Biomedical subjects

V Kühlkamp

Publications and source records attributed to V Kühlkamp.

At least 55 records · Page 3Linked to original sources

PubMed1997

Efficacy and proarrhythmia with the use of d,l-sotalol for sustained ventricular tachyarrhythmias.

This study prospectively evaluated the clinical efficacy, the incidence of torsades de pointes, and the presumable risk factors for torsades de pointes in patients treated with d,l-sotalol for sustained ventricular tachyarrhythmias. Eighty-one consecutive patients (54 with coronary artery disease, and 20 with dilated cardiomyopathy) with inducible sustained ventricular tachycardia or ventricular fibrillation received oral d,l-sotalol to prevent induction of the ventricular tachyarrhythmia. During oral loading with d,l-sotalol, continuous electrocardiographic (ECG) monitoring was performed. Those patients in whom d,l-sotalol prevented induction of ventricular tachycardia or ventricular fibrillation were discharged with the drug and followed up on an outpatient basis for 21 +/- 18 months. Induction of the ventricular tachyarrhythmia was prevented by oral d,l-sotalol in 35 (43%) patients; the ventricular tachyarrhythmia remained inducible in 40 (49%) patients; and two (2.5%) patients did not tolerate even 40 mg of d,l-sotalol once daily. Four (5%) patients had from torsades de pointes during the initial oral treatment with d,l-sotalol. Neither ECG [sinus-cycle length (SCL), QT or QTc interval, or U wave] nor clinical parameters identified patients at risk for torsades de pointes. However, the oral dose of d,l-sotalol was significantly lower in patients with torsades de pointes (200 +/- 46 vs. 328 +/- 53 mg/day; p = 0.0017). Risk factors associated with the development of torsades de pointes were the appearance of an U wave (p = 0.049), female gender (p = 0.015), and significant dose-corrected changes of SCL, QT interval, and QTc interval (p < 0.05). During follow-up, seven (20%) patients had a nonfatal ventricular tachycardia recurrence, and two (6%) patients died suddenly. One female patient with stable cardiac disease had recurrent torsades de pointes after 2 years of successful treatment with d,l-sotalol. Torsades de pointes occurred early during treatment even with low doses of oral d,l-sotalol. Pronounced changes in the surface ECG (cycle length, QT, and QTc) in relation to the dose of oral d,l-sotalol might identify a subgroup of patients with an increased risk for torsades de pointes. Other ECG parameters before the application of d,l-sotalol did not identify patients at increased risk for torsades de pointes. Recurrence rates of ventricular tachyarrhythmias are high despite complete suppression of the arrhythmia during programmed stimulation. Therefore programmed electrical stimulation in the case of d,l-sotalol seems to be of limited prognostic value.

Adult↗

PubMed1996

Manifestation of severe coronary heart disease after anabolic drug abuse.

Anabolic steroids are frequently abused, thus increasing the risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles. We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease. Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronary artery, and hypokinetic regions corresponded to posterolateral and anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2-year abuse of the anabolic steroid stanazolol. No report published so far has shown possible atherogenic consequences of long-term abuse of stanazolol.

Adult↗

PubMed1996

Quantitation of pentisomide and its metabolite by high-pressure liquid chromatography in human serum.

A rapid, inexpensive, and accurate high-performance liquid chromatographic method for the simultaneous determination of pentisomide and its major mono-N-dealkylated metabolite has been developed. After a simple and inexpensive solvent extraction procedure, the unchanged drug, its metabolite, and the internal standard are separated using a C18 reversed-phase column with a 5-microns particle size. The eluent is monitored with ultraviolet detection at 260 nm. Endogenous substances or a variety of drugs do not interfere with the assay. The mean recoveries of pentisomide and its metabolite are 92.6% and 92.2%, respectively. The limit of detection of the assay is 28 ng/mL for both drugs. Serum levels of pentisomide and its metabolite in patients on oral therapy for supraventricular tachycardia are reported.

Anti-Arrhythmia Agents↗

PubMed1996

[Shock-induced, but not terminated ventricular tachycardia in a patient with implantable defibrillator].

A 62-year-old male patient with coronary artery disease and drug refractory sustained ventricular tachycardia received an implantable cardioverter defibrillator (PRX III, model 1720, CPI) with a transvenous lead system (Endotak, model 0115, CPI) in combination with a subcutaneous array electrode (SQ array, model 049, CPI). The intraoperative defibrillation threshold was 15 J and was confirmed 1 week later at the hospital discharge test. Three months after discharge from hospital the patient reported 5 shocks during moderate physical exertion followed by a tachycardia associated with dizziness which terminated spontaneously. The print out of the stored electrogram showed a supraventricular tachycardia (probably sinus tachycardia) with a heart rate of 154/min which activated the device. Antitachycardia pacing did not terminate the supraventricular tachycardia, and hence shock therapy was delivered. The first shock (34 J) converted the supraventricular tachycardia to a ventricular tachycardia with a heart rate of 178/min, which was not terminated by four consecutive 34 J DC shocks. There was no hint of a device or lead failure. Determination of the defibrillation threshold reconfirmed the 15 J value for termination of ventricular fibrillation. However, neither a 1 J shock nor a 34 J shock terminated a monomorphic sustained ventricular tachycardia (cycle length 340 ms) induced by noninvasive programmed electrical stimulation. The ventricular tachycardia was, however, reproducibly terminate by antitachycardia pacing. It is concluded that an inappropriate high-energy DC shock might induce a sustained ventricular tachycardia. However, a sufficient defibrillation threshold for the termination of ventricular fibrillation does not necessarily mean that a sustained ventricular tachycardia will be terminated by a high-energy DC shock.

Coronary Disease↗

PubMed1995

Long-term efficacy of d/l sotalol in patients with sustained ventricular tachycardia refractory to class I antiarrhythmic drugs.

The efficacy of d/l sotalol was investigated in 50 patients (43 men, seven women; 33 with coronary artery disease, 15 with dilated cardiomyopathy; ejection fraction 33 +/- 10%) with inducible sustained ventricular tachycardia. Before d/l sotalol a mean of 2 +/- 1 (1 to 4) class I antiarrhythmic drugs were ineffective. In 24 patients (48%) oral d/l sotalol (320 +/- 47 mg.day-1) prevented induction of the ventricular tachycardia; in 23 patients the ventricular tachycardia remained inducible (d/l sotalol 326 +/- 50 mg.day-1). The electrophysiological effects of d/l sotalol did not differ between patients in whom d/l sotalol prevented induction of ventricular tachycardia and those in whom the ventricular tachycardia remained inducible. In two patients, torsade des pointes developed after oral application of d/l sotalol; one patient suffered from severe hypotension even with 80 mg of sotalol per day. During long-term follow-up (27 +/- 12 months) 5/24 patients (21%) had a non-fatal recurrence of ventricular tachycardia (1 week to 21 months), one patient died suddenly and another from progressive heart failure. In patients in whom the ventricular tachycardia could be induced despite oral application of d/l sotalol, control of the ventricular tachyarrhythmia was attempted by the use of sotalol in combination with mexiletine (n = 2), amiodarone (n = 9), catheter ablation (n = 2), antitachycardia surgery (n = 1) or the implantation of an automatic cardioverter defibrillator (n = 12). Recurrence of ventricular tachycardia was observed in four patients without an implanted cardioverter defibrillator. Seven out of 12 patients with an implanted cardioverter defibrillator received appropriate shocks or successful antitachycardia pacing. Although no patient died suddenly, overall mortality was 17% in this group. It is concluded that d/l sotalol is highly effective in the suppression of sustained monomorphic ventricular tachycardia inducible by programmed electrical stimulation. However during a mean follow-up of 27 +/- 12 months a recurrence of ventricular tachycardia was seen in 21% of patients, and one patient died suddenly.

Administration, Oral↗

PubMed1995

[Early after-depolarization in polymorphic ventricular tachycardia without QT prolongation].

Endocardial monophasic action potentials (MAP) were recorded at different sites of the right ventricle in a patient with a history of syncope and recurrent polymorphic ventricular tachycardia (pVT) without QT prolongation. The MAP recording from the infero-septal wall demonstrated persisting early afterdepolarizations (EAD) during sinus rhythm with no cycle length dependence. Programmed ventricular stimulation at this site provoked a pVT rapidly degenerating into ventricular fibrillation. Iodine-123-meta-iodobenzylguanidine (MIBG) scintigraphy indicated a defective sympathetic innervation in inferior and apical sectors of the left ventricle. Intravenous verapamil resulted in marked sinus bradycardia and nevertheless completely suppressed the pVT. These observations support the hypothesis that the mechanism of pVT is EAD-induced triggered activity that is due to an intrinsic defect of the myocardial cell with alteration of the calcium channels. This regulation defect of ionic channels might possibly be induced by an abnormality in the sympathetic innervation. Both conditions may lead to dispersion of repolarization causing triggered activity. In our case the regionally restricted findings explain the absence of QT prolongation. The effect of verapamil provides evidence that bradycardia is not an essential condition in the genesis of pVT.

Calcium Channels↗

PubMed1995

[Catheter ablation in sinus node tachycardia].

Sinus node tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia. Of those patients who were referred to our clinic for electrophysiologic evaluation and catheter ablation, four patients (1 male, 3 female) were found to have sinus node tachycardia. The diagnosis of sinus node tachycardia required all of the following: The P-wave during sinus rhythm had to be similar to the P-wave during the tachycardia, the atrial activation sequence during sinus rhythm and tachycardia had to be similar, the origin of the tachycardia had to be in the high right atrium. In one patient the tachycardia was incessant. The other three patients had paroxysmal sinus node tachycardia that could be induced by programmed atrial stimulation. No patient had overt cardiac disease. One patient had an inducible av nodal reentrant tachycardia and one patient had a second atrial tachycardia originating from the basal right atrium. Activation mapping during tachycardia was performed in all patients. Local atrial activation at the site of successful ablation preceded the P-wave in the surface electrocardiogram by 54 +/- 43 ms. In three patients the interval from the local atrial activation at the site of successful catheter ablation to the onset of the signal from the high right atrium (HRA) ranged from 25 ms to 125 ms, in one patient the signal from the high right atrium was the earliest recorded signal during tachycardia. In all patients the tachycardia was terminated with the application of radiofrequency current. Two to a maximum of 12 radiofrequency current applications were necessary; complications were not observed. In all patients a second electrophysiologic study was performed 8 +/- 2 weeks after successful catheter ablation; no patient had inducible sinus node or atrial tachycardia. During a follow-up of 5 +/- 2 months, no patient had a recurrence of sinus node tachycardia or required antiarrhythmic medication. It is concluded that catheter ablation in patients with sinus node tachycardia is an effective and safe treatment.

Adult↗

PubMed1994

[Electrocardiographic diagnosis of atrial fibrillation and flutter].

The key for the diagnosis of atrial fibrillation is the complete irregularity of the R-R intervals in the absence of P waves. In atrial flutter, the analysis of the flutter waves itself is important. In doing so, common and uncommon flutter can be distinguished. The A-V conduction and therefore the R-R intervals can be constant or irregular. If widened QRS complexes are registered intermittently, aberrant conduction has to be differentiated from ventricular premature beats. In this context die analysis of the width and the shape of the QRS complexes as well as the R-R intervals preceding and following the abnormal beats are important criteria. In principle, this holds true as well for the diagnosis of WPW syndrome in the presence of AF. If the surface ECG does not allow a clear-cut diagnosis, the indication for invasive electrophysiological testing may be given in a few cases.

Atrial Fibrillation↗

PubMed1993

[Ventricular tachyarrhythmia. Drug therapy and evaluation of success].

In principle, all antiarrhythmic drugs (classes 1-3) are useful in the treatment of ventricular tachyarrhythmias. In special cases even Ca-antagonists (class 4) can be effective. Holter monitoring and programmed ventricular stimulation are clinical tools for predicting efficacy and controlling proarrhythmic effects. However, only in a limited number of patients are the prerequisites given for testing with one or the other method. Using long-term tape recording the suppression of ventricular salvoes by an antiarrhythmic drug seems to predict a good prognosis. In the electrophysiological lab complete or partial suppression of inducibility of the arrhythmias during programmed stimulation under antiarrhythmic treatment has a high predictive value as far as recurrence during follow-up is concerned. Using Holter criteria the efficacy of antiarrhythmic drugs is higher than with programmed stimulation. However, invasive electrophysiological testing has a higher sensitivity, i.e., a low rate of false-positive results. As the results of two newer studies question the value of both methods, a definitive answer of the problem of optimal control of antiarrhythmic therapy cannot be given today.

Anti-Arrhythmia Agents↗

PubMed1993

[Syncope in bradycardic cardiac arrhythmias].

Bradyarrhythmias, depending on the patient population, are the cause of syncope in 3 to 10%. Marked bradycardia or asystole can be due to impaired function of the sinus node (sinus node syndrome) or high-grade AV-conduction block as well as carotid sinus syndrome and pathologic vasodepressor reactions. In particular, in the presence of high-grade AV-block, the diagnosis of bradyarrhythmia-induced syncope can frequently be established on the basis of a standard ECG. One of the most common causes of syncope is functional impairment of the sinus node, in particular, an inadequate permanent sinus bradycardia, sinus node arrest or SA-block and paroxysmal atrial tachycardia alternating with atrial bradycardia. The method of choice for detecting suspected paroxysmal arrthythmias is ambulatory ECG monitoring but interpretation may be encumbered by the absence of concomitant symptoms during the registration. Frequently, the use of non-invasive methods alone, such as detailed history, ambulatory ECG and ECG exercise testing, will not render confirmatory findings to document the cause of syncope, that is, > 3 s pause in sinus rhythm or high-grade AV-block. In this situation, the question arises which patients should undergo electrophysiologic examination. Several studies have shown that in patients with a pathologic resting ECG (first degree AV-block, bundle branch block, inadequate sinus bradycardia) and cardiac disease, electrophysiologic studies will document a cause of syncope in more than 30%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bradycardia↗

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

[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

Value of a modified continuity equation method to quantify mitral valve area in patients with mitral stenosis and sinus rhythm.

To quantify valve area in mitral stenosis, a modified continuity equation method using continuous wave Doppler and thermodilution measurements was applied. In 14 patients with mitral stenosis and sinus rhythm (age: 49 +/- 11 years), transmitral flow velocity was recorded by continuous wave Doppler during right and left heart catheterization. Mitral valve area was calculated by three different methods: 1. According to the continuity equation, stroke volume (thermodilution technique) was divided by the registered time velocity integral of the mitral stenotic jet (continuous wave Doppler). 2. Mitral valve area was calculated by the pressure half-time method. 3. Simultaneous pulmonary capillary wedge and left ventricular pressure measurements were used for determination of mitral valve area according to the Gorlin formula. The mitral valve area determined by application of the continuity equation (y) showed a close correlation to the valve area calculated by the Gorlin equation (x): y = 0.73x + 0.12, SEE = 0.11 cm2, r = 0.88, P less than 0.001. In contrast, the correlation between mitral valve area determined by pressure half-time (y) and the Gorlin formula (x) was not as good: y = 0.77x + 0.11, SEE = 0.26 cm2, r = 0.65, P less than 0.05. Thus, the continuity equation method using combined continuous wave Doppler and thermodilution technique allows a valid determination of mitral valve area. In patients with mitral stenosis and sinus rhythm, this technique is superior to the noninvasive determination of mitral valve area by the conventional pressure half-time method.

Adult↗

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

Pharmacokinetic profile and tolerability of pimobendan in patients with terminal renal insufficiency.

The pharmacokinetics of an i.v. bolus of pimobendan (P) 2.5 mg and 5.0 mg, its tolerability and the effect on heart rate and blood pressure have been studied in 12 subjects (42-70 y) suffering from severe terminal renal impairment. Plasma level data were compared with those obtained in a previous investigation in healthy volunteers. Pharmacokinetics were dose linear and were comparable to those in healthy subjects. No adjustment of the dose of P is necessary in patients with severe renal impairment. Tolerability of P, observed by means of blood pressure monitoring, clinical chemistry tests, electrocardiography and subjective judgement resulted in 4 complaints out of 12 patients: three suffered from orthostatic problems and vomiting, and one patient had nausea. Mean heart rate was elevated by 19% (2.5 mg) and 16% (5.0 mg). Blood pressure was significantly reduced after 2.5 mg P (23% systolic and 26% diastolic pressure), and after 5.0 mg P by 25% systolic and 23% diastolic pressure.

Adult↗

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↗