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Biomedical subjects

M Manz

Publications and source records attributed to M Manz.

At least 109 records · Page 6Linked to original sources
PubMed1990

New aspects of the clinical use of anti-arrhythmia agents with special reference to acute therapy of ventricular tachycardia (lidocaine vs. ajmaline).

Antiarrhythmic treatment is based on the hypothesis that ventricular premature beats (VPBs), in the presence of underlying cardiac disease and impaired ventricular function, may predispose to sudden cardiac death. The effectiveness of treatment, however, has not been proven. For acute treatment of paroxysmal ventricular tachycardia, on comparison of the effectiveness of lidocaine and ajmaline, some new aspects have been rendered. VENTRICULAR PREMATURE BEATS (VPB): Isolated VPBs can be found in 40 to 75% of healthy subjects; if their number is substantial, investigation is warranted. For VPBs with subjective symptoms, beta-receptor blockers or specific antiarrhythmic agents, if necessary in combination, may be given. In several studies it has been shown that the prognosis of patients with frequent and complex VPBs, that is couplets and salvos, without heart disease is not compromised. In one long-term study over an average of 6.5 years, sudden death was observed in only one of 70 subjects who had 566 VPBs/24 hours, 60% additionally couplets and 26% salvos in the Holter ECG. Accordingly, treatment for the sake of prognosis is not warranted. For patients with mitral valve prolapse or only mildly impaired ventricular function and asymptomatic arrhythmias, treatment is not necessary since it has not been shown to be beneficial. Coronary artery disease is the most frequent cause of ventricular arrhythmias and sudden death. In numerous studies in patients after myocardial infarction, a relationship has been recognized between frequent and complex VPBs and overall mortality as well as sudden death. Particularly at risk are patients with very frequent and complex VPBs with additional impairment of ejection fraction to less than 30 to 40% but this group only accounts for 10% of patients after infarction. Only in one interventional study, carried out with aprindine, there was a significant reduction in overall mortality from 12.5 to 7.8% with an adverse reaction rate, however, of 21%. In high-risk patients with a low ejection fraction and numerous, complex VPBs as well, in a further study with aprindine, after one year, there was no decrease in overall mortality as compared with the placebo group. The cause for the insufficient effectiveness of the antiarrhythmic agents in various interventional studies has been attributed to a limited number of patients, rigid dosing regimens, inadequate suppression of VPBs and a high incidence of adverse reactions. In the multicenter, randomized, placebo-controlled CAST study with newer substances, a total of 2309 patients with essentially asymptomatic VPBs at a rate of more than 6/hour and an ejection fraction less than 55% or 40% admitted more than 90 days after infarction, respectively, were followed from six days to two years after myocardial infarction to determine if the significant suppression of VPBs in patients with coronary artery disease with antiarrhythmic agents leads to a reduction in arrhythmia-associated deaths. Flecainide, encainide and moricizine led to a significant suppression of VPBs in 75% of the patients. After an average of ten months, the rate of arrhythmia-induced deaths of 4.5% in those treated with encainide or flecainide was significantly higher than the 1.2% observed in the placebo group. These results appear attributable to a proarrhythmic effect of the class IC drugs during long-term treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Ajmaline↗
PubMed1990

[Indications for pacemaker therapy in ophthalmoplegia plus and Kearns-Sayre syndrome].

Mitochondrial myopathies can affect the skeletal muscle, the central or peripheral nervous system, and they may be associated with chronic progressive external ophthalmoplegia (CPEO). In 7/29 patients with mitochondrial myopathies and CPEO a cardiac involvement (Kearns-Sayre syndrome) was found: incomplete right bundle branch block (n = 1), right bundle branch block (n = 1), left anterior fascicular block and right bundle branch block (n = 2), complete atrioventricular block (n = 3); congestive cardiac failure (ejection fraction 40%) (n = 2); 3/10 patients had prolonged infranodal conduction on His-bundle electrography (HV-interval 60 ms). The cardiac involvement in ophthalmoplegia plus is characterized by progressive impairment of fascicular conduction. The need for prophylactic pacemaker implantation appears to exist in patients with bifascicular block and prolonged His-ventricle conduction.

Adolescent↗
PubMed1989

Role of antitachycardia devices in the treatment of ventricular tachyarrhythmias.

Chronic recurrent ventricular tachycardia (VT) can be terminated reproducibly by programmed endocardial right ventricular stimulation. However, antitachycardia pacing is associated with possible acceleration of VT, while frequent occurrence of VT and discomfort of the patient can limit treatment with an automatic implantable cardioverter/defibrillator (AICD; Cardiac Pacemakers Inc.). The combined use of antitachycardia pacing (Tachylog pacemaker; Siemens-Elema) and AICD was therefore evaluated in 6 of 35 patients (aged 50 to 70 years, mean 60.1 +/- 7.7) in whom AICD had been implanted because of VT, which could be terminated by temporary overdrive pacing. With the interactive mode of the Tachylog, termination of VT by the pacemaker as well as by the AICD was assessed after implantation. In the automatic mode, the Tachylog functioned as a bipolar ventricular inhibited (VVI) device with antitachycardia burst stimulation: 2 to 5 stimuli, interval 260 to 300 ms, 1 to 2 interventions. During follow-up of 32 +/- 17 months, the Tachylog terminated VT reliably 50 to 505 times per patient. When burst stimulation accelerated VT, termination was achieved by AICD discharge. Thus, drug-resistant VT can be terminated by antitachycardia pacing avoiding patient discomfort. In case of acceleration, VT can be controlled by the AICD. A universal pacemaker should combine antibradycardia and antitachycardia pacing with backup cardioversion/defibrillation mode.

Electric Countershock↗
PubMed1989

[Arrhythmogenic effect of flecainide--treatment with i.v. magnesium].

We report on a 46-year-old woman with ventricular tachycardia and ventricular fibrillation after starting antiarrhythmic drug therapy with flecainide. The flecainide acetate plasma levels were always in the normal range. A successful therapeutical intervention was induced with two i.v. applications of 1,000 mg magnesium glutamate. A persistent suppression of ventricular rhythm disturbance was accomplished by continuous i.v. application of 4 mg magnesium glutamate/min.

Electrocardiography↗
PubMed1989

[Cibenzoline: electrophysiologic effects of a new class I anti-arrhythmia agents in supraventricular tachycardia].

Cibenzoline, an imidazoline derivate, is a new class 1 antiarrhythmic agent. The electrophysiologic effects and antiarrhythmic properties of cibenzoline (100 mg i.v.) were evaluated in 22 patients with paroxysmal supraventricular tachycardia: 12x Wolff-Parkinson-White Syndrome, 9x AV nodal reentrant tachycardia, 1x atrial tachycardia. Cibenzoline shortened the sinus cycle length from 742 +/- 103 ms to 661 +/- 87 ms (p less than 0.001) and the sinus node recovery time from 1026 +/- 106 ms to 926 +/- 135 ms (p less than 0.001). The substance lengthened the AH interval from 93 +/- 19 ms to 112 +/- 24 ms (p less than 0.001) and the HV interval from 42 +/- 12 ms to 61 +/- 14 ms (p less than 0.001). The effective refractory periods of the atrium and right ventricle did not change significantly, but the effective refractory period of the AV node in antegrade (269 +/- 42 ms vs 278 +/- 46 ms; p less than 0.05) and retrograde direction (281 +/- 57 ms vs 413 +/- 124 ms; p less than 0.001) increased markedly. Cibenzoline prolonged the effective refractory period of the accessory pathway in retrograde direction from 263 +/- 41 ms to 428 +/- 101 ms (p less than 0.001). The effective refractory period of the antegrade accessory pathway did not change. During atrial stimulation inducibility of the reentrant tachycardia was suppressed in 14 of 22 patients and the inducibility of atrial fibrillation in 7 of 12 patients. The RR interval of the reentrant tachycardia was prolonged from 353 +/- 57 ms to 420 +/- 57 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Emergency therapy of ventricular tachycardias: lidocaine versus ajmaline].

The efficacy of ajmaline (50-75 mg i.v.) or lidocaine (100-200 mg i.v.) in terminating persistent, haemodynamically stable ventricular tachycardia (VT) was compared in a prospective, randomized trial of 31 patients. There were no significant differences as to age, underlying heart disease, ejection fraction and rate of ventricular tachycardia between the two treatment groups. Ajmaline terminated VT in 10 of the 15 patients receiving it, lidocaine in only 2 of 16 (P less than 0.01). The frequency of VT was not significantly changed by lidocaine, while mean cycle length during VT changed under ajmaline from 369 +/- 82 ms to 452 +/- 11 ms (P less than 0.01). In contrast to lidocaine, QRS duration under ajmaline lengthened from 166 +/- 18 ms to 200 ms +/- 28 ms (P less than 0.01), but return cycles after tachycardia termination were similar (ajmaline, 863 +/- 296 ms; lidocaine, 917 +/- 367 ms). Both drugs were equally well tolerated, but in this series ajmaline was more effective in the acute treatment of persistent VT.

Ajmaline↗
PubMed1988

Electrophysiologic effects of dextro- and levo-verapamil on sinus node and AV node function in humans.

The electrophysiologic effects of dextro (d)- and levo (l)-verapamil on sinoatrial (SA) and atrioventricular (AV) node function were studied in ten patients undergoing electrophysiologic evaluation of their supraventricular tachyarrhythmias. Both isomers elicited a significant prolongation of sinus node recovery time (SNRT) and AH interval. No difference between d- and l-verapamil regarding the magnitude of the effects were observed. However, 50 mg d-verapamil was required to elicit the same electrophysiologic effects as 5 mg l-verapamil. The d- and l-verapamil plasma concentrations associated with the maximum effect on AH interval and SNRT showed a more than 20-fold difference (d: 380 ng/ml; l: 19 ng/ml). These data demonstrate that both verapamil isomers possess qualitatively similar slow channel blocking effects on the SA and AV node in humans, but the l isomer is 20 times more potent than the d isomer.

Adult↗
PubMed1988

[Hemodynamics in ventricular arrhythmias and in their treatment].

The hemodynamic consequences of ventricular tachyarrhythmias are influenced by age, underlying cardiac disease, left ventricular ejection fraction, and possibly by atrial natriuretic peptide. Severity and frequency of the rhythm disorder play, of course, a major role, e.g., monomorphic or polymorphic ventricular premature complexes (VPC), rare or frequent VPC, ventricular tachycardia, ventricular flutter or fibrillation, torsade de pointes, and tachycardia, etc. The therapeutic approach with antiarrhythmic drugs or cardiac pacemakers in cases of conduction disturbances have an additional impact on cardiac performance. Compared to ventricular pacing, a significant higher cardiac output was observed during AV sequential (so called "physiological") pacing evaluated by radionuclide ventriculography. Especially in patients with a reduced left ventricular ejection fraction, the negative inotropic effects of antiarrhythmic drugs are of major importance. A decrease of cardiac output may occur under beta-blocking agents, propafenone, flecainide and particularly disopyramide. On the other hand, amiodarone does not impair cardiac output significantly during acute high dose loading and longterm therapy. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia.

Amiodarone↗
PubMed1988

[Supraventricular tachycardia: therapy with a variable antitachycardia stimulation program].

Modern, microprocessor-controlled antitachycardia pacemakers are available with extended detection and termination programs for the treatment of supraventricular tachycardias. Using the "InterTach 262-12" we examined a universal antitachycardia pacing mode in the chronic state. Based on the individual electrophysiologic parameters, a defined burst stimulation mode was used for the first intervention and, consecutively, a determined scanning mode. The InterTach device was implanted in 17 patients with a mean age of 50 +/- 15 years: 10 with AV-nodal reentrant tachycardia, 6 with Wolff-Parkinson-White syndrome, 1 with reentrant tachycardia with Mahaim fibers. The mean tachycardia rate was 178 +/- 23/min and the follow-up 10 +/- 4 months. Every 3 months the efficacy of the termination mode was tested by programmed stimulation in supine and upright body position or during physical activity. In these tests, a rate of 95-100% successful terminations was observed. In the chronic state, 26 persistent tachycardias in 11 patients were noted; 21 episodes could be referred to an insufficient tachycardia detection. Only four persistent tachycardias were due to ineffective antitachycardia pacing. The introduction of extended variable termination programs, including consecutive, flexible pacing modes, can be considered as a marked advancement in the antitachycardia pacemaker therapy for supraventricular tachycardias.

Adult↗
PubMed1988

[Noninvasive diagnosis of bilocular left atrial and right ventricular myxoma of the heart].

Bilateral cardiac myxomas are very rare and therefore mostly overlooked. In most cases the diagnosis has been made intraoperatively or at postmortem examination. We report on a 60-year-old woman with a left atrial and right ventricular myxoma where diagnosis was made by echocardiography and computer tomography, and confirmed histologically after successful surgical and therapeutic aspects are discussed.

Echocardiography↗
PubMed1987

[Combination of sotalol with the class I B substances mexiletine or tocainide in complex ventricular extrasystole].

In 34 patients with ventricular tachyarrhythmias the effect of the antiarrhythmic therapy of sotalol (160-320 mg p.o.) in combination with the type-I-B-agent mexiletine (600-800 mg p.o.) or tocainide (800-1200 mg p.o.) was studied by Holter monitoring. In all patients 2.2 +/- 1.1 drugs trials had failed, including amiodarone in 8 patients and beta blocking substances in 15 patients. The combination of sotalol with mexiletine or tocainide reduced ventricular ectopic beats by 79% and complex ventricular arrhythmias (pairs and salvoes) by 85%. A significant reduction of ventricular ectopic beats (greater than 80%) was reached in 74% of the patients, of pairs and salvoes (greater than 90%) in 79%. There was no difference in the antiarrhythmic efficacy between the combination of sotalol/mexiletine and sotalol/tocainide. Intervals of the resting ECG or laboratory values did not change significantly. In 5 patients with sotalol/tocainide and 1 patient with sotalol/mexiletine, side effects were observed which necessitated discontinuation of the treatment. The results show that sotalol, in combination with mexiletine or tocainide, has a potent antiarrhythmic effect in patients with otherwise drug-refractory ventricular arrhythmias.

Adult↗