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Biomedical subjects

N El-Sherif

Publications and source records attributed to N El-Sherif.

At least 91 records · Page 5Linked to original sources
PubMed1978

Apparent malfunction of demand pacemakers due to spurious potentials generated by contact between two endocardial electrodes.

Malfunction of both temporary and permanent demand transvenous pacemakers was caused by contact between the two endocardial electrodes. Contact between these electrodes created spurious potentials which resulted in irregular inhibition of both demand units. The potentials were demonstrated by recording from the temporary wire. There was no interference with either pacemaker in the fixed rate mode and malfunction ceased when the temporary wire was removed.

Aged↗
PubMed1978

Atypical Wenckebach periodicity simulating Mobitz II AV block.

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a 'classical' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.

Aged↗
PubMed1978

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 5. Mechanism of action of diphenylhydantoin.

The mechanism of action of diphenylhydantoin (DPH) on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery utilizing direct recordings of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). DPH in a therapeutic dose consistently prolonged refractoriness of potentially RP in the IZ. This resulted in further impairment and/or block of conduction in the RP and was directly responsible for DPH ability to abolish RVA. On the other hand, DPH had no significant effect on conduction in the adjacent normal zone. Prior to abolition of RVA initiated by premature beats (PBs), DPH resulted in: 1) narrowing of the critical range of coupling intervals of PBs that resulted in re-entry (i.e., the re-entry zone), 2) shift of the narrowed re-entry zone to longer cardiac cycle lengths, and 3) lengthening of the coupling interval of the first re-entrant beat, as well as slowing the rate of re-entrant tachycardia. Thus DPH, similar to lidocaine, owes its antiarrhythmic action in RVS to its selective depressant effect on ischemic cells forming part of the RP.

Animals↗
PubMed1978

Normalization of bundle branch block patterns by distal His bundle pacing. Clinical and experimental evidence of longitudinal dissociation in the pathologic his bundle.

Clinical and experimental observations in which bundle branch block patterns (BBBP) in ECG leads were normalized by distal His bundle (H) pacing are reported. The clinical material includes four patients with acute right BBBP secondary to anterior wall myocardial infarction and three patients with chronic left BBBP. Six of the seven patients had a prolonged H-V interval (60-85 msec) including three who showed evidence of an intra-H conduction delay (IHCD) with split H (H and H'). Distal H pacing from a right-sided electrode catheter normalized the BBBP with a stimulus-to-QRS (PI-V) interval 20-35 msec shorter than the H-V interval and almost identical to the H'-V interval in the three patients with documented IHCD. In 18 dogs ligation of the anterior septal artery resulted in IHCF with split H associated with right or left BBBP. Distal H pacing from catheter and/or plunge wire electrodes normalized the BBBP in 12 experiments (67%) with a PI-V interval identical to the H'-V interval. H pacing was selective and direct stimulation of myocardium was excluded by monitoring the high ventricular septal electrogram. The clinical and experimental observations are discussed as evidence that functional longitudinal dissociation is probably only operative in the pathologic H due to selectively greater depression of conduction in the transverse interconnections.

Animals↗
PubMed1978

Reentrant ventricular arrhythmias in the late myocardial infarction period. 6. Effect of the autonomic system.

The effect of the autonomic system on conduction disorders in the infarction zone (IZ) and related reentrant ventricular arrhythmias (RVA) in the late myocardial infarction period in the dog was studied utilizing averaged recordings of the reentrant pathways from the epicardial surface of the IZ. Vagal (V) stimulation was found to have no significant direct electrophysiologic effect while sympathetic (S) stimulation resulted in a direct slight improvement of conduction in the IZ. However, because of the marked rate-dependency of conduction in the IZ, the effects of both V and S stimulation were modified through changes in the heart rate. The bradycardia produced by V stimulation resulted in improvement of conduction in the IZ and disappearance of RVA, while the tachycardia induced by S stimulation resulted in worsening of conduction in the IZ and the occurrence of RVA. Thus, in spite of its slight enhancing effect on conduction in the IZ, the propensity of S stimulation to induce RVA was primarily due to its tachycardiac effect.

Animals↗
PubMed1977

Continuous concealed ventricular arrhythmias.

Twenty dogs were studied 3 to 9 days after myocardial infarction. None had ventricular arrhythmias during sinus rhythm, and ventricular automaticity (as revealed by sinus nodal crush procedure or vagal stimulation, or both) was within the normal range. With regular atrial pacing or pacing with long-short cycle sequences it was possible to induce ventricular arrhythmias in all animals. Quadrigeminal and pentageminal rhythms (19 of 20 dogs) and trigeminal (17 of 20) and bigeminal ventricular rhythms (8 of 20) were observed. These rhythms which were manifest or partially or entirely concealed were always associated with delayed and fractionated electrical activity within the "infarcted" subepicardium. Continuous electrical activity (electrical activity that bridged the interval between two or more successive beats) was recorded from the infarct zone. Such activity either was manifest as ventricular arrhythmia during atrial pacing or remained concealed until atrial pacing was stopped and then was manifest as ventricular tachycardia.

Animals↗
PubMed1977

Coronary artery aneurysms: study of the etiology, clinical course and effect on left ventricular function and prognosis.

Coronary artery aneurysms were found in 16 men between 37 and 62 years of age, mean 51 years. Aneurysms were of two types: saccular and fusiform. They involved the right coronary artery in 13 (87 per cent), the circumflex artery in eight (50 per cent) and the left anterior descending artery in five (31 per cent). In some patients, more than one vessel was involved. Twelve patients presented with angina pectoris, three with congestive heart failure and one with both. Five were in functional class II, eight were in class III and three were in class IV at the beginning of the study. The electrocardiogram showed evidence of previous myocardial infarction in four patients; four patients had left ventricular hypertrophy, one had left axis deviation, one had left bundle branch block, one had right bundle branch block, two had first degree atrioventricular block and seven had abnormalities in the S-T segment and T wave. Obstructive coronary disease was present in all; the obstruction score was from 1 to 4 in three patients, from 5 to 9 in four patients and from 10 to 14 in the remaining nine. Similar aneurysms were found in the pulmonary artery of one patient and in the abdominal aorta of three patients; in seven of 14 patients with adequate venous angiograms, varicosities of the coronary venous tree were observed. Left ventricular dysfunction and angina pectoris were noted in patients with significant obstructive coronary disease (greater than 70 per cent) and also in patients without obstruction but with coronary aneurysms. Ten patients were treated surgically; nine underwent aortocoronary bypass and one mitral valve replacement. Criteria for bypass was the presence of obstructive disease and medically unresponsive angina pectoris. All but one surgically treated patient showed improvement. The functional class in medically treated patients was unchanged. Fourteen patients were still alive at the completion of the study. The findings of this study suggest that angina pectoris and left ventricular dysfunction can occur with coronary artery aneurysm without coronary artery obstructions. Coronary aneurysms may be a subset of atherosclerosis, and this process may involve other vascular territories. The prognosis in those patients appears to be no worse than in patients with obstructive coronary disease and no aneurysms.

Adult↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 1. Conduction characteristics in the infarction zone.

Dogs 3-7 days following ligation of the anterior descending coronary artery representing a remarkably stable model for re-entrant ventricular arrhythmias (RVA) and allowed detailed electrophysiologic studies of the re-entrant mechanism. In these dogs, we could regularly illustrate the presence of continuous electrical activity originating from the infarction zone (IZ) and bridging the diastolic interval between the initiating and re-entrant beats as well as between consecutive re-entrant beats. Conduction in the IZ was highly complex, with multiple potentially re-entrant pathways, functionally dissociated areas, and areas of localized ventricular fibrillation. Conduction disorders in ischemic myocardium were consistently tachycardia-dependent with the spontaneous onset of RVA specifically associated with a Wenckebach-like conduction pattern in a potentially re-entrant pathway. Both manifest and concealed re-entry, as well as re-entrant beats with regular extrasystolic grouping, constant or variable coupling, uniform multiform and bidirectional QRS configurations, were related to characteristic conduction patterns in the IZ. In summary, the study provides the first direct in vivo evidence of ventricular re-entry and demonstrates propensity for RVA and sudden death in the late myocardial infarction period.

Animals↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 2. Patterns of initiation and termination of re-entry.

The electrophysiologic mechanisms for the initiation and termination of re-entrant ventricular arrhythmias (RVA) were critically analyzed in dogs 3-7 days following ligation of the anterior descending coronary artery, utilizing direct recordings of the re-entrant pathway (RP) from the epicardial surface of the infarction zone. Re-entry could occur during a regular cardiac rhythm if the heart rate is within the narrow critical range during which conduction in a potentially RP exhibits a Wenckebach-like (W) pattern with a beat-to-beat increment of conduction delay until the activation waveform is sufficiently delayed to re-excite normal myocardium. If a regular cardiac rhythm is associated with limited conduction delay in a potentially RP, premature beats within a critical range of coupling intervals could result in sufficient conduction delay to induce re-entry. Re-entrant ventricular arrhythmias may be unmasked on abrupt termination of a critical fast rate of cardiac pacing only if pacing was terminated during those beats of a W pattern associated with marked conduction delay in a RP. RVA could be ended by one or more properly timed premature beats that would pre-excite part of the RP. An electrophysiologic mechanism for R-on-T and its relationship to onset of ventricular fibrillation was shown, based on markedly delayed RP conduction of the beat prior to the one apparently coupled to the premature beat.

Animals↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 3. Manifest and concealed extrasystolic grouping.

Re-entrant beats with regular extrasystolic grouping were seen in 44- of dogs 3--7 days following ligation of the anterior descending coronary artery. Utilizing direct recording of the re-entrant pathway (RP) from the epicardial surface of the infarction zone, we found extrasystolic grouping to be based on the infarction tachycardia-dependent conduction disorders in a potentially RP. Trigeminy and quadrigeminy were related, respectively, to a 3:2 and 4:3 Wenckebach-like conduction cycle in a RP. However, quadrigeminy could also be due to an underlying bigeminal rhythm with concealment of alternate re-entrant beats, i.e., concealed bigeminy. A bigeminal rhythm was the result of a 2:1 conduction pattern in a re-entrant pathway with a sufficient degree of conduction delay during the conducted beat of the 2:1 cycle to result in re-entry. A trigeminal or quadrigeminal rhythm could change to a bigeminal rhythm on critical shortening of the cardiac cycle. Fixed and variable coupling were related, respectively, to stable and changing conduction pattern in a re-entrant pathway. On the other hand, extrasystolic grouping could be concealed due to either block in the re-entrant pathway or entrapment in a small area of the closely bordering normal zone.

Animals↗
PubMed1977

Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine.

The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed.

Animals↗
PubMed1977

Second-degree atrioventricular block in the His-Purkinje system following acute myocardial infarction. Clinical observations on its evolution.

The evolution of second-degree atrioventricular block in the His-Purkinje system was studied in four patients with acute myocardial infarction, utilizing continuous electrocardiographic monitoring and serial His bundle recordings. Three patients had anterior wall infarction; all developed acute right bundle-branch block and two also showed a left anterior hemiblock one to four hours prior to onset of second-degree atrioventricular block. The fourth patient had an old anteroseptal infarction and chronic right bundle-branch block and left anterior hemiblock; he developed second-degree atrioventricular block following an acute lateroposterior infarction. His bundle electrograms were obtained during the insertion of a temporary ventricular pacemaker within the first 24 hours of onset of chest pain. A second His bundle electrogram was obtained during removal of the temporary paceemaker 7 to 14 days after the first recording. In all cases the block was localized in the His-Purkinje system. In three patients the first His bundle recording showed second-degree atrioventricular block with minimal increment of delay in conduction (3 to 10 msec) prior to the blocked beat (equivalent of Mobitz type 2 block). The second His bundle electrogram showed the development of significant increment of delay in conduction (35 to 210 msec) prior to block (equivalent of Wenckebach conduction). The fourth patient illustrated the reverse order of the observations seen in the other three. Three patients showed resumption of 1:1 atrioventricular conduction; however, when one patient was challenged with rapid atrial pacing, he developed repetitive block in the His-Purkinje system.

Aged↗
PubMed1977

Long-term clinical and hemodynamic studies after ventricular aneurysmectomy and aorta-coronary bypass.

Late clinical and hemodynamic evaluations in 18 patients with ventricular aneurysmectomy and aorta-coronary bypass are presented. Tne patients had significant obstructive lesions in two major vessels (55 per cent), and 6 had extensive three vessel disease (33 per cent). In 13 patients, 21 aorta-coronary saphenous bypass grafts were performed in addition to aneurysmectomy. The operative mortality rate was 11 per cent. One patient died suddenly 5 months after the operation (one year mortality rate 17 per cent). The 15 surviving patients have been followed up for 12 to 41 months (average 24 months). Clinical results were considered excellent in 2 patients who have been asymptomatic (Class I, N.Y.H.A.). Nine others were considered to have good clinical results (Class II). Five patients have continued to have congestive heart failure and angina on minimal effort (Class III or IV). Six of the 11 patients considered to have excellent or good results underwent postoperative hemodynamic studies 6 to 34 months after the operation. A significant increase in cardiac index was documented in all 6 patients. Paradoxic movement was not detected in any of the postoperative ventriculograms. Five of the seven venous grafts inserted were patent. Elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index, and a persistent dyskinetic area in the left ventricle were found in 2 patients considered to have poor clinical results. Clinical and hemodynamic evaluations have shown a significant improvement in most patients surviving ventricular aneurysmectomy. However, postoperative systemic embolism, myocardial infarction, progression of coronary artery disease, transient cerebral ischemic attacks, graft occlusion, arrhythmias, and mitral regurgitation in previously prolapsed mitral valve leaflets account for progressive disability and limited activity after a successful operation.

Adult↗
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↗