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Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 19 recordsLinked to original sources
PubMed1992

Effects of chronic amiodarone therapy on defibrillation threshold.

In a prospective and parallel, randomized study, the long-term stability of epicardial defibrillation threshold was evaluated in 22 patients, using a patch-patch lead configuration at the time of implantation and generator replacement. The concomitant antiarrhythmic drug treatment consisted of either mexiletine (720 mg/day) or amiodarone (400 mg/day) and was administered to patients in a randomized and parallel manner. During a mean follow-up of 24 +/- 6 months, the defibrillation threshold increased significantly from 14.3 +/- 2.8 to 17.9 +/- 5.3 J (p < 0.05) for the entire patient group. The increase in the chronic defibrillation threshold was due to a marked increase in defibrillation energy needs in the subgroup of patients receiving amiodarone. Whereas no significant change in the defibrillation threshold was documented in the subgroup of patients receiving mexiletine, the mean defibrillation threshold increased from 14.1 +/- 3.0 to 20.9 +/- 5.4 J (p < 0.001) in those receiving amiodarone. In all patients with increased defibrillation thresholds, reevaluation showed a reduction in the defibrillation threshold after discontinuation of antiarrhythmic drug therapy. The only variable associated with an increase in the chronic defibrillation threshold was amiodarone treatment. These findings suggest that the defibrillation threshold should be measured at each generator replacement and in case of a change in antiarrhythmic drug treatment. In particular, if amiodarone treatment is initiated, it is recommended that the defibrillation threshold should be reevaluated to ensure an adequate margin of safety.

Amiodarone↗
PubMed1992

Pharmacologic treatment of supraventricular tachycardia: the German experience.

Tachyarrhythmias that originate above the bifurcation of the bundle of His or in tissue proximal to it are classified as supraventricular tachyarrhythmias (SVTs). Primary treatment of SVT tries to influence the underlying disease. Symptomatic therapy is subdivided into drug therapy, electrotherapeutic tools (e.g., antitachycardia pacemakers, catheter ablation), and antiarrhythmic surgery. Antiarrhythmic agents that slow conduction and suppress premature beats are efficient for emergency and long-term treatment of SVTs. We evaluated some of the most relevant antiarrhythmic drugs in SVT, including propafenone, diprafenone, cibenzoline, sotalol, and diltiazem; in addition, usage and efficacy of quinidine/verapamil, disopyramide, amiodarone, ajmaline, adenosine, and flecainide are summarized. In 1990, the case load of supraventricular arrhythmias per physician in Germany was more than 30 patients seen per month. About 50% of them were treated with drug therapy; i.e., approximately 17 patients were treated with antiarrhythmic drugs per month per physician for supraventricular arrhythmias. The most important antiarrhythmic agents used in Germany are propafenone (40%), combination of quinidine and verapamil (23%), sotalol (12%), disopyramide (6%), flecainide (6%), and other (13%).

Anti-Arrhythmia Agents↗
PubMed1992

Hemodynamic effects of amiodarone during acute and chronic treatment in patients with recurrent sustained ventricular tachycardia.

In 15 patients with recurrent ventricular tachycardia, the hemodynamic effects of amiodarone were evaluated under oral loading (1000 mg/day for 14-16 days) and during chronic treatment (600 mg/day for a further 10 weeks). In all patients, coronary artery disease was present with a mean ejection fraction of 37%+/- 10%. The cardiac output during the sinus rhythm, as determined by thermodilution, did not change significantly during loading with amiodarone. During ventricular tachycardia, the cardiac output increased from 3.7 +/- 1.3 to 4.5 +/- 1.6 1/min under the influence of amiodarone in 5 patients. Echocardiographic measurements of the left ventricle dimensions did not show a directed change of the enddiastolic and endsystolic diameters and the fraction shortening at the end of the loading period and after 3 months of maintenance therapy. No negative inotropic effect of amiodarone could be demonstrated in patients with recurrent ventricular tachycardia and impaired left ventricular function due to coronary artery disease.

Aged↗
PubMed1992

Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia.

The electrophysiological and haemodynamic effects of lidocaine (100 mg) and ajmaline (50 mg) were evaluated while attempting to interrupt sustained ventricular tachycardia. The study was performed as a prospective, non-blinded, randomized investigation in 61 patients. Lidocaine terminated ventricular tachycardia in four of 31 patients, ajmaline in 19 of 30 patients (P less than 0.001). QRS and RR intervals during ventricular tachycardia were prolonged by ajmaline from 164 +/- 28 ms to 214 +/- 49 ms and from 371 +/- 86 ms to 479 +/- 137 ms (P less than 0.001), respectively; lidocaine did not influence these parameters. The duration of the return cycles after termination of ventricular tachycardia did not differ between the two groups. Lidocaine did not change cardiac output during ventricular tachycardia whereas cardiac output increased significantly under ajmaline from 3.5 +/- 1.21.min-1 to 5.5 +/- 1.91.min-1 (P less than 0.001). It is concluded that anti-arrhythmic agents such as ajmaline, which slow conduction velocity and prolong refractoriness, are more effective than lidocaine in the medical treatment of haemodynamically stable, sustained ventricular tachycardia.

Ajmaline↗
PubMed1992

Long-term therapy of antitachycardia pacing for supraventricular tachycardia.

Long-term antitachycardia pacing therapy with the InterTach 262-12 and 262-16 was evaluated in 32 consecutive patients (mean age 50 +/- 13 years) with recurrent, drug refractory supraventricular tachycardia. AV nodal reentrant tachycardia was present in 20 patients, Wolff-Parkinson-White syndrome in ten patients, and a reentrant tachycardia due to Mahaim fibers in one patient. During follow-up of 39 +/- 17 months, 250 persistent tachycardia episodes occurred in 22 patients. By adjusting detection and termination mode, recurrent supraventricular tachycardia could be controlled in 19 of 32 patients (60%) by antitachycardia pacing alone. Concomitant antiarrhythmic drug therapy was required in ten of 32 patients (30%). During follow-up antitachycardia pacing became ineffective in three patients (10%). Thus, chronic antitachycardia pacing proved to be safe and effective in selected patients with drug refractory supraventricular tachycardia and could significantly improve quality of life by rapid termination of recurrent supraventricular tachycardia episodes.

Algorithms↗
PubMed1992

Failure of an implantable cardioverter-defibrillator to redetect ventricular fibrillation in patients with a nonthoracotomy lead system.

BACKGROUND: Shock delivery of an implantable defibrillator may cause a change in the amplitude of endocardial electrograms and impair the detection of ventricular fibrillation. Thus, the effects of shock discharges on the amplitude of endocardial electrograms were evaluated in five patients undergoing implantation of a cardioverter-defibrillator in combination with a new nonthoracotomy lead system. METHODS AND RESULTS: At implant, bipolar endocardial electrograms were recorded before each shock application, during ventricular fibrillation, during redetection of ventricular fibrillation in case the applied shock was ineffective, and at intervals of 5, 10, 20, 30, 60, and 120 seconds after each shock delivery. The amplitude of the endocardial electrograms decreased from 10.5 +/- 3.8 mV during sinus rhythm to 6.3 +/- 1.9 mV during initial ventricular fibrillation and declined to 2.2 +/- 1.3 mV during redetection of ventricular fibrillation. After successful termination, the following bipolar electrograms could be obtained at the predetermined intervals: 1.9 +/- 1.2 mV, 3.1 +/- 1.8 mV, 4.5 +/- 1.9 mV, 6.5 +/- 2.9 mV, 9.5 +/- 3.3 mV, and 10.4 +/- 3.8 mV. At predischarge testing, failure of redetection of ventricular fibrillation could be documented in two patients, requiring rescue external defibrillation in both cases to restore sinus rhythm. CONCLUSIONS: These findings demonstrate that the implantable cardioverter-defibrillator did not ensure reliable redetection of ventricular fibrillation in patients using the implanted nonthoracotomy lead system. Thus, the potential risk of sudden cardiac death may persist in these patients despite defibrillator therapy.

Cardiomyopathy, Dilated↗
PubMed1992

[Combination anti-arrhythmic drug therapy].

Antiarrhythmic treatment with single agents is often ineffective and can be limited by dose-dependent side-effects. Therefore, combinations of antiarrhythmic drugs in smaller and well-tolerated doses are advocated in cases refractory to single antiarrhythmic drugs. Basically, substances belonging to the same electrophysiologic class should not be combined. A combination of beta-adrenoreceptor blockers with class I antiarrhythmic drugs may be effective, mainly in cases in which the arrhythmia is dependent on adrenergic stimulation. As shown in our study, the combination of class III and I B-substances can be useful in some cases, from the electrophysiological and clinical points of view. Among the successful combinations of this type are amiodarone and mexiletine, sotalol and mexiletine, and sotalol and tocainide. In patients refractory to amiodarone alone or to a combination with mexiletine, the combined treatment with amiodarone and class-I-C drugs such as flecainide and encainide prolongs the cycle length of ventricular tachycardia, but does not suppress induction of ventricular tachycardia during programmed stimulation. Combination therapy with amiodarone and encainide is associated with a remarkable incidence of proarrhythmic effects. Nevertheless, a combination of antiarrhythmic drugs improves efficacy of therapy in selected patients. However, a close monitoring is mandatory because of the risk of proarrhythmia.

Amiodarone↗
PubMed1992

[Wolff-Parkinson-White syndrome: regional endocardial potential and efficacy of high frequency ablation].

The aim of the study was the evaluation of results of radiofrequency (RF) catheter ablation in relation to characteristics of regional endocardial potential morphology. 418 RF current deliveries in 26 patients with anterogradely conducting left-sided accessory pathways (AP) were investigated. A large regional atrial deflection (> 1/4 of ventricular potential) prior to RF discharge is a prerequisite for ablation success using the ventricular approach. A failing or extremely short (< 10 ms) isoelectric interval between atrial and ventricular deflections of the regional potential predicts a block of the AP. A persistent block can be expected if the regional electrogram contains an AP potential and the AP block occurs early (< 5 s) during onset of RF current.

Adult↗
PubMed1992

[Doppler echocardiography imaging of construction-induced regurgitation of technical heart valve prostheses].

The normal leakage flow in modern technical heart valve prostheses can be visualized by color-coded Doppler-echocardiography, provided that an adequate ultrasonic image quality can be achieved. Sometimes it may be difficult, however, to distinguish such a normal leakage flow from pathological regurgitation. We therefore mounted new specimens of five different types of prostheses (Bjørk-Shiley monostrut, Medtronic-Hall, Omnicarbon, Saint Jude Medical, Duromedics) into an invitro model, where the leakage flows could directly be visualized as emerging water jets. When the system was completely filled, the jets could also be registered by two-dimensional Doppler-echocardiography. For each valve, characteristic patterns for the localization of the principal jets were found. Besides the relative broad central jet in the Medtronic-Hall valve, all other jets arose mainly at the ring. They were detected at the hinges or the basis of the larger struts, respectively, and with asymmetrical mono-disc valves at the side of the smaller opening. The length and the orientation of the jets were found to change significantly with minimal variations of the position of the closing discs. This variability could be confirmed, when in a separate model the overall leakage flows were repeatedly measured. For patient examinations it seems useful to refer mainly to the localization of the jet origins. The comparison with reference values of jet-dimensions in Doppler images will rarely enable the examiner to distinguish between normal and pathological jets.

Echocardiography, Doppler↗
PubMed1992

[Who should be referred for electrophysiologic studies?].

Prerequisite of a rational antiarrhythmic therapy is the correct diagnosis of the given cardiac rhythm disorder. The majority of intermittent and latent cardiac arrhythmias can be reliably induced and analyzed during the electrophysiologic study (EPS). In case of bradyarrhythmias, the method is indicated in patients with suspected sinus node disease or high-grade AV conduction disturbances, as far as the cause of clinical symptoms cannot be settled by Holter recordings. Since patients with paroxysmal supraventricular tachycardias (WPW syndrome and AV nodal reentrant tachycardia) can be cured by transvenous ablation techniques, EPS is indicating in this setting in all symptomatic patients for the diagnosis and the treatment of the given arrhythmia. In patients with recurrent ventricular tachyarrhythmias, EPS should be performed to establish the diagnosis and to control medical treatment; in addition, EPS is a prerequisite for nonpharmacologic treatment modalities such as defibrillator therapy and transvenous or surgical ablation techniques. In survivors of cardiac arrest without new Q-wave myocardial infarction, persistent ventricular tachyarrhythmias can be induced in some 50% of the patients. Patients should be evaluated by EPS in case the reasons for significant clinical symptoms cannot be determined otherwise, given the likelihood, that brady- or tachyarrhythmias are the cause of the clinical symptoms; this includes patients with organic heart disease and with unexplained syncopes.

Arrhythmias, Cardiac↗
PubMed1992

[Clinical assessment and indications for automatic defibrillation].

A variety of therapeutic options including pharmacological treatment, surgical procedures, ablation interventions and electrotherapy are available for the management of patients who are subject to symptomatic ventricular tachyarrhythmias. Patients with documented sustained ventricular tachycardia or ventricular fibrillation are usually controlled by serial electrophysiological studies. About 30 to 60% of these patients respond to antiarrhythmic drugs during serial electrophysiological testing. Patients with severe left-ventricular function respond less frequently than those of well-preserved function. Long-term follow-up studies have demonstrated that, if ventricular tachyarrhythmias can no longer be induced on antiarrhythmic drugs or if inducibility is at least rendered more difficult, the rate of recurrences is low. In contrast, patients with still inducible ventricular tachyarrhythmias may have a poor prognosis and may suffer from frequent recurrences or may even die suddenly. Thus, nonpharmacological strategies such as an implantable cardioverter/defibrillator, transvenous catheter ablation and map-guided antitachycardia surgery have become important alternatives for drug refractory patients. Since the introduction of the implantable cardioverter/defibrillator using a nonthoracotomy approach, the intraoperative and perioperative mortality and morbidity has been significantly reduced. A widespread use of these newer devices required the establishment of guidelines for the appropriate application of this new treatment modality. Surgical, medical and economic considerations make it imperative that defibrillator therapy should be chosen on a basis of careful patient selection. The presenting clinical arrhythmia and its hemodynamic stability, underlying heart disease and left-ventricular ejection fraction should be taken into consideration.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric Countershock↗
PubMed1992

[Transluminal coronary extraction atherectomy. Method, acute results, angiographic and clinical follow-up].

Transluminal coronary extraction-endarterectomy is an alternative interventional approach for treatment of coronary artery disease. The atherectomy system consists of a catheter assembly including a cutter and torque tube which is rotated at a relatively low rate of 750 rotations per minute, when introduced to the coronary artery over a guide-wire via a guiding catheter. Excised tissue is withdrawn from the coronary artery by suction applied through the catheter by means of an attached vacuum bottle. We report acute results in 18 patients and the clinical outcome of 14 patients who up to now underwent angiographic follow-up catheterization after 6 months. Initial angiographic success (residual stenosis less than 50%) using TEC-atherectomy alone was obtained in 6/18 patients (33%), 11/18 patients (60%) required additional PTCA in order to achieve primary success (9/18) or to treat total occlusion (2/18) after TEC-atherectomy. Major complications consisted in 1-vessel perforation with non-Q-wave-infarction but no need of surgical intervention and 2 occlusions due to dissection (treated with PTCA). 14 patients underwent angiographic follow-up (6 months) and restenosis (greater than 50%) was confirmed in 7 patients (50%). Considering the low primary success rate of TEC-atherectomy alone and the tendency to high restenosis rate, we cannot recommend it as an alternative to conventional PTCA in general clinical practice. Further studies should be designed to directly compare TEC-atherectomy to PTCA in specific patient subgroups (e.g. bypass grafts, intraluminal thrombus, diffuse disease) in order to define the role of this interventional device.

Adult↗
PubMed1992

[Measuring blood flow velocity in the coronary sinus with Doppler catheters].

Measurements of the coronary sinus blood flow velocity with Doppler catheters (Medtronic Floscan; Millar DC201) were performed to assess coronary flow reserve and significance of coronary artery stenosis. In seven patients with normal coronary angiogram coronary sinus blood flow velocity (Doppler catheters) and coronary sinus blood flow volume (thermodilution) were simultaneously recorded. Coronary flow reserve was calculated as the quotient of the peak flow velocity (peak flow volume) and resting flow velocity (resting flow volume) after infusion of 0.5 mg/kg dipyridamole intravenously. The correlation coefficient was r = 0.88. Coronary sinus blood flow velocity was measured in 31 patients at resting conditions and after injection of contrast media during coronary angiography. At resting conditions blood flow velocity was 3.6 +/- 1.5 cm/s (n = 31), 3.5 +/- 1.8 cm/s (n = 9; controls), and 3.6 +/- 1.1 cm/s (n = 9; significant stenosis of the left anterior descending; not significant). After injection of contrast media flow velocity amounted to 2.2-fold resting flow in controls and to 1.5-fold resting flow in patients with stenoses of the left anterior descending artery (p less than 0.01). Measurement of coronary sinus blood flow velocity with Doppler catheters is a valuable adjunct for determination of coronary flow reserve and for assessment of stenosis severity of the left anterior descending artery. Continuous on-line monitoring of phasic flow velocity provides important information of the myocardial perfusion, e.g., during angioplasty.

Blood Flow Velocity↗
PubMed1992

[Sudden cardiac death--possibilities and limits of drug therapy].

Sudden cardiac death is a challenge for primary prevention efforts, the rescue system, and the prophylactic antiarrhythmic medical therapy. A prerequisite for the successful prevention is insight into the pathophysiologic interaction of the arrhythmogenic substrate, the ischemic events, the autonomous nervous system, ventricular premature beats, left-ventricular function, etc. Latest results of prophylactic antiarrhythmic therapy indicate that the benefit under a specific antiarrhythmic treatment depends on the ratio of antiarrhythmic to proarrhythmic effects and the prevalence of sudden cardiac death in a given population. In diseased hearts with ventricular tachycardia or ventricular fibrillation the chance of sudden cardiac death is high, therefore, antiarrhythmic therapy is indicated and should be controlled by programmed stimulation. In patients with a low likelihood of sudden cardiac death after myocardial infarction, beta receptor blockers should be given; in certain higher risk patients (non-sustained ventricular tachycardia, reduced left-ventricular function) class-III antiarrhythmic agents are recommended. In hypertrophic cardiomyopathy (less in dilative cardiomyopathy) a beneficial effect of amiodarone becomes apparent in subgroups with high risk. Treatment of symptomatic ventricular premature beats remains empiric; in case of no or minimal structural heart disease, the arrhythmogenic potential is low. For the management of recurrent ventricular tachycardia new concepts are proposed that include antiarrhythmic agents and magnesium.

Anti-Arrhythmia Agents↗