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Biomedical subjects

J Brachmann

Publications and source records attributed to J Brachmann.

At least 109 records · Page 6Linked to original sources
PubMed1986

[Neuroradiologic findings in tumors of ventricles I-III].

In the period from 1953-1983, apart from the computer tomography the following neurodiagnostic methods were employed for the diagnosis of ventricular tumours: native radiography of the skull, PEG, ventriculography, positive ventriculography, angiography and cerebral scintigraphy. This study shows that a clear change in the importance of the various methods has taken place in the above mentioned period of time. The X-ray pictures of the skull taken without a contrast medium have become less important in the last few years although they showed direct and indirect signs of the tumours in almost all ventricular tumours. The former paramount importance of the presentation of the tumours with negative or positive contrast media has decreased considerably. From 1980, for example, practically no pneumo-encephalograms and no air ventriculography have been carried out. The unreliable filling in PEG and the considerable stress for the patients, especially in classic ventriculography, and thus the relatively high rate of wrong diagnoses are the reasons for this change. Only the direct positive representation of the third ventricle, e.g. in case of pinealoma, are still attached the same importance as computer tomography. Carotid angiography which shows almost every ventricular tumour in our patients and can yield information about the vascular supply, has maintained its importance in the neuroradiological scheme of diagnostics.

Cerebral Ventricle Neoplasms↗
PubMed1985

Ventricular arrhythmias following one-stage and two-stage coronary reperfusion: evidence for both reentry and enhanced automaticity.

We studied the effects of reperfusion in 60 dogs following a 30-45 minute period of left anterior descending coronary artery occlusion using electrocardiograms and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 seconds. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 +/- 8/min) did not prevent ventricular fibrillation (eight of eight dogs) and escape beats were often followed by one or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (six of six dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in two stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within two minutes after reperfusion and lasting 20-30 minutes. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 +/- 10/min versus 55 +/- 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (less than 90 sec) restored normal sinus rhythm and suppressed automaticity (72 +/- 11/min) as did left anterior descending artery reocclusion (52 +/- 6/min). We conclude that both reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.

Animals↗
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↗
PubMed1985

Day to day variations in morphology and duration of fragmented ventricular potentials during the late post-myocardial infarction phase in conscious dogs.

The relationship between the inducibility of ventricular tachyarrhythmias and the presence of fractionated epicardial ventricular electrograms ('late potentials') was studied daily between days 3 and 8 after experimental myocardial infarction in 15 conscious dogs. Before each programmed stimulation, epicardial infarct zone electrograms were recorded from implanted 'composite' electrodes during sinus rhythm. There was considerable daily variation in the morphology and duration of delayed ventricular activation, but no significant difference in duration of infarct zone electrograms was seen between studies resulting in ventricular fibrillation (108 +/- 62 ms, mean +/- SD), sustained ventricular tachycardia (87 +/- 18 ms), nonsustained (94 +/- 41 ms) or no tachycardia (78 +/- 5 ms). Although fractionated ventricular electrograms were commonly recorded early after infarction, their presence and duration could not predict the inducibility of malignant ventricular tachyarrhythmias. Similar limitations may apply in clinical practice to the use of surface signal averaging of ventricular late potentials in the early post-myocardial infarction period.

Animals↗
PubMed1985

Simultaneous recording of atrial and ventricular monophasic action potentials: monophasic action potential duration during atrial pacing, ventricular pacing, and ventricular fibrillation.

A newly developed transvenous suction electrode was used in dogs to record monophasic action potentials (MAPs) from the right atrium and right ventricle simultaneously. Continuous MAP recordings could be made from the same endocardial site for test periods of 1.5 hours. Left ventricular pacing at increasing heart rates resulted in a statistically significant decrease of right ventricular MAP duration. A high degree of correlation was found between right ventricular MAP duration at 90% of repolarization and the QT interval during both right atrial and left ventricular pacing. At the onset of ventricular fibrillation (VF), right ventricular MAP duration shortened to 25% of the value obtained during left ventricular pacing at a cycle length of 250 ms. A cyclic alternation in amplitude of the right ventricular MAPs was observed during VF. Fast Fourier Transform Analysis of right ventricular MAPs during VF showed a significant dominant frequency at 12 Hz, with no levels of interest beyond this frequency. This observation might prove to be useful in elaborating a new algorithm for the automatic detection of ventricular fibrillation.

Action Potentials↗
PubMed1985

Day-to-day variations in inducibility of ventricular tachyarrhythmias during the late postmyocardial infarction phase in conscious dogs.

The inducibility of ventricular tachyarrhythmias was studied daily on days 3 through 8 after experimental myocardial infarction in 15 conscious dogs. Although a sustained ventricular tachyarrhythmia was produced on one or more occasions in 11 of 15 dogs (73%), there was marked daily variation in the results of programmed stimulation. Ventricular fibrillation or sustained ventricular tachycardia was elicited in six dogs on day 3 after infarction. In two of these dogs, no sustained tachycardia could be induced by day 7. In nine dogs sustained ventricular arrhythmias were not inducible on day 3. By day 6 to 7, sustained ventricular tachycardia was inducible in five of these dogs. In clinical practice similar variation in the inducibility of sustained ventricular arrhythmias may conceivably complicate the use of results of programmed ventricular stimulation as determinants of risk of sudden death after myocardial infarction.

Animals↗
PubMed1985

[Computer tomography of tumors of the lateral and 3d ventricle].

In the diagnosis of tumours of the supratentorial ventricles, CT leaves some questions unanswered. This is true of the differential-diagnostic demarkation and the determination of the initial site of the tumour. Frequently, ventriculography cannot be renounced for an additional clearing-up of the last mentioned question.

Cerebral Ventricle Neoplasms↗
PubMed1984

Actions of disopyramide on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs during the late post-myocardial infarction phase.

The effect of intravenous disopyramide (plasma level 3.7 +/- 1.6 micrograms/ml, mean +/- standard deviation) on reentrant ventricular tachyarrhythmias was studied by programmed ventricular stimulation in 11 conscious dogs 3 to 8 days after experimental myocardial infarction. Sustained ventricular tachycardia (VT) was induced in 4 dogs (mean cycle length 173 +/- 14 ms) and nonsustained VT in 7 (8 +/- 4 beats, mean cycle length 136 +/- 18 ms). Disopyramide prevented induction of VT in 1 of 4 dogs with sustained VT and 3 of 7 with nonsustained VT, and increased VT cycle length by more than 30% in 2 dogs with sustained VT and 2 of 7 with nonsustained VT. Disopyramide prolonged refractoriness in the infarct zone, measured by analysis of electrograms from an implanted "composite" electrode, by 38 to 53%, depending on the mode of pacing. These values were significantly greater than the increase produced by disopyramide in ventricular effective refractory period (13 +/- 12%), QRS duration and QT interval. Disopyramide has a selective effect on potential reentry circuits in ischemic myocardium, and prolongs refractoriness in abnormal myocardium to a greater extent than its effect on the normal ventricle.

Animals↗
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

Mechanisms of ventricular arrhythmias in multivessel coronary disease: the effects of collateral zone ischemia.

We studied 15 anesthetized dogs with 4-day-old anterior wall infarctions caused by previous ligation of the left anterior descending coronary artery. Left circumflex artery (LCA) stenosis induced an average 41% decrease in collateral-dependent flow to the surviving anterior wall (epicardium) and only a 10% decrease to the normal posterior epicardial wall. Electrogram changes in 12 dogs consisted of fractionation and delay of anterior wall electrograms leading to bridging electrical activity between sinus beats and ventricular ectopic beats in five dogs. No similar electrogram changes were noted in posterior wall recordings. Ventricular paced beats induced ventricular tachycardia arising from the anterior wall in four dogs only after LCA stenosis. LCA stenosis in anterior myocardial infarction may be arrhythmogenic because of increased sensitivity of the surviving tissues, which have been electrically deranged by the ischemic/infarction process.

Angina Pectoris↗
PubMed1984

Synthesis, conformational analysis, and antiarrhythmic properties of 7-benzyl-3-thia-7-azabicyclo[3.3.1]nonan-9-one, 7-benzyl-3-thia-7-azabicyclo[3.3.1]nonane hydroperchlorate, and 7-benzyl-9-phenyl-3-thia-7-azabicyclo[3.3.1]nonan-9-ol hydroperchlorate and derivatives: single-crystal X-ray diffraction analysis and evidence for chair-chair and chair-boat conformers in the solid state.

The synthesis of the title ketone has been completed via a type of Mannich reaction starting from 4- thianone . An X-ray diffraction analysis has revealed that the solid system is a chair-boat conformer with the sulfur atom in the boat portion of the bicyclic ring compound. Wolff- Kishner reduction of the ketone group gave 7-benzyl-3-thia-7-azabicyclo [3.3.1]nonane, which was isolated as the hydroperchlorate . However, X-ray diffraction analysis of the salt showed this solid to be a chair-chair conformer. Addition of phenylmagnesium bromide to the ketone gave a tertiary alcohol with the C-C6H5 bond being equatorial with respect to the thiane ring and axial with respect to the piperidine ring. The reaction of the Grignard reagent with the ketone to give this alcohol seems to be very stereospecific. An X-ray analysis of the hydroperchlorate of the alcohol confirmed the system to be a chair-chair form in the solid. The title compounds were screened for antiarrhythmic activity in anesthetized mongrel dogs in which myocardial infarctions had been created when the left anterior descending coronary artery was ligated. Vagal-induced slowing of the sinus mode firing rate was used to determine the underlying ventricular automaticity in the dogs, which averaged 164 +/- 27 beats/min. Ventricular pacing was initiated to rates between 240 and 390/min. This technique resulted in the induction of rapid and sustained ventricular tachycardia. At doses of 3 and 6 mg/kg of body weight, 7-benzyl-3-thia-7-azabicyclo [3.3.1]nonane hydroperchlorate in alcohol (the solution was administered intravenously) was able to suppress markedly the induced ventricular tachycardia in five of six dogs. The compound also caused a 10-15% increase in blood pressure within a few minutes. The antiarrhythmic properties of this compound and others of related structure are discussed, and some comparison is made with the action of lidocaine in similar dog preparations.

Animals↗
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

Mechanisms of spontaneous and induced ventricular arrhythmias in the 24-hour infarcted dog heart.

The incidence and types of ventricular arrhythmias were evaluated in 14 dogs, 24 hours after occlusion of the left anterior descending coronary artery. After induction of anesthesia and left thoracotomy, standard electrocardiographic leads and electrograms from the His bundle and the left ventricular endocardium and epicardium (both infarct and normal zones) were recorded. Spontaneous ventricular tachycardia presumably due to abnormal automaticity was consistently observed (average rate 154 +/- 26 beats/min). These arrhythmias were irregular and multiform. In this same group of dogs 3 ventricular paced beats at rates above 300 beats/min induced rapid and uniform reentrant ventricular tachycardias (average rate 345 +/- 17 beats/min) that were difficult to terminate by premature beats or overdrive pacing. During this sustained ventricular tachycardia, continuous electrical activity was recorded from composite electrodes on the epicardial surface overlying the infarcted zone. Such interectopic activity was not observed during the spontaneous, automatic arrhythmias. Two of the 14 dogs showed only ventricular fibrillation in response to the provocative stimuli. These data confirm previous findings that 24 hours after acute myocardial infarction in the dog heart multiform ventricular rhythms can result from enhanced automaticity. In addition, it was found that ventricular tachycardia can be induced in the same dog heart by a standard ventricular pacing procedure. Continuous electrical activity bridging the interectopic intervals only during the latter tachycardia provides strong evidence for the reentrant basis of these induced arrhythmias. These experimental findings are comparable to the 2 different forms of ventricular arrhythmias described clinically, at the same stage of myocardial infarction. The direct myocardial recordings also provide new insights into the phenomenon of entrainment of tachyarrhythmias by overdrive pacing.

Animals↗