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Biomedical subjects

F L Meijler

Publications and source records attributed to F L Meijler.

At least 19 recordsLinked to original sources
PubMed2001

Supraventricular escape rhythms during transient episodes of bradycardia in preterm infants.

OBJECTIVE: To evaluate the origin of transient episodes of sinus bradycardia, atrial escape rhythm, and atrioventricular nodal escape rhythm in preterm infants. MATERIAL AND METHODS: The study was observational, and was carried out in a third level neonatal intensive care unit. We studied 19 spontaneously breathing infants born healthy but prior to term, the examinations being carried out between the ages of 3 and 28 days. The mean gestational age was 29.2 +/- 1.9 weeks, and the mean birth weight was 1154 +/- 264 g. Transient episodes of bradycardia were defined as a decline in heart rate equal to or greater than 25% from baseline, lasting for at least 3 successive RR-intervals. To discriminate between different types of escape mechanisms, we used the P wave and the P axis of the electrocardiogram. Sinus bradycardia was diagnosed when the P axis was from +0 to +90 degrees; atrial escape rhythm when it was from +91 to +359 degrees, and atrioventricular nodal escape rhythm when the P wave was absent, hidden, or followed the QRS complex. RESULTS: The mean P axis was +50 +/- 11 degrees. We observed 60 transient episodes of bradycardia in 11 of the 19 infants. Of these, 34 (57%) were classified as sinus bradycardia, and 13 (22%) as atrial escapes. Atrioventricular nodal escapes developed during 6 episodes (10%), while 7 episodes (11%) could not be classified. CONCLUSIONS: Atrial excitation as evidenced by the P axis during sinus rhythm is similar in very preterm infants to that seen in children and adults. Escape rhythms with different origins occur during transient episodes of bradycardia in healthy preterm infants. In at least one third, the episodes are due to atrial or atrioventricular nodal escape.

Atrial Premature Complexes↗
PubMed1999

[Electrophysiology of the atrioventricular node during atrial fibrillation. I. Ventricular rhythm].

Atrial fibrillation (AF) occurs in 0.9% of the population, in 6% of persons over 65 and in 10% of persons over 80. It is an important independent risk factor for thromboembolism, especially cerebral infarctions. The functions of the atrioventricular (AV) node are: (a) optimal adjustment of the time between the contractions of atria and ventricles; (b) protection of the ventricles against excessively high frequencies of atrial tachycardia; (c) a pacemaker function in case of atrial arrest. AF is an irregular, disorganized electrical activity of the atria. On the ECG, P waves are absent and the baseline shows wavelets constantly changing in shape, duration, amplitude and direction. Development and existence of AF are correlated with a sufficiently large number of myocardial cells and a sufficient degree of difference between the electrical properties of the myocardial cells. In the absence of an AV conduction block, the resulting ventricular rhythm is completely irregular. The constant irregularity of the ventricular rhythm is independent of ventricular frequency and independent of cardiac and other characteristics of the patient. Electrical stimulation of the right ventricle leads to complete AV block.

Adult↗
PubMed1999

[Electrophysiology of the atrioventricular node during atrial fibrillation. II. The influence of atrial impulses].

An atrial impulse that is not conducted to the ventricle may slow down the conduction of the next atrial impulse. A ventricular extrasystole may also affect the conduction through the AV node. This phenomenon is called 'concealed conduction'. At least three mechanisms are possible to explain concealed conduction, but neither weakening of the impulse as the conduction proceeds nor electrotonic modulation of the pacemaker function of the AV node is in accordance with the observed constant irregularity of atrial fibrillation. The most probable mechanism to explain the ventricular rhythm during atrial fibrillation is the electrotonic change (inhibition) by atrial impulses of the conduction properties of the AV node.

Adult↗
PubMed1999

ECG of the "newborn" mouse (Mus domesticus) with specific reference to comparative AV transmission.

INTRODUCTION: The objective of this study was to record the ECG of the smallest living mammal to extend the domain of data for comparative AV nodal electrophysiologic purposes. These data are needed to establish the relationship between the PR interval and heart size in mammalian species of all sizes. METHODS AND RESULTS: In recently born mice (age 1.5 to 8 weeks) weighing between 2.5 and 10 g and with estimated heart weights between 15 and 60 mg, ECGs, using bipolar limb leads, were recorded during general anesthesia. The PR interval, representing AV transmission time was about 40 msec, which is quite long for hearts of this size. On the basis of detailed analysis of the data, we postulate the presence of a fixed delay or discontinuous propagation in the AV node not only in newborn mice, but in mammals of all sizes. CONCLUSION: AV transmission times obtained in mammals (including humans) cannot be explained on the basis of generally accepted, classic AV conduction theories. The acceptance of the presence of a fixed delay in the AV node may ultimately be of value to better understand AV node function during sinus rhythm and supraventricular arrhythmias.

Animals↗
PubMed1998

Pharmacological classification of adenosine receptors in the sinoatrial and atrioventricular nodes of the guinea-pig.

1. The effects of seven agonist and three antagonist adenosine receptor ligands were compared on the guinea-pig sinoatrial (SA) node (isolated right atrium) and atrioventricular (AV) node (perfused whole heart). Single agonist concentration-effect curves were obtained to 5'-N-ethylcarboxamidoadenosine (NECA), R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA), N6-cyclohexyladenosine (CHA), 2-chloroadenosine (CADO),),S(+)-N6-(2-phenylisopropyl)adenosine (L-PIA), 2-phenylaminoadenosine (CV 1808) and N6-aminoadenosine (MeAdo). Adenosine and/or NECA curves were obtained in the absence and presence of the antagonists 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), 9-chloro-2 (2-furanyl)-5,6-dihydro-1,2,4-triazolo[1,5-c]quinazolin-5-imine (CGS15943) and N6-(endonorbornan-2-yl)-9-methyladenine (N-0861). 2. A formal comparison of the agonist and antagonist potency data was made by fitting the data to a straight line using a least squares procedure based on principal components analysis to account for the variance on both axes. The antagonist affinity estimates made on the two assays did not deviate significantly from the line of identity. 3. The agonist p[A]50 data obtained on the two assays did not deviate from the line of identity, indicating that there were no significant differences in potencies between the two assays. The p[A]50 ratio of R-PIA and S-PIA was 1.24+/-0.09 in the SA node and 1.36+/-0.11 in the AV node, indicating no difference in the stereoselectivity of the PIA isomers between the two tissues. 4. The agonist potency and antagonist affinity data obtained are consistent with previous findings showing that the AV and SA node data are pharmacologically indistinguishable and belong to the adenosine A1-receptor class. No evidence for the reported A3-receptor was found.

Adenosine↗