28, 90, 180, 360 postimplant, sensing threshold (up to 7.0 mV, measuring range 1-14 mV on day 360 only) and the strength duration curve (0.5-4.0 V; 0.03-1.5 ms; steps: 0.5 V; 0.01 ms, respectively) were determined, the minimum charge delivered per pulse (charge threshold), and the impedance were taken from pacemaker telemetry (Intermedics 294-03). Data were compared with those of an earlier series of 20 unipolar, tined TIR-leads (Biotronik) with a surface area of 10 mm2 and a @actal" coating of titanium nitride. With the model SD-V137 versus TIR, intraoperative electrogram amplitudes were 15.1 +/- 6.1 versus 14.4 +/- 3.9 mV (NS), slew rates 3.45 +/- 1.57 versus 1.94 +/- 1.06 V/s (P < 0.05), pacing thresholds 0.16 +/- 0.05 versus 0.52 +/- 0.15 V (P < 0.01) and impedance measurements 1,136 +/- 175 versus 441 +/- 73 omega (P < 0.0001), respectively. During follow-up, sensing thresholds were the same with both leads. Differences in pulse width thresholds lost its significance on day 28 but resumed on day 360 (SD-V137; 0.08 +/- 0.04 ms; TIR: 0.16 +/- 0.06 ms at 2.5 V; P < 0.01). With an electrode surface of 1.3 mm2, charge per pulse and impedance consistently differed from control, being 0.15 +/- versus 0.66 +/- 0.20 microC (P < 0.001) and 1,344 +/- 376 versus 538 +/- 79 omega respectively, one year after implantation (P < 0.0001). In summary, "fractally" coated small surface electrodes do not compromise sensing; by more than doubling impedance against controls they offer pacing thresholds (mainly in terms of charge) that are significantly lower than with the reference electrode.

Rate adaptive atrial pacing in the bradycardia tachycardia syndrome.

In 42 patients (26 men, 16 women; mean age 69 +/- 10 years), who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome, chronotropic response and AV conduction with rapid atrial pacing during exercise were studied. Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval < or = 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest with an AAI pacing rate of 5 beats/min above the sinus rate (SQ-R + 5), and at the end of exercise with 110 beats/min (SQ-E110). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol with the pacemakers being programmed to AAI with a fixed rate of 60 beats/min. Chronotropic incompetence was defined as peak exercise heart rate: (1) < 100 beats/min; (2) < 75% of the maximum predicted heart rate; or (3) the heart rate at half the maximum workload < 60 + 2 beats/min per mL O2/kg per minute (calculated O2 consumption). During exercise, one patient developed atrial fibrillation. Chronotropic incompetence was present in 71% (29/41) of the patients according to definition 2, and in 76% (31/41) according to definition 1 or 3. Ten out of 41 patients (24%) exhibited a second-degree AV block with atrial pacing at 110 beats/min at the end of exercise. Only 9 out of the remaining 31 patients (29%) showed a physiological adaptation of the SQ-E110, and 21 patients (68%) exhibited a paradoxical increase of the SQ interval with rapid atrial pacing at the end of exercise as compared to the SQ-R + 5. These observations indicate that the pacing system to be used in most patients paced and medicated for the bradycardia tachycardia syndrome should be dual chamber, and the option of rate adaptation should be considered.

Chronic ventricular pacing using an output amplitude of 1.0 volt.

Thirty-seven patients (21 male, 16 female, mean age 71 years) received identical DDD pacemakers. They also received the same bipolar ventricular passive fixation electrode, which has a microporous tip of platinum-iridium, a surface area of 5.8 mm2, and steroid elution. Eighteen months after implantation the ventricular charge threshold [microC] was measured telemetrically at 0.5, 1.0, and 2.0 V, respectively. For the 1.0 and 2.0 V amplitudes the pulse duration was increased until the charge per pulse [microC] was twice the threshold value, thus giving a 100% safety margin in terms of charge ("safety charge"). Patients who had ventricular capture at 0.5 V were permanently programmed to 1.0 V (30/37 patients), while those who did not capture at 0.5 V were set to 2.0 V (7/37 patients). In both cases, the pulse duration was programmed according to the rationale of "safety charge." During a routine follow-up period of 6 months, no complications were observed and none of the patients suffered from symptoms indicating loss of ventricular capture. Twenty-four-hour Holter recordings, obtained from all patients at the end of the follow-up with the output parameters unchanged, revealed constant ventricular capture. In patients with chronic stable pacing thresholds and steroid-eluting low threshold leads who have capture at 0.5 V, chronic ventricular pacing at an output amplitude of 1.0 V is feasible, and it seems to be safe if the pacing threshold is measured as charge delivered per pulse and a 100% safety margin in terms of charge is programmed. Reducing the output amplitude to well below the battery voltage may increase pacemaker longevity.

Influence of neutrophil separation on the expression of adhesion molecules.

In many assays of polymorphonuclear neutrophil (PMN) function the first step is separation of PMN from whole blood. In the present investigation it was examined if PMN separation leads to an altered expression of neutrophil surface membrane adhesion molecules. Samples have been taken from 20 healthy volunteers (10 male, 10 female; 39.7 +/- 11.8 years of age). PMN activation was measured cytometrically using the following antibodies against PMN surface membrane receptors: L-selectin (CD 62 L), beta-2-integrin Mac-1 (CD 11b) and Intercellular Adhesion Molecule 1 (CD54). PMN activation was determined in whole blood and after separation of PMN using density gradients. After PMN separation all three adhesion molecules appeared increased but the effect was only statistically significant for CD 54 (Wilcoxon test). Data (mean fluorescence intensity in arbitrary units) were: CD 62 L: 62 +/- 37 in whole blood, 82 +/- 28 after separation; p = 0.0674, CD 11b: 94 +/- 55 in whole blood, 111 +/- 47 after separation; p = 0.1454, CD 54; 13 +/- 12 in whole blood, 81 +/- 35 after separation; p < 0.0001. With the present data available it can be assumed that separation of PMN from whole blood can influence the results of flow cytometric assays.

A new steroid-eluting screw-in electrode.

A new lead design was tested that combined a small microporous steroid-eluting electrode with an insulated, exposed helix for active fixation. This lead (model 5078, Medtronic, Inc., group I, n = 10) was compared to a conventional model (model Y 60 BP, Biotronik) with a larger surface of polished platinum-iridium, equipped with a fixed, noninsulated screw but without steroid elution (group II, n = 10). The two lead models were studied in the atrial position of dual chamber pacing systems, which all had a tined ventricular lead (model 5024, Medtronic, Inc.), with essentially the same steroid-eluting tip as the new active fixation lead design. Sensing and pacing data were recorded acutely and during 1 year of follow-up, via the telemetry of a Relay pulse generator (Intermedics, Inc.). Intraoperatively, unfiltered atrial electrogram amplitudes did not differ between groups (group I: 7.12 +/- 2.56 mV vs group II: 6.42 +/- 1.87 mV; P > 0.05), nor did sensing thresholds 1 year after implantation (group I: 5.33 +/- 1.70 mV vs group II: 4.26 +/- 1.40 mV; P > 0.05). Atrial pacing thresholds as measured during surgery at a pulse width of 0.5 msec were lower in group I (0.49 +/- 0.15 V) than in group II (0.68 +/- 0.19 V; P < 0.05). From day 5 through day 360 of follow-up, the difference in atrial pacing thresholds was highly significant (P < 0.01), with a smaller peaking of early thresholds and a much lower scattering of data for the steroid screw-in leads than for controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Reliability of an automatic sensing algorithm.

Automatic adaptation of the atrial sensitivity was evaluated in 18 patients with dual chamber pacemakers (Intermedics, Inc., Relay) in the unipolar mode. After atrial sensitivity was stabilized in the upright position, patients underwent a 1.0 W/kg body weight exercise for 5 minutes. A 24-hour Holter ECG was recorded, and the maximum and minimum atrial sensitivity values reached were stored in the memory of the pulse generator. In a second series of 12 patients, Holter ECGs were recorded twice, starting with the same sensitivity but with automatic adaptation alternately switched "on" or "off." Results of the exercise test: mean atrial sensitivity declined from 2.30 +/- 0.77 mV to 2.03 +/- 0.68 mV. There was no change in five patients, a slight increase in two patients, and lowering of the atrial sensitivity was observed in 11 patients, the difference ranging from 0.2 to 1.0 mV. A total of two P waves in two patients were missed by the atrial amplifier. The minimum and maximum sensitivity reached during Holter monitoring averaged 2.31 +/- 0.67 mV versus 1.72 +/- 0.71 mV (difference 0-1.7 mV). Normal pacemaker function was found in six patients, including one patient without any intrinsic atrial activity. Malsensing of less than five P waves occurred in four patients. More than 50 sensing defects resulted from ectopic atrial beats (four patients). We observed atrial oversensing in three cases; one patient showed atrial over- and undersensing. The comparison between fixed and variable sensitivity did not reveal any superiority of automatic adaptation.(ABSTRACT TRUNCATED AT 250 WORDS)

Threshold and polarization properties of modern active fixation atrial leads.

The purpose of the study was to compare the stimulation characteristics of two modern active fixation leads (Ela 583F, vitreous carbon tip [ELA] and Intermedics 82-0008-1601, iridium oxide tip [IROX]) with a standard lead (Osypka KY 67 VC, carbon-covered elgiloy tip [OSY]). In three groups of ten patients each, minimum charge threshold delta Qmin and polarization properties were determined via charge telemetry of the pacemaker (Intermedics Cosmos II and Relay) 0, 2, 5, 10, 28, 90, and 180 days after implant (dai). The polarization parameters global capacitance Cg, global resistance Rg, polarization voltage U(p), and a time constant t* (t* = Cg.Rg) were obtained by nonlinear regression. U(p) was always significantly (sig) lower in ELA and IROX (0.04-0.10 V) compared to OSY (0.54-0.76 V). Rg was sig lower in ELA (330-437 omega) compared to OSY and IROX (414-588 omega) from 0 to 28 dai. From 2 to 10 dai, Cg was sig higher in ELA and IROX (3.8-4.2 microF) compared to OSY (3.3-3.4 microF). In the three groups, delta Qmin reached a comparable maximum (1-1.2 microC) at 5 dai. Therefore, vitreous carbon and iridium oxide atrial fixation leads exhibit low chronic polarization effects compared to a standard elgiloy lead, but do not show a sig reduction in charge threshold.