His bundle electrocardiography in manifest and concealed right bundle branch extrasystoles.

His bundle electrocardiography was helpful in the diagnosis of impulse formation in the right bundle branch. Ten patients with narrow QRS complexes had ectopic beats with an "incomplete" left bundle branch pattern and almost simultaneous activation of His bundle and ventricles. Both QRS morphology and H- - V intervals depended on the more proximal or distal location of the ectopic focus. In four patients with "complete" right bundle branch block the morphology of ectopic ventricular complexes and H- - V intervals also depeneded on the presence or absence of retrograde block and differential degrees of forward and/or retrograde conduction delays. Nine patients with "complete" right bundle branch block and four with "complete" left bundle branch block had premature beats which could have originated in the proximal right bundle branch, proximal left bundle branch, or distal His bundle. In one patient with "complete" left bundle branch block, "concealed" His bundle depolarizations (probably originating in an ectopic focus located in the right bundle branch) produced pseudo Type II (Mobitz) A-V block. Although lidocaine appeared to have been more effective in patients with bundle branch block than in those with narrow QRS complexes, further studies are necessary to corroborate this impression.     

Anomalous origin of the left anterior descending coronary artery from the pulmonary artery

Three children were identified as having anomalous origin of the left anterior descending coronary artery (LAD) from the pulmonary artery (PA). Two had had congestive heart failure in infancy with clinical diagnosis of endocardial fibroelastosis and all had abnormal ECGs. The correct diagnosis was delayed in each case, and two patients required selective coronary angiography. Surgery was accomplished in the three children although ECG abnormalities have persisted and one child has dyskinesis of the left ventricular apex. Because this diagnosis may be difficult to make when intercoronary anastomoses are inadequate to outline the left anterior descending coronary flow into the PA, patients with clinical findings suggestive of anomalous coronary artery may require selective coronary studies to exclude this anomaly.     

Detection of pulmonary venous flow by pulsed Doppler echocardiography in children

Parasternal pulsed Doppler echocardiographic examinations of the left atrium were prospectively performed in 14 pediatric patients, aged 2 weeks to 8 years, in order to characterize the left atrial flow pattern in children. None of the patients had clinical or cardiac catheterization evidence (9 of 14 patients) of either mitral regurgitation, right-to-left shunts at the atrial level, or anomalies of pulmonary venous drainage. In all 14 patients, a systolic-diastolic positive velocity pattern could be recorded within the left atrium. Furthermore, this pattern was more readily detected in those children with left-to-right shunts. We conclude that continuous positive velocity patterns are commonly recorded in the left atria of children and probably represent pulmonary venous return. Demonstration of this signal is contingent on proper orientation of the transducer with respect to pulmonary venous flow.     

Effects of bundle branch block on experimental A-V reentrant tachycardia

The effects of bundle branch block on experimental A-V reentrant tachycardia (PSVT) were studied in 17 dogs using an anomalous pathway simulatory (APS). The APS was a programmable digital electronic circuit with ability for ventricular sensing, retrograde conduction with programmable conduction time, and atrial stimulation. Close bipolar electrodes were positioned at seven contiguous atrial and ventricular sites (V_l) along the A-V ring, these being; anterior, lateral, and posterior right (AR, LR, PR), septal (S), and posterior, lateral and anterior left (PL, LL, AL). Right (R) (seven dogs) and left (L) (10 dogs) bundle branch block (BBB) were produced with transcardiac needle. After BBB, cycle length (CL) of A-V reentrant PSVT was significantly increased only with ipsilateral sites. Thus, with RBBB, CL of PSVT increased by 37 ± 3 msec., 27 ± 3 msec., and 23 ± 4 msec. (P < 0.001), at AR, LR, and PR sites respectively. With LBBB, CL of PSVT increased only with left-sided sites. Thus, CL increased by 34 ± 2.6 msec., 38 ± 4.6 msec., and 32 ± 3.3 msec., (P < 0.001) with PL, LL, and AL sites, respectively. PSVT CL and septal site did not change significantly after either R or LBBB. The increase in CL was explicable in terms of corresponding increases in intraventricular conduction time (H-V_l). There were slight compensatory decreases in A-H intervals for the increases in H-V_l. These studies confirm findings suggested by clinical electrophysiological observation.     

Electrophysiologic effects of Tween 80 in the myocardium and specialized conduction system of the canine heart

Amiodarone, a wide spectrum antiarrhythmic agent, has been associated with hypotensive reactions in man as well as in dogs after intravenous use. This hypotensive effect has been attributed to Tween 80, the diluent in the commercially available form of amiodarone. We studied the electrophysiologic effects of Tween 80 in the cardiac conduction system of the dog. Electrophysiologic studies were conducted in anesthetized adult dogs before and after the administration of 10 and 20 mg/kg of Tween 80, equivalent to the amount of diluent in 5 and 10 mg/kg respectively of commercial intravenous amiodarone. In addition to a drop of 60% in systolic blood pressure and 66% in diastolic blood pressure (p less than 0.005), 10 mg/kg of Tween 80 induced a decrease in heart rate (sinus cycle length increased from 523 +/- 57 msec to 662 +/- 27 msec, p less than 0.025), prolongation of sinus node recovery time (652 +/- 77 msec to 804 +/- 45 msec, p less than 0.05), depression of AV nodal function manifested by induction of Wenckebach at longer cycle length (from 208 +/- 18 msec to 266 +/- 14 msec, p less than 0.005), and increase in atrial ERP (from 138 +/- 7 msec to 176 +/- 14 msec, p less than 0.025) and FRP (from 180 +/- 14 msec to 209 +/- 12 msec, p less than 0.025). No further significant changes were observed after the second Tween 80 dose. The ventricular ERP increased significantly (from 168 +/- 18 msec to 20 +/- 16 msec, p less than 0.025) following the 20 mg/kg dose. It is demonstrated that Tween 80 is a potent depressant of the cardiac conduction system in the dog, capable of causing electrophysiologic changes similar to those produced by amiodarone in humans and dogs.     

Effects of the pacing site in sinus node reentrant tachycardia.

His bundle recordings and premature atrial stimulation from coronary sinus, mid-right atrium and high-right atrium were performed in a patient with repetitive supraventricular tachycardias. Regardless of the paced site, there was a range of coupling intervals during which testing stimuli elicited short runs of premature beats. The corresponding P waves were positive in leads I, II and III and had a high-to-low right atrial activation sequence. Their morphology was similar to that of sinus beats. However, sustained tachycardia occurred only when pacing was performed from the coronary sinus. Therefore, it is postulated that the site of stimulation might be important in the genesis and (perhaps) perpetuation of this arrhythmia by changing the site and (or) mode of entry into the area where this type of tachycardia occurs. Though sinus node reentry was the most likely mechanism, it could not be determined whether the circuit involved the sinus node per se or the so called perinodal fibers.     

Restorative effect of epinephrine on the electrophysiologic properties of depressed human atrial tissue

The effects of epinephrine on the electrophysiologic properties of human right atrial tissue, obtained at cardiac surgery, were evaluated utilizing standard microelectrode techniques. In studies of electrophysiology, epinephrine had little effect on the resting membrane potential and transmembrane action potentials of normal atrial fibers. Epinephrine enhanced phase-4 depolarization and increased automaticity in normal fibers but hyperpolarized partially depolarized atrial fibers and decreased automaticity. The hyperpolarizing action of epinephrine resulted in a increase in action potential amplitude and dV/dt and enhanced conduction. Active force increased 40–230% in depressed tissues when exposed to epinephrine. Epinephrine-induced hyperpolarization of depressed atrial fibers may have a beneficial effect on atrial arrhythmias and depressed contractility encountered clinically.     

Site of functional right bundle branch block

An in vivo canine heart was prepared by utilizing a temporary right heart bypass system to place close bipolar electrodes along the course of the right bundle branch. Activation within the right bundle could be recorded in up to six locations along the right bundle with premature supraventricular stimulation that caused functional right bundle branch block. The loss of activation recordings was found to occur in the proximal 0 to 6 mm. of the right bundle branch in every instance and in nine different preparations.     

Effects of proximal intra-atrial Wenckebach on distal atrioventricular nodal, and His-Purkinje, block with special reference to the theory of alternating Wenckebach periods

Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.     

The R-on-T phenomenon during supraventricular tachycardia in childhood.

The electrocardiographic R-on-T phenomenon was observed in the absence of Wolff-Parkinson-White syndrome during recurrent episodes of supraventricular tachycardia (SVT) with rates between 240 to 275 per minute in a 5 year old boy. The rapid ventricular response during SVT corroborates the recent finding of a short refractory period of the A-V node in children. The demonstration of the R-on-T phenomenon in this child may be important in attempting to understand the pathogenesis of sudden death in children.     

Left ventricular hypertrophy in left bundle branch block

The detection of left ventricular hypertrophy (LVH) in the presence of left bundle branch block (LBBB) remains a difficult clinical problem. Its prevalence and significance have not previously been studied in a group of living patients. M-mode echocardiography was utilized to determine the prevalence of anatomic LVH in 28 patients with LBBB. Various ECG and chest x-ray criteria as predictors of LVH were assessed. Anatomic LVH was present in 89% by echocardiography. A left atrial abnormality on ECG and a cardio-thoracic ratio greater than .50 were the best predictors of LVH. Hypertension and/or ischemic heart disease was present in 78.5% of the patients while only one patient was free of any evidence of cardiovascular disease.     

Left isomerism and complete atrioventricular block: A report of six cases

Six children, aged 12 days to 13 years, with left isomerism and complete atrioventricular (A-V) block are presented. In all six patients the diagnosis of left isomerism was suggested by an interrupted inferior vena cava found during cardiac catheterization and angiocardiography;four patients had complex heart disease consisting of endocardial cushion defect, five had a common atrium, three had pulmonary stenosis, three had patent ductus arteriosus and two had dextrocardia. Further anatomic abnormalities included situs inversus of the viscera (four patients) as well as partial malrotation of the bowel. Of the six patients, four had congenital complete A-V block, whereas the remaining two had A-V conduction disturbances documented during early infancy that progressed to complete A-V block later in life. All six patients required pacemaker implantation and five of the six patients died. This report discusses the clinical presentation of complete A-V block and left isomerism and reviews the literature.     

Second degree His-Purkinje block during his bundle pacing

This report presents, for the first time, clear evidence supporting the occurrence of Wenckebach and 2:1 H-V block during His bundle pacing. The simultaneous recording of various intracardiac electrograms, as well as the comparison of the effects produced by selective His bundle pacing and high right atrial pacing at the same rates, permitted the identification of conduction disturbances located distal to the paced His bundle site. This could be done although one criterion usually required to diagnose selective His bundle pacing (namely, stimulus-V intervals of constant duration) was not present.     

Modulation of ventricular parasystole by extraneous depolarizations

The ectopic cycle length of a ventricular parasystole was influenced in a predictable fashion (modulated) by nonparasystolic beats. Although the interectopic intervals were not multiples of the ectopic cycle length (as in "classical" parasystole), the diagnosis could be established because: a) nonparasystolic beats falling during the first half of the cycle produced an 8-12% shortening of the ectopic cycle length; and b) nonparasystolic beats occurring during the second half of the cycle decreased the ectopic cycle length by 9-14%. The events occurring in this case are further proof that the classical criteria for the diagnosis of parasystole have to be reevaluated.     

Hemodynamics and intracardiac conduction after operative repair of tetralogy of Fallot

Electrophysiologic studies were performed in 47 children aged 3 to 18 years, 15 of whom had cardiac arrhythmias 1 to 15 years after repair of tetralogy of Fallot. Six exhibited sinus or atrioventricular nodal dysfunction, 8 had ventricular extrasystoles, and 1 had supraventricular tachycardia. Hemodynamic and electrophysiologic data were obtained at postoperative catheterization. Although electrophysiologic responses were abnormal in a proportion of both the children with and those without arrhythmia, hemodynamic values were similar. Three of 6 children with impaired sinus impulse generation or atrioventricular nodal conduction had a prolonged A-H interval, and in 3 Wenckebach heart block developed at low pacing rates. Ventricular ectopic rhythm was not associated with any particular abnormality of basic intracardiac conduction intervals. Thus, arrhythmias and conduction abnormalities are not consistently related to residual right ventricular hypertension. Abnormalities in electrophysiologic function are common after repair of tetralogy of Fallot in patients with sinus rhythm and may have prognostic implications for these patients.     

Abnormal quinidine binding in survivors of prehospital cardiac arrest

Quinidine binding was studied in 15 survivors of prehospital cardiac arrest and was compared to 18 normal individuals and 20 patients with coronary artery disease. The unbound quinidine fraction was 6.3 ± 2.8% in the survivors of prehospital cardiac arrest, a value significantly lower than normal individuals (unbound quinidine fraction = 9.9 ± 3.0%, p < 0.005). Furthermore, unbound quinidine fraction correlated with interdose quinidine half-life in the six survivors of prehospital cardiac arrest where this could be measured (r = 0.79, p < 0.05). The resultant quinidine interdose half-life was significantly prolonged (10 ± 3 hours) when compared to normal (6 ± 2 hours, p < 0.02). The reduction in free drug fraction in cardiac arrest survivors was a nonspecific finding in that free drug fraction was also reduced in the patients with coronary artery disease (unbound quinidine fraction = 7.4 ± 3%) and was independent of the α-1-glycoprotein concentration. Therefore survivors of prehospital cardiac arrest have a mean 40% reduction in free quinidine drug fraction which results in less free drug at any given total drug concentration and may relate to quinidine pharmacokinetics and pharmacodynamics in this patient group.