Biomedical subjects
Publications and source records attributed to N El-Sherif.
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.
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.
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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.
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.
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.
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.
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.
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.
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.
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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.
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.
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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.
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.
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.