Search PubMed⌕ Search

Biomedical subjects

N El-Sherif

Publications and source records attributed to N El-Sherif.

At least 55 records · Page 3Linked to original sources
PubMed1984

Electrophysiologic effects and mechanisms of termination of supraventricular tachycardia by intravenous amiodarone.

Electrophysiologic studies were performed in nine patients with reentrant paroxysmal supraventricular tachycardia (PSVT) during a control period and following 5 mg/kg body weight of intravenous amiodarone (Cordarone, Labaz) administered as a slow continuous infusion over 15 to 20 minutes. All nine patients had induction of sustained PSVT during control studies. In seven of nine patients (group 1) the tachycardia was due to atrioventricular (AV) nodal reentry, and in two of nine patients (group 2) a concealed retrograde bypass tract was incorporated in the reentrant process. In group 1, following amiodarone, all seven patients lost the ability to sustain PSVT with either absence of atrial echoes (one patient) or induction of less than or equal to 3 echo beats (six patients) with termination of PSVT in the antegrade pathway (three patients) or retrograde pathway (two patients) or both (one patient). In group 2, following amiodarone, both patients lost the ability to sustain PSVT with absence of atrial echoes (one patient) on induction of a single echo beat (one patient) with block in the retrograde pathway (i.e., the concealed retrograde bypass tract). Amiodarone significantly increased (1) atrial cycle length for AV nodal Wenckebach block, (2) antegrade functional refractory period of the AV node, (3) antegrade effective refractory period of the AV node, (4) ventricular paced cycle length for ventricular atrial block, and (5) the retrograde functional refractory period of the ventricular-atrial conducting system.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Nonrandom occurrence of single-vessel coronary artery disease.

The location of obstructive coronary artery lesions in single-vessel disease is nonrandom. The circumflex coronary artery is protected relative to the right coronary artery. This may have important implications regarding the causation of coronary obstructive lesions.

Coronary Angiography↗
PubMed1984

Atrioventricular block. Mechanism, clinical presentation, and therapy.

The mechanism of AV block and bifascicular block and the role of His bundle electrocardiography in localizing the site of AV block are reviewed. The clinical presentation and therapy of the different types of AV block and the indications for permanent pacing are discussed.

Atrioventricular Node↗
PubMed1984

Reentrant ventricular arrhythmias in the late myocardial infarction period. II. Burst pacing versus multiple premature stimulation in the induction of reentry.

Isochronal maps of ventricular activation were analyzed in dogs 1 to 5 days after infarction utilizing a 64 channel multiplexer. Only dogs in which circus movement reentry could not be induced by a single premature stimulus were analyzed. Reentrant rhythms could be successfully induced equally by multiple (double or triple) premature stimuli and by burst pacing. Successive premature stimuli as well as successive beats during burst pacing resulted in progressively longer arcs of functional conduction block or slower circulating wave fronts, or both, that succeeded in reexciting myocardial zones on the proximal side of the arc of block to initiate reentry. However, for manifest reentry to be induced by burst pacing, the paced run had to be terminated after the beat that resulted in a critical degree of conduction delay. Otherwise, reentrant activation could be confined (concealed) by the subsequent paced wave front, which could also arrive earlier to the reentrant circuit zone of slow conduction resulting in block and interruption of reentry. Termination of a paced run after this beat would not result in reentry. If the paced run was extended past this beat, a new sequence of ventricular activation patterns characterized by progressively longer arcs of block or slower conduction, or both, developed again. The number of beats in a paced run that could initiate reentry varied with the cycle length of pacing, as well as in different experiments, and was difficult to standardize. It is therefore concluded that random burst pacing as a technique for induction of reentrant rhythms should probably be abandoned in favor of multiple premature stimulation.

Animals↗
PubMed1984

Effects of diltiazem on triggered activity in canine 1 day old infarction.

Triggered activity arising from a delayed after-depolarisation occurs in canine subendocardial Purkinje fibres 1 day following infarction. Standard microelectrode techniques were used to study small preparations (less than 50 mm2) in vitro. Diltiazem, 1 mg X litre-1, reversibly suppressed triggered activity by reducing maximum diastolic potential, action potential amplitude and the rate of depolarisation of the delayed after-depolarisation. Complete quiescence or exit block resulted. The effects of diltiazem were antagonised by elevating extracellular Ca ion concentration. These results suggest that automatic ectopic rhythms 1 day following myocardial infarction, that are the result of triggered activity, are dependent on transmembrane Ca ion movement which diltiazem can directly antagonise.

Action Potentials↗
PubMed1984

Asynchronized direct-current electrical energy causing acceleration of ventricular tachycardia.

Asynchronized direct-current (DC) shock was delivered inadvertently to a 67-year-old man with ventricular tachycardia. The electrical shock, which fell on the T-wave of the ECG, accelerated the tachycardia. A synchronized DC shock then converted the accelerated tachycardia to sinus rhythm. This case emphasizes the importance of synchronizing the electrical energy delivered during ventricular tachycardia.

Aged↗
PubMed1984

Recurrent pulmonary embolization following implantation of transvenous pacemaker.

A 44-year-old man developed recurrent pulmonary embolization after implantation of a permanent transvenous DVI pacemaker connected to polyurethane leads. Thrombus was found in the left innominate and subclavian veins around the pacemaker leads, but not in the right atrium or in the venous system of the pelvis and the lower extremities. The recurrence of pulmonary embolization followed discontinuation of treatment with Coumadin. This case demonstrates that lifelong anticoagulation is indicated in patients who have had pulmonary embolization and/or venous thrombosis around the pacemaker leads.

Adult↗
PubMed1984

Recording of diastolic slope with catheters during junctional rhythm in humans.

Junctional diastolic slopes were recorded in 11 of 15 patients (73.3%) with junctional rhythm that occurred spontaneously, after intravenous administration of atropine (1 mg), or during carotid sinus massage. The diastolic slopes were recorded through a unipolar lead consisting of a terminal of an electrode catheter placed in the His bundle area paired with an indifferent terminal on the superior vena cava. The slope of these diastolic deflections -0.18 +/- 0.06 m V/sec (mean +/- SD). Overdrive atrial and ventricular stimulations were followed by slowing of the junctional rate and decrease in the diastolic slope. Strong negative correlations (r values from -.71 to -.95) were found between the junctional cycle lengths and the diastolic slopes after atrial or ventricular pacing. Carotid sinus massage decreased the junctional rate and the junctional diastolic slope, whereas atropine increased the junctional rate and the junctional diastolic slope. Since prolongation of junctional cycle lengths after atrial pacing did not depend on frequency of impulse penetration into the His bundle, we postulate that the junctional pacemaker responsible for the junctional rhythm in some of our patients was in the N region of the AV node. Application of this recording method should help in the identification and characterization of automatic junctional pacemakers.

Aged↗
PubMed1984

Programmed electrical stimulation in patients with high-grade ventricular ectopy: electrophysiologic findings and prognosis for survival.

The significance and treatment of ventricular premature beats (VPBs) in patients without sustained ventricular tachycardia (VT), sudden death, or syncope remains unclear. We undertook a prospective study of programmed electrical stimulation (up to two extrastimuli and burst pacing) in 73 patients (age 60 +/- 10 years) with high-grade VPBs who had no evidence of sustained VT, sudden death, or syncope as determined by 48 hr of monitoring in the cardiac care unit and 48 hr Holter monitoring. Fifty-six patients (76.7%) had atherosclerotic heart disease, 10 (13.7%) had cardiomyopathy or valvular heart disease, and seven (9.6%) had no evident heart disease. Thirty-seven patients (50.7%) had Lown grade IVB VPBs, 30 (41.1%) had Lown grade IVA VPBs, and six (8.2%) had Lown grade III VPBs. Programmed electrical stimulation identified two groups of subjects: group 1 comprised 20 patients (27%) in whom VT or ventricular fibrillation was induced, group 2 comprised 53 patients (73%) in whom no ventricular arrhythmia or only two to four repetitive ventricular responses were induced. There was a significant difference between the presence of atherosclerotic heart disease, old myocardial infarction, and ejection fraction of less than 40% in group 1 compared with group 2. However, there was no significant difference in the grade of VPBs between the two groups. Seventeen of 20 patients from group 1 were placed on antiarrhythmic therapy (defined by programmed electrical stimulation), whereas group 2 patients were randomly assigned to prophylactic antiarrhythmic therapy. A total of 70 patients were followed up for 30 +/- 15 months. The incidence of sustained VT and/or sudden death (31.5% vs 2%; p less than .001) was significantly higher in group 1 compared with group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Appraisal of a Low Noise Electrocardiogram.

Two low noise electrocardiographic systems were designed to record low amplitude His-Purkinje potentials in the PR segment and delayed depolarization potentials in the ST-T segment from the body surface on a beat to beat basis. In one system, a bipolar electrode was utilized and the noise level was optimally reduced to 2 to 2.5 microV by a combination of noise reduction techniques. In the second system, better noise reduction (1 to 1.5 microV) was achieved by utilizing spatial averaging from 16 pairs of electrodes and a specially designed volume conductor electrode. The low noise electrocardiogram using the volume conductor electrode identified the His-Purkinje potential (up to 6 microV in amplitude) in 43% of patients compared with 71% recorded in the signal-averaged electrograms from the same patients. However, in contrast to the signal-averaged electrogram, only the low noise electrocardiogram could identify the His-Purkinje potential when moment to moment dynamic changes of the temporal relation of the P wave and QRS complex occurred. On the other hand, the low noise electrocardiogram recorded low amplitude, late diastolic potentials in the ST-T segment of postinfarction patients who showed a propensity to develop ventricular tachyarrhythmias. The diastolic potentials either: 1) remained constant in successive sinus beats, 2) varied in configuration, amplitude and timing in successive sinus beats, or 3) were only recorded in the diastolic interval preceding possible "reentrant" ventricular beats. The present study proves the feasibility of recording low amplitude His-Purkinje potentials and late diastolic potentials on the body surface on a beat to beat basis utilizing low noise electrocardiographic systems. Recording of late diastolic potentials on a beat to beat basis has the exciting potential of directly identifying malignant "reentrant" versus benign "focal" ventricular rhythms. However, the clinical relevance of these potentials remains to be established.

Adult↗
PubMed1983

Reentrant ventricular arrhythmias in the late myocardial infarction period. 9. Electrophysiologic-anatomic correlation of reentrant circuits.

We studied isochronal maps of ventricular activation during ventricular arrhythmias induced by programmed premature stimulation in dogs 3-5 days after ligation of the left anterior descending coronary artery. The entire epicardial surface and selective intramural sites were recorded using a computerized multiplexing technique. The electrophysiologic data were correlated with the anatomic characteristics of the infarction. In nine of 17 dogs (55%), the induced ventricular rhythm was due to reentrant activation in the surviving epicardial layer overlying the infarction. The irregular epicardial layer (up to 4 mm thick) had grossly intact myocardial fibers on microscopic examination but showed abnormal electrophysiologic characteristics. The stimulated premature beat that initiated reentry produced a continuous arc of functional conduction block within the surviving epicardial layer. The activation wave front circulated slowly around both ends of the arc of block, rejoined on the distal side of the arc before breaking through the arc to reactivate an area proximal to the block. This resulted in splitting of the initial single arc of block into two arcs. Reentrant activation continued as two synchronous circuits that traveled clockwise around one arc and counterwise around the other. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue, resulting in the coalescence of the two arcs of block into one. The present study may increase the understanding of the electrophysiologic mechanism of some ventricular repetitive responses and tachyarrhythmias induced by programmed premature stimulation in the clinical laboratory.

Animals↗
PubMed1983

Catecholamine-dependent atrioventricular nodal reentrant tachycardia.

An unusual case of atrioventricular nodal reentrant tachycardia precipitated by ethanol ingestion is presented. Programmed atrial and ventricular stimulation failed to induce the tachycardia during control conditions or after atropine administration. This failure to induce tachycardia was related to the absence of ventriculoatrial conduction. A low-dose isoproterenol infusion allowed induction of atrioventricular nodal reentrant tachycardia by the enhancement of ventriculoatrial conduction. This report suggests that programmed stimulation during isoproterenol infusion can be used to induce paroxysmal supraventricular tachycardia in suspected cases in whom induction during control conditions or after atropine administration is not possible.

Aged↗
PubMed1983

Reentrant ventricular arrhythmias in the late myocardial infarction period. Interruption of reentrant circuits by cryothermal techniques.

Both sustained and nonsustained ventricular tachycardias were reproducibly induced in dogs 3 to 5 days after ligation of the left anterior descending coronary artery. Isochronal maps of ventricular activation were constructed from close bipolar electrograms recorded from the entire epicardial surface and selected intramural sites by a computerized multiplexing technique. The electrophysiologic data were correlated with the anatomic characteristics of the infarction. The induced tachycardias were due to reentrant activation in the surviving epicardial layer overlying the infarction. Cooling or cryoablation was applied to localized epicardial sites along the reentrant circuit to reversibly or permanently interrupt reentrant activation. The reentrant circuit could be consistently interrupted when cooling or cryoablation was applied to the distal part of the common reentrant wave front proximal to the site of earliest reactivation. Localized cooling of the site of earliest reactivation usually failed to interrupt reentry because the common reentrant wave front reactivated other sites close to the original reactivation site. Before interruption of reentry, cooling resulted in characteristic changes in conduction of the reentrant wave front. The study (1) fulfills Mines' criteria that circus movement reentry is the mechanism of the induced rhythms in this canine experimental model and (2) identifies the critical site along the reentrant circuit at which cryothermal ablation (or surgical interruption) of reentrant activation could be successfully accomplished.

Animals↗
PubMed1983

Triggered ventricular rhythms in 1-day-old myocardial infarction in the dog.

Triggered activity developed in depolarized Purkinje fibers (maximum diastolic potential -59.3 +/- 9.9 mV) during superfusion with normal Tyrode's solution in 84% of subendocardial preparations from 1-day-old canine infarct. Triggered activity occurred when a delayed afterdepolarization attained threshold potential and spontaneously terminated after a subthreshold delayed afterdepolarization. Triggered activity was initiated either by stimulated beats or by the background slow Purkinje automaticity. When multiple stimulated beats were required, the amplitude of the afterdepolarization increased and the coupling interval decreased when the stimulation frequency and/or the number of stimulated beats increased. Varying degrees of entrance and exit block around sites of triggered activity were common, and some triggered activity manifested as a parasystolic rhythm. In preparations showing subthreshold delayed afterdepolarizations, both epinephrine (2.5 x 10(-6) M) and increasing [Ca++]o, (from 2.7 to 8.1 mM) increased the amplitude of afterdepolarizations and resulted in triggered activity. On the other hand, verapamil (2.2 x 10(-6) M) resulted in exit block around sites of triggered activity and/or completely suppressed afterdepolarizations and triggered activity. Isochronal mapping of endocardial activation during the initiation and perpetuation of triggered activity elucidated a focal site of origin from Purkinje fibers overlying the infarct and showed no evidence of a circus movement of excitation. The in vitro triggered activity may explain the spontaneous multiform ventricular rhythms seen in the intact heart.

Action Potentials↗
PubMed1983

Aortico-right ventricular shunt following aortic valve replacement.

A 58-year-old man developed cardiac decompensation following aortic valve replacement as a result of an aortico-right ventricular fistula. Serial hemodynamic and electrocardiographic changes are presented. Attention is drawn to this rare complication as a cause of hemodynamic deterioration following aortic valve surgery.

Aortic Diseases↗