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Michiel J. Janse

Researcher at University of Amsterdam

Publications -  227
Citations -  21845

Michiel J. Janse is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Ischemia & Ventricular tachycardia. The author has an hindex of 70, co-authored 227 publications receiving 21183 citations. Previous affiliations of Michiel J. Janse include University of Bern & Columbia University.

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Total Excitation of the Isolated Human Heart

TL;DR: In this paper, isolated human heart measurements were made from as many as 870 intramural terminals to obtain information concerning the time course and instantaneous distribution of the excitatory process of the normal human heart.
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The Lambeth Conventions: guidelines for the study of arrhythmias in ischaemia, infarction, and reperfusion

TL;DR: The Lambeth Conventions are guidelines intended to be of practical value in the investigation of arrhythmias induced by ischaemia, infarction, and reperfusion and are encouraged to adopt in the hope that this will improve uniformity and interlaboratory comparisons.
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Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT

TL;DR: The findings do not support the systematic prophylactic use of amiodarone in all patients with depressed left-ventricular function after myocardial infarction, but the lack of proarrhythmia and the reduction in arrhythmic death support the use of the drug in patients for whom antiarrhythmmic therapy is indicated.
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Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation.

TL;DR: The majority of evidence supports the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass in patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction.
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Slow conduction in the infarcted human heart. 'Zigzag' course of activation.

TL;DR: Slow conduction perpendicular to the fiber direction in infarcted myocardial tissue is caused by a "zigzag" course of activation at high speed.