Antiarrhythmische Therapie bei Herzinfarkt

Lüderitz, Berndt; d’Alnoncourt, C. Naumann

doi:10.1007/978-3-642-68872-0_18

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…Aus dieser arrhythmogenen Verfinderung k6nnen sich Herzrhythmusst6rungen aufgrund fokaler Reizbildung durch Verletzungsstrom und kreisender Erregung (Reentry) im ischfimischen Myokard entwickeln [9]. Die Repolarisationsverspfitung fiihrt zu einer negativen T-Welle im extrazellulfiren Elektrogramm.…”

Section: Herzrhythmusstfrungen Und Stumme Ischiimieunclassified

Die stumme Myokardisch�mie

Lüderitz

1991

Eur J Clin Pharmacol

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Eight normal subjects (3 females and 5 males) were studied using intravenous L-[11C] deprenyl and positron emission tomography. In a single blind study one subject received tracer alone, one subject received an oral pre-dose of 20 mg of L-deprenyl and 6 subjects received oral pre-doses of 10 to 50 mg of a novel reversible MAO-B inhibitor (Ro 19-6327). Dynamic PET scans beginning 12 h after the oral dose were collected over 90 min and arterial blood was continuously sampled. Data analysis was modelled for two tissue compartments and using an iterative curve fitting technique the value of the rate constant for irreversible binding of L-[11C] deprenyl to MAO-B (k3) in whole brain was obtained for each subject. The dose response curves obtained indicated that a dose of at least 0.48 mg.kg-1 of Ro 19-6327 was necessary for greater than 90% decrease in whole brain k3. Inhibition of MAO-B in platelets isolated from blood samples taken at the time of scanning correlated strongly with decrease in whole brain k3 (r = 0.949). The results indicate that PET can be used to determine the dose of Ro 19-6327 necessary to inhibit greater than 90% of brain MAO-B. This technique is an attractive alternative to traditional large scale patient-based dose-finding studies. Moreover it is shown that inhibition of platelet MAO-B can be used as a marker for central MAO-B inhibition with Ro 19-6327.

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Section: Herzrhythmusstfrungen Und Stumme Ischiimieunclassified

Die stumme Myokardisch�mie

Lüderitz

1991

Eur J Clin Pharmacol

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“…The delay in repolarization leads to a negative T-wave in the extracellular ECG. Cardiac arrhythmias may develop due to these arrhythmogenic changes and focal ectopy because of current in the damaged tissue and re-entry circuits in the ischemic myocardium [9].…”

Section: Cardiac Arrhythmias and Silent Ischemiamentioning

confidence: 99%

Silent myocardial ischemia: A special aspect of coronary artery disease

Lüderitz

1990

Eur J Clin Pharmacol

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Silent myocardial ischemia is a serious progressive disease which deserves continuous surveillance. It is characterized by painless ST-segment depression based on coronary artery disease. The mechanisms responsible for producing this condition do not differ from stable angina pectoris. The prognostic implications of silent ischemia are not yet completely clarified. However it could be argued that patients die--whether or not angina pectoris is present--because they develop myocardial infarction or ischemic ventricular arrhythmias. Complex ventricular arrhythmias seem to occur not at a higher rate than in patients with angina pectoris. On the other hand there is no doubt about a present arrhythmogenic potential of a silent myocardial ischemia, but there is so far no clinical evidence that the prognostic significance is different to symptomatic myocardial ischemia. In order to reduce or eliminate ischemic episodes intensive combination medical therapy should be used. If symptoms recur or ischemic changes are persistent, consideration should be given to revascularisation. Nevertheless, the optimal way of treating silent ischemia is still to be defined.

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Antiarrhythmische Therapie bei Herzinfarkt

Cited by 2 publications

References 24 publications

Die stumme Myokardisch�mie

Die stumme Myokardisch�mie

Silent myocardial ischemia: A special aspect of coronary artery disease

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