Ole-Jørgen Ohm

Automatic Adjustment of Pacemaker Stimulation Output Correlated with Continuously Monitored Capture Thresholds: A Multicenter Study

Pacing threshold is affected by many factors. A pacing system able to confirm capture at each beat and automatically adjust its output close to the actual pacing threshold is highly desirable. This study evaluates the safety and efficacy of the Autocapture function of the Pacesetter Microny SR+. One hundred thirteen patients were recruited from 16 centers in 7 European countries and followed up for 1 year. All pacemakers were implanted with Pacesetters low polarization, bipolar leads. The key feature of Autocapture is the immediate delivery of a 4.5 V safety backup pulse 62.5 ms after any ineffective ongoing low output pulse. Holter recordings confirmed total reliability of this feature without any exit block. The measured evoked response (ER) signal was stable over time. Acute and chronic pacing thresholds measured by VARIO and Autocapture tests correlated (r > 0.79) over the period of the study. The incidence of backup pulses was 1.1% during pacing. With Autocapture programmed ON, the overall total current consumption was 4.1 μA for VVI and 5.0 μA for VVIR pacing. Tbis study proved that the Autocapture safely and reliably regulates the pacemakers output according to the prevailing threshold thus providing maximum patient safety and prolonging service life.

A time-related study of the hemodynamic benefit of atrioventricular synchronous pacing evaluated by Doppler echocardiography.

We have used Doppler echocardiography to estimate the stroke volume (SV) in a study of 13 patients equipped with DDD pacemakers. SV was measured both during DDD and WI pacing after observation times of 1,3, 6, and 12 months of DDD pacing. SV was also measured at seven atrioventricular (AV) intervals (75–250 ms) in the search for optimal AV intervals. Mitral flow velocity was investigated to see if DDD pacing resulted in synchronous atrial contraction, and if mitral insufficiency existed at any of the pacing modes. Compared with the VVI mode, DDD pacing resulted in a mean increase in SV of 21 ± 2% for the four observation periods. Two patients with severe left ventricular failure had no significanl increase in SV during DDD vs VVI pacing. In each patient, an optimal AV inlerval ranging between 100–250 ms for the SV was found. Velocity profiles of mitral flow showed synchronous atrial contraction during DDD pacing, but not during VVI pacing. Mitral insufficiency was not seen in any pacing mode. DDD pacing resulted in a reduction in SV during the first 6 months, and was constant thereafter. Doppler echocardiography can be used repeatedly to evaluate the hemodynamic response of DDD pacing vs VVI pacing, and to find which AV interval gives the highest SV in the individual patient. Our study further shows that the hemodynamic benefit of DDD pacing is present after short‐term as well as after long‐term DDD pacing.

Electrophysiologic effects of flecainide acetate in patients with sinus nodal dysfunction.

Flecainide acetate (R818) is a new antiarrhythmic agent for oral and intravenous use; it has predominantly class I properties and a long plasma half-life. Electrophysiologic effects were evaluated in 11 patients with sinus nodal dysfunction before administration of flecainide acetate and 15 to 60 minutes after intravenous administration of 1.5 mg/kg body weight of flecainide acetate given over 15 minutes. In 8 of 11 patients with maximal sinus nodal recovery time increased after flecainide acetate. However, the mean maximal sinus nodal recovery time was not statistically significantly increased from 1,929 +/- 184 (mean +/- standard error of the mean [SEM]) to 2,770 +/- 500 ms (p less than 0.10). The corrected sinus nodal recovery time increased from 875 +/- 181 before to 1,727 +/- 507 ms after administration of flecainide acetate (p less than 0.05). The sinus cycle length and sinoatrial conduction time were not significantly changed. Flecainide acetate induced a marked prolongation of the H-V interval (from 41 +/- 3 to 52 +/- 4 mg [p less than 0.01]) as well as a significant increase in the A-H interval, QRS duration, and QT100 interval. The effective and functional refractory periods of the atria increased by 12% (p less than 0.01) and 11% (p less than 0.01), respectively. The atrioventricular (AV) nodal functional refractory period increased significantly by 7% (p less than 0.01), whereas the 9% prolongation of the effective refractory period was not statistically significant. No side effects were observed. It is concluded that flecainide acetate prolongs atrial and ventricular conduction and refractoriness, and thus appears to be a potent antiarrhythmic agent. However, the sinus nodal function is depressed, and thus caution is advised in the use of flecainide acetate in patients with sinus nodal dysfunction.

Long-term comparison of unipolar and bipolar pacing and sensing, using a new multiprogrammable pacemaker system.

Over a six‐month period a comparison was made between uni‐ and bipolar myocardial stimulation thresholds and R‐wave sensitivity in 15 consecutive pacemaker patients. The patients received a new multiprogrammable Cordis 336 A pulse generator, that could be programmed with either uni‐ or bipolar circuitry. In addition, rale, output, sensitivity and pacing mode could be noninvasively programmed. The occurrence of myopotential interference at different sensitivity levels was also studied. Cordis 325–161 bipolar endocardial leads were used in all patients. In one patient, the current output sometimes had to be programmed higher bipolarly than unipolarly to capture the ventricles, otherwise no differences in threshold were found. Acutely, R‐wave sensitivity was superior in 9 patients (60%) in the bipolar mode. Unipolar and bipolar electrograms were equal in 4 (26.7%), whereas unipolar R‐wave sensitivity was best in only 2 (13.3%) of the patients. At a six‐month follow‐up, the same tendency was found. In 5 patients, bipolar sensing was superior to unipolar, while uni‐and bipolar sensitivily was equal in the remaining patients. Myopotential inhibition was never seen in the bipolar mode at highest sensitivity (0.8 mV) even during provocative tests (n = 35) or 24‐hour Holter monitoring (n = 12). In the unipolar mode, 14/15 patients (93.3%) showed inhibition during provocative tests and 12/32 patients (100%) during monitoring at a programmed sensitivity of 0.8 mV. No patients had myopotential inlerference at a sensitivity level of 3.5 mV. All patients have theirpacemakers programmed in the bipolar mode after six months. This study con firms earlier acute data that the bipolar pacing mode is superior to the unipolar mode for permanent pacemaker therapy.

Colour tissue velocity imaging can show resynchronisation of longitudinal left ventricular contraction pattern by biventricular pacing in patients with severe heart failure

Objective: To quantify ventricular resynchronisation by biventricular pacing using colour tissue Doppler velocity imaging (c-TVI). Design and patients: c-TVI shows regional tissue velocity profiles with a very high time resolution (10 ms). Eighteen patients were studied from an apical four chamber view at baseline and after a one month follow up of biventricular pacing. Regional left ventricular peak tissue velocities and regional time differences during the cardiac cycle were compared in the basal and mid interventricular septal segments of the left ventricle, and in the corresponding segments in the left ventricular free wall. Results: From baseline to follow up, mean peak tissue velocities changed only during isovolumic contraction in the basal interventricular septum and the left ventricular free wall. At baseline the peak main systolic tissue velocities in the left ventricular free wall were typically delayed by an average of 42 ms in the basal left ventricular site and by 14 ms in the mid left ventricular site compared with the corresponding sites in the interventricular septum. After resynchronisation by biventricular pacing those regional movements were separated by an average of only 7 ms at the basal site, but there was still a 21 ms earlier movement of the left ventricular free wall in the mid left ventricular site. The diastolic movement pattern remained unchanged from baseline to follow up. Conclusions: c-TVI showed a significant asynchronous regional longitudinal movement of basal left ventricular sites at baseline. A change to a more synchronous longitudinal left ventricular movement pattern during biventricular pacing was demonstrated.

Pacing Threshold Trends and Variability in Modern Tined Leads Assessed Using High Resolution Automatic Measurements: Conversion of Pulse Width into Voltage Thresholds

With the aid of an algorithm for automatic pacing threshold (T) measurement in the atrium and ventricle, downloadable into implanted Thera pacemakers (Medtronic Inc.), we studied T evolution during lead maturation, T variation during activities of daily living, and various types of beat‐to‐beat T variations in three tined bipolar leads: 5.6‐mm2 steroid‐eluting (Medtronic Inc. models 4524 atrial‐J [n = 8] and 4024 ventricular [n = 8]), 1.2‐mm2 steroid‐eluting (Medtronic Inc. models 5534 atrial‐J [n = 9] and 5034 ventricular [n = 9]), and 8‐mm2 without steroid (Intermedics models 432–04 atrial‐J [n = 7] and 430–10 ventricular [n = 7]). The leads were implanted in 24 consecutive patients with intact AV conduction (required by the algorithm) and followed for up to 13–25 months after implantation. Since the algorithm determined pulse width Ts at different amplitudes that, depending upon T level, could range from 0.5 to 5.0 V, we invented a methodology for conversion of pulse width Ts into voltage Ts at 0.5 ms, to pool and present T data on a universal scale. Frequent, high resolution T measurements revealed details on the lead maturation process that we divided into three stages: initial T subsiding, first wave of T peaking, and a new, quicker or slower, T rise. Although there were notable differences in duration and magnitude of T peaking on the individual basis, differences between the three lead types and between the atrium and ventricle were demonstrable. The 1.2‐mm2 leads exhibited less T peaking than their predecessors 5.6‐mm2 leads and excellent positional stability, whereas 8‐mm2 leads demonstrated the most intensive T peaking and highest mean chronic T values. T changes during activities of daily living showed some tendencies—higher T during night and lower T during exercise —yet with a number of exceptions. The overall magnitude of daily T fluctuations was < 0.2 V in all but one lead, and 50% daily voltage safety margin would be sufficient. A 100% voltage safety margin may be inadequate for a 1‐year period during the chronic phase (after 6 months of implantation). A scheme for calculation of pulse width safety margins equivalent to voltage safety margins is given. Some leads can exhibit very large beat‐to‐beat T variations before, during, and after T peaking, and prospective algorithms for automatic T measurement should verify T values through more than 1–2 captured beats to obviate a great underestimation of the T providing consistent capture. T dependence upon pacing rate was negligible. Consistent‐capture hysteresis may, in conjunction with lead instability, be as much as 0.25 V. Therefore, it is better to use an incremental approach from below to T level during automatic T measurements.

Time Domain and Spectral Analysis of Electrograms in Man During Regular Ventricular Activity and Ventricular Fibrillation

Electrogram signals from intramyocardially placed wire electrodes were recorded in 24 open heart surgery patients during regular heart activity (RHA) and ventricular fibrillation (VF). Time domain parameters, maximal amplitudes (AMAX, UMAX), maximal derivatives (DMAX, SMAX), and power spectra in the frequency region up to 100 Hz were analyzed off-line on a digital computer. DMAX, AMAX, SMAX, and UMAX were significantly lower postoperatively than during the operation in RHA, median values reduced by 37, 23, 54, and 50 percent. Corresponding reductions in median values of 64, 39, 58, and 30 percent occurred in the transition from RHA to VF during the operation (peroperatively).

Assessment of the Work Capacity and Relationship Between Rate Response and Exercise Tolerance Associated With Activity-Sensing Rate-Responsive Ventricular Pacing

The relationship between rate response and exercise tolerance was studied by measuring the symptom‐limited maximum treadmill time (MTT) both during fixed rate VVI pacing and during VVI + activity mode pacing (RRP) in 15 patients (mean age, 73 years) who had received rate‐responsive ventricular pacemakers. Their indications were atrioventricular block, sino‐atrial block, and atrial fibrillation with slow ventricular response. Basic rate was programmed to 60 ppm in both pacing modes; rate response and activity threshold were programmed to 5 and medium, respectively. The order in which the two pacing modes were tested was randomly determined. The MTT was, on average, 29% longer in RRP than in WI mode with a mean of 12 minutes in VVI and 14.8 minutes in RRP(p < 0.001). For the subgroup of eight patients with paced‐only rhythm the average increase in MTT was 38% with a mean of 9.5 minutes in VVI and 12.8 minutes in RRP (p < 0.01). Seven patients who showed episodes of spontaneous rhythm, increased their average MTT by 17% (mean in VVI, 14.9 minutes; in RRP, 17.1 minutes; p < 0.02). During RRP, a significant positive correlation existed between MTT and the increase in heart rate (N = 15; r = 0.83; p < 0.001). In 12 patients with paced‐only rhythm, the pacing rate remained at the programmed basic rate when the patients were lying, sitting, and standing and increased to 86 ± 4 ppm during casual walking, and to 101 ± 4 ppm during jumping up and down with the pacemaker programmed to the above‐mentioned parameters. The maximum pacing rate during jumping corresponded with the maximum pacing rates measured from Holter recordings during normal daily activities.

Color Doppler tissue velocity imaging can disclose systolic left ventricular asynchrony independent of the QRS morphology in patients with severe heart failure.

A QRS width greater than 120 ms is assumed to be a marker of inter‐ and intraventricular asynchrony in severe heart failure (HF) patients. Color Doppler tissue velocity imaging (c‐TVI) with a time resolution of 10 ms was used to study regional left ventricular (LV) longitudinal systolic contraction pattern in HF patients with left and right bundle branch block (LBBB and RBBB) and in patients with normal QRS width. We studied 12 women and 23 men with severe HF, with a mean age of 66 ± 11 years in New York Heart Association functional Class 2.9 ± 0.6. Twenty patients had LBBB and 10 of those were accepted for cardiac resynchronization therapy by biventricular pacing (CRT). Ten patients had normal QRS width, and five had RBBB. In the echocardiographic apical four chamber view, regional peak LV tissue velocities and regional LV time differences of peak tissue velocities were compared at basal and mid‐LV segments. There were no significant differences in regional mean peak tissue velocities among the patient groups. In patients with LBBB accepted for CRT, the LV lateral free‐wall movement at basal LV was 29 ms delayed during main systole, almost significantly different from LBBB patients not accepted for CRT (P = 0.075). Even in HF patients with normal QRS width or RBBB, significant asynchronous longitudinal LV contraction was observed. Conclusions: For the detection of regional longitudinal LV contraction asynchrony in patients with severe HF, supplementary methods to the surface ECG, such as c‐TVI, are strongly recommended. (PACE 2004; 27:460–467)

Long‐Term Clinical Performance of a Central Venous Oxygen Saturation Sensor for Rate Adaptive Cardiac Pacing

Rate adaptive ventricular pacemakers using central venous oxygen saturation (O2Sat) to control the pacing rate have been implanted in 14 patients (mean age 71 years), with a mean follow‐up period of 44 months (range 2–63 months). In eight patients the pacemakers were replaced due to signs of battery depletion after an implant duration of 39–58 months. During bicycle exercise testing the O2Sat decreased on average from 61%± 4% at rest to 36%± 4% (P < 0,0001) at peak exercise, and the maximum pacing rate was 122 ± 5 beats/min. The time delay until the O2Sat bad dropped 10%, 65%, and 90% of the total reduction during exercise was 4.8 ± 0.9 seconds, 39.8 ± 3.8 seconds, and 71.3 ± 7.5 seconds, respectively. The O2Sat decreased 9.4%± 2% (P <0.005) from resting supine to resting sitting. Oxygen breathing increased the telemetered O2Sat from the pacemaker by 8.4 %± 1 % (P < 0.001). During follow‐up the O2Sats were relatively stable in 50% of the patients, but demonstrated significant fluctuations in the others. At 1‐year invasive follow‐up O2Sat measured by the pacemaker decreased 22%± 2%, and in blood samples from the right ventricle 22%± 2% from rest to 3 minutes exercise at 25 watts. There was a significant correlation between O2Sat measured by the pacemaker and in blood samples from right ventricle (n = 105; r = 0.73; P < 0.001). In two patients the O2Sat dropped significantly during pneumonia. In another patient episodes of angina pectoris was associated with low O2Sat and a concomitant fast pacing rate.