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K Michels

Publications and source records attributed to K Michels.

18 recordsLinked to original sources
PubMed1998

A prospective randomized comparison between fixed rate response programming and automatic rate response optimization in activity-triggered DDDR pacemakers. Thera Pacemaker Study Group.

Activity rate response programming depends on the physician's experience and on the limited knowledge of patient's daily activities. The present investigation compares a new continuous automatic adjustment of the activity rate response called rate response optimization (OPT) with fixed activity rate response programming (FIXED). At hospital discharge 37 patients with Thera DR pacemakers (Medtronic) were randomized either to FIXED (n = 20; 65 +/- 12 years, male n = 12) or to OPT (n = 17; 65 +/- 12 years, male n = 13). After 1 month's follow-up occurrence of complaints related to rate-responsive pacing and the percentage of pacing were assessed. Other activity sensor parameters were programmed according to clinical judgement and similarly distributed in the two groups. Activity rate response was 7.1 +/- 1.4 (FIXED) and 7.2 +/- 1.7 (OPT), activity threshold was medium in 9 (FIXED) and 8 (OPT), and medium/low in 11 (FIXED) and 9 (OPT) patients, respectively. No patient with FIXED had any complaints with respect to activity-triggered rate response. One patient with OPT reported palpitations due to rapid changes in the pacing rate leading to reprogramming of the pacemaker. Atrium and ventricle were paced in 56 +/- 31% (FIXED) and in 58 +/- 35% (OPT; not significant) and the atrium only in 4 +/- 10% (FIXED) and 0% (OPT; not significant), respectively. In the 17 patients programmed to OPT the pacemaker increased activity rate response in 5 and decreased activity rate response in 3 patients. In conclusion, as only 1 (3%) patient had complaints related to the activity rate response and fixed rate response programming according to clinical judgement already resulting in symptom-free DDDR pacing, no differences could be detected between the fixed rate response programming and rate response optimization.

Aged↗
PubMed1997

[Frequency of atrial pacing in patients with intermittent atrial fibrillation and 2nd or 3rd degree atrioventricular block. Thera DR Pacemaker Study Group].

UNLABELLED: Patients with 2nd or 3rd degree AV-block and paroxysmal atrial fibrillation could be suitable for VDDR pacemakers, if they are not or rarely paced in the atrium. We studied in 23 of these patients 1 month after DDDR pacemaker implantation, how often they were paced in the atrium with usual pacemaker programmings; patients with < 10% atrial pacing were compared with patients with > or = 10% atrial pacing. In case automatic mode switch was programmed, the number of mode switch episodes was assessed as a marker for the frequency of atrial tachyarrhythmias. Atrial pacing < 10% of the time occurred in seven, pacing from 10 to 19% in six, from 20 to 29% in two, and > or = 30% of the time in eight patients. Five of the seven patients with < 10% atrial pacing were paced in the DDD mode, but only four of 16 patients with > or = 10%. Usual clinical findings were unable to predict patients with rare atrial pacing. Patients with < 10% as well as with > or = 10% atrial pacing had < 10 mode switch episodes in 67% each. CONCLUSIONS: During short-term follow-up after DDDR pacemaker implantation 30% of the patients with paroxysmal atrial fibrillation and second or third degree AV-block, with present usual pacemaker programmings, rarely had atrial pacing, that means < 10% of the time. These patients would be probably suitable for VDDR pacemakers. Rare atrial pacing had no influence on the occurrence of automatic mode switch episodes.

Adult↗
PubMed1997

Comparison of electrical characteristics between a steroid-eluting single-pass VDD lead and a standard steroid-eluting ventricular lead. Thera Pacemaker Study Group.

Compared to regular ventricular leads, single-pass VDD leads have two additional floating electrodes proximal to the ventricular tip, which enables them to detect atrial signals. Because of the latter, VDD leads are thicker than ventricular leads, which could affect ventricular pacing. The purpose of the present study was to compare ventricular pacing of a steroid-eluting single-pass VDD lead (CapSure VDD, Medtronic; n = 107) with the same steroid-eluting regular lead (CapSure SP, Medtronic; n = 39) implanted in the ventricle; both leads were connected to the same types of pacemakers. At implantation, pacing thresholds were measured at 0.5-ms pulse duration and impedance by means with the PSA. At discharge, as well as after 1 and 3 months, pulse duration thresholds were determined at 2.5 V pulse amplitude and impedance by telemetry. At implantation, pacing thresholds and impedance were not different in the VDD (0.38 +/- 0.16 V; 691 +/- 122 omega) and ventricular lead group (0.44 +/- 0.17 V; 648 +/- 150 omega). During follow-ups, no differences in pulse duration threshold were detected between the two groups neither at discharge (VDD = 0.05 +/- 0.03 ms; ventricular 0.05 +/- 0.02 ms), nor after 1 (VDD = 0.05 +/- 0.02 ms; ventricular 0.08 +/- 0.07 ms) and 3 months (VDD = 0.06 +/- 0.03 ms; ventricular 0.09 +/- 0.10 ms). There were also no significant differences for impedance at discharge (VDD = 675 +/- 113 omega; ventricular = 594 +/- 113 omega), after 1 (VDD = 678 +/- 131 omega; ventricular = 627 +/- 112 omega) and 3 months (VDD = 652 +/- 99 omega; ventricular = 628 +/- 105 omega). Pacing thresholds and impedance were neither significantly different at implantation nor during follow-ups between patients with steroid-eluting VDD leads and patients with an equivalent ventricular lead indicating that the thicker VDD lead does not affect ventricular pacing.

Aged↗
PubMed1996

[Low stimulation impedance in pacemaker patients with cardiac diseases. The Thera Pacemaker Study Group].

BACKGROUND AND AIM OF THE STUDY: As increasing impedance of the pacing impulse decreases pacing current, high pacing impedance lowers pacing current and subsequently prolongs pacemaker longevity. The present assumption of a standard 500 ohms impedance disregards interindividual differences. In the present study, the interindividual range of pacing impedance was assessed at implantation. Additionally clinical parameters of patients with low pacing impedance were compared to those of patients with high values. PATIENTS AND METHODS: The same lead and the same pacemaker (CapSure VDD; Thera VDD; Medtronic) were implanted in 126 patients (79 men, 47 women, mean age 65 +/- 16 years). Patients with an impedance below or similar to the median were compared to patients with an impedance above the median in respect to clinical (age, gender, arterial hypertension, cardiac diseases such as coronary heart disease, valvular heart disease, cardiomyopathy) and electrical parameters (pacing threshold at 0.5 ms pulse duration, R-wave amplitude). RESULTS: Mean impedance was 687 +/- 121 ohms with a range from 333 to 1040 ohms and a median of 670 ohms. 64 patients had an impedance < or = 670 ohms and 62 patients > 670 ohms. Mean age, gender and the occurrence of arterial hypertension were similar in the two groups. Cardiac diseases occurred significantly (P < 0.01) more often in patients with lower (n = 23) than with higher impedance (n = 9). Intraoperative pacing thresholds and R-wave amplitudes were not different between the two groups. CONCLUSIONS: The range of pacing impedance was 707 ohms for the studied lead. Under consideration of permanent pacing with 2.5 V pulse amplitude and 0.5 ms pulse duration this would vary expected longevity of the implanted pacemaker from 7.8 to 9.3 years. Patients with lower impedance more often had cardiac diseases than patients with higher impedance.

Adult↗
PubMed1996

Present day pacemakers for pulse generator exchange: is 3.5 V a sufficient nominal setting for the pulse amplitude? Thera Pacemaker Study Group.

Projected pacemaker longevity is calculated according to the nominal setting, which is 3.5 V for pulse amplitude in most present day pacemakers. The aim of this study was to test whether the nominal ventricular output setting of 3.5 V and 0.4 ms provides a 100% safety margin if these pacemakers are connected to implanted ventricular pacing leads. The study included 24 patients undergoing pulse generator exchange. The new pacemaker was either a Thera DR (n = 21) or Thera SR (n = 3) device. Ventricular pacing leads were implanted 70 +/- 38 months previously. Intraoperative measurements included pacing threshold at 0.5-ms pulse duration, impedance, and R wave amplitude. To achieve a 100% safety margin with 3.5 V, the cut-off pacing threshold is 1.7 V. At discharge it was assessed whether ventricular pulse amplitude remained at < or = 3.5 V or was programmed to > 3.5 V. At pulse generator exchange, pacing threshold was 1.2 +/- 0.5 V, including four patients with pacing thresholds > 1.7 V. Impedance was 587 +/- 189 omega and R wave amplitude was 12.8 +/- 4.8 mV. At discharge, ventricular pulse amplitude remained at the nominal setting in 13 patients, including 2 patients with high pacing thresholds at pacemaker exchange, and was programmed to < 3.5 V in 7 patients. Ventricular pulse amplitude was programmed to > 3.5 V in four patients. Two of these patients had high pacing thresholds (> 1.7 V/0.5 ms) at pulse generator exchange; the other two patients were programmed to > 3.5 V, although 3.5 V already provided a 100% safety margin. After pulse generator exchange, 92% of the patients could be paced with a 3.5-V pulse amplitude. Pacemakers were programmed in four patients > 3.5 V, but in only two of them to obtain a sufficient safety margin. High pacing thresholds at pulse generator exchange did not generally predict high pacing thresholds at discharge.

Aged↗
PubMed1996

[Intermittent atrial fibrillation/flutter: contraindication for implantation of a dual chamber pacemaker?].

UNLABELLED: The programming of dualchamber pacemakers to DDD(R) mode is not recommended in patients with paroxysmal atrial fibrillation/flutter, because the pacemaker detects atrial fibrillation/flutter and paces the ventricle up to the pacemaker's upper tracking rate. Some newer pacemakers have the feature to switch automatically from DDD(R) to DDIR mode at the onset of atrial tachyarrhythmias. The aim of the study was to assess how many patients who received such a new DDDR pacemaker with automatic mode switch can be programmed to DDD(R) mode during follow-up. The dual-chamber pacemaker Thera DR (Medtronic) was implanted for clinical evaluation in 142 patients (65 +/- 16 years, male n = 86; female n = 56). Paroxysmal atrial fibrillation/flutter was present in 54 patients, with an additional 2nd or 3rd degree AV-block in 13 and no high-degree AV block in 22 cases; an AV node ablation was performed in 19 patients. Pacemakers were programmed to DDD(R) mode at discharge in 52 of 53, at month 1 in 44 of 46, and at month 3 in 28 of 30 cases. In respect to the programming to DDD(R) mode there were no statistically significant differences to patients without paroxysmal atrial fibrillation/flutter. CONCLUSION: Paroxysmal atrial fibrillation/flutter was present in 38% of the studied patients. During follow up more than 90% of the patients were paced in the DDD(R) mode.

Aged↗
PubMed1996

[Comparison of active and passive fixation of steroid emitting atrial electrodes].

UNLABELLED: Steroid-eluting screw-in leads (CapSure Fix 4068, Medtronic; n = 14) were compared to the same lead as a J-shaped tined electrode (CapSure SP 4524, Medtronic; n = 27, implanted in the atrium in patients receiving dual-chamber pacemakers. Follow-up were at discharge and after 1 month. Implantation (screw-in lead: 84 +/- 18 min; tined lead: 81 +/-29 min) and fluoroscopy times (screw-in lead: 7.3 +/- 4.9 min; tined lead 9.2 +/- 7.0 min) were similar in the two groups. At implant, P-wave amplitudes were similar with 4.8 +/- 1.6 mV (screw-in lead) and 4.0 +/- 2.6 mV (tinted lead), respectively. Compared to tined leads, the screw-in leads had higher pacing thresholds at 0.5 ms pulse duration (screw-in lead: 0.74 +/- 0.32 V; tined lead: 0.55 +/- 0.15 V; p = 0.02) as well as higher impedance (screw-in lead: 566 +/- 93 ohms; tined lead: 470 +/- 99 ohms; p = 0.01). Pulse duration thresholds at 2.5 V pulse amplitude were neither different at discharge (screw-in lead: 0.07 +/- 0.04 ms; tined lead: 0.06 +/- 0.05 ms) nor after 1 month (screw-in lead: 0.09 +/- 0.04 ms; tined lead: 0.06 +/- 0.06 ms). P-wave amplitudes > or = mV were observed at discharge in 14/14 (screw-in lead) 21/27 patients (tined lead), respectively, and after 1 month in 13/14 (screw-in lead) and 22/27 (tined lead) patients, respectively. Impedance of the screw-in lead was significantly higher with 693 +/- 84 ohms at discharge and 691 +/- 79 ohms after 1 month compared to the tined lead with 520 +/- 81 and 574 +/- 62 ohms (p = 0.001). No lead dislodgment was reported during follow-up. CONCLUSIONS: For the studied steroid-eluting leads active and passive fixation had neither at implantation nor during 1-month follow up any influence on P-wave amplitude. At similar pulse duration thresholds, impedance of the screw-in lead was significantly higher than for the tined lead. Higher impedance additionally reduces pacing current, if similar pacing impulses are delivered.

Administration, Topical↗
PubMed1994

Partition of insulin-like growth factor (IGF)-binding sites between the IGF-I and IGF-II receptors and IGF-binding proteins in the human kidney.

Quantitative ligand binding autoradiography and in situ hybridization were employed to analyze [125I]insulin-like growth factor-I ([125I] IGF-I) and [125I]IGF-II-binding sites in human kidney sections. Binding sites for both ligands were concentrated in the inner medulla and glomeruli, with low levels present in the tubulo-interstitial cortex. Competition with cold IGF-I, IGF-II, and insulin was used to determine nonspecific binding and differentiate binding of ligands to the IGF-I and IGF-II receptors and IGF-binding proteins (IGFBPs). Nonspecific binding was less than 20% of the total for both ligands. Insulin (10(-5) mol/L), which binds to the IGF-I receptor, but not to the IGF-II receptor or IGFBPs, displaced 39 +/- 8% of [125I]IGF-I binding in glomeruli, 60 +/- 7% in the tubulo-interstitial cortex, and 32 +/- 7% in the medulla. Insulin produced no detectable decrease in [125I]IGF-II binding in any region. IGF-I (10(-8) mol/L), which binds strongly to IGFBPs, but not appreciably to the IGF-II receptor, produced reductions of 46 +/- 9%, 35 +/- 8%, and 39 +/- 12% in [125I]IGF-II binding in glomeruli, tubulo-interstitial cortex, and medulla, respectively. In situ hybridization showed that IGFBP-1-5 mRNAs were all expressed in glomeruli. IGFBP-2 mRNA was abundant in medullary collecting duct epithelium, whereas IGFBP-3, -4, and -5 mRNAs were localized in interstitial and vascular cells throughout the kidney. IGF-I and -II receptor mRNAs were widely distributed in renal epithelium. The abundance of local IGFBP gene expression was positively correlated with insulin-nondisplaceable IGF binding in specific kidney regions. In summary, [125I]IGF-I binding appears to be partitioned largely to IGFBPs in glomeruli and largely to the IGF-I receptor in the tubulo-interstitial cortex, with binding in the medulla more evenly divided. The proportion and regional distribution of [125I]IGF-II binding to IGFBPs are similar, but the balance appears to be primarily associated with the IGF-II, rather than the IGF-I, receptor. Finally, this study shows that [125I]IGF binding autoradiography combined with in situ hybridization can be used to localize and potentially quantitative expression of IGFBPs in tissue sections.

Adult↗
PubMed1985

Antitumor activity of 1.3-diketonato zirconium (IV) and hafnium (IV) complexes.

Ten six-coordinate dihalogenobis (1.3-diketonato)zirconium (IV) and hafnium (IV) complexes as well as seven halogenotris(1.3-diketonato) zirconium(IV) and hafnium(IV) species were prepared and characterized by their elemental analysis, IR- and NMR-spectra. Their antitumor activity was tested using the intraperitoneally transplanted Sarcoma 180 tumor system in mice. Cisplatin was used in several doses as positive control compound. Seven complexes were highly active. The ratio of median survival time of treated to untreated control animals ranged up to 3 (T/C = 300%; the experiment was interrupted after that time) for these compounds. Significance according to Kruskal-Wallis test, long-time survivors, and animals which are dead on day 5 and day 30 are given. The possible mechanism of action compared to cisplatin is discussed.

Animals↗
PubMed1983

Small cytoplasmic RNAs from rat liver mRNP particles. Studies on their structure and function.

Free cytoplasmic 40S mRNP particles from rat liver were treated with EDTA and separated into two populations of RNP particles with sedimentation maxima of 20S and 35S, respectively. A characteristic set of distinct scRNAs is found for 20S and 35S RNP particles. The sequences of two of the most abundant scRNAs from 20S RNP particles with chain lengths of 104 (alpha 1-RNA) and 124 (beta 1-RNA) nucleotides, respectively, are presented. alpha 1-RNA shows a high sequence homology to the 3'-end of 18S rRNA. Since alpha 1-RNA carries a cap, it cannot be a degradation product of 18S rRNA. The beta 1-RNA is strongly post-transcriptionally modified, but uncapped. When the individual scRNAs of 20S and 35S RNP particles isolated from preparative polyacrylamide gels were assayed for their capability to inhibit in vitro protein synthesis, several potent translational inhibitory RNAs were detected. Particularly, the scRNAs of 147,203 and 263 nucleotide length associated with the 35S RNP particles turned out to be strong inhibitors of protein synthesis.

Animals↗
PubMed1982

Effect of amphetamine and cocaine on seizure in lead treated mice.

Mice, genetically selected for differences in brain weight were employed. Lead administration (0.5% lead acetate) from conception increased the proportion of 21 day old mice exhibiting seizures; total duration of observed seizures was also increased. Mice from the low brain weight line more frequently exhibited seizures than either mice from the high brain weight line or the Binghamton heterogeneous stock. Although genome and lead administration after bodyweight, the inability of bodyweight to predict seizure occurrence and/or total duration of seizure within conditions also was noted. Lead administration from conception through testing increased the probability and duration of transcorneally induced electroconvulsive seizures of 21 day old mice within all three genotypes, and both cocaine and amphetamine injections 15 min prior to ECS reduced the number of animals exhibiting seizures as well as the duration of seizures in both lead treated and control mice.

Animals↗
PubMed1982

Acetylcholinesterase distribution in axotomized frog motoneurons.

The distribution of acetylcholinesterase (AChE; EC 3.1.1.7) activity was examined in the perikarya and proximal axonal stumps of frog motoneurons injured by ventral root transection. Based upon measurements of net AChE accumulation in the proximal stumps of transected ventral roots, and upon orthograde clearances of AChE reported by others, it was determined that an amount of AChE equivalent to at least 0.7-2 times the perikaryal content of this enzyme enters the motor axon each day. A progressive decrease in the rate of AChE accumulation in transected axons during the first 3 days after ventral rhizotomy raised the possibility that excess enzyme might accumulate elsewhere within the axotomized motoneurons. However, AChE accumulation was detected only near the cut ends of the ventral roots and was not appreciably increased within injured motoneuronal cell bodies and proximal dendrites, which were isolated by a new method combining bulk and single-cell isolation techniques. These data suggest that AChE turnover is altered rapidly in response to axonal injury, thereby avoiding large perikaryal accumulations of this enzyme.

Acetylcholinesterase↗
PubMedDate not supplied

DDD(R) pacing with automatic mode switch in patients with paroxysmal atrial fibrillation following AV nodal ablation.

Optimal pacing in patients with paroxysmal atrial fibrillation/flutter following AV node ablation remains to be determined because VVIR pacing cannot restore AV synchronization and conventional DDD(R) pacing cannot properly cope with atrial tachyarrhythmias. The objective of the present investigation was to study the clinical outcome of 16 of these patients who received a new DDDR pacemaker with an automatic mode switch (Thera DR; Medtronic) immediately after AV node ablation. Arrhythmia-related symptoms before ablation were palpitations in 12, dizziness in 10, exercise intolerance in 8, and syncope in 6 patients. Pacing modes at hospital discharge were DDDR (n = 14) and DDD (n = 2) with an activated mode switch in all patients. After 1 month 12 patients were symptom free. Clinical events occurred in 4 patients (palpitations in 2, dizziness in 1, chest pain in 1, and fatigue in 1), which could be relieved in 3 patients. At discharge as well as at the 1-month follow-up, Holter ECG recorded a total of 12 episodes of atrial fibrillation in 5 patients, which were correctly detected by the pacemaker and followed by mode switching. At the 3-month follow-up (n = 14), 12 patients were symptom free and 2 continued to report symptoms which could not be resolved. All patients remained on an automatic mode switch in either the DDDR (n = 12) or DDD (n = 2) mode. There were no hints of inappropriate mode switching or reports of pacemaker syndrome, and there were no new symptoms related to automatic mode switching. The patients studied were highly symptomatic before implantation due to paroxysmal atrial fibrillation/flutter. After the first follow-up, 81% of the patients reported no symptoms. Paroxysmal atrial fibrillation/flutter combined with a high-degree AV-block seems no longer to be a contraindication for AV-synchronous pacing.

Atrial Fibrillation↗
PubMedDate not supplied

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Humans↗