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Biomedical subjects

M J Janse

Publications and source records attributed to M J Janse.

At least 163 records · Page 9Linked to original sources
PubMed1978

[Surgical interruption of the accessory pathway in a case of WPW-syndrome with persistent supraventricular tachycardia provoked by sinus node suppression (author's transl)].

This is a case report of a 60-year-old woman with a WPW-syndrome Type A developing persistent supraventricular tachycardia refractory to medical treatment. The re-entry mechanism was based on av-junction escape beats leading to retrograde conduction through the accessory pathway in presence of sinus node dysfunction i.e. long periods of sinus arrest probably enhanced through antiarrhythmic drug therapy and/or digitalis. With the aid of electrophysiological examinations and intraoperative epicardial mapping the accessory pathway was located in the upper lateral region of the left ventricle and interrupted by an incision in the av-groove from inside of the lfet atrium. Although an additional accessory pathway, not interrupted by surgery was suggested by the postoperative electrophysiological study, the patient remained free from tachycardia over more than 18 months, except for one episode terminated promptly by overdrive pacing from the right atrium. Postoperatively sinus bradycardia and av-junctional escape rhythm prevailed.

Accessory Nerve↗
PubMed1978

Mechanisms of tachyarrhythmias, past and present.

Several hypotheses, developed in the early years of arrhythmology, and frequently used for the explanation of many types of clinical tachyarrhythmias, are often based on experiments on unusual models, unphysiologic interventions, or, in some instances, on erroneously interpreted histologic findings. However, it can be demonstrated that several of these hypotheses are valid. Focal activity, unidirectional block, extremely slow conduction velocity, differences in conduction velocity in closely adjacent regions, reentry of the excitation wave, circulating excitation waves in small or large regions of the heart and other postulated mechanisms as, for example, entrance and exit block, local ventricular fibrillation, appear to be involved in the causative mechanisms of clinical tachyarrhythmias. A multicausal genesis of at least some of these must be considered seriously, particularly those which occur in acute or chronic coronary heart disease. A recent suggestion that the injury current might be involved in the genesis of ventricular tachyarrhythmias in acute myocardial ischemia and infarction is supported by observations on several properties of this current. Progress has been made in recent years but large gaps in our knowledge of mechanisms causing arrhythmias are still present.

Animals↗
PubMed1977

The effect of "ischemic" blood on transmembrane potentials of normal porcine ventricular myocardium.

"Ischemic" blood was obtained in pigs from a local coronary vein on release of coronary artery occlusion. The effects of this blood on transmembrane potentials of muscle strips taken from the same heart were compared with control blood. Whereas action potentials remained stable in control blood, ischemic blood collected after more than 15 minutes of coronary occlusion produced shortening of action potential duration, reduction of resting potential, upstroke velocity and amplitude, then postrepolarization refractoriness and finally unresponsiveness. Ischemic blood collected after shorter periods of coronary occlusion produced only mild effects (shortening of action potential and postrepolarization refractoriness). These effects of ischemic blood could not be attributed to increased potassium concentration even in combination with acidosis, hypoxia and hypoglycemia. It appears that during ischemia unidentified factors are released which have potent depressant effects on the excitability of even normal myocardium.

Action Potentials↗
PubMed1977

The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart.

Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.

Action Potentials↗
PubMed1976

Pathophysiological basis of tachyarrhythmias--re-entry.

A description is given of the principles of re-entry and circus movement, which were originally formulated on the basis of experiments on jellyfish and play an important role in cardiac arrhythmias. The essential features of re-entry are 1) the existence of two conducting pathways which communicate at their proximal and distal ends, and 2) the occurrence of uni-directional block in one pathway while conduction is maintained in the other. A retrograde wavefront may then be set up in the pathway where block was present, and the tissue from which the impulse came may be re-excited. Once this sequence is set up it may continue as a circus movement leading to tachycardia. Long re-entry circuits are present in Wolff-Parkinson-White syndrome, in which two connections between atria and ventricles exist. Micro-re-entry may occur in a variety of cardiac tissues. An example of supraventricular tachycardia due to micro-re-entry in the atrio-ventricular node of an isolated rabbit heart is shown, in which simultaneous recording of transmembrane potentials of AV nodal cells unraveled the events. The principles of the termination of circus movement tachycardias by electrically induced premature beats are discussed.

Atrioventricular Node↗
PubMed1976

Cycle-length-dependent properties of AV nodal activation in rabbit hearts.

Cycle-length-dependent changes in AV nodal cell activation were studied in isolated preparations from rabbit hearts. Transmembrane action potentials were recorded from the node while it was propagating impulses initiated in the atrium with an accelerating train of stimuli. This train consisting of five successive stimuli separated by progressively shorter intervals was uniformly repeated at every 10th basic beat, each time reproducing a sequence of five different increasing AV nodal delays. The AN and NH cells were found to contribute only slightly to the cycle-length-dependent AV nodal delay which developed mainly in the small N zone, located centrally in the AV node. With the increasing delay, the action potentials from this N zone typically dissociated into two components synchronous with late AN and early NH activity, respectively. The amplitude of the first component decreased, wheareas that of the second increased progressively in N cells activated progressively later. No cells were activated at an intermediate time between the two components. This dissociation was not accompanied by changes in the activation pattern of the AV node. The different nodal cells classified according to their response to the accelerating train delineated functional zones corresponding to different anatomic structures. The possible mechanisms which would explain the cycle-length-dependent AV nodal delay are discussed.

Action Potentials↗