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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.

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.

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 (Δ) in QRS duration between apical and septal stimulation (Δxyz) was correlated with the difference in phase distribution (ΔAuC) and ejection parameters (ΔEF, ΔEC). 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 (Δxyz) and phase distribution (ΔAuC: r = 0.66393, p = 0.010) and a significant negative correlation to systolic function (ΔEF: r = 0.70931, p = 0.004; ΔEC: 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.

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.

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; p0.05), in phagocyting neutrophil activation (39+/-18 to 25+/-14%; p0.05), and in resting neutrophil activation (9+/-7 to 3+/-4%; p0.05). 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; p0.05), 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; p0.05) during thrombolysis. Systemic thrombolysis in acute myocardial infarction is accompanied by a reduction in neutrophil adhesion and activation dependent on thrombolytic success.

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.

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-aluting 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. Chronic thresholds as measured 1 year postimplant in terms of minimum charge delivered for capture were 0.20 ± 0.03 μC in group I versus 0.54 ± 0.11 μC in group II (P < 0.01). There was no difference between groups on the ventricular level, both acutely and during follow-up. If the active fixation atrial lead was compared to its tined ventricular counterpart in group I, pacing thresholds only differed within the early days postimplant, but they were virtually identical from week 3 through 1 year. It is concluded that the novel pacing lead design effectively combines low energy pacing with more versatility in electrode positioning by use of the active fixation mechanism.

A logic error in the software of Cosmos II results in apparent malsensing of atrial signals at high rather than low sensitivity settings. The paradoxical function was found in 54 out of 87 units tested (= 62%) if the atrial sensitivity was increased and in 54 out of 87 units tested (= 62%) if the atrial sensitivity was increased and the ventricular refractory period was lengthened beyond critical limits that could be defined individually. The problem inherent in both unipolar (66%) and bipolar systems (54%) is attributed to a summation of a physiological signal and internal noise, which has to be detected at the atrial level within a specific timing window to disable atrial sensing for the next pacing cycle. The malfunction virtually disappears if the ventricular refractory period does not exceed 210 msec. It is recommended, therefore, that Cosmos II pacemakers be left at their nominal ventricular refractory value (200 msec).

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.

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.

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.

Study objective – The aim of the study was to investigate the use of an optimised function to approximate and interpolate the time course of serum creatine kinase and creatine kinase-MB values after thrombolytic therapy in acute myocardial infarction. Design – A three parameter interpolating function was developed which approximates the time course of serum enzyme levels. In the proposed function, time to peak creatine kinase and maximum of creatine kinase determined from raw data were used as starting parameters of the non-linear interpolation routine, thus providing ideal starting conditions for the iteration. The efficacy of the function was compared with that of three other functions cited in published reports (log-normal distribution function, modified gamma density function, three compartment function). Subjects – Serum enzyme data from 20 patients with acute myocardial infarction were used in the comparisons. The patients have all been treated with anisoylated plasminogen streptokinase activator complex. Results – In comparison with the other models, deviations of the experimental model function from the raw data were minimal. The fit remained stable for time intervals between blood samples of up to 6 h. Conclusions – Due to its numerical stability, the function outlined in this study is suitable for large clinical reperfusion trials. In the case of uncomplicated infarctions without thrombolytic therapy, the area under the creatine kinase activity curve could be directly calculated in terms of maximum activity and time to peak.

In spite of equivalent clinical efficacy of various thrombolytic agents for the treatment of acute myocardial infarction there is evidence of different drug-depending influences on the haemostatic and fibrinolytic system. In the present study 40 patients with acute myocardial infarction have been investigated. 20 patients received 750,000 and 1.5 mio U streptokinase (SK), respectively, 10 patients 30 mg anisoylated plasminogen streptokinase activator complex (BRL 26921) and 10 patients a combination of 200,000 U urokinase (UK) and 4.5 mio U pro-urokinase (PUK) as a short-term intravenous treatment. Reperfusion of coronary arteries has been achieved in 70 to 100 percent. Major not fatal bleedings occurred in 2 patients. One patient died within 72 hours after beginning of the myocardial infarction. The longest duration of fibrinolytic activity was observed in the BRL 26921 group (half-disappearance time close to 2 h). It was significantly shorter in the SK groups showing a dose-dependency. Plasma concentration of fibrinogen dropped beyond normal levels following SK and BRL 26921, but not under UK/PUK. Plasma viscosity correlated with fibrinogen decrease and displayed a dose-depending relationship with the presence of SK. Haemorheological effects are suggested to be important for the clinical efficacy of thrombolytic therapy in myocardial infarction.

To give some explanation for atrial malsensing in dual chamber pacing that occurs only during exercise, atrial electrograms from 33 patients were telemetrically recorded and analyzed in both the time and frequency domains. During exercise, an overall decrease from 6.4 +/- 1.9 to 5.6 +/- 1.9 mV (-11%) in the atrial signal amplitude was noted. Despite considerable variability among patients, marked changes occurred in 15 patients whose signals diminished by 11 to 49%. Slew rates showed a similar decrease from 1.35 +/- 0.45 to 1.18 +/- 0.45 V/s (-10.8%), with individual changes of as much as -51%. Signal attenuation in the time domain correlated well with frequency data, exhibiting a highly significant reduction of signal energy between 25 and 105 Hz. However, spectral distribution changed from rest to exercise, with a relative increase of signal energy in the range between 5 and 25 Hz and a decrease at higher frequencies. Individual changes differed widely when low (15 to 65 Hz) and high (65 to 115 Hz) frequencies were compared, but in a group of 11 patients signal attenuation in the high frequency band was more pronounced (-45%) than in the low frequency band (-23%). The clinical impact of the change in frequency distribution during ergometry was visualized by computer simulation of two different (low and high bandpass) filters. Although in individual patients, both characteristics may be favorable with respect to atrial sensing, it was observed in 11 patients that high pass filtering attenuates signal amplitudes by 10 to 24% in excess of the variation without filtering.(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate the atrial sensing function of dual chamber pacemakers during exercise, we studied 57 patients aged 12 to 81 years (m = 65). They were paced for sinoatrial disorders (n = 15), second or third degree AV block (n = 37), or binodal disease (n = 11). The examination was performed 3-24 months (m = 11) after pacemaker implantation. Individual sensing thresholds were determined at rest in the supine position, and proper detection of atrial signals at the programmed sensitivity level was verified during a period of 5-9 minutes (m = 5.8). Without a change in the program of the unit, symptom-limited bicycle ergometry was performed at a maximum load of 25-200 Watts (m = 95) and 6-channel chest wall electrocardiograms were continuously recorded throughout the test, including recovery. During exercise, 25/57 patients (44%) exhibited poor atrial sensing of the pulse generator; after termination of exercise in 16 of the 25 patients, proper atrial sensing resumed within 1 to 7 minutes of recovery. In the remaining nine cases, ergometry was continued after lowering the sensitivity threshold to half the initial setting or, depending on the pacemaker model, by a value of 0.4 mV. This resulted in normal function of the pulse generator in all patients but one, who needed a sensitivity adjustment of another 0.4 mV. In a subgroup of 25 patients, telemetric atrial electrogram recordings were monitored during ergometry, 19 of which could be evaluated quantitatively. Besides random atrial signal variations, presumably due to ectopic beats or runs, a systematic decrease of the peak-to-peak amplitude by 0.1 to 1.6 mV (3-30%) was observed in 16/19 patients during exercise. Mean signal reduction amounted to 11.8% and was statistically significant at the 0.1% level. It is concluded from these findings that, besides testing of atrial sensing at rest, the follow-up of dual chamber pacemakers should include an exercise test.