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Biomedical subjects

V Kühlkamp

Publications and source records attributed to V Kühlkamp.

At least 37 records · Page 2Linked to original sources
PubMed2000

Antibiotic prophylaxis in percutaneous endoscopic gastrostomy (PEG)--results from a prospective randomized multicenter trial.

OBJECTIVE: To determine the efficacy of antibiotic prophylaxis in percutaneous endoscopic gastrostomy (PEG) as a part of a standardized regimen. METHODS: An open prospective randomised multicenter study in 216 patients. 106 received ceftriaxone 1 g i.v. 30 min preinterventionally and 110 no study medication. A standardized protocol was followed for PEG preparation, insertion, and aftercare; all patients received a 15 French gastrostomy tube. Follow-up of local and systemic infection and clinical course was continued to postintervention day 10. An aggregate erythema and exudation score > 3 or the presence of pus was taken as indicative of peristomal infection. The pharmacoeconomics of antibiotic use were also examined. RESULTS: In no-prophylaxis patients, wound infection rates were 23.6% on day 4 and 24.5% on day 10 vs. 7.6% (p < 0.05) and 11.4% (p < 0.05), respectively, in prophylaxis patients. Results were disproportionally better in tumor patients in comparison with neurological patients. Patients systemic infection rates were 11.8% vs. 1.9% in noprophylaxis vs. prophylaxis (p < 0.05), and overall infection rates 36.3% vs. 13.3%, respectively (p < 0.05). Pneumonia was more frequent in patients with underlying neurological disease and reduced in the prophylaxis group. Antibiotic and application costs were similar in both groups (p = 0.400). CONCLUSIONS: Single-dose ceftriaxone 1 g is a effective prophylaxis against local and systemic infection after PEG and should be a part of a standard regimen.

Aged↗
PubMed2000

Molecular remodeling of Kv4.3 potassium channels in human atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) is associated with important alterations in cardiac ion channels that cause shortening and impaired rate adaptation of atrial repolarization. The mechanisms underlying potassium current remodeling in human AF are not clear. We investigated the effects of AF on the gene expression of the Kv4.3, Kv1.4, and Kv1.5 potassium channel subunits and correlated the findings with the transient outward (Ito) and the sustained outward (Isus or I(Kur)) potassium current. METHODS AND RESULTS: Semiquantitative reverse transcription-polymerase chain reaction was used to evaluate mRNA expression, and ion currents were studied with the patch clamp technique in right atrial appendages from patients in AF and compared with those from patients in stable sinus rhythm (SR). The presence of AF was associated with a 61% reduction in Kv4.3 mRNA expression (P < 0.001 vs SR), which was paralleled by a reduction in Ito current densities in this group of patients (i.e., at +50 mV: 7.44+/-0.76 pA/pF in SR and 1.24+/-0.28 pA/pF in AF; P < 0.001 vs SR). mRNA levels of Kv1.4 were identical in the two groups. AF did not affect either the gene expression of Kv1.5 or the current densities of Isus. CONCLUSION: Chronic AF in humans reduces Ito by transcriptional down-regulation of the Kv4.3 potassium channel. Altered gene expression is an important component of the electrical remodeling process and may contribute to repolarization abnormalities in AF.

Aged↗
PubMed1999

Effect of amiodarone and sotalol on the defibrillation threshold in comparison to patients without antiarrhythmic drug treatment.

AIM OF THE STUDY: It is generally accepted that chronic therapy with antiarrhythmic drugs might increase the defibrillation threshold at implantation of an implantable cardioverter defibrillator. A recently published animal study showed a minor effect of the class 1 antiarrhythmic drug lidocaine on the defibrillation threshold if biphasic shocks were used. METHODS AND RESULTS: We therefore performed a retrospective analysis in 89 patients who received an ICD capable of monophasic (n=18) or biphasic (n=71) shocks with a transvenous lead system. In all patients the defibrillation threshold was determined according to the same step down protocol. In the 18 patients with a monophasic device the effects of chronic therapy with amiodarone (n=7) on the defibrillation threshold were evaluated in comparison to a group without antiarrhythmic treatment (n=11). In those patients receiving a biphasic device the effects of chronic therapy with amiodarone (n=29), sotalol (n=20) or no antiarrhythmic medication (n=22) on the defibrillation threshold were evaluated. The groups receiving a monophasic device did not differ in respect to age, sex, underlying cardiac disease, clinical arrhythmia (VT/VF), clinical functional status, left ventricular ejection fraction and the number of patients with additional subcutaneous electrodes. These parameters as well as the type of implanted device were not different between patient groups receiving a biphasic device. Patients on chronic amiodarone therapy receiving a monophasic device had a significantly higher defibrillation threshold (29.1 +/- 8.8 J) than patients without antiarrhythmic treatment (19.1 +/- 5.1 J, P = 0.021). The groups did not differ significantly in respect to the impedance measured at the shocking lead (P = 0.13). In three patients on chronic amiodarone an epicardiac lead system had to be implanted due to an inadequate monophasic defibrillation threshold compared to no patient without antiarrhythmic drug treatment (P = 0.043). In the patients with a biphasic device the intraoperative defibrillation threshold was not significantly different between the three study groups (P = 0.44). No patient received an epicardiac lead system. The defibrillation threshold in the amiodarone group was 15.3 +/- 7.3 J, in the sotalol group 14.4 +/- 7.2 J and in the patients without antiarrhythmic drug treatment 17 +/- 6.1 J. As well, no significant difference was seen between the groups in respect of the impedance of the high voltage electrode (P = 0.2). CONCLUSION: With the use of a biphasic device in combination with a transvenous lead system the intraoperative defibrillation threshold is not significantly different between patients on chronic amiodarone in comparison to patients without antiarrhythmic drug treatment or patients on chronic oral sotalol. This is in contrast to our findings with a monophasic device.

Aged↗
PubMed1999

[Implantation of a dual chamber pacemaker-defibrillator (DDD-ICD) in a patient with hypertrophic obstructive cardiomyopathy].

A 70-year-old woman with severely symptomatic hypertrophic obstructive cardiomyopathy was unresponsive to drug treatment. She had recurrent ventricular tachyarrhythmias and syncope and was at high risk for sudden death; a dual chamber pacemaker defibrillator (DDD-ICD) was implanted. Her initial left ventricular outflow tract gradient was 80 mm Hg and fell to 40 mm Hg during dual-chamber pacing at an atrial ventricular delay of 140 ms. In the follow-up over six months she was asymptomatic with respect to angina pectoris; ventricular tachycardias could be successfully terminated by antitachycardia pacing or by shocks. A dual chamber pacemaker defibrillator is an important therapeutic option for patients with symptomatic hypertrophic obstructive cardiomyopathy and ventricular tachyarrhythmias.

Aged↗
PubMed1999

Ionic mechanisms of electrical remodeling in human atrial fibrillation.

OBJECTIVES: Atrial fibrillation (AF) is associated with a decrease in atrial ERP and ERP adaptation to rate as well as changes in atrial conduction velocity. The cellular changes in repolarization and the underlying ionic mechanisms in human AF are only poorly understood. METHODS: Action potentials (AP) and ionic currents were studied with the patch clamp technique in single atrial myocytes from patients in chronic AF and compared to those from patients in stable sinus rhythm (SR). RESULTS: The presence of AF was associated with a marked shortening of the AP duration and a decreased rate response of atrial repolarization. L-type calcium current (ICa,L) and the transient outward current (Ito) were both reduced about 70% in AF, whereas an increased steady-state outward current was detectable at test potentials between -30 and 0 mV. The inward rectifier potassium current (IKI) and the acetylcholine-activated potassium current (IKACh) were increased in AF at hyperpolarizing potentials. Voltage-dependent inactivation of the fast sodium current (INa) was shifted to more positive voltages in AF. CONCLUSIONS: AF in humans leads to important changes in atrial potassium and calcium currents that likely contribute to the decrease in APD and APD rate adaptation. These changes contribute to electrical remodeling in AF and are therefore important factors for the perpetuation of the arrhythmia.

Acetylcholine↗
PubMed1999

Suppression of sustained ventricular tachyarrhythmias: a comparison of d,l-sotalol with no antiarrhythmic drug treatment.

OBJECTIVES: This study evaluates the clinical efficacy of d,l-sotalol in patients with sustained ventricular tachyarrhythmias. BACKGROUND: D,l-sotalol is an important antiarrhythmic agent to prevent recurrences of sustained ventricular tachyarrhythmias (VT/VF). However, evidence is lacking that an antiarrhythmic agent like d,l-sotalol can reduce the incidence of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment. METHODS: A prospective study was performed in 146 consecutive patients with inducible sustained ventricular tachycardia or ventricular fibrillation. In 53 patients, oral d,l-sotalol prevented induction of VT/VF during electrophysiological testing and patients were discharged on oral d,l-sotalol (sotalol group). In 93 patients, VT/VF remained inducible and a defibrillator (ICD) was implanted. After implantation of the device patients were randomly assigned to oral treatment with d,l-sotalol (ICD/sotalol group, n=46) or no antiarrhythmic medication (n=47, ICD-only group). RESULTS: During follow-up, 25 patients (53.2%) in the ICD-only group had a VT/VF recurrence in comparison to 15 patients (28.3%) in the sotalol group and 15 patients (32.6%) in the ICD/sotalol group (p=0.0013). Therapy with d,l-sotalol, amiodarone or metoprolol was instituted in 12 patients (25.5%) of the ICD-only group due to frequent VT/VF recurrences or symptomatic supraventricular tachyarrhythmias. In nine patients, 17% of the sotalol group, an ICD was implanted after VT/VF recurrence, three patients (5.7%) received amiodarone. Total mortality was not different between the three groups. CONCLUSIONS: D,l-sotalol significantly reduces the incidence of recurrences of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.

Administration, Oral↗
PubMed1999

Long-term reproducibility of electrophysiologically guided therapy with sotalol in patients with ventricular tachyarrhythmias.

OBJECTIVES: Goal of this study was to assess the long-term reproducibility of electrophysiologic drug testing in patients with ventricular tachyarrhythmias (VT/VF). BACKGROUND: Programmed ventricular stimulation (PVS) is still widely used to guide antiarrhythmic therapy in patients with sustained ventricular tachycardia/fibrillation (VT/VF). Sotalol is considered as one of the most effective drugs for VT/VF. Because there is no proof of long-term reproducibility of a successful drug test with sotalol, we investigated the long-term reproducibility of drug testing with sotalol. METHODS: Thirty patients with VT/VF (age: 57+/-11 years, 20 patients with coronary heart disease, 7 patients with no structural heart disease, 3 with others) and reproducible induction of VT/VF (28 patients VT, two patients VF) in a baseline PVS, were suppressible with sotalol (mean dosage 395+/-137 mg) in a subsequent PVS. After a mean follow-up of 13+/-10 months a PVS was again performed in patients, who had no evidence of progressive cardiac disease, who did not experience any arrhythmia recurrences or who were drug compliant. Irrespective of the inducibility after long-term therapy with sotalol, all patients were kept on the initial sotalol regimen. All 30 patients had a stable cardiac condition, were free of VT/VF recurrences and were drug compliant. RESULTS: Despite the clinical efficacy of sotalol, in 12 patients (40%) VT/VF could again be induced after 13+/-10.2 months. Inducibility was independent of age, heart disease, ejection fraction and follow-up time. During a further follow-up of 22.1+/-10.9 months, five patients experienced nonfatal VT recurrences independently of the prior inducibility. CONCLUSIONS: This study shows a lacking long-term reproducibility of an initial effective PVS with sotalol. Despite an uneventful clinical follow-up, late electrophysiologic testing showed a VT/VF inducibility in a high portion of patients. Hence, electrophysiologic testing performed late after the initial drug test may no longer be predictive of outcome.

Anti-Arrhythmia Agents↗
PubMed1999

Ambasilide prolongs the action potential and blocks multiple potassium currents in human atrium.

Ambasilide (LU 47110) is a new class III antiarrhythmic drug with a unique profile of action in mammals; however, the effects on human atrial repolarization are not known. We tested the effects of ambasilide on action potentials and repolarizing potassium currents in single atrial myocytes. Ambasilide delayed all phases of repolarization in a concentration-dependent manner [i.e., 10 microM prolonged the action potential duration to 90% repolarization at 1 Hz from 217.8 +/- 34.1 to 360.6 +/- 63.0 ms (p < 0.05 vs. control)]. Action-potential prolongation was independent of the applied stimulation frequency over a range of 0.5-2 Hz; the drug therefore did not display reverse use dependence. Ambasilide produced a concentration-dependent block of the inward rectifier potassium current (IK1) and the acetylcholine-activated potassium current (IKACh) with a median effective concentration (EC50) of 6.0 and 2.3 microM, respectively. Ambasilide also led to a concentration-dependent inhibition of the transient outward current (Ito1; EC50 = 5.7 microM) and the sustained potassium outward current (ISO; EC50 = 43.6 microM). The effect of ambasilide was independent of the step voltage (in the range of +20 to +60 mV) or the applied stimulation frequency (0.5-2 Hz). Inactivation kinetics were not altered. Ambasilide is a new class III antiarrhythmic drug with a distinct profile of action. Its frequency-independent prolongation of the human atrial action potential makes this group of compounds a promising alternative to currently available class III antiarrhythmic drugs.

Action Potentials↗
PubMed1999

A randomized controlled clinical trial comparing ventricular fibrillation detection time between two transvenous defibrillator models. The Acute Ventak AV investigator group.

The Ventak AV is an implantable cardioverter defibrillator with dual chamber pacing capability. Features include detection and treatment of ventricular arrhythmias, detection of atrial arrhythmias, as well as dual chamber pacing. The objective of the investigation was to verify the efficacy of the Ventak AV in detecting ventricular fibrillation in the presence of dual chamber pacing. Thirty-three patients, who were to receive an implantable defibrillator were randomized (1:1) in a paired comparison study to the Ventak AV (study device) and the Ventak Mini (control) during defibrillation threshold testing. In order to create a "worst case scenario" for sensing of ventricular fibrillation, pacing was performed at high lower rate limit values (Ventak AV DDD pacing at 150/min, Ventak Mini at VVI 100/min). Ventricularfibrillation was induced and the randomized device was allowed to detect and treat the arrhythmia. This test was repeated for each patient using the alternate device in a randomized order, such that all patients were tested with both devices. The mean ventricular fibrillation detection time for the Ventak AV was 2.0+/-0.11 seconds and for the control device the detection time was 1.8+/-0.11 seconds (P = 0.26). Appropriate tachyarrhythmia therapy decision was documented in all episodes for both devices. The study patient population demonstrated equivalent ventricular fibrillation detection time between the Ventak AV and the Ventak Mini. The Ventak AV demonstrated effectiveness in detecting ventricular fibrillation in the presence of high rate dual chamber pacing.

Adult↗
PubMed1999

Clinical experience with the new detection algorithms for atrial fibrillation of a defibrillator with dual chamber sensing and pacing.

INTRODUCTION: A major drawback of therapy with an implantable defibrillator is the nonspecificity of detection. Theoretically, adding atrial sensing information to a decision algorithm could improve specificity of detection. METHODS AND RESULTS: This open-label nonrandomized study compares the detection algorithm of the Ventak AV and the Ventak Mini implantable defibrillators. The Ventak AV (n = 39) uses dual chamber detection as opposed to single chamber detection (with rate stability) in the Ventak Mini (n = 55). Programmed zone configurations, rate thresholds, and stability criteria were identical in all patients. In the Ventak AV group, 235 ventricular tachyarrhythmias were adequately detected and treated by the device. In the Mini group, 699 episodes of ventricular fibrillation/tachycardia occurred. All but six of the latter episodes were correctly identified and treated: one patient with incessant ventricular tachycardia had five episodes not terminated by the device, another episode occurred in a patient with a device/lead defect. In the Ventak AV group, 33 episodes of sinus tachycardia and 166 episodes of atrial fibrillation/flutter activated the device; inappropriate therapy was applied to 41% of atrial fibrillation/flutter episodes. In the Ventak Mini group, 226 supraventricular tachyarrhythmias activated the device, eight of which were sinus tachycardia and 218 were atrial fibrillation or flutter; of the atrial fibrillation/ flutter episodes 24% were treated inappropriately (fewer vs Ventak AV, P < 0.001). CONCLUSION: The new detection algorithm incorporated in the Ventak AV did not inadvertently withhold therapy for ventricular tachyarrhythmias, but at the same time the number of inappropriate therapies for atrial fibrillation was not decreased in comparison to a single chamber device.

Aged↗
PubMed1998

Late outcome of survivors of idiopathic ventricular fibrillation.

This report describes clinical, hemodynamic, and electrophysiologic characteristics of 18 consecutive survivors of sudden cardiac arrest due to idiopathic ventricular fibrillation (VF) between 1986 and 1996. Long-term data in relation to the prescribed therapy are presented. The mean age of the 18 patients was 48 +/- 14 years (median 49). Electrophysiologic studies showed a low inducibility of sustained ventricular tachyarrhythmias in 4 patients (22%). Treatment consisted of class III agents, beta blockers, or implantable cardioverter-defibrillators. Two patients were discharged without any therapy. Therapy control was undertaken either by serial drug testing or by the empirical approach. Serious complications of therapy occurred in 2 patients: 1 patient experienced a proarrhythmic effect of antiarrhythmic drug therapy, and the other patient received multiple inadequate defibrillator discharges due to a defect in the transvenous lead. All but 1 patient (94%) remained free of recurrences of sudden cardiac arrest during a follow-up time of 45 +/- 29 months (median 41). One patient died 2 weeks after surviving cardiac arrest due to intractable VF while receiving sotalol treatment. Therapy guided by electrophysiologic studies did not have any impact on survival. Adverse effects or noncompliance led to discontinuation of drug therapy in 7 patients after a mean period of 31 +/- 30 months. Without any treatment 9 patients remained without recurrences over 45 +/- 33 months. Because of the absence of risk factors for arrhythmia recurrence and criteria to select therapy, randomized prospective studies are warranted to assess the optimal therapies in these young, ostensibly healthy patients.

Adrenergic beta-Antagonists↗
PubMed1998

[Twiddler-Syndrome in a subpectoral implanted unipolar cardioverter-defibrillator].

Twiddler's syndrome is a rare complication in patients with pacemakers. We report this very rare syndrome in a patient with pectoral implanted unipolar cardioverter defibrillator. This syndrome was detected because the patient presented in the 3 month routine visit an exitblock with an increased pacing impedance. The defibrillation threshold remained unchanged. The chest x-ray revealed an inferolaterally migrated generator with a multiply rotated lead. The intraoperative exploration showed a generator which was rotated nine-fold around its longitudinal axis with a multiple twisted unipolar lead. The lead was substituted and the aggregate fixed with a suture to the underlying muscle fascia. An atrophy of the pectoralis muscle was found in this patient which previously resulted from a long hospital stay. This atrophy was identified as a possible risk factor for the development of Twiddler's syndrome. This report illustrates that Twiddler's syndrome, a rare complication in patients with pectoral ICD, may become a significant problem in these patients as it is for pacemaker patients but with more serious possible consequences.

Aged↗
PubMed1998

Effect of a single element subcutaneous array electrode added to a transvenous electrode configuration on the defibrillation field and the defibrillation threshold.

Even with the use of biphasic shocks, up to 5% of patients need an additional subcutaneous lead to obtain a defibrillation safety margin of at least 10 J. The number of patients requiring additional subcutaneous leads may even increase, because recent generation devices have a < 34 J maximum output in order to decrease their size. In 20 consecutive patients, a single element subcutaneous array lead was implanted in addition to a transvenous lead system consisting of a right ventricular (RV) and a vena cava superior lead using a single infraclavicular incision. The RV lead acted as the cathode; the subcutaneous lead and the lead in the subclavian vein acted as the anode. The biphasic defibrillation threshold was determined using a binary search protocol. Patients were randomized as to whether to start them with the transvenous lead configuration or the combination of the transvenous lead and the subcutaneous lead. In addition, a simplified assessment of the defibrillation field was performed by determining the interelectrode area for the transvenous lead only and the transvenous lead in combination with the subcutaneous lead from a biplane chest X ray. The intraoperative defibrillation threshold was reconfirmed after 1 week, after 3 months, and after 12 months. The mean defibrillation threshold with the additional subcutaneous lead was significantly (P = 0.0001) lower (5.7 +/- 2.9 J) than for the transvenous lead system (9.5 +/- 4.6 J). With the subcutaneous lead, the impedance of the high voltage circuit decreased from 48.9 +/- 7.4 omega to 39.2 +/- 5.0 omega. In the frontal plane, the interelectrode area increased by 11.3% +/- 5.5% (P < 0.0001) and in the lateral plane by 29.5% +/- 12.4% (P < 0.0001). The defibrillation threshold did not increase during follow-up. Complications with the subcutaneous electrode were not observed during a follow-up of 15.8 +/- 2 months. The single finger array lead is useful in order to lower the defibrillation threshold and can be used in order to lower the defibrillation threshold.

Aged↗
PubMed1997

[High incidence of isolator fractures in transvenous implantation of cardioverter defibrillators].

With the growing complexity of transvenous ICD-lead systems the incidence of lead complications might increase in comparison to usual pacemaker leads. The incidence of insulation defects of transvenous leads was determined during a mean follow-up time of 23.8 +/- 10.9 months. Among 130 transvenous ICD-patients, eight insulation-breaks in seven patients (6%) could be identified after a mean follow-up of 28 +/- 13 months. After a follow-up period of 12 months no lead defect was identified, after 24 months 96.3 +/- 1.8% of all transvenous leads were free of complications, after 36 months 87.9 +/- 6% and after 48 months in 61.2 +/- 18.7% of all leads no isolator fracture was found. In seven cases an operative revision was required. All insulation-defects were exclusively found in abdominally implanted silicone lead-systems type Endotak/CPI (Cardiac Pacemakers, Inc., USA): isolator fractures occurred in 12% of all Endotak leads used, 19% of the Endotak C models 62, 64, 72 and 74 were affected. In none of 66 implanted Transvene lead systems (Medtronic, Inc., USA) were isolator defects found. In six patients the proximal part of the sensing lead near the device was affected. All of these patients experienced potentially harmful repetitive device discharges. In one patient during elective ICD-replacement an isolation break of the proximal shock electrode was found, in another patient between the proximal and distal shock-electrode. Despite regular follow-ups with impedance-measurements, only in one case was the insulation break foreseeable. Stored electrograms were helpful to disclose insulation defects. With increasing age of the transvenous lead systems a growing number of insulation defects has to be expected. Especially the isolators of the first Endotak C models 60-74 seem to create major problems with increasing age.

Aged↗
PubMed1997

Single-incision and single-element array electrode to lower the defibrillation threshold.

Occasional patients have excessive defibrillation energy requirements despite appropriate transvenous defibrillation lead position and the use of biphasic shocks. A single-element subcutaneous array electrode was implanted in 2 patients with a high defibrillation threshold. The array electrode was implanted through the same infraclavicular incision that was used for implantation of the transvenous lead. The defibrillation threshold decreased from 30 J to 15 J and from 24 J to 9 J with the subcutaneous array electrode.

Cardiomyopathy, Dilated↗