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Biomedical subjects

J Senges

Publications and source records attributed to J Senges.

At least 145 records · Page 8Linked to original sources
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↗
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

Ventricular arrhythmias in idiopathic dilated cardiomyopathy.

Twenty four hour ambulatory electrocardiograms were recorded in 60 patients with idiopathic dilated cardiomyopathy. The diagnosis was based on clinical, laboratory, and cardiac catheterisation findings. All patients had a left ventricular ejection fraction less than 0.55; in 39 it was less than 0.40. Ventricular extrasystoles were evident in all patients: they were rare in 11 (18%), moderately frequent in 24 (40%), and frequent in 25 (42%). Multiform extrasystoles were recorded in 57 patients (95%), paired ventricular extrasystoles in 47 (78%), and non-sustained ventricular tachycardias consisting of three to 19 beats in 25 (42%) of the 60 patients studied. Eight patients had more than five episodes of ventricular tachycardia a day. Patients with atrial fibrillation had the same frequency and grade of ventricular arrhythmias as those with sinus rhythm. Patients with infrequent and frequent ventricular extrasystoles could not be differentiated on the basis of the clinical or haemodynamic findings. The mean values of NYHA functional class, cardiac index, left ventricular end diastolic pressure, and ejection fraction were, however, significantly different in patients with and without ventricular tachycardia. During follow up of 12 +/- 5 months seven patients died; all seven had an ejection fraction less than 0.40. In four patients who died of congestive heart failure, but in only one of the three patients who died a sudden cardiac death, ventricular tachycardia was recorded during ambulatory monitoring. High grade ventricular arrhythmias are often seen in patients with idiopathic dilated cardiomyopathy; patients with ventricular tachycardia have more impairment of left ventricular function than patients without ventricular tachycardia; and ambulatory monitoring may be of little help in identifying patients at increased risk of sudden cardiac death.

Adolescent↗
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↗
PubMed1983

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase.

Sotalol is a beta-adrenergic blocker that also prolongs action potential duration and myocardial refractoriness over the short term (class III effect). Its short-term antiarrhythmic effects were compared with those of metoprolol, which has neither short-term class III nor membrane-stabilizing action, on reentrant ventricular arrhythmias produced by programmed stimulation in 17 conscious dogs 3 to 8 days after myocardial infarction. Ventricular arrhythmias were prevented or significantly slowed by sotalol in 11 of 19 studies (58%) compared with in one of 14 (7%) studies with metoprolol. Sotalol prolonged refractoriness in the infarct zone, measured from an implanted "composite" electrode, by 41 +/- 45% (mean +/- SD, p less than .01), which was significantly greater than the increases it produced in effective refractory period of the normal ventricle (14.0 +/- 5.5%) or QT interval (12.5 +/- 7.8%). Metoprolol had no effect on infarct-zone refractoriness. Sotalol differentially increases refractoriness in potential reentry circuits in ischemic myocardium. Its antiarrhythmic effect in this model is not due to beta-blockade, and is presumably related to prolongation of action potential duration.

Action Potentials↗
PubMed1982

Electrophysiological effects of glucose-insulin-potassium on sinus node function in patients with and without sinus node dysfunction.

The electrophysiological effects of glucose (100 g)-insulin (20 U)-potassium (10 mmol X litre-1) infusion (GIK) on three parameters of sinus node function were studied in 14 control subjects (mean age 53 +/- 14 yr) and 11 patients (mean age 50 +/- 17 yr) with sinus node dysfunction (SND). In a first series of experiments the response to GIK was examined in nine control and 11 SND patients. Following GIK, the mean spontaneous cycle length decreased by 17% (671 to 560 ms; P less than 0.01) in the control group and by 33% (1066 to 715 ms; P less than 0.001) in the SND patients; this difference between both groups was statistically significant (P less than 0.01). In the control group mean corrected sinus node recovery time (CRST) and calculated sinoatrial conduction time (SACT; n = 6) were not significantly altered after GIK. In SND patients GIK decreased the mean value of CSRT by 40% (693 to 416 ms; P less than 0.05) and of calculated SACT (n = 6) by 27% (130 to 95 ms; P less than 0.05); prolonged secondary pauses following termination of rapid atrial pacing in SND patients were also shortened. In a second series of experiments, mannitol (100 g, iv) was administered in five control patients but had no significant effect on the electrophysiological parameters tested. Plasma levels of glucose were significantly increased, by 500% (P less than 0.01), after GIK; plasma potassium and sodium concentrations decreased by 7 and 5% (P less than 0.05). The results indicate that GIK had a beneficial effect on sinus node dysfunction.

Adult↗