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Biomedical subjects

L Seipel

Publications and source records attributed to L Seipel.

At least 19 recordsLinked to original sources
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↗
PubMed1992

Atrial vulnerability and electrophysiology determined in patients with and without paroxysmal atrial fibrillation.

For elucidation of atrial electrophysiology and vulnerability an electrophysiological study was performed in 45 patients with documented paroxysmal atrial fibrillation and a control group (n = 46). Atrial vulnerability was assessed by programmed atrial stimulation with up to two extrastimuli during sinus rhythm and paced cycle lengths of 600 msec, 430 msec and 330 msec. Sustained atrial fibrillation or flutter was induced in 37/45 patients with paroxysmal atrial fibrillation in contrast to 9/46 patients in the control group (P less than 0.001). Left atrial diameter (M-mode echocardiogram), P wave duration, sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly different between the two study groups. Intraatrial conduction time from the high right atrium (HRA) to the basal right atrium (A) and the functional refractory period of the right atrium were significantly longer in patients with paroxysmal atrial fibrillation.

Atrial Fibrillation↗
PubMed1992

Hemodynamic effects of cibenzoline on normal myocardium and after pretreatment with DL-sotalol.

The circulatory and myocardial effects of cibenzoline were investigated in 78 open-chest rats during and after a 7-min intravenous (i.v.) infusion. Measurements were performed in the intact circulation, and myocardial function was also examined by isovolumic registrations independent of circulatory changes. In the first part of the study, the dose-dependent effects of cibenzoline were investigated (2, 4, and 8 mg/kg vs. NaCl controls). Cibenzoline caused a dose-dependent decrease in heart rate (HR) (-16, -34, -37% vs. preinfusion values), mean aortic blood pressure (AoPm) (-8, -20, -30%), cardiac output (CO) (-6, -29, -39%), and dP/dtmax (+1, -21, -59%). The isovolumic peak left ventricular systolic BP (LVSBP) (-6, -6, -17%) and peak dP/dtmax (-8, -18, -54%) were also reduced. In the second part of the study, we examined the effects of 2 mg cibenzoline/kg after pretreatment with 2 mg DL-sotalol/kg: HR was -22% AoPm was -12%, CO was -29%, dP/dtmax was -40%, isovolumic LV pressure (LVP) was -12%, and peak dP/dtmax was -41%. Cibenzoline caused dose-dependent bradycardia, which cannot be explained by beta-adrenoceptor blockade. The auxotonic and isovolumic measurements indicate that cibenzoline possesses a dose-dependent negative inotropic effect: 2 mg cibenzoline/kg caused only a slight decrease in myocardial performance, but this effect was aggravated after pretreatment with DL-sotalol. Cibenzoline also increased peripheral resistance. The observed combination of negative inotropism and vasoconstriction caused by cibenzoline should be taken into consideration especially in patients with reduced LV function. This is of particular importance if cibenzoline is combined with DL-sotalol.

Animals↗
PubMed1992

[Hemodynamic effects of anti-arrhythmia substances].

Medical treatment of cardiac arrhythmias is limited by several side effects. Haemodynamic and proarrhythmic effects are the most important limitations of antiarrhythmic drug therapy. In this paper we present data from several studies on the haemodynamic side effects of antiarrhythmic drugs of Class I and III according to Vaughan-Williams. The results were discussed with special regard to the influence of these drugs on myocardial contractility. From the results presented it is concluded that there are no important differences in the negative inotropic effects among the Class I drugs. The clinically observed more marked cardiodepressant action of some of these drugs is probably due to their unfavourable effects on pre- and afterload of the left ventricle. From a theoretical point of view, Class III drugs should have a more favourable haemodynamic profile. However, after acute administration the commercially available Class III drugs also had a cardiodepressant action. A possible explanation for this finding might be other side effects of the Class III drugs currently available, since a pure Class III drug does not exist at present. Therefore, the special haemodynamic profile of each drug should be taken into consideration for antiarrhythmic treatment.

Animals↗
PubMed1992

[Drug therapy of atrioventricular tachycardia].

All types of antiarrhythmic drugs are suitable for the treatment of junctional and AV-reentry Tachycardias. Betablocker, calcium antagonist and digitalis are mainly influencing the conductivity in the AV node, leaving other structures unaltered. In contrast, class-antiarrhythmic drugs slow conduction and prolong the refractor effect in the accessory pathway. In addition, drugs of subclass 1c can influence especially the 'fast' pathway in dual AV-node conduction. Class-3 drugs prolong refractoring in all compartments of the heart by preventing re-entry in both, AV nodal tachycardias and AV re-entry in the WPW syndrome. The clinical indication for one of these drugs is mainly influenced by the potential side-effects and by pharmacokinetic considerations.

Anti-Arrhythmia Agents↗
PubMed1992

[Anti-arrhythmic drug prevention of sudden cardiac death--the status after the CAST study].

Sudden cardiac death is caused by ventricular tachyarrhythmias. Therefore, antiarrhythmic drugs have been widely used in the prophylaxis of this lethal event. However, all studies using "classical" antiarrhythmic drugs (class 1) for this purpose have shown an enhanced mortality in the patients treated. One of the major causes for these disappointing results are probably proarrhythmic effects, which are especially observed in patients with reduced left ventricular function. Obviously a normal Holter ECG during the titration phase cannot exclude proarrhythmic events during long-term follow-up. In addition, the suppression of ventricular premature beats by an antiarrhythmic agent seems not to be an useful criterium as far as the prophylaxis of sudden death is concerned. The crucial prerequisit for the induction of the lethal arrhythmia is the "arrhythmogenic substrate" which clinically can only incompletely analysed by recording of late potentials or programmed ventricular stimulation. From the therapeutical point of view we need drugs which can modulate this arrhythmogenic substrate i.e. antifibrillatory acting drugs and not antiarrhythmic drugs in the classical sense. Beta blockers and class 3 drugs are the first step in this direction.

Anti-Arrhythmia Agents↗
PubMed1991

Simplified, rapid and inexpensive extraction procedure for a high-performance liquid chromatographic method for determination of disopyramide and its main metabolite mono-N-dealkylated disopyramide in serum.

A simplified, rapid and inexpensive extraction procedure for the determination of the antiarrhythmic drug disopyramide and its main metabolite mono-N-desalkylated disopyramide in serum by high-performance liquid chromatography has been developed. The analysis uses ultraviolet detection at 254 nm, and a 5 micron reversed-phase column with a mobile phase of water-triethylamine-acetonitrile-PIC-B8 reagent. Serum extraction is performed with dichloromethane and 1 M sodium hydroxide. p-Chlorodisopyramide is used as internal standard. Recovery rates were 94.5% (S.D. 5.7%) for disopyramide, 96.8% (S.D. 2.2%) for mono-N-desalkylated disopyramide and 97.9% (S.D. 2.8%) for the internal standard.

Chromatography, High Pressure Liquid↗
PubMed1991

Hemodynamic effects of the D- and L-isomers of sotalol on normal myocardium.

This study investigated the hemodynamic effects of the D-isomer of sotalol in open-chest rats and compared this to the action of the L-isomer and the racemic DL-sotalol. Hemodynamic and additional isovolumic maximum measurements were registered at the end and 5 minutes after an intravenous infusion period of 7 minutes. DL- (1 and 2 mg/kg) and L-sotalol (2 mg/kg) caused a significant reduction in the heart rate and in the indices of contractility during and after infusion. D-sotalol (2, 4, and 8 mg/kg), however, decreased the contractility only transiently after very high doses at high plasma concentrations. Thus, while the effects of the beta-blocking L-isomer were comparable to those of DL-sotalol, only a slight and transient hemodynamic action of comparable doses of D-sotalol was found. These findings may be of significance for the proposed use of the D-isomer as a class-III antiarrhythmic agent.

Animals↗
PubMed1991

Electrophysiologic effects of the calcium antagonist isradipine, a double-blind placebo-controlled study.

The electrophysiologic effects of the calcium channel antagonist isradipine in comparison to placebo were evaluated in a double-blind study with 9 patients in each group. The two patient groups were not different with respect to their cardiac disease, baseline electrophysiologic parameters, or blood pressure. Isradipine significantly decreased the systolic (P less than 0.01) and diastolic (P less than 0.05) blood pressure, whereas sinus cycle length was significantly (P less than 0.05) decreased in the placebo group and the isradipine group with no difference between the groups. The influence of isradipine and placebo on sinus node recovery time, effective refractory period of the atrioventricular node, intranodal conduction time (AH interval) and PR interval were not significant. In conclusion, isradipine significantly decreased systolic and diastolic blood pressure. The decrease in sinus cycle length after intravenous isradipine was not significantly different from the decrease seen in the placebo group. Atrioventricular conduction was not significantly affected.

Blood Pressure↗
PubMed1991

Randomized comparison of flecainide and cibenzoline in the conversion of atrial fibrillation.

The efficacy of oral cibenzoline (260 mg/day and 320 mg/day) and flecainide (200 mg/day and 300 mg/day) in the conversion of chronic atrial fibrillation to sinus rhythm were compared in 31 patients in a randomized order. If sinus rhythm was not restored on the 5th day of oral treatment with either cibenzoline or flecainide (phase of initial treatment) patients were switched to a second phase of treatment with the drug not given in the first phase after a washout phase of 3 days. Sinus rhythm was restored in 7/28 treatment trials with cibenzoline and in 7/23 treatment trials with flecainide (not significant). Trough levels of cibenzoline and flecainide in the plasma were not significantly different between patients in whom sinus rhythm was restored and patients with persisting atrial fibrillation. In patients successfully converted to sinus rhythm, long-term treatment was instituted with flecainide (n = 6) or cibenzoline (n = 6). Atrial fibrillation developed in 2 patients in each group of patients within 3 months. In all other patients, sinus rhythm was maintained during the follow-up period of 12 months. Non-cardiac side effects were observed in 2 patients during treatment with cibenzoline and flecainide respectively. With flecainide, one patient developed sinus arrest up to 5.6 seconds.

Adult↗
PubMed1991

Effects of the new class-III antiarrhythmic drug D-sotalol on contractile function of postischemic myocardium.

The hemodynamic effects of the new class-III antiarrhythmic drug D-sotalol (2 mg/kg i.v.) on postischemic myocardium were investigated in comparison with the actions of the racemic D,L-sotalol (2 mg/kg i.v.) in rats. Drug infusion (7 min) was started 20 min after 3 x 4 min of global ischemic injury (oxygen deficiency). The left ventricular isovolumic pressure-generating capacity at the beginning of infusion was reduced by 15%, indicating postischemic dysfunction. Infusion of D-sotalol caused a highly significant (p less than 0.01) reduction of the left ventricular pressure-generating capacity (to 58 +/- 5%), as well as of the dp/dtmax (to 21 +/- 3%). Stroke volume (to 66 +/- 6%), ejection fraction (to 62 +/- 7%), and cardiac output (to 51 +/- 6%) were also decreased (p less than 0.01). Fifteen minutes after infusion a partial renormalization of the hemodynamic measures (dp/dtmax 41 +/- 5%; stroke volume 94 +/- 8%) was observed. Infusion of the racemic D,L-sotalol caused similar hemodynamic changes (left ventricular pressure-generating capacity 60 +/- 2%, dp/dtmax 25 +/- 2%), indicating its cardiodepressant action. In contrast to prior findings on normal myocardium, our present results indicate that D-sotalol, a potential new class-III antiarrhythmic drug, has a considerable negative inotropic effect on postischemic myocardium.

Animals↗
PubMed1991

Selenium as a protector of diastolic function during oxidant stress.

Interventional studies yielded conflicting results on reperfusion injury. They are unable to discriminate between lesions due to ischemia or to additional damage during reoxygenation. Since reactive oxygen metabolites have been implicated as a major cause of reperfusion injury, 375 nmol/min of hydrogen peroxide was infused in a Langendorff rat heart preparation as a model of oxidant stress without previous ischemic contractile dysfunction. Impaired endogenous defense was remodeled, using selenium-deficient hearts with reduced glutathione peroxidase activity. Measurements of hemodynamic parameters demonstrate increased myocardial susceptibility to oxidant stress in hearts with decreased antioxidant defense. Defined concentrations of hydrogen peroxide produce isolated impairment of active and passive diastolic properties of the ventricle in this model.

Animals↗
PubMed1991

[Comparison of lisinopril and captopril in treatment of severe heart failure (NYHA III-IV) in high risk patients. Preliminary results of the trial].

We present preliminary data of a study comparing captopril, a short acting, with lisinopril, a long acting ACE-inhibitor in 8 of 12 projected patients with severe chronic heart failure (NYHA III-IV) and one additional risk factor (e.g. diabetes mellitus, renal failure). The 8 patients were treated in a cross over design for 12 weeks with either drug. While lisinopril improved NYHA-class in all patients, captopril reached this goal in only 3. Renal function was stable in all patients. Captopril influenced hormones (renin, aldosterone, norepinephrine, epinephrine) and microalbuminuria less than lisinopril. The number of adverse reactions was smaller in lisinopril treated patients. These preliminary data demonstrate at least an equal efficacy of lisinopril compared to captopril in high risk patients with severe chronic heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Value of diagnostic methods in conduction disorders for pacemaker indications and choice of a suitable stimulation mode].

Sinus node syndrome: In patients with sinus node dysfunction, additional conduction disturbances may be present in the AV-node thereby precluding the possibility for basically-desirable atrial stimulation. Systematic electrophysiologic studies have shown that, overall, conduction disturbances are uncommon, albeit more frequently than in normal subjects and most are incurred a high rate of stimulation. In practice, invasive electrophysiologic studies are not required to clarify this question. If there is no high-grade AV-block on Holter monitoring, diagnostic atrial stimulation can be carried out at the time of pacemaker implantation via the atrial electrode. A low rate should be used initially then increased gradually. On 1:1 conduction to 130 to 140 b/min permanent atrial pacing is possible since under these conditions it is very unlikely that high-grade AV-block will occur. If AV-block is observed at an atrial rate of 130 b/min, an additional ventricular electrode for two-chamber pacing should be implanted. If there is intact retrograde ventriculo-atrial (V-A) conduction, isolated ventricular stimulation should not be carried out because of the possibility of hemodynamically-unfavorable pacemaker syndrome. Possible problems with intact V-A conduction currently have only negligible importance since the development of modern programmable two-chamber systems. Carotid sinus syndrome: On manipulation of the hypersensitive carotid sinus, the invariably-present functional compromise of the AV-node is masked by the marked bradycardia but can be detected by atrial stimulation. This examination is not routinely necessary however, since in carotid sinus syndrome isolated atrial stimulation is not carried out.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

[Low-dose enalapril in severe chronic heart failure].

In a prospective, controlled trial, the clinical course of 40 patients with severe chronic heart failure (NYHA III-IV) was followed for 1 year. In addition to digitalis and diuretics, 20 patients were treated with low-dose enalapril (5 mg/d; group E), while the previous therapy including conventional vasodilators was continued in the other 20 patients (group K). After 1 year in group E, the functional degree of heart failure decreased significantly compared to group K (p less than 0.02): 65% of group E patients improved by at least one NYHA functional class vs only 5% in group K. Parallel to the clinical changes in group E, cardiac size decreased significantly compared to group K, when measured as either a decrease in the cardiac thoracic ratio of the chest x-ray from 0.55 +/- 0.07 to 0.52 +/- 0.11 (p less than 0.02) or in the echocardiographically determined left ventricular end-diastolic diameter from 72 +/- 9 to 65 +/- 7 mm (p less than 0.01). Severe side effects or complications occurred in 15% of the patients in group E and in 10% of group K, showing no significant difference between the two groups. During the 1-year observation period, two patients died in group E, and nine patients died in group K, resulting in a significantly (p less than 0.025) different mortality rate of 10% in group E compared to 45% in group K. Thus, additional treatment with low dose enalapril had lasting favorable influences on the clinical course of patients with severe chronic heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗