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Biomedical subjects

R Gmeiner

Publications and source records attributed to R Gmeiner.

At least 19 recordsLinked to original sources
PubMed1995

[High frequency catheter ablation in AV-nodal reentry tachycardia: clinical significance of slow pathway potentials and junctional tachycardia].

During slow pathway-ablation of AV nodal reentrant tachycardia (AVNRT) with a mean cycle length of 355 +/- 70 ms the clinical significance of slow pathway electrograms (SP-EGM) and junctional tachycardias (JT) was evaluated in 39 patients (9 male, 30 female; mean age 57 +/- 15 years). After two patients were excluded from further investigation because of inadvertent procedural complete heart block, typical SP-EGM were recorded in 30/37 patients (81%) before successful RF administration in the posteroseptal portion of the right atrium. Signals were recorded 61 +/- 22 and 34 +/- 24 ms after atrial activation in the His bundle and proximal coronary sinus catheter, respectively. Additionally, timing was noted 15 +/- 10 ms before the His spike; the duration of SP-EGM was 27 +/- 7 ms, and the A/V relation of the SP-EGM was calculated as 0.59 +/- 0.51 in the ablation bipole. JT was observed in 24/37 patients (78%), with a mean cycle length of 511 +/- 92 ms. The first tachycardia beat appeared initially 4.1 +/- 3.8 s after delivery of the successful RF administration and lasted 18 +/- 8 s. In 14/37 patients (38%) either SP-EGM or JT was missing; in one patient neither of these two was recorded despite successful ablative therapy. The success rate, defined by noninducibility of AVNRT, was 95% (35/37). In 11% (4/37) AVNRT recurred during a mean follow-up of 5 +/- 4 months. In summary, SP-EGM and JT were recorded reproducibly and proved to be a useful tool as electrographic mapping approach of slow pathway ablation in AVNRT.

Adult↗
PubMed1994

Successful radiofrequency ablation of adenosine-sensitive right ventricular outflow tract tachycardia.

We report on a patient without evidence of structural heart disease who presented with adenosine-sensitive sustained ventricular tachycardia with left bundle branch block and right axis QRS morphology. Endocardial catheter mapping revealed the origin of ventricular tachycardia to be located in the right ventricular outflow tract, where the earliest endocardial activation during ventricular tachycardia was registered 30-40 ms prior to onset of QRS complex in the surface ECG. Pace-mapping provided no additional information; we found a good match between 12 lead surface ECGs registered during spontaneous episodes of ventricular tachycardia and those recorded during pacing in a relatively large area in the right ventricular outflow tract. The 10th application of radiofrequency current abolished ventricular tachycardia temporarily, but it recurred within 30 min. After the 28th radiofrequency current delivery ventricular tachycardia was permanently abolished.

Adenosine↗
PubMed1987

[Treatment of aluminum-induced osteopathy with desferrioxamine in dialysis-dependent renal failure].

Presenting two patients on long-term dialysis with marked osteopathy due to aluminium intoxication we described the symptoms, pathogenesis and therapy of the disease. Two patients were treated with the chelating agent desferrioxamine which lead to a striking improvement in clinical symptoms and removal of aluminium from bone. Osteopathy due to aluminium intoxication is refractory to Vitamin D and its metabolites. Using reversed osmosis in dialysis the high aluminium levels in bone result mainly from the long-term use of phosphate binders. Therapy of choice is the treatment with desferrioxamine.

Adult↗
PubMed1987

Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report.

We observed a dangerous increase of ventricular rate following the intravenous administration of amiodarone in a patient with atrial fibrillation and rapid ventricular response associated with the Wolff-Parkinson-White syndrome. The mechanism of enhanced accessory pathway conduction remains speculative. A possible explanation for the shortened antegrade effective refractory period of the accessory pathway is afforded by the hypotensive action of amiodarone or its dissolvent which might trigger beta-adrenergic reflexes. Intravenous amiodarone should be used with caution in patients with atrial fibrillation and rapid ventricular response via an accessory pathway.

Amiodarone↗
PubMed1985

[Ventriculo-cardiac shunt in an adult with a fatal complication: diagnostic and therapeutic aspects. Case report].

A 29-year-old patient with a Pudenz-Heyer-shunt was assigned to examination because of exercise-induced dyspnea after 10 years of uncomplicated follow-up. Echocardiography established the diagnosis of advanced cor pulmonale, the cause being multiple pulmonary embolism produced by thrombotic layers on the shunt-tube. During anticoagulant therapy right heart decompensation with fatal outcome occurred.

Adult↗
PubMed1984

[Conservative therapy of supraventricular tachycardias].

The conservative management of supraventricular tachycardias is briefly surveyed and described. For exact treatment a description of different ways of origin of tachycardias such as focal activity or reentry-mechanisms is given. A diagram at the end shows the site of influence of different antiarrhythmic drugs in the atria and the AV-node as well as the accessory pathways in preexcitation. A list of antiarrhythmics according to their classification of Vaughan Williams and of Tournboul completes this survey.

Adrenergic beta-Antagonists↗
PubMed1984

[Non-secreting myeloma. Case report with immunohistologic and electron microscopic studies].

Immunological, immunofluorescence and electromicroscopic studies were performed in a case of atypical myeloma. The 77-year-old patient presented with skeletal pain, multiple osteolytic lesions and bone marrow infiltration by atypical plasma cells. Monoclonal light chains kappa were confined to the plasma cells, as shown by immunofluorescence. No monoclonal immunoglobulin or fragments were detected in plasma or concentrated urine, even by highly sensitive immunological methods. The concentration of the immunoglobulins G, A and M in the plasma was markedly reduced. The plasma cells contained very little sarcoplasmatic reticulum. The simultaneous occurrence of monoclonal light chains kappa in the plasma cells and the absence of monoclonal immunoglobulins or fragments in plasma and urine suggest a non-secretory myeloma.

Diagnosis, Differential↗
PubMed1984

Tachycardia caused by an accessory nodoventricular tract: a clinico-pathologic correlation.

Paroxysmal tachycardia with widened QRS complexes was recorded in an eleven-year old boy who had suffered from brain damage, which had resulted from an episode of ventricular fibrillation. Atrial stimulation produced an increased AV conduction, sudden disappearance of the His bundle deflection and a complete left bundle branch block pattern. Tachycardias of this morphology were initiated by early atrial and ventricular premature beats. The findings suggested the presence of a macro re-entry circuit, utilizing a slow AV node- nodoventricular bypass tract as the anterograde limb and the His-Purkinje system--fast AV node as the retrograde limb. This supposition found further support by serial sectioning of the AV junctional area of the heart, which revealed a nodoventricular tract, which originated from the posterior extension of the compact part of the atrioventricular node and inserted into the crest of the ventricular septum.

Brain Damage, Chronic↗
PubMed1983

[Therapy of paroxysmal supraventricular tachycardias by rapid patient-activated atrial stimulation].

Recurrent, drug refractory supraventricular tachycardia may present a therapeutic challenge. Following invasive electrophysiological study and the prospectively controlled therapeutic failure of all available drugs 3 patients were treated by permanent implantation of a system for atrial burst stimulation. The system consists of an implanted receiver with electrodes connected to the right atrium and a radiofrequency stimulator that requires patient activation for burst pacing. During a follow-up period of 6 to 39 months numerous attacks of recurrent tachycardia were successfully terminated without complication. The therapeutic approach which has allowed stoppage of all antiarrhythmic drugs and has obviated the need for frequent hospital admissions has met with patient approval and is highly regarded as providing an improvement in quality of life.

Adult↗
PubMed1982

[Clinical and electrophysiological observations in a case of Romano-Ward syndrome ].

Syncope associated with atypical ventricular tachycardia of the "torsades de pointes" type was observed in a 16 year-old girl with hereditary QT prolongation. The arrhythmia occurred only during maximal prolongation of the QTc to 0.77 sec, which had possibly been aggravated by exercise and hypokalaemia. Electrophysiological studies were performed when the QTc was 0.59 sec. Incremental as well as premature ventricular pacing with single or double premature ventricular beats did not initiate ventricular arrhythmias, but revealed AV nodal and bundle branch reentry. It is postulated that these types of macroreentry are involved in the twisting of the QRS complexes in the surface ECG in torsades de pointes.

Adolescent↗
PubMed1982

Electrophysiology of tiapamil in concealed accessory pathways.

The effect of 2 mg/kg intravenous tiapamil was studied by programmed stimulation of the heart in 6 patients. Before tiapamil, sustained tachycardias were initiated in 5, and only atrial echoes in 1. In all patients, the reentrant circuit involved an accessory pathway conducting only in the ventriculoatrial direction. When administered during tachycardia, tiapamil promptly terminated the arrhythmia in 5 cases. Tiapamil lengthened the atrio-His (A-H) interval and the effective refractory period of the A-V node. As a result of these changes, it was not possible to initiate the tachycardia in 1 patient. In 1 case, tiapamil permitted the induction of sustained tachycardia, while only echoes had been initiated before the drug. In 2 cases, the tachycardia zone narrowed, in 2 others it widened following tiapamil. The ability to sustain the arrhythmia was lost in 1 patient. Tiapamil may be useful for the termination of reentrant supraventricular tachycardia involving concealed accessory pathways. Whether tiapamil prevents or favors the initiation of tachycardia in these patients depends on the interplay between the prolongation of the effective A-V nodal refractory period and the prolongation of the transnodal conduction time in individual patients.

Adult↗
PubMed1982

Effect of tiapamil in the preexcitation syndrome.

The effects of tiapamil were studied in 10 patients with antegrade preexcitation using programmed stimulation of the heart. Before administration of the drug, it was possible to initiate sustained orthodromic tachycardia in 7 patients, antidromic tachycardia in 2 and atrial echoes in 1 case by premature atrial and/or ventricular stimulation. An intravenous bolus of 2 mg/kg tiapamil terminated the tachycardia in 7 out of 8 cases by blocking the A-V node. The tachycardia continued at a reduced heart rate in 1 case with a nodoventricular bypass. Tiapamil lengthened the effective A-V nodal refractory period in 1 patient in whom it could be measured and the atrial effective refractory period in 1 case but did not prolong the antegrade or retrograde refractory periods of the accessory pathway. Only in 1 case was the antegrade effective refractory period of the accessory pathway shortened by tiapamil. The A-V nodal conduction time (A-H interval) was prolonged. Following tiapamil it was not possible to initiate the tachycardia in 4 cases and atrial echoes in 1 case; in 2 patients the tachycardia zone widened and in 3 it was not altered. In the latter, the cycle length of the tachycardia increased. Tiapamil appears to be of therapeutic value for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the initiation of tachycardia. The delayed A-V nodal conduction during sinus rhythm augments the area of ventricular preexcitation which may facilitate the electrocardiographic localization of the accessory pathway.

Adolescent↗
PubMed1981

Demonstration of multiple antegrade and retrograde atrioventricular pathways.

A patient with paroxysmal supraventricular tachycardia had discontinuous antegrade (1a-A2, H1-H2) and retrograde (V1-V2, A1-A2) conduction curves suggesting dual A-V nodal pathways in both directions. Atrial echoes occurred with premature atrial pacing only at short A1-A2 coupling intervals after long antegrade (A2-H2) and retrograde (H2-A3) conduction intervals. Premature ventricular stimulation revealed ventricular echoes simultaneously with a sudden increase in the V2-A2 interval. The echo zone coincided with the slow pathway curve. Following atropine the echo zone was extended over the slow and fast pathway curves. Slow pathway conduction was observed at long and sort V1-V2 coupling intervals. Following isoproterenol ventricular stimulation initiated two cycles of ventricular echoes with relatively long retrograde (V2-A2, Ve-Ae) and short antegrade (A2-He, Ae-He) conduction times, the earliest atrial activation being observed in the low right atrium before the left atrium and the high right atrium. Antegrade fast and slow pathways as well as retrograde fast pathway conduction appeared to be confined to the A-V node. Retrograde slow pathway conduction may progress through a slow or fast A-V nodal pathway slowed by antegrade concealed conduction. However, an accessory pathway with long conduction times located near the septum cannot be ruled out entirely.

Atrioventricular Node↗
PubMed1979

Intracardiac electrophysiological effects of lorcainide in man.

The electrophysiological effects of lorcainide 1.25 or 2.5 mg/kg given iv over 2 or 4 min, were studied in 21 patients with normal and diseased impulse formation and conduction, by means of intracardiac recording and stimulation. Sinus rate and the effective atrial refractory period rose following both doses of lorcainide. The corrected sinus node recovery time rose only after lorcainide 2.5 mg/kg and then most markedly in patients with sinus node dysfunction. The P-A interval remained unchanged following the drug. The A-H interval during sinus rhythm, and the pooled A-H intervals during atrial pacing, increased slightly, and the functional and effective A-V nodal refactory period changed variably. Wenckebach periods above the bundle of His occurred at lower atrial pacing rates following both doses of lorcainide in 7 patients, at the same atrial pacing rate in 9 and at higher rates in 3. H-V intervals, pooled H-V intervals and QRS-width lengthened in all patients, most markedly in cases with a conduction delay below the His bundle, who had received lorcainide 2.5 mg/kg. Thus, lorcainide shares some electrophysiological properties with procainamide and aprindine. Higher doses should be used with caution in patients with pre-existing conduction delay below the bundle His.

Acetanilides↗
PubMed1979

Concealed accessory pathway and dual AV conduction: drug-dependent reentrant tachycardia.

Electrophysiological studies were performed in a patient with paroxysmal supraventricular tachycardia and a normal surface ECG at the time of the study. Premature atrial stimulation revealed dual AV conduction and an echo zone during AV conduction over the fast and the slow pathway. The prolongation of the AV conduction time by a calcium antagonist, Ro 11-1781, permitted the induction of tachycardias via both pathways. Premature ventricular stimulation yielded constant VA conduction times with activation of the low right atrium before the high right atrium before the left atrium. During the tachycardia, premature right ventricular beats conducted to the atrium at a time when the AV node and the His bundle would be refractory. The study suggests the simultaneous occurrence of an occult accessory bundle connecting the right ventricle to the right atrium and dual AV conduction.

Adult↗
PubMed1979

Effect on paroxysmal re-entrant supraventricular tachycardia of a drug affecting calcium transport (Ro 11-1781).

The effect of Ro 11-1781, a drug that affects calcium transport, in 10 patients with paroxysmal supraventricular tachycardia (PSVT), was studied by intracardiac recording and stimulation. The re-entry circuit involved an accessory pathway that conducted only in the ventriculo-atrial direction in 5 patients, and was confined to the A-V node in 5 cases. Prior to administration of Ro 11-1781 tachycardia could be initiated in all patients. An intravenous bolus of 2 mg/kg during PSVT terminated the tachycardia in all cases by blockade in the A-V node. Ro 11-1781 lengthened the A-V nodal conduction time as well as the functional and effective refractory period of the A-V node. The effective refractory period of the "fast" pathway was variably changed. After Ro 11-1781 the tachycardia zone was abolished in 3 cases, reduced in 3, increased in 3 and was converted to an echo zone in 1. The ability to sustain the PSVT was lost in one subject. The heart rate during PSVT was slowed following Ro 11-1781. Ro 11-1781 appears to be useful for the termination of PSVT, but its ability to prevent PSVT varies. Beneficial effects include abolition or narrowing of the tachycardia zone, loss of the ability to sustain PSVT and a reduction in heart rate during PSVT. The widening of the tachycardia zone may be harmful.

Adult↗
PubMed1979

The effect of a new calcium antagonist (Ro 11-1781) on the cardiac conduction system in man.

Using His bundle electrograms and atrial pacing the effects of Ro 11-1781, a new calcium antagonist, was studied in 13 patients with normal A--V conduction. Following an intravenous bolus of 2 mg/kg Ro 11-1781 the A--V nodal conduction time (A--H interval) was prolonged in all patients during sinus rhythm, atrial incremental and premature pacing. Wenckebach periods above the bundle of His occurred at lower atrial driving rates following the drug. The functional and effective refractory period of the A--V node were prolonged after the administration of Ro 11-1781. No significant effect of Ro 11-1781 on the remainder of the conduction system was observed. Heart rate and the corrected sinus node recovery time changed variably. The increase of the A--H time in response to Ro 11-1781 was completely reversed by Atropine.

Adolescent↗