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Biomedical subjects

C Mewis

Publications and source records attributed to C Mewis.

At least 37 records · Page 2Linked to original sources
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

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

Efficacy and proarrhythmia with the use of d,l-sotalol for sustained ventricular tachyarrhythmias.

This study prospectively evaluated the clinical efficacy, the incidence of torsades de pointes, and the presumable risk factors for torsades de pointes in patients treated with d,l-sotalol for sustained ventricular tachyarrhythmias. Eighty-one consecutive patients (54 with coronary artery disease, and 20 with dilated cardiomyopathy) with inducible sustained ventricular tachycardia or ventricular fibrillation received oral d,l-sotalol to prevent induction of the ventricular tachyarrhythmia. During oral loading with d,l-sotalol, continuous electrocardiographic (ECG) monitoring was performed. Those patients in whom d,l-sotalol prevented induction of ventricular tachycardia or ventricular fibrillation were discharged with the drug and followed up on an outpatient basis for 21 +/- 18 months. Induction of the ventricular tachyarrhythmia was prevented by oral d,l-sotalol in 35 (43%) patients; the ventricular tachyarrhythmia remained inducible in 40 (49%) patients; and two (2.5%) patients did not tolerate even 40 mg of d,l-sotalol once daily. Four (5%) patients had from torsades de pointes during the initial oral treatment with d,l-sotalol. Neither ECG [sinus-cycle length (SCL), QT or QTc interval, or U wave] nor clinical parameters identified patients at risk for torsades de pointes. However, the oral dose of d,l-sotalol was significantly lower in patients with torsades de pointes (200 +/- 46 vs. 328 +/- 53 mg/day; p = 0.0017). Risk factors associated with the development of torsades de pointes were the appearance of an U wave (p = 0.049), female gender (p = 0.015), and significant dose-corrected changes of SCL, QT interval, and QTc interval (p < 0.05). During follow-up, seven (20%) patients had a nonfatal ventricular tachycardia recurrence, and two (6%) patients died suddenly. One female patient with stable cardiac disease had recurrent torsades de pointes after 2 years of successful treatment with d,l-sotalol. Torsades de pointes occurred early during treatment even with low doses of oral d,l-sotalol. Pronounced changes in the surface ECG (cycle length, QT, and QTc) in relation to the dose of oral d,l-sotalol might identify a subgroup of patients with an increased risk for torsades de pointes. Other ECG parameters before the application of d,l-sotalol did not identify patients at increased risk for torsades de pointes. Recurrence rates of ventricular tachyarrhythmias are high despite complete suppression of the arrhythmia during programmed stimulation. Therefore programmed electrical stimulation in the case of d,l-sotalol seems to be of limited prognostic value.

Adult↗
PubMed1996

Manifestation of severe coronary heart disease after anabolic drug abuse.

Anabolic steroids are frequently abused, thus increasing the risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles. We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease. Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronary artery, and hypokinetic regions corresponded to posterolateral and anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2-year abuse of the anabolic steroid stanazolol. No report published so far has shown possible atherogenic consequences of long-term abuse of stanazolol.

Adult↗
PubMed1996

Quantitation of pentisomide and its metabolite by high-pressure liquid chromatography in human serum.

A rapid, inexpensive, and accurate high-performance liquid chromatographic method for the simultaneous determination of pentisomide and its major mono-N-dealkylated metabolite has been developed. After a simple and inexpensive solvent extraction procedure, the unchanged drug, its metabolite, and the internal standard are separated using a C18 reversed-phase column with a 5-microns particle size. The eluent is monitored with ultraviolet detection at 260 nm. Endogenous substances or a variety of drugs do not interfere with the assay. The mean recoveries of pentisomide and its metabolite are 92.6% and 92.2%, respectively. The limit of detection of the assay is 28 ng/mL for both drugs. Serum levels of pentisomide and its metabolite in patients on oral therapy for supraventricular tachycardia are reported.

Anti-Arrhythmia Agents↗
PubMed1996

[Shock-induced, but not terminated ventricular tachycardia in a patient with implantable defibrillator].

A 62-year-old male patient with coronary artery disease and drug refractory sustained ventricular tachycardia received an implantable cardioverter defibrillator (PRX III, model 1720, CPI) with a transvenous lead system (Endotak, model 0115, CPI) in combination with a subcutaneous array electrode (SQ array, model 049, CPI). The intraoperative defibrillation threshold was 15 J and was confirmed 1 week later at the hospital discharge test. Three months after discharge from hospital the patient reported 5 shocks during moderate physical exertion followed by a tachycardia associated with dizziness which terminated spontaneously. The print out of the stored electrogram showed a supraventricular tachycardia (probably sinus tachycardia) with a heart rate of 154/min which activated the device. Antitachycardia pacing did not terminate the supraventricular tachycardia, and hence shock therapy was delivered. The first shock (34 J) converted the supraventricular tachycardia to a ventricular tachycardia with a heart rate of 178/min, which was not terminated by four consecutive 34 J DC shocks. There was no hint of a device or lead failure. Determination of the defibrillation threshold reconfirmed the 15 J value for termination of ventricular fibrillation. However, neither a 1 J shock nor a 34 J shock terminated a monomorphic sustained ventricular tachycardia (cycle length 340 ms) induced by noninvasive programmed electrical stimulation. The ventricular tachycardia was, however, reproducibly terminate by antitachycardia pacing. It is concluded that an inappropriate high-energy DC shock might induce a sustained ventricular tachycardia. However, a sufficient defibrillation threshold for the termination of ventricular fibrillation does not necessarily mean that a sustained ventricular tachycardia will be terminated by a high-energy DC shock.

Coronary Disease↗
PubMed1996

Tricuspid valve endocarditis due to a jet lesion detected by echocardiography in a 27-year old man with congenital ventricular septal defect.

The case of an non-addict young caucasian with isolated tricuspid valve endocarditis in congenital ventricular septal defect (VSD) is presented. Despite antibiotic treatment the patient suffered from recurrent right sided pneumonias. A computed tomography of the chest revealed an abscess localized in the right lower lung with signs of cavitation. Echocardiography identified a vegetation located at the anterior tricuspid leaflet due to a jet lesion through the VSD. ECG-gated MRI revealed normal left ventricular function and localized the septal defect and a jet against the anterior tricuspid valve leaflet. The patient underwent open heart surgery and the VSD was closed. Now, two years later, the patient is free from any symptoms or complications. This case illustrates that noninvasive techniques like echocardiography and ECG-gated MRI can not only accurately image cardiac anatomy in patients with ventricular septal defect but additionally provide information about the pathomechanism of the development of jet lesions resulting in valvular vegetations. Operative correction of underlying cardiac disease in nonaddicts with complicating tricuspid valve endocarditis might be a favourable treatment especially when antibiotic treatment fails to cure the infection.

Adult↗
PubMed1995

Long-term efficacy of d/l sotalol in patients with sustained ventricular tachycardia refractory to class I antiarrhythmic drugs.

The efficacy of d/l sotalol was investigated in 50 patients (43 men, seven women; 33 with coronary artery disease, 15 with dilated cardiomyopathy; ejection fraction 33 +/- 10%) with inducible sustained ventricular tachycardia. Before d/l sotalol a mean of 2 +/- 1 (1 to 4) class I antiarrhythmic drugs were ineffective. In 24 patients (48%) oral d/l sotalol (320 +/- 47 mg.day-1) prevented induction of the ventricular tachycardia; in 23 patients the ventricular tachycardia remained inducible (d/l sotalol 326 +/- 50 mg.day-1). The electrophysiological effects of d/l sotalol did not differ between patients in whom d/l sotalol prevented induction of ventricular tachycardia and those in whom the ventricular tachycardia remained inducible. In two patients, torsade des pointes developed after oral application of d/l sotalol; one patient suffered from severe hypotension even with 80 mg of sotalol per day. During long-term follow-up (27 +/- 12 months) 5/24 patients (21%) had a non-fatal recurrence of ventricular tachycardia (1 week to 21 months), one patient died suddenly and another from progressive heart failure. In patients in whom the ventricular tachycardia could be induced despite oral application of d/l sotalol, control of the ventricular tachyarrhythmia was attempted by the use of sotalol in combination with mexiletine (n = 2), amiodarone (n = 9), catheter ablation (n = 2), antitachycardia surgery (n = 1) or the implantation of an automatic cardioverter defibrillator (n = 12). Recurrence of ventricular tachycardia was observed in four patients without an implanted cardioverter defibrillator. Seven out of 12 patients with an implanted cardioverter defibrillator received appropriate shocks or successful antitachycardia pacing. Although no patient died suddenly, overall mortality was 17% in this group. It is concluded that d/l sotalol is highly effective in the suppression of sustained monomorphic ventricular tachycardia inducible by programmed electrical stimulation. However during a mean follow-up of 27 +/- 12 months a recurrence of ventricular tachycardia was seen in 21% of patients, and one patient died suddenly.

Administration, Oral↗
PubMed1995

[Catheter ablation in sinus node tachycardia].

Sinus node tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia. Of those patients who were referred to our clinic for electrophysiologic evaluation and catheter ablation, four patients (1 male, 3 female) were found to have sinus node tachycardia. The diagnosis of sinus node tachycardia required all of the following: The P-wave during sinus rhythm had to be similar to the P-wave during the tachycardia, the atrial activation sequence during sinus rhythm and tachycardia had to be similar, the origin of the tachycardia had to be in the high right atrium. In one patient the tachycardia was incessant. The other three patients had paroxysmal sinus node tachycardia that could be induced by programmed atrial stimulation. No patient had overt cardiac disease. One patient had an inducible av nodal reentrant tachycardia and one patient had a second atrial tachycardia originating from the basal right atrium. Activation mapping during tachycardia was performed in all patients. Local atrial activation at the site of successful ablation preceded the P-wave in the surface electrocardiogram by 54 +/- 43 ms. In three patients the interval from the local atrial activation at the site of successful catheter ablation to the onset of the signal from the high right atrium (HRA) ranged from 25 ms to 125 ms, in one patient the signal from the high right atrium was the earliest recorded signal during tachycardia. In all patients the tachycardia was terminated with the application of radiofrequency current. Two to a maximum of 12 radiofrequency current applications were necessary; complications were not observed. In all patients a second electrophysiologic study was performed 8 +/- 2 weeks after successful catheter ablation; no patient had inducible sinus node or atrial tachycardia. During a follow-up of 5 +/- 2 months, no patient had a recurrence of sinus node tachycardia or required antiarrhythmic medication. It is concluded that catheter ablation in patients with sinus node tachycardia is an effective and safe treatment.

Adult↗
PubMed1992

Electrophysiology and long-term efficacy of pentisomide in patients with supraventricular tachycardia.

The electrophysiologic effects of pentisomide were investigated after intravenous (5 mg/kg) and oral (900-1200 mg three times a day) application in 9 patients with drug refractory atrioventricular nodal tachycardia and 6 patients with orthodromic atrioventricular re-entrant tachycardia. Pentisomide did not change sinus cycle length, effective refractory period of the right ventricle and the atrioventricular node. AH, HV interval, effective refractory period of the right atrium, QRS duration and QTc duration were (p less than or equal to 0.01) increased. Tachycardia cycle length was only increased after intravenous application of pentisomide, antegrade effective refractory periods of the accessory pathways and shortest fully pre-excited R-R intervals during atrial fibrillation were increased after the oral treatment phase (p = 0.054). Intravenous pentisomide prevented tachycardia in 6/9 patients with atrioventricular nodal tachycardia and in 2/6 patients with atrioventricular re-entrant tachycardia. If intravenous pentisomide did not prevent induction of the tachycardia, oral pentisomide was not effective either. During long-term follow-up 2/7 patients with atrioventricular nodal tachycardia and 1/4 patient with atrioventricular re-entrant tachycardia had a recurrence. Long-term treatment with pentisomide had to be discontinued because of possible side effects in 2 patients. It is concluded, that the electrophysiological effects of pentisomide are similar to those of flecainide and propafenone.

Administration, Oral↗
PubMed1990

[Electrophysiologic effects of penticainide in patients with supraventricular tachycardia].

The electrophysiologic effects of the new class-I antiarrhythmic drug pentisomide were investigated after intravenous (5 mg/kg) application in nine patients with atrioventricular nodal reentrant tachycardia and six patients with atrioventricular tachycardia. Pentisomide did not change sinus cycle length, effective refractory period of the right ventricle (ERP-RV), the AV-node (ERP-AVN) and QT interval. Intranodal (AH-interval) and infranodal conduction time (HV-interval), effective refractory period of the right atrium (ERP-A), QRS duration, antegrade effective refractory period of the accessory pathway (ERP-Kent), ventricular cycle length during atrial fibrillation and tachycardia cycle length were significantly (P less than 0.05) increased. Intravenous pentisomide prevented induction of the tachycardia in 5/9 patients with atrioventricular nodal tachycardia and in 2/6 patients with atrioventricular tachycardia. The electrophysiologic properties of pentisomide indicate that it might be a useful drug in the treatment of supraventricular tachycardia.

Adult↗