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Biomedical subjects

R Jauernig

Publications and source records attributed to R Jauernig.

12 recordsLinked to original sources
PubMed1985

Late pulmonary embolization of a retained pacemaker electrode fragment after attempted transatrial extraction.

Embolization of pacemaker electrode fragments into the pulmonary circulation is a rare complication following transvenous pacemaker implantation. One such case is reported here. In a 67-year-old patient, a battery pocket infection developed after transvenous pacemaker implantation and subsequent surgical revision. After removal of the pacemaker and ventricular pacing lead, the atrial lead broke within the superior vena cava when prolonged traction was applied after frustrating attempts to extract the electrode. Attempts to extract the fragment transvenously using endoscopic forceps were unsuccessful. Due to firm fixation of the electrode by extensive fibrous scar tissue in the atrial wall, a further attempt to remove the retained electrode fragment by atriotomy also failed. On the first postoperative day, the fragment migrated to the left pulmonary artery, from where it was successfully extracted by means of a Dormier basket.

Aged↗
PubMed1985

Contribution of delayed ventricular repolarization to the anti-arrhythmic efficacy of sotalol.

Eighteen patients with sustained ventricular tachycardia underwent serial electrophysiological studies to establish the therapeutic efficacy of sotalol as compared to other available anti-arrhythmic agents. One or more acutely effective drug was found in 14 of the 18 patients (78%). Sotalol was tested in all 18 patients and was effective in 12 of them (67%). For assessment of the prophylactic efficacy of other anti-arrhythmic agents, an average of 3.5 additional studies per patient were performed resulting in successful prevention of ventricular tachycardia in a total of 10 of 63 (16%) additional trials. Nine patients were placed on chronic oral therapy with sotalol. In these nine patients long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 9.6 months (range 2-18 months). The study suggests that sotalol can provide effective prophylaxis against ventricular tachycardia in a significant proportion of patients refractory to other available drugs and that this prophylactic efficacy is predominantly due to its Class III anti-arrhythmic properties. Experimental studies were performed in eight conscious dogs 3-7 days following proximal LAD ligation. Epicardial recordings were obtained using implanted composite electrodes. Sotalol prevented sustained VT by a predominant increase in refractoriness of the infarcted zone. In vitro, sotalol caused a significant prolongation of the action potential of epicardial and endocardial fibres within both the infarcted and noninfarcted myocardium. Refractoriness of epicardial ventricular fibres was significantly more prolonged in ischemically damaged cells as compared to normal fibres.

Animals↗
PubMed1985

Intraindividual comparison of intravenous ajmaline and quinidine in patients with sustained ventricular tachycardia: effects on normal myocardium and on arrhythmia characteristics.

Intraindividual comparison of the acute response to intravenous quinidine and to intravenous ajmaline was performed in 23 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Inducibility of sustained VT was prevented after quinidine in 6 of the 23 patients (26%) and after ajmaline in 8 of the same 23 cases (35%). Agreement between the effects of both drugs was not significant: 2 patients had a similar response to both quinidine and ajmaline and 11 patients did not have a response to either of the two drugs, resulting in a total of only 13 patients (57%) who had a similar response to both drugs. In the 11 non-responders with inducible sustained VT before and after both drugs, quinidine and ajmaline caused qualitatively and quantitatively similar alterations of VT characteristics including a significant prolongation of the interval between the initiation extrastimulus and the first beat of VT by 38 and 42% (P less than 0.01), an increase in VT cycle length by 15 and 22% (P less than 0.01) and a prolongation of the QRS duration during VT by 15 and 18% (P less than 0.01), respectively. In all 23 patients, quinidine and ajmaline caused a quantitatively similar prolongation of ventricular refractoriness by 11 and 9% (P less than 0.05), of the QRS duration at sinus rhythm by 10 and 15% (P less than 0.01) and of the QTc interval by 13 and 10% (P less than 0.05), respectively. Thus, ajmaline and quinidine appear to have similar electrophysiological effects on both normal myocardium and on indirect parameters of reentry; in individual patients with sustained VT, however, such electrophysiological similarities do not result in significant agreement of preventive responses.

Adult↗
PubMed1984

Differential effects of sotalol and metoprolol on induction of paroxysmal supraventricular tachycardia.

Seventeen patients with recurrent paroxysmal supraventricular tachycardia (SVT) underwent serial electrophysiologic studies to compare the effects of i.v. sotalol (1.5 mg/kg) and i.v. metoprolol (0.15 mg/kg). The plasma concentrations of sotalol (2.1 +/- 1.1 microgram/ml) and metoprolol (67 +/- 15 ng/ml) were within the therapeutic range. Before drug administration, sustained SVT could be reproducibly induced in all patients. Sotalol prevented induction of sustained SVT in 10 of 17 patients (59%) and metoprolol in 4 (28%) (p less than 0.05). In 6 of 8 patients with atrioventricular (AV) nodal reentrance, the site of action of sotalol was the anterograde or the retrograde limb, reflecting an increase in refractoriness in both pathways of the circus movement. In 4 of 9 patients with AV reentrance, the site of action of sotalol was exclusively the AV nodal pathway; conduction through the extranodal accessory tract appeared to be unchanged, but its anterograde effective refractory period was prolonged (from 285 +/- 25 to 322 +/- 28 ms, p less than 0.001; mean +/- standard deviation). In the 7 patients in whom sotalol did not prevent sustained SVT, the tachycardia cycle length increased from 347 +/- 42 to 392 +/- 45 ms (p less than 0.01). Compared with sotalol, metoprolol had qualitatively similar but quantitatively less potent effects on the AV nodal pathways; however, different from sotalol, metoprolol had no effect on extranodal accessory tracts. The study suggests that at therapeutic plasma concentrations, sotalol would be effective in preventing clinical SVT in a significant proportion of patients refractory to metoprolol; because sotalol not only has beta-blocking properties but also results in acute prolongation of the action potential duration, this combination of class II and III activity may contribute to its superior prophylactic efficacy compared with pure beta blockade.

Adult↗
PubMed1984

Electrophysiologic testing in assessment of therapy with sotalol for sustained ventricular tachycardia.

Eighteen patients with sustained ventricular tachycardia underwent electrophysiologic studies to establish the therapeutic efficacy of sotalol. In each patient ventricular tachycardia could be reproducibly initiated by programmed stimulation during control studies. Sotalol prevented induction of sustained ventricular tachycardia in 12 of the 18 patients (67%). Prolongation of the QTC interval and of ventricular refractoriness was regularly observed after sotalol but did not reliably predict prophylactic efficacy. Severe adverse effects, including congestive heart failure and sinus node dysfunction, were noted early during sotalol therapy in three patients. Nine patients were placed on long-term oral treatment with sotalol and four patients on another effective agent. In these 13 patients, complete (12 patients) or partial (one patient) long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 16 months (range 8 to 24). The study suggests that sotalol can provide effective prophylaxis against sustained ventricular tachycardia; this prophylactic efficacy is not typical for pure beta-adrenergic antagonism but may at least partly result from experimentally observed prolongation of the ventricular action potential duration.

Administration, Oral↗
PubMed1984

[Programmed stimulation in patients with malignant ventricular arrhythmias. I: Diagnostic value].

Sudden cardiac death is a leading cause of death in industrially developed countries and accounts for approximately 90 000 deaths yearly in the FRG. While the majority of victims have severe coronary heart disease, sudden cardiac death is infrequently caused by acute myocardial infarction (20%) but is predominantly related to malignant ventricular arrhythmias (i.e., ventricular fibrillation or sustained ventricular tachycardia). Patients with a history of such malignant ventricular arrhythmias are at high risk for sudden death. Spontaneous occurrence of sustained ventricular tachycardia and of ventricular fibrillation is critically related to two factors: 1. trigger-arrhythmias consisting usually of complex ventricular extrasystoles (Lown classification IV to V); 2. increased vulnerability of the myocardium representing the target organ for trigger-arrhythmias. While trigger-arrhythmias can be easily recorded by noninvasive techniques including Holter monitoring or exercise and stress ECG, ventricular vulnerability is more difficult to determine and often requires ventricular stimulation with intracardiac electrocatheters. In patients with documented spontaneous malignant ventricular arrhythmias, two aspects of programmed stimulation must be considered: 1. diagnostic, and more importantly, 2. therapeutic purposes of this method. Diagnostic purposes include determination of the mode of initiation and unequivocal ventricular localization of the tachycardia excluding other arrhythmias with broad QRS complex. In patients with spontaneous sustained ventricular tachycardia, programmed stimulation can reproducibly initiate the clinical arrhythmia in 85% (sensitivity and specificity of the method approximately 90%). In patients with cardiac arrest due to ventricular fibrillation, programmed stimulation is less reliable (50%). However, the main purpose of programmed stimulation in patients with documented clinical malignant arrhythmias is not diagnostic or prognostic evaluation but is serial electrophysiological studies for individual optimization of antiarrhythmic therapy.

Arrhythmias, Cardiac↗
PubMed1984

[Programmed stimulation in patients with malignant ventricular arrhythmia. II: Individual optimization of anti-arrhythmia therapy].

The major purpose of programmed ventricular stimulation in patients with malignant ventricular arrhythmias (sustained ventricular tachycardia/ventricular fibrillation) is not the diagnostic or prognostic evaluation but the individual optimization of antiarrhythmic therapy. For successful antiarrhythmic treatment, the choice of an adequate parameter of efficacy is of outstanding relevance: in patients with frequent daily episodes of malignant ventricular arrhythmias, proper treatment can be based on Holter monitoring; however, in patients with infrequent but life-threatening attacks, Holter monitory appears to be inadequate and programmed stimulation is the method of choice for proper treatment decisions. A total of 394 serial pharmaco-electrophysiological studies was performed in 82 patients with inducible sustained ventricular tachycardia or ventricular fibrillation. During the acute serial studies, one drug was tested each subsequent day using short-term intravenous infusions. The only criterion for drug efficacy was prevention of inducible sustained ventricular tachycardia or ventricular fibrillation that had been reproducibly initiated under control conditions before antiarrhythmic treatment. At least one preventive drug was found in approximately 2/3rd of the patients. Following serial acute studies using intravenous administration, an effective agent was selected and given orally. Programmed stimulation was repeated usually after three days demonstrating reproducibility of preventive efficacy in 90% of the trials. During a subsequent follow-up period of an average of 15 months, the number of acute events (9%) including sudden death or life-threatening recurrences of malignant ventricular arrhythmias was significantly reduced as compared to patients with non-optimized therapy (54%; p less than 0.05). The number of cardiac deaths due to progressive heart failures was not significantly different in patients placed on optimized or non-optimized antiarrhythmic treatment.

Administration, Oral↗
PubMed1983

Effect of nifedipine and AQ-A 39 on the sinoatrial and atrioventricular nodes of the rabbit and their antiarrhythmic action on atrioventricular nodal reentrant tachycardia.

The effects of two drugs that apparently block slow inward current--nifedipine and the new compound AQ-A 39--were studied on the isolated sinoatrial (SA) and atrioventricular (AV) nodes of the rabbit heart using intracellular microelectrodes. Nifedipine and AQ-A 39 both slowed the sinus rate associated with a decrease in the rate of diastolic depolarisation. Conduction through the AV node was consistently impaired; this effect was enhanced with increasing atrial rates or with decreasing coupling intervals of premature beats. The action potential amplitude was significantly reduced in SA nodal and upper (AN) AV nodal fibres but was not significantly affected in lower (NH) AV nodal and in atrial fibres. The maximum diastolic potential showed little or no alteration. In all fibre types studied, the action potential duration was shortened with nifedipine but was significantly prolonged with AQ-A 39. Prevention of AV nodal reentrant tachycardia by nifedipine was related to an increase in the effective refractory period of the AV node. AQ-A 39 prevented the tachycardia by both slowing of AV nodal conduction and by prolongation of action potential duration in the AV nodal and atrial compartments of the reentrant circuit associated with the appearance of different gap phenomena of the AV conduction. The maximum possible A-H interval was, however, not shortened by either drug and single atrial echo beats could still be initiated. The results suggest that nifedipine and AQ-A 39 both have a direct depressant action on the slow inward current-dependent electrical activity of the SA and AV node but have opposite effects on the repolarisation phase resulting in different antiarrhythmic mechanisms.

Action Potentials↗