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Biomedical subjects

N El-Sherif

Publications and source records attributed to N El-Sherif.

At least 73 records · Page 4Linked to original sources
PubMed1982

Noninvasive His Bundle electrogram: value of three vector lead recordings.

Studies were conducted in 45 patients to determine whether the reliability of the measurement of the His bundle potential from the body surface was increased by signal averaging of three simultaneously recorded electrocardiographic potentials from horizontal (X), frontal (Y) and sagittial (Z) axes as opposed to recording of any of these. Potentials from the X, Y and Z leads were amplified by 250,000, filtered between 80 hertz (12 dB/octave) and 200 hertz (24 dB/octave) and signal averaging of 1,000 beats was performed. The His bundle potential could be clearly defined in 25 of the 45 patients in the X, Y, or Z lead. His bundle potentials were evident in the X lead in 17 (68 percent) of these 25 patients, in the Y lead in 19 (77 percent) and in the Z lead in 11 (44 percent). No single lead gave satisfactory His bundle electrographic potentials in all patients. In 20 patients the His bundle electrogram could not be recorded because terminal atrial activity overlapped activity of the His bundle potential. The three lead system defined the His bundle potential in a significantly greater number of patients than did the best single lead because it (1) displayed the vectorial lead with the largest His bundle potential, (2) permitted validation of the His bundle potential in more than one lead, and (3) displayed the vectorial lead with the most isoelectric terminal P wave. It is concluded that reliable His bundle potential measurements are obtained in a significantly greater number of patients with use of the simultaneous three lead system than with use of any single lead.

Bundle of His↗
PubMed1982

Procainamide in the induction and perpetuation of ventricular tachycardia in man.

The effects of a single intravenous infusion of 750 mg of procainamide was studied in 12 patients with symptomatic chronic recurrent ventricular tachycardia in whom arrhythmias could reproducibly be initiated and terminated by programmed electrical stimulation of the heart. Sustained ventricular tachycardia was induced in 6 patients and non-sustained tachycardia was induced in the remaining 6 patients during control studies. Following procainamide (plasma level 10.3 +/- 3.7 mcg/ml), ventricular tachycardia could be induced in 10/12 patients, sustained in 4 patients and non-sustained in the remaining 6 patients. In 8/12 patients (66%), induction of ventricular tachycardia was facilitated as demonstrated by: (1) tachycardia zone was widened in 4 patients and was unchanged in another 3 patients; (2) non-sustained ventricular tachycardia was sustained ventricular tachycardia in one patient. the ventricular tachycardia had a faster rate and a different QRS morphology; (3) in 4 patients tachycardia was inducible with a lesser number of extrastimuli and/or by spontaneously occurring ventricular premature depolarization and; (4) increase of the number of induced ventricular responses of non-sustained ventricular tachycardia. In 4/12 patients (33%), procainamide abolished or modified the induction of ventricular tachycardia as demonstrated by: (1) inability to induce ventricular tachycardia in 2 patients; (2) narrowing of the tachycardia zone and conversion from sustained into non-sustained ventricular tachycardia (one patient) and; (3) decrease in the number of induced ventricular responses in one patient. The response to procainamide could not be predicted from rates of spontaneous ventricular tachycardia, induced ventricular tachycardia during control studies, degree of slowing of ventricular tachycardia or from prolongation of the coupling interval after procainamide. These results suggest that instead of abolishing the arrhythmia, procainamide in frequently employed doses in patients with chronic recurrent ventricular tachycardia can facilitate its initiation sometimes at even faster rates. Patients not responsive to the usual doses of procainamide should undergo acute drug trials to determine the optimal dose/drug levels.

Aged↗
PubMed1982

Ventricular activation patterns of spontaneous and induced ventricular rhythms in canine one-day-old myocardial infarction. Evidence for focal and reentrant mechanisms.

We studied isochronal maps of ventricular activation during spontaneous multiform ventricular rhythms (rates 120-190/min) and pacing-induced ventricular tachyarrhythmias (rate 230-450/min) in dogs 1 day after myocardial infarction. Recordings were obtained from the entire epicardial surface and from selected endocardial and intramural sites utilizing a computerized multiplexing technique. Spontaneous ventricular rhythms had a focal origin from the surviving subendocardial Purkinje network underlying the infarction and showed frequent shift of the pacemaker site. On the other hand, fast ventricular tachyarrhythmias were consistently induced in the same dogs by bursts of rapid ventricular pacing or programmed premature stimulation and had a tendency to degenerate into ventricular fibrillation. Pacing-induced rhythms were due to reentrant activation that developed mainly in the surviving, electrophysiologically abnormal, epicardial layer overlying the infarction. The last stimulated heat that initiated reentry resulted in a continuous arc of functional conduction block and two slowly circulating activation fronts around both ends of the arc of block. The activation fronts rejoined on the distal side of the arc of block 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 separate arcs. Reentrant activation subsequently continued as two synchronous circuits which conducted in clockwise and counterclockwise directions, respectively. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue and failed to advance. The presence of two synchronous circuits was the hallmark of a stable reentrant activation. The development of three or more asynchronous circuits resulted in an activation pattern that was "prefibrillatory." This pattern was seen to develop during pleomorphic ventricular rhythms and ventricular tachycardias of the torsades de pointes type that degenerated into ventricular fibrillation. Ventricular fibrillation was maintained by continuously changing multiple asynchronous circuits. The transition from a stable reentrant activation pattern to that of ventricular fibrillation was probably related to nonhomogeneous shortening of refractoriness in different parts of the myocardium.

Animals↗
PubMed1981

Effects of digitalis on the human sick sinus node after pharmacologic autonomic blockade.

To study the effects of digitalis on the sinus node and the mechanisms involved, 16 patients with the sick sinus syndrome had electrophysiologic assessment of sinus nodal function during (1) control study, (2) after pharmacologic autonomic blockade with propranolol (0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously), and (3) 10 minutes after 0.01 mg/kg of intravenous ouabain. The study was completed within 30 minutes of pharmacologic autonomic blockade. During the control study 50 percent of patients had an abnormal corrected sinus nodal recovery time or abnormal sinoatrial conduction time, or both. The effects of ouabain on sinus nodal function were compared with those after pharmacologic autonomic blockade. Ouabain significantly increased both intrinsic sinus cycle length (ouabain 975 +/- 194 ms [mean +/- standard deviation]; autonomic blockade 1,025 +/- 218 ms, probability [p] less than 0.001) and corrected sinus nodal recovery time (ouabain 615 +/- 503 ms; autonomic blockade 575 +/- 536 ms, p less than 0.05). In contrast there was no significant change in sinoatrial conduction time after ouabain (ouabain 141 +/- 56 ms; autonomic blockade 132 +/- 45 ms; difference not significant). The effects of ouabain were similar in patients with both normal and abnormal sinus nodal function. These findings suggest that (1) digitalis in therapeutic doses has a depressant effect on intrinsic sinus nodal automaticity in patients with normal as well as abnormal sinus nodal function; (2) digitalis has no significant effects on sinoatrial conduction; and (3) the effects of digitalis on sinus nodal automaticity are primary and independent of its vagal and antiadrenergic effects.

Aged↗
PubMed1981

Coexistence of sick sinus rhythm and atrial flutter-fibrillation.

A 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we could assess sinus node function by overdrive stimulation of the area of sinus node-activity. Sinus node function studied revealed an underlying sick sinus syndrome.

Atrial Fibrillation↗
PubMed1981

Canine ventricular arrhythmias in the late myocardial infarction period. 8. Epicardial mapping of reentrant circuits.

We made simultaneous recordings from 48 bipolar electrodes to obtain epicardial isochronal maps during induced ventricular arrhythmias in dogs 3-5 days after ligation of the left anterior descending artery. There was strong evidence of a reentrant circuit (RC) that was discernible largely on the epicardial surface in 21% of ectopic beats that were analyzed. Epicardial recordings were of limited value in analyzing the arrhythmia in other beats. The reentrant circuit consisted of an arc of conduction block around which the activation front advanced in a circular fashion at slow but uneven speeds while the rest of the ventricle was activated by radial spread. The arc of conduction block around which the RC was formed was usually functional in nature, since the same area of myocardium was excitable at relatively long cardiac cycle lengths. Both the length of the arc of conduction block which defines the length of the reentrant circuit and the degree of conduction delay were crucial factors for the occurrence of reentry. A premature beat that initiated reentry resulted in a longer arc of conduction block and slower conduction compared to one that failed to induce reentry.

Animals↗
PubMed1980

Myocardial infarction following acute aortic dissection.

Acute aortic dissection may present a clinical picture simulating myocardial infarction, including electrocardiographic changes. The mechanism underlying this mode of presentation has not heretofore been documented during life. We present here for the first time, a patient with acute aortic dissection and the clinical picture of acute myocardial infarction, where the mechanism of infarction has been demonstrated, by preoperative angiographic studies, probably to be due to compression of the extramural portion of the right coronary artery by the false channel of the dissecting hematoma.

Aortic Dissection↗
PubMed1980

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide.

UNLABELLED: Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anteriograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. IN CONCLUSION: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, oine for anterograde and the other for retrograde conduction.

Aged↗
PubMed1979

Ventricular pacing from the middle cardiac vein mimicking supraventricular morphology.

A case is described in which ventricular pacing from the middle cardiac vein produced an electrocardiographic pattern which mimicked the morphology of the normally conducted beats. The possible etiologies of this unusual phenomenon and its implications concerning the functional anatomy of the normal conduction system in the human heart are discussed.

Aged↗
PubMed1979

Reentrant ventricular arrhythmias in the late myocardial infarction period. 7. Effect of verapamil and D-600 and the role of the "slow channel".

Reentrant ventricular arrhythmias (RVA) were analyzed in dogs 3--7 days after ligation of the anterior descending coronary artery using averaged "composite" recordings of electrical activity of reentrant pathways (RP) from the epicardial surface of the infarction zone (IZ). Verapamil (V) and D-600 (D) (0.2--0.5 mg/kg i.v.) resulted in slight-to-moderate improvement of conduction in RP with abolition of spontaneous RVA and RVA initiated by premature depolarizations. The effect of V was not blocked by pretreatment with propranolol (0.5 mg/kg i.v.). Using a standard microelectrode technique and strips of epicardial muscle from the IZ, D (0.5--1 X 10(-6) g/ml) slightly improved the upstroke velocity and membrane responses of depressed ischemic cells. In contrast, tetrodotoxin (5 X 10(-7) g/ml) further depressed or abolished action potentials of ischemic cells. We conclude: 1) the moderate antiarrhythmic effect of V and D on RVA is the result of improved conduction in RP; 2) this action is partly explained by improvement of a depressed sodium channel and is not related to catecholamine release; 3) slow-response action potentials play no significant role in the genesis of ischemia-related RVA, which probably results from depression of the fast response.

Action Potentials↗
PubMed1978

Functional significance of electrocardiographic changes after left ventricular aneurysmectomy.

Electrocardiographic (ECG) changes after left ventricular aneurysmectomy were analyzed in 20 patients, thirteen of whom had additional aorto coronary saphenous vein bypass surgery. ECG changes were correlated with postoperative clinical and hemodynamic results. Out of 14 patients (Group I) who showed hemodynamic and/or clinical improvement, eight had decrease of chronic ST segment elevation that was associated in five with loss of pathologic Q waves. In the remaining six patients (Group II) who showed no hemodynamic or clinical improvement as well as in six patients in Group I, chronic ST segment elevation persisted or increased and in some, new pathologic Q waves developed after surgery. The study suggests that loss of pathologic Q waves and/or decrease of chronic ST segment elevation in patients who undergo a left ventricular aneurysmectomy with aorto coronary saphenous vein bypass surgery may reflect postoperative clinical, hemodynamic and angiographic improvement. On the other hand, failure of these ECG changes to occur or, conversely, increased ST segment elevation and/or appearance of new Q waves may have no predictive value. The mechanisms for these ECG changes are discussed.

Adult↗
PubMed1978

The significance of dissociation of conduction in the canine His bundle. Electrophysiological studies in vivo and in vitro.

Fractionated His bundle potentials were induced by ischemia or trauma in 30 anesthetized dogs, in vivo. Functional dissociation, i.e., alteration of the activation sequence of portions of these His bundle potentials was demonstrated in vivo as well as in 10 in vitro preparations of the His-Purkinje system. In vivo, plunge wire and electrode catheters were utilized to record from portions of the His bundle. During vagal-induced slowing of the heart rate, atrial pacing or His bundle pacing, His-Purkinje conduction as measured by the H-V interval was constant over a wide range of heart rates, 50-300/min. One or two hours after anterior septal artery ligation, His bundle damage manifested as split His bundle potentials (H, H'). Atrial pacing or proximal His bundle pacing induced H-H' delays with concomitant right or left bundle branch block patterns in ECG leads. However, distal His bundle pacing at comparable or even higher rates produced normal QRS complexes. In other cases, during atrial pacing or with progressive ischemia at a constant rate, H' progressively delayed during the H-V interval or even disappeared into the QRS complex with a concomitant occurrence of right or left bundle branch block. In vitro, a dissected septal preparation was studied containing the His bundle, proximal and distal right bundle and left bundle branches. Normal conduction throughout the His-Purkinje system was observed at pacing rates of 30-220/min. Punctate lesions, anatomically placed above the branching His bundle caused tachycardia-dependent, complete bundle branch blocked with concurrent temporal reversal of proximal and distal His bundle action potentials. These data suggest that ischemic or traumatic lesions in the His bundle may manifest on the electrocardiogram as bundle branch block patterns. From a clinical point of view, a critical site of lesion would markedly increase the liability for A-V blocked although the electrocardiogram alone would not indicate the actual site of lesion. Predestination of fiber tracts and alternative proposals to the pedestination theory are considered to explain QRS aberration due to exclusive His bundle lesions.

Action Potentials↗