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Biomedical subjects

B Befeler

Publications and source records attributed to B Befeler.

At least 37 records · Page 2Linked to original sources
PubMed1976

Mitral valve prolapse. Recent concepts and observations.

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.

Animals↗
PubMed1976

Effects of the pacing site in sinus node reentrant tachycardia.

His bundle recordings and premature atrial stimulation from coronary sinus, mid-right atrium and high-right atrium were performed in a patient with repetitive supraventricular tachycardias. Regardless of the paced site, there was a range of coupling intervals during which testing stimuli elicited short runs of premature beats. The corresponding P waves were positive in leads I, II and III and had a high-to-low right atrial activation sequence. Their morphology was similar to that of sinus beats. However, sustained tachycardia occurred only when pacing was performed from the coronary sinus. Therefore, it is postulated that the site of stimulation might be important in the genesis and (perhaps) perpetuation of this arrhythmia by changing the site and (or) mode of entry into the area where this type of tachycardia occurs. Though sinus node reentry was the most likely mechanism, it could not be determined whether the circuit involved the sinus node per se or the so called perinodal fibers.

Cardiac Catheterization↗
PubMed1976

His bundle recordings in diagnosis of impulse formation in Kent and Mahaim tracts.

His bundle electrograms were recorded in 2 patients with ectopic beats arising in accessory atrioventricular tracts. Case 1 had Wolff-Parkinson-White (WPW) type A and a left-sided Kent tract with a short effective refractory period. Though ectopic impulse formation most probably occurred within the Kent tract itself, a vulnerability-related origin in the ventricular muscle close to the distal end of the Kent tract could not be excluded. In Case 2, with a Mahaim tract extending from His bundle to ventricles, there were three types of QRS morphologies resulting from : (a) atrioventricular conduction exclusively through the normal pathways; (b) atrioventricular conduction through both, normal pathway, and Mahaim tract; and (c) ectopic impulse formation in the Mahim tract. Specialized electrophysiological studies were essential to diagnose these unusual arrhythmias.

Adult↗
PubMed1976

Intermittent bundle-branch block in patients with accessory atrio-His or atrio-AV nodal pathways. Variants of the Lown-Ganong-Levine syndrome.

Intracardiac electrophysiological studies were performed in two patients with a documented history of repetitive supraventricular tachyarrhythmias. Case 1, with short PR interval and narrow QRS complexes had a short AH interval and intermittent right bundle-branch block. Thus the short PR wide QRS syndrome is not always a result of the Wolff-Parkinson-White syndrome but can also be seen in the Lown-Ganong-Levine syndrome coexisting with bundle-branch block. Case 2, with normal PR and AH at the lower limits of normal, showed the dual pathway response to atrial pacing that can occur in patients with Lown-Ganong-Levine syndrome. He also had tachycardia-dependent right bundle-branch block and left posterior hemiblock. Therefore, neither the short PR interval nor the narrow QRS complexes characterized these forms of pre-excitation. The constant features were, from the clinical viewpoint, the occurrence of repetitive supraventricular tachyarrhythmias, and electrophysiologically the abnormal response to atrial stimulation.

Arrhythmias, Cardiac↗
PubMed1976

Retrograde His bundle deflection in bundle-branch re-entry.

Atrial echo beats resulting from a reciprocating mechanism involving the bundle-branches were produced by premature atrial impulses in a patient with an A-V nodal bypass tract. The mechanism of the arrhythmia was suggested by the presence of a retrograde His bundle deflection which appeared 'sandwiched' in between a QRS complex with complete right bundle-branch morphology and a negative P wave. Though at a shorter cycle length the His bundle was still activated retrogradely echo beats were not seen because the retrograde H deflection occurred too early, when both bypass tract and A-V node were still effectively refractory. At the faster driven rate concealed retrograde activation of the right branch (by the premature impulse) was responsible for the right bundle-branch block patterns shown by the post-premature driven beat.

Adult↗
PubMed1976

Effects of pacing site on QRS morphology in Wolff-Parkinson-White syndrome, with special reference to 'pseudo-tachycardia-dependent block in accessory pathway and 'atrial gap'.

In a patient with a Wolff-Parkinson-White (WPW) syndrome type A mid-right atrial stimulation at a rate of 73/min produced a lesser degree of ventricular pre-excitation than when a slower sinus rhythm was present. This paradoxical effect was not related to tachycardia-dependent block in the accessory pathway because pre-excitation again increased at faster pacing rates. It was partly the result of a (proportionally) greater prolongation of intra-atrial conduction time to the accessory pathway than to the atrioventricular node and partly of a faster atrioventricular nodal conduction time. The latter, in turn, could be attributed either to later-than-normal arrival of excitation at the atrioventricular node, at a time when this structure was more recovered, or to a change in the site or mode of entry into the atrioventricular node. A gap in the atria was present because at a St1-St2 interval shorter than that which A2 had been blocked in the accessory pathway conduction was again possible, but with longer A1-A2 intervals. Finally, at similar, short, coupling intervals the impulse penetrated the atrioventricular node from the mid-right atrium but not from the coronary sinus. The unusual findings in this case support a recent assumption that in patients with WPW type A atrial stimulation should be performed from the coronary sinus to minimize the potential sources of error which can be produced by intra-atrial delay.

Atrioventricular Node↗
PubMed1976

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Arrhythmias, Cardiac↗
PubMed1976

Effects of the pacing site on A-H conduction and refractoriness in patients with short P-R intervals.

His bundle recordings were studied in four patients with short P-R and A-H intervals, and narrow QRS complexes, who had experienced several episodes of supraventricular tachyarrhythmias. The heart was paced from the high right atrium (HRA) and the coronary sinus (CS). In three patients the A-H Wenckebach phenomenon occurred at higher rates (greater than 200 pacing beats/min) when the CS was paced than when pacing was performed from the HRA. Moreover, CS stimulation produced smaller increments in the A-H interval than did pacing from HRA. The extrastimulus method of testing was done. In cases 1 and 2 the functional refractory period of the A-H tissues was 15 to 25 msec shorter during CS pacing than when pacing from the HRA. In case 3, the low right atrium (LRA) as well as the other two sites were paced. A type 1 gap was seen from HRA, a type 2 gap from CS, and both types appeared when the LRA was paced. Case 4, in which the mid-right atrium (MRA) was also stimulated, had a double pathway from HRA and CS with conduction through the accessory pathway late in the cycle and through the A-V node earlier in the cycle. However, the A-V node could not be penetrated during MRA stimulation. It appeared that the pacing site influenced the A-H conduction pattern and refractoriness, possibly by changing the site and/or mode of entry of the stimulus into the pathways that are responsible for this syndrome.

Atrioventricular Node↗
PubMed1976

Re-entry due to manifest and concealed. His bundle ectopic systoles. Report of a case.

Concealed (C) His bundle ectopic systoles (H') have been shown in man to give rise to first and second degree atrioventricular (A-V) block and to simulate nonconducted atrial premature beats (P'). This report outlines a hitherto undescribed electrophysiologic consequence of H' in a 69-year-old man with arteriosclerotic heart disease and a Wenckebach type second degree A-V block in the His-Purkinje system. During a His bundle study, H' were shown to conduct either to the atria and ventricles with varying relationships to P' and QRS, or to conduct only to the atria, simulating nonconducted P' or atrial fusion beats. Both types of H' could initiate a re-entrant arrhythmia during retrograde conduction. Of particular interest are late coupled H' that failed to conduct to the ventricles and also failed to activate the atria because of prior capture by the sinus impulse (CH'). These CH' could also initiate re-entry by conducting retrogradely to engage the subatrial re-entry circuit. Evidence is presented to suggest re-entry occurs by way of a retrograde concealed accessory pathway and antegrade conduction in the atrioventricular node.

Aged↗
PubMed1976

The His-Purkinje electrocardiogram in man: an initial assessment of its uses and limitations.

A methodology is described for noninvasive recording of the electrical activity generated by the His-Purkinje system of man utilizing filtering, high amplification, and signal averaging. A waveform ranging between 1 and 10mu V was observed during the P-R segment. In many individuals, there was temporal overlap between the terminal P wave and the initial portion of the His-Purkinje waveform. In ten patients with long P-R intervals there was a strong correlation (r greater than 0.95) between the H-V time measured by electrode catheter and the duration of the His-Purkinje waveform. In two patients with atrial fibrillation the resultant His-Purkinje waveform was similar in morphology and duration to those observed in the ten patients. In each group H-V time was determined noninvasively and a waveform associated with electrical activation of the major portions of the His-Purkinje system was obtained.

Action Potentials↗
PubMed1976

Regional refractoriness within the ventricular conduction system. An evaluation of the "gate" hypothesis.

We studied the refractoriness of Purkinje fibers with the intent of localizing critical sites of block of premature impulses. To preserve the ventricular conducting system (VCS) nearly intact in vitro, we used a modification of the Elizari preparation. This was superfused with a physiologic salt solution. Action potential durations increased progressively from the His bundle to the distal Purkinje fibers along three pathways: (1) the main right bundle branch and moderator band; (2) the anterior border fibers of the left bundle and anterior false tendons; (3) the posterior border fibers of the left bundle and posterior false tendons. The action potential durations near the terminations of the false tendons were the longest ones found. The interior fibers of the left bundle branch had action potentials of shorter duration and greater variability than those of simultaneously activated fibers in the right bundle branch or the border fibers of the left bundle branch. Similarly, on the right side, the septal branches of the right bundle had action potentials of shorter duration than those of the moderator band. We also found that the fibers with short action potential durations provided the quickest pathways to septal myocardium. When extrastimuli were applied to the His bundle, block in a bundle branch always occurred in the proximal 1 or 2 cm of the main bundle branch. Experiments performed in vivo in which extrastimuli were delivered to the atrium or His bundle and recordings made from the terminations of false tendons and the distal ends of the main right bundle branch confirmed the finding that the critical sites of block were located in the proximal main bundle branches.

Action Potentials↗