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Biomedical subjects

N el-Sherif

Publications and source records attributed to N el-Sherif.

At least 109 records · Page 6Linked to original sources
PubMed1987

Antiarrhythmic effects of oral indecainide in patients with ventricular tachyarrhythmias.

In order to assess the efficacy and safety of oral indecainide in patients with serious ventricular arrhythmias we studied 11 patients with high-grade ventricular ectopy and ventricular tachycardia (VT) which were refractory to therapy with at least one standard antiarrhythmic drug. Spontaneous arrhythmias were quantitated by 24-h Holter monitor before and during therapy with indecainide. Spontaneous VT was sustained in 4 patients and nonsustained in 7. Ten patients underwent baseline electrophysiologic study (EPS) and VT was induced in 9. The mean ejection fraction was 25 +/- 14%. Indecainide was given orally at a dose of 211 +/- 118 mg/day. The frequency of ventricular premature beats (VPBs) was significantly (greater than 85%) decreased in 90% of patients, while ventricular couplets frequency decreased in 78%. Spontaneous VT was abolished in 5 of 11 (45%). Sustained VT was induced in 5 of 7 (71%) patients who underwent follow-up EPS. The QRS duration was significantly prolonged during therapy (0.13 +/- 0.04 s) compared to control (0.10 +/- 0.02 s). The PR, QTc, and JTc intervals were not significantly changed. Indecainide was well tolerated, but 2 patients died of ventricular tachyarrhythmias while receiving the drug. Indecainide suppressed VPBs in a high percentage of patients, but was much less successful in controlling VT. Caution is necessary when using this drug because of its potential for exacerbation of arrhythmia.

Aged↗
PubMed1987

Reentrant ventricular arrhythmias in the late myocardial infarction period: 14. Mechanisms of resetting, entrainment, acceleration, or termination of reentrant tachycardia by programmed electrical stimulation.

The mechanisms of resetting, entrainment, acceleration, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post-infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure-eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachycardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefront could reach this zone in time for conduction block were: the cycle length of stimulation; the number of stimulated beats; and the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration, and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new balance of refractoriness and conduction velocity in the reentrant pathway. This could perpetuate the reentrant process at the shorter cycle length of the stimulated train and spontaneous reentry would resume on termination of the train (entrainment). The study provides better understanding of the mechanisms of action of programmed electrical stimulation on reentrant ventricular tachycardia.

Animals↗
PubMed1987

Signal processing options for detecting conduction abnormalities in ischemic ventricles.

Sources of error in averaging for late ventricular potentials include variations in the magnitude and timing of late potentials as well as variability in the temporal alignment of successive cardiac cycles during averaging. Since these errors can both attenuate high frequency signals and add artifactual components to the ECG, we developed methods to estimate and minimize them. Studies on patients indicated that small misalignments can obliterate high frequency components of the QRS, while broadening the low amplitude tail of the QRS, possibly leading to erroneous interpretations. The digital cross-correlation method of alignment was evaluated using simulated signals, and was shown to be relatively insensitive to gross variations in waveshape, and appeared to be less accurate than real-time pattern recognition schemes. A real-time alignment method based on a mathematical model was developed that could measure its accuracy, and was implemented in hardware. Our method improves alignment and average fidelity. Direct recordings from human and canine ventricles revealed that beat-to-beat variability in activation patterns of ischemic regions often followed a regular pattern such as 2:1 block. Spectral analysis of ECG recordings showed that a sub-harmonic, indicative of a 2:1 pattern, could be detected in the ECG during periods when ischemic regions of the ventricle were experiencing 2:1 block. These results suggest the possible utility of sub-harmonic analysis as a tool for detection of abnormal electrophysiological conduction.

Animals↗
PubMed1986

Catheter ablation for control of ventricular tachycardia: a report of the percutaneous cardiac mapping and ablation registry.

Catheter ablation of ventricular tachycardia is a procedure of last resort in critically ill patients. The Percutaneous Cardiac Mapping and Ablation Registry was able to collect data on 88 patients undergoing ablation of ventricular tachycardia foci. The mean following interval for the group was 10 +/- 8 months. Results were divided into three categories: Group I patients remained asymptomatic and were on no antiarrhythmic medications (33%); Group II remained asymptomatic and took antiarrhythmic agents (38%); Group III patients were considered unsuccessful and consisted of 29 percent of the total. More than one-third of patients received two shocks; the remainder received from one to five shocks. Overall mortality included four procedure-related deaths and total follow-up mortality was 25 percent. Catheter ablation for ventricular tachycardia should be undertaken only in highly specialized centers with an expert and experienced electrophysiologist with immediate surgical back-up available.

Adolescent↗
PubMed1985

Autonomic dependence of ventriculoatrial conduction.

To evaluate the effects of isoproterenol and atropine on patients with poor ventriculoatrial (VA) conduction, 17 patients were studied who did not have 1-to-1 VA conduction during ventricular pacing at a rate slightly faster than sinus rate (group I) and 11 patients were studied who had 1-to-1 VA conduction, but only at constant ventricular pacing cycle lengths longer than 600 ms (group II). Isoproterenol infusion at a rate causing a 20 to 30% increase in sinus rate or up to 4 micrograms/min shortened the ventricular pacing cycle lengths that induced VA block in all group II patients. Atropine administration at a dose causing a 20 to 30% increase in sinus rate or up to a total dose of 2 mg also shortened the ventricular pacing cycle lengths that induced VA block in all group II patients. At similar pacing cycle lengths, isoproterenol and atropine induced shorter VA intervals than control. Nine of 17 group I patients had demonstrable 1-to-1 VA conduction either during isoproterenol infusion or after atropine administration. Of these 9 patients, 1-to-1 VA conduction could be found only during isoproterenol infusion in 3 patients and only after atropine administration in 4 patients. The improvement of VA conduction by these drugs was related to their effects on the atrioventricular node. The change in VA conduction mediated by autonomic changes induced by these drugs may explain why some patients without demonstrable VA conduction during rest may have, under certain circumstances, "endless-loop" tachycardia or paroxysmal supraventricular tachycardia using atrioventricular nodal conduction as the retrograde limb.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The radiographic appearance of arterial sheath kinking.

A case of arterial sheath kinking is reported. Radiographically, sheath kinking has some features which mimic sheath fracture. The radiographic appearance of sheath kinking is, however, distinctive and clearly separable from sheath fracture, the hallmark of which is extravasation of contrast at the fracture site.

Angioplasty, Balloon↗
PubMed1985

Effect of labetalol on exercise tolerance and double product in mild to moderate essential hypertension.

Maximal exercise capacity after control of resting blood pressure with labetalol was studied in nine hypertensive men aged 34 to 69 years (average 52 years). Subjects exercised to exhaustion on an upright cycle ergometer with workload increased as a step function by 25 watts every three minutes, both before and after control of blood pressure was obtained. Mean exercise capacity expressed as total time of exercise until exhaustion was 936 seconds prior to control of the resting blood pressure and 884 seconds (no significant difference) after control of resting blood pressure with labetalol. Double product at peak exercise fell from 254 X 10(2) mm Hg beats per minute prior to blood pressure control to 183 X 10(2) mm Hg beats per minute (p = 0.006) after control of blood pressure with labetalol. The difference in the means of resting heart rate and both peak blood pressure and peak heart rate with exercise were all statistically significant after control of blood pressure with labetalol. These findings suggest that labetalol has an ideal exercise profile affording a cardioprotective effect by decreasing double product but without sacrificing exercise capacity.

Adult↗
PubMed1985

Reentrant ventricular arrhythmias in the late myocardial infarction period. 12. Spontaneous versus induced reentry and intramural versus epicardial circuits.

One to 5 days after one-stage ligation of the left anterior descending coronary artery in dogs, reentrant excitation can be induced by programmed premature stimulation in the surviving electrophysiologically abnormal, thin epicardial layer overlying the infarct. In experiments in four dogs, reentrant excitation occurred "spontaneously" during a regular sinus or atrial rhythm. A tachycardia-dependent Wenckebach conduction sequence in a potentially reentrant pathway was the initiating mechanism for spontaneous reentrant tachycardias and was the basis for both manifest and concealed reentrant extrasystolic rhythms. In all dogs showing spontaneous reentry, reentrant excitation could also be induced by premature stimulation at cycle lengths much shorter than those associated with spontaneous reentry, and induced reentrant circuits were always different from those during spontaneous reentry. In two dogs, the reentrant circuit was located intramurally in close proximity to a patchy septal infarction. The study illustrates that irrespective of the anatomic localization of reentrant circuits (epicardial or intramural), their dimension (large or small) or their mechanism of initiation (programmed premature stimulation or "spontaneous"), reentrant excitation always occurred in a figure 8 configuration (or a modification thereof). The figure 8 model, rather than the ring model or the leading circle model, may be the common model of reentry in the mammalian heart.

Animals↗
PubMed1985

Late potentials and arrhythmogenesis.

There are three current prognostic indicators of ventricular electrical instability: categorization and stratification of spontaneous ventricular arrhythmias from standard ECG recordings; programmed electrical stimulation; direct recording of delayed depolarization potentials, usually referred to as late potentials. Of the three, the latter offers a new and promising approach. Late potentials represent delayed activation potentials of diseased myocardial zones and may prove to be a strong independent marker of the propensity to develop reentrant ventricular arrhythmias and sudden cardiac electrical death. The problem in identifying late potentials on the body surface is that the signal is smaller than the electrical noise produced by various sources. Two different techniques have been utilized to improve the signal-to-noise ratio: first, signal averaging, which is applicable to regular repetitive electrocardiographic signals but cannot detect moment-to-moment dynamic changes in the signal; second, low-noise or high-resolution electrocardiography that utilizes spatial averaging techniques as well as other noise-reducing measures to record the late potentials on a beat-to-beat basis. This technique has the potential of directly identifying malignant "reentrant" versus benign "focal" ventricular rhythms. The present report discusses the electrophysiologic basis of late potentials and the clinical results of both signal-averaged and low-noise recordings for evaluation of ventricular electrical instability, particularly in patients with ischemic heart disease.

Aged↗
PubMed1985

Quantitative analysis of the high-frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: a prospective study.

We performed a prospective study of the high-frequency components of the terminal portion of the QRS complex in 50 patients with acute myocardial infarction (AMI) (mean age 63 +/- 10 years) within 3.25 +/- 2.45 days of the acute event. Signal averaging (400 beats) at a filter setting of 80 to 300 Hz was performed and the duration of the low-amplitude signals of less than 40 microV in the terminal portion of the QRS, the root-mean-square (RMS) voltage of the terminal 40 msec of the QRS complex, and the total duration of the signal-averaged QRS vector complex were measured. The low-amplitude signals were abnormally prolonged in 22 of 50 patients (44%); the RMS-V was abnormal (less than 20 microV) in 21 of 50 patients (58%), and the signal-averaged vector complex was abnormal (greater than 120 msec) in 15 of 46 patients (33%) without bundle branch block. There was no significant correlation between any of the signal-averaged parameters and site of AMI or total creatine kinase (CK) and CK-MB values. On the basis of the occurrence of spontaneous ventricular tachycardia in the acute and postcoronary care phase of AMI, the patients were divided into two groups. Group I consisted of 31 patients (62%) who had no documented ventricular tachycardia and group II consisted of 19 patients (38%) who had one or more runs of ventricular tachycardia. Fourteen of the 19 patients in group II (73.6%) had nonsustained ventricular tachycardia and five patients (26.3%) suffered sustained ventricular tachycardia/ventricular fibrillation or sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Reentrant ventricular arrhythmias in the late myocardial infarction period in the dog. 13. Correlation of activation and refractory maps.

Isochronal maps of ventricular activation were analyzed in dogs 3-5 days after ligation of the left anterior descending coronary artery utilizing a 64-channel multiplexer. Isochronal maps of the effective refractory period were determined from 62 epicardial sites and correlated with the activation maps. The ischemia occurring in the surviving epicardial layer prolonged refractoriness in a spatially nonuniform manner. The resulting pattern of refractoriness on the epicardial surface resembled concentric rings of isorefractoriness which increased in duration from the normal zone to the center of the ischemic zone. The formation of an arc of functional unidirectional conduction block occurred along the gradient of refractoriness and the exact location of the arc depended on the S1-S2 interval. When a short S1-S2 failed to induce reentry, fewer adjacent sites with sufficiently disparate refractoriness formed a smaller arc of block. A subsequent S3 encountered further nonuniformly shortened refractoriness (normal areas had shortened refractoriness greater than ischemic areas) and the arc of block was lengthened. This required a longer time for the wavefront to circulate around the arc. When it then reached the distal side of the arc, refractoriness had expired proximal to the arc and reentry occurred. Similarly, nonuniform shortening of refractoriness explained why one reentrant beat may or may not produce successive reentrant beats. Therefore, the spatial pattern of refractoriness forms the substrate for the arc of unidirectional conduction block that is fundamental to the development of ventricular reentry in this experimental model.

Animals↗