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Biomedical subjects

M J Janse

Publications and source records attributed to M J Janse.

At least 145 records · Page 8Linked to original sources

Endocardial mapping by simultaneous recording of endocardial electrograms during cardiac surgery for ventricular aneurysm.

A technique was developed for the simultaneous recording of 30 endocardial electrograms during cardiac surgery in patients undergoing aneurysmectomy or endocardial resection, or both, for medically intractable ventricular tachycardia. An inflatable balloon covered with 30 terminals at distances of 1.5 to 2 cm was used to record from the entire endocardial surface; a smaller silicone rubber sheet with 30 terminals at distances of 0.7 cm was used to obtain a better spatial resolution. The multielectrodes were inserted into the left ventricular cavity by way of an incision in the aneurysm. A transportable minicomputer was used for the acquisition and analysis of the signals. After initiation of ventricular tachycardia by programmed stimulation, signals of a 1.5 second period were stored and analyzed. The earliest activated terminal could be determined within 2 to 5 minutes. The technique was applied in 32 patients and proved especially useful in those patients in whom sustained tachycardia could not be evoked and in whom conventional mapping with a roving electrode would have been impossible or very time consuming. In all patients, the isochronic maps showed that the ectopic impulses originated from a rather localized area and no evidence was found for large endocardial circus movements, thereby excluding these as a mechanism underlying the tachycardia. Isochronic maps, depicting activation sequences during consecutive ectopic beats with the same QRS morphologic features, showed the same site of origin in all but six patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

The calcium paradox: an electrophysiological study in the isolated rabbit heart.

In Langendorff perfused rabbit heart (37 degrees C) transmembrane potentials were recorded from the left ventricle with 'floating' microelectrodes. During calcium-free perfusion, action potential duration lengthened by 55.4 +/- 34.9% (n = 8). AV conduction time increased, until Wenckebach and 2 : 1 AV block occurred. Heart rate initially decreased, and later increased although control values were not reached. Upon reperfusion with normal calcium-containing fluid, a few vigorous contractions occurred, which dislodged the intracellular microelectrode. As far as could be established, cells depolarized within 6-60s to values less than -50 mV, and no action potentials could be recorded. During low-calcium (50 mumol l-1) perfusion (n = 5), action potential duration initially increased, but later decreased. When perfusion with normal calcium-containing fluid was resumed when action potentials were still longer than normal, the action potentials shortened initially but returned later to control values. In these hearts, contractions reappeared. However, when perfusion with normal calcium-containing fluid was resumed when action potential duration was shorter than normal, no contractions reappeared, and action potentials remained short during the entire reperfusion period. In six experiments, creatine kinase release was determined during both low-calcium and calcium-free perfusion, and during subsequent periods with normal calcium-containing fluid. During 10 min of low-calcium perfusion, 107 +/- 31 IU g-1 dry weight appeared in the perfusate, and in the subsequent normal calcium perfusion period of 15 min, 438 +/- 88 IU were released. During the 10 min calcium-free period, 141 +/- 40 IU were released, and during 15 min of reperfusion, 2773 +/- 258 IU appeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Effect of changes in perfusion pressure on the position of the electrophysiologic border zone in acute regional ischemia in isolated perfused dog and pig hearts.

In isolated, Langendorff perfused hearts, 60 direct-current extracellular electrograms were simultaneously recorded from the left ventricular epicardium. In each experiment, the left circumflex branch and the left anterior descending coronary artery were successively occluded for 15 minutes, each occlusion separated by a long reperfusion period. During the occlusion, perfusion pressure to the nonoccluded arteries was changed from a high to a low value and vice versa, and the position of the electrophysiologic border (the zone where T-Q segment potentials became negative) was determined. In some experiments tissue biopsy samples were taken from recording sites and analyzed for lactate and creatine phosphate. In all experiments the metabolic border correlated well with the electrophysiologic border. In other experiments, the coronary arteries were injected with barium sulfate; epicardial collateral channels were found in dogs hearts, but not in pig hearts. In seven of eight dog hearts, the border could be shifted by changing perfusion pressure; in seven of eight collateral channels, changes in perfusion pressure could enlarge or reduce the area showing ischemic changes. Despite species differences, not all hearts within one species behaved the same: One pig heart behaved as a dog heart, one dog heart as a pig heart.

Animals↗

Electrotonic interactions across an inexcitable region as a cause of ectopic activity in acute regional myocardial ischemia. A study in intact porcine and canine hearts and computer models.

We recorded 60 DC simultaneous electrograms from isolated porcine and canine hearts in the first minutes after coronary occlusion. Ventricular premature beats (VPB) originated from the normal side of the ischemic border, which was frequently separated from the central ischemic area showing delayed activity by a small zone of inexcitable tissue. We attempted in a computer model to generate VPB's at one side of an area showing conduction block. In computer simulations,,, the presence of elements capable of automatic activity greatly facilitated the induction of VPB's. By coupling automatic elements to nonautomatic elements, overt pacemaking activity could be suppressed. Subthreshold depolarizations transmitted through a zone of conduction block could, when properly timed, trigger the latent automatic elements into overt automatic activity, resulting in single or repetitive VPB's. The ventricular premature beats in the intact hearts with acute regional ischemia may be caused by "triggered automaticity" in which the trigger is provided by the "injury current" flowing from ischemic cells showing delayed repolarization via a segment of inexcitable ischemic cells in the border zone to normally perfused cells with suppressed automaticity.

Animals↗

Effects of tocainide on ectopic impulse formation in isolated cardiac tissue.

The effect of tocainide on enhanced automaticity if Purkinje fibers was studied under the influence of epinephrine (0.2 microgram/ml) by means of intracellular recordings with microglass electrodes. In the presence of tocainide 5 microgram/ml and 10 microgram/ml cycle length of enhanced automaticity was increased in the range of 10.6% and 34.9% and in the range of 26.3% and 108.7% respectively. Repetitive impulse formation in ventricular myocardium was generated by creating a potential difference in a papillary muscle mounted in a partition chamber. One chamber was connected to ground, the potential of the other chamber could be changed in the range of 0 to 500 mV. By progressively increasing the voltage difference across the papillary muscle repetitive rhythmic impulse formation was induced. The threshold voltage gradient increased in the presence of tocainide (100 microgram/ml) from--285 to--335 mV. The results suggest that tocainide is suitable to suppress arrhythmias due to enhanced automaticity of Purkinje fibers.

Action Potentials↗

Clinical relevance of experimentally obtained electrophysiologic data on antiarrhythmic drugs.

An extrapolation of electrophysiological findings to a specific clinical situation is not always feasible since successful arrhythmia analysis frequently is not achieved and even in the presence of a known arrhythmic mechanism, the predominant effect of a given antiarrhythmic agent cannot be predicted with respect to therapeutic relevance. These assertions are additionally supported by the fact that the effects of antiarrhythmic agents, which have been primarily studied in healthy myocardium, may be entirely different in the presence of myocardial ischemia. Furthermore, in spite of a certain degree of agreement among data of experimentally-induced and clinical myocardial ischemia, the findings do not imply complete applicability. Theoretical considerations indicate that a reentry mechanism may not only be favourable influenced by an agent rendering improved conduction velocity and shortened refractory periods but also influenced by an agent effecting oppositely directed changes. Although an effective therapeutic regimen can generally be achieved with no exact knowledge of the arrhythmic mechanism or of the specific action of a given drug, future investigations hould augment existing information to yield a more rational means of treatment and prevention of arrhythmias as well as to aid in the development of new antiarrhythmic agents.

Animals↗

Efficacy of lidocaine in preventing primary ventricular fibrillation within 1 hour after a 300 mg intramuscular injection. A double-blind, randomized study of 300 hospitalized patients with acute myocardial infarction.

The effectiveness of intramuscular lidocaine in preventing in-hospital primary ventricular fibrillation within 1 hour after injection of the drug in patients with acute myocardial infarction was assessed in a double-blind randomized study performed in 300 such patients admitted within 6 hours of myocardial infarction. Six of 147 patients treated with 300 mg of intamuscular lidocaine had ventricular fibrillation compared with 4 of 153 control subjects. The lidocaine blood level of the patients who experienced ventricular fibrillation was 1.4 +/- 0.7 microgram/ml (mean +/- standard deviation) at the time of fibrillation, a value not significantly different from that of treated patients who did not experience fibrillation. Lidocaine blood levels in the latter were 1.9 +/- 1.1, 2.1 +/- 1.1, 2.1 +/- 1.1 and 1.7 +/- 0.7 microgram/ml, respectively, 7, 15, 30 and 60 minutes after injection. In this study intramuscular lidocaine was ineffective in preventing ventricular fibrillation, possibly because the given dose, 300 mg, prevented attainment of adequqte blood levels of the drug.

Adult↗