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Biomedical subjects

E N Moore

Publications and source records attributed to E N Moore.

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

Electrophysiologic studies on atrioventricular nodal Wenckebach cycles.

Wenckebach cycles with a 4:3 ratio, produced by rapid atrial pacing, were studied in 27 anesthetized denervated dogs using programmed stimulation. A test stimulus (S') could be inserted after any preselected beat of the Wenckebach cycle. An on-line computer measured the atrial (A) to His bundle (H) intervals. In all dogs a progressive increase in atrioventricular (A-V) nodal refractoriness was seen in the effective refractory period for each beat and a rightward shift of the A'-H' relative to the A-A' refractory curves. Atypical Wenckebach cycles could be produced by small changes in the basic cycle length. No evidence for reentry was found from the refractory curves of Wenckebach cycles and by interruption of stimulation after the third stimulus of a 4:3 Wenckebach cycle. Analysis of the A'-H' relative to the H-A' refractory curves did not confirm a positive feedback mechanism. In order to mimic a Wenckebach cycle, a blocked premature beat was inserted during stressed 1:1 conduction. The changes in the refractory curves for successive beats after the premature beat were rate-dependent and similar to those in Wenckebach cycles but smaller in magnitude. In Wenckebach cycles there is a progressive increase in refractoriness, caused by cumulative effect similar to that seen after a blocked beat during stressed 1:1 conduction, until block occurs and the cycle resets.

Animals↗
PubMed1978

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Adolescent↗
PubMed1978

The limitations of epicardial mapping as a guide to the surgical therapy of ventricular tachycardia.

The adequacy of intraoperative epicardial mapping as a guide to surgical procedures performed to terminate ventricular arrhythmias was investigated. Ligation of the anterior septal or left anterior descending coronary artery in 28 dogs produced ventricular arrhythmias that were studied 24-36 hours following occlusion. The sites of origin of 26 tachycardias were determined to be in the subendocardium by using extensive epicardial, endocardial and intramural mapping techniques and were verified by demonstrating unaltered activation sequences during pacing from these earliest sites. Epicardial breakthrough followed earliest directly recordable ventricular activity by as little as 7 msec. Without endocardial mapping many of these tachycardias would have been incorrectly identified as originating in the fascicles or epicardium. The sites of epicardial breakthrough were anatomically distant from the sites of origin by a markedly varying extent (5mm to 6cm). Two rhythms might be close in their sites of earliest epicardial appearance yet distant on the endocardium or vice versa. We conclude that epicardial mapping may not be sufficient to identify or predict the origins of many ventricular tachycardias and that the success of surgery to abolish these arrhythmias may be enhanced by preoperative and intraoperative endocardial mapping.

Animals↗
PubMed1977

The origin of ventricular arrhythmias 24 hours following experimental anterior septal coronary artery occlusion.

The anterior septal coronary artery was acutely ligated in 16 open-chest anesthetized dogs to produce an infarct of the septal myocardium. Twenty-four hours following occlusion complete epicardial mapping and extensive plunge electrode recording techniques were used to localize the sites of origin and patterns of activation of the ventricular tachyarrhythmias that developed during recovery. The earliest electrical activity for 13 individual rhythms was recorded from surviving septal subendocardial Purkinje fibers at the margins of the infarct, in the right or left ventricle, directly underlying the sites of earliest epicardial breakthrough. The sites of origin were verified by demonstrating unchanged activation sequences during pacing through the electrode sites which recorded the earliest activity. None of the arrhythmias arose from the His bundle or bundle branches despite the fact that these tissues course directly through the necrotic septum. The data presented supports the hypothesis that ventricular arrhythmias occuring in the 24-36 hour post acute infarction period may originate in the surviving subendocardial Purkinje system. Our experimental model shows that in cases in which a malignant rhythm arises from a focus, whether it is due to enhanced automaticity or local re-entry, epicardial mapping alone may not identify the source of the arrhythmias. Extensive endocardial mapping may provide a more rational basis for surgical interventions designed to abolish these arrhythmias.

Animals↗
PubMed1976

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

In 12 anesthetized open-chest dogs, ventricular epicardial activation maps were constructed and electrograms were recorded from the bundle of His, left bundle branch, and subendocardial Purkinje fibers 24 hours following Harris 2-stage ligation of the left anterior descending coronary artery. All animals developed ectopic ventricular depolarizations and/or ventricular tachycardia. The earliest area of epicardial activation was located along the border of the infarct in the left ventricle in all animals. Bipolar recording from various levels of the conduction system and ventricular myocardium revealed that the earliest recorded electrical activity originated in subendocardial Purkinje fibers which had survived the acute myocardial infarction. The origin of these arrhythmias was further studied by pacing through the electrode which had recorded the early Purkinje activity and comparing the surface ECG and activation sequence with that of the spontaneous rhythm. These data tend to support the hypothesis that ventricular arrhythmias occurring 24-72 hours following acute myocardial infarction have their origin in the subendocardial Purkinje network which has survived the infarction.

Animals↗
PubMed1975

Effects of aminophylline on the threshold for initiating ventricular fibrillation during respiratory failure.

Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.

Acid-Base Equilibrium↗
PubMed1975

Intraventricular conduction in man studied with an endocardial electrode catheter mapping technique. Patients with normal QRS and right bundle branch block.

The sequence of intraventricular conduction has been studied in a total of 60 patients, 38 of whom had normal QRS morphology and 37 of whom had right bundle branch block (RBBB) either present continuously or produced as functional aberrant RBBB by the introduction of atrial premature depolarizations or by rapid atrial pacing. Activation times were measured by intracardiac electrode catheters positioned at the right ventricular inflow tract (RVIT), right ventricular apex (RVA), right ventricular outflow tract (RVOT), left ventricular apex (LVA) and left ventricular outflow tract (LVOT). The activation after beginning of QRS in milliseconds plus or minus 1 SD and the number of patients studied at each location were: RVIT--normal 23 plus or minus 13 (15 patients); RVIT-RBBB 49 plus or minus 16 (15 patients); RVA--normal 18 plus or minus 9 (28 patients); RVA-RBBB 54 plus or minus 16 (30 patients); RVOT--normal 40 plus or minus 10 (28 patients); RVOT-RBBB 78 plus or minus 21 (30 patients);LVA--normal 9 plus or minus 9 (18 patients); LVA-RBBB 6 plus or minus 10 (10 patients); LVOT--normal 45 plus or minus 13 (10 patients); LVOT-RBBB 32 plus or minus 9 (7 patients). Significant differences observed were: RVA-normal versus RVA-RBBB P smaller than 0.001; RVOT-RBBB P smaller than 0.001; RVA-normal versus LVA-normal P smaller than 0.005; LVA-normal versus LVA-RBBB NS, LVOT-normal versus LVOT-RBBB P smaller than 0.05. The LVOT change was unexpected and suggests changes in left ventricular depolarization may occur when right bundle branch block develops. In patients with RBBB the activation of the RVA (r equals 0.82) and of the RVOT (r equals 0.68) was directly related to the duration of QRS. Changes in activation time when RBBB was induced by rapid atrial pacing or by introduction of atrial premature depolarizations were: RVA (7 patients) 19 plus or minus 11 to 56 plus or minus 16 (P smaller than 0.001); RVOT (9 patients) 41 plus or minus 10 to 77 plus or minus 22 (P SMALLER THAN 0.001); LVA (5 patients) and LVOT (2 patients), small insignigicant changes. These data indicate that endocardial activation changes can be evaluated in the catheterization laboratory, that right ventricular conduction becomes slower in RBBB as a direct function of total QRS and that left ventricular conduction may be affected when RBBB develops.

Action Potentials↗
PubMed1975

The differences in atrioventricular conduction of premature beats in young and adult goats.

Atrioventricular (AV) conduction was studied in anesthetized, open-chest, 1-35-day-old goats. Atrial, bundle of His, and ventricular bipolar electrograms were recorded, and the functional refractory periods of the AV conduction system and the ventricles were determined. Supraventricular premature excitation invaded the ventricles during their vulnerable period. This AV conduction property is different from that of the adult goat heart; thus, the existence of a lateral accessory bypass tract was investigated. Electrocardiographic leads I, aVF, and V10 revealed no delta waves indicative of ventricular preexcitation. Bundle of His electrograms showed that: (1) bundle of His excitation always preceded the onset of ventricular depolarization, (2) no shortening occurred in the bundle of His to ventricular activation time following early atrial premature beats, and (3) the functional refractory period of the AV node was less than that of the ventricle. The ventricular epicardial excitation sequence indicated no involvement of a lateral bypass tract in the AV conduction of basic or premature beats. Interruption of the bundle of His caused complete AV block. Therefore, no functional lateral accessory bypass tracts are present in the young goat heart, and the AV node and the ventricular specialized conduction system of the young goat are capable of conducting premature atrial excitation to the ventricles within plus or minus 10 msec of the expiration of the ventricular functional refractory period.

Animals↗