Conduction disturbances in the middle internodal tract of the rabbit heart

Conduction properties between the sinus node and the septal branch of the crista terminalis, the so-called middle internodal tract, were studied in the isolated rabbit right atrium. Recordings were obtained from two simultaneously impaled microelec-trodes using the extrastimulation technique after cutting the anterior and posterior internodal tracts. Several types of conduction block were observed associated with steplike prepotentials and distortions of perinodal fibers in the absence of pharmacological intervention. Prolongation of sino-septal conduction time occurred with decreasing coupling intervals. The return cycle of the atria gradually increased with prolongation of the retrograde conduction time of premature impulses to the SN until entrance block was seen. Several observations in this data demonstrate the influence of concealed or manifest retrograde conduction into the perinodal fibers of the sinus node after premature stimulation of the atria, as critical delay within the perinodal region could alter conduction time of the premature depolarization, reset the sinus node, and influence subsequent antegrade conduction alone or in various combinations.     

Parathyroid activity and bone formation.

Patients of both sexes with primary hyperparathyroidism showed increments in the total subperiosteal diameter and the medullary cavity diameter of the second metacarpal bone. When two groups of females of similar age were compared, those with hyperparathyroidism had significantly greater total metacarpal area and medullary area than that of hypoparathyroid patients. An increased subperiosteal apposition has therefore been found in primary hyperparathyroidism. This might be due to a direct stimulation of PTH on bone formation at the subperiosteal surface or to a nonspecific compensatory response to endosteal resorption.     

Efficacy of amiodarone during long-term treatment of potentially dangerous ventricular arrhythmias in patients with chronic stable ischemic heart disease

Amiodarone was administered orally to 30 patients with chronic stable coronary artery disease and severe ventricular arrhythmias. Control studies revealed frequent (more than 30/hr) ventricular premature beats (VPBs) (27 patients), bigeminy (21 patients), couplets (29 patients), R-on-T phenomenon (14 patients), ventricular tachycardia (16 patients), and ventricular fibrillation (1 patient). Two 24-hour Holter recordings and stress tests were performed before treatment, and an average of 3.6 per patient were done during treatment. Amiodarone caused suppression of all ventricular arrhythmias in 13 (43%) of the 30 patients and suppression of all complex forms and greater than 90% reduction of VPB number in 14 patients (47%) during a follow-up of 12.4 months. The mean dose was 590 mg/day in the 27 responders and 300 mg/day in the three nonresponders. A similar antiarrhythmic response was observed during stress testing. One of the 30 patients died due to massive pulmonary embolism and no arrhythmias were detected. In addition, amiodarone suppressed the occurrence of anginal pain and effort-induced ST changes in 9 of 10 patients and in 11 of 13 patients, respectively. The rate—pressure product and peak heart rate were significantly reduced in all patients. Our results suggest that amiodarone may be ideally suited for treatment of ventricular arrhythmias and for possible prevention of sudden death in patients with ischemic heart disease.     

Conduction system examination in a case of spontaneous heart block in a dog

This is a serial-section study of the conduction system in a 2-year-old boxer with electrocardiographic evidence of complete A-V block. The following findings were present: a lack of communication between the atria and the A-V node, atrophy of the A-V node, and tenuous connections between the A-V node and the A-V bundle. These were accompanied by acute degenerative changes in the conduction system. These changes are considered to be the result of arteriolosclerotic heart disease.     

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 block 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 block although the electrocardiogram alone would not indicate the actual site of lesion. Predestination of fiber tracts and alternative proposals to the predestination theory are considered to explain QRS aberration due to exclusive His bundle lesions.     

Usefulness of the ajmaline test in patients with latent bundle branch block

Twelve patients were studied with intermittent bundle branch block whose conduction disturbance disappeared completely and could no longer be recorded even after provoked changes in heart rate. Premature atrial stimulation and atrial pacing at rapid rates were performed in nine patients; in none of these nine were these procedures able to evoke the complete bundle branch block pattern that all patients exhibited before the spontaneous normalization of conduction. In marked contrast, the administration of ajmaline (1 mg/kg body weight, intravenously in 90 seconds) caused the bundle branch block pattern to reappear in 10 (83.3 percent) of the 12 patients 30 to 120 seconds after the end of the injection, and in 11 patients (91.6 percent) when additional atrial stimulation was performed in 1 of the 2 “failures.” This pharmacologie test was much more rapid and simple than electrophysiologic testing and it was noninvasive. Results of this study suggest that some form of subclinical fascicular injury was present (or had persisted) at a time when intraventricular conduction was persistently normal even though no significant physiologic alteration could be demonstrated by the atrial stimulation techniques. The ajmaline test may become a valuable tool for uncovering cases of latent bundle branch block and furthering our knowledge of the early natural history of intraventricular block.     

The response of the canine heart to double pulses of short duration: a simple addition principle

Experiments are done with rectified and opposite double pulses I₁ and I₂ with a duration of 10 microseconds each applied to the right ventricle of the dog heart.The double pulse with a time interval θ between the pulses is applied after a certain time delay ν after the R-wave in the heart cycle of the dog. Care is taken that the double pulse was not administered during the T-wave.If a certain combination of amplitudes I₁ and I₂ with a fixed θ was followed by one electrical ventricular extrasystole, a (+) was entered in the graphic representation. If not, a (?) was entered.Graphic representations of the stimulation threshold in the (I₁, I₂) plane were made up with the respective time interval θ between the pulses as parameters.From the experiments it is concluded: (1) for θ < 50 μs the addition principle for the heart is nearly valid, (2) for θ > 500 μs the pulses I₁ and I₂ are working independently on the heart, and (3) for θ > 1000 μs the pulses I₁ and I₂ are working independently with a 2 per cent KCl solution disturbance.The “memory time” is, possibly, a parameter to detect abnormalities in ion concentrations in the heart muscle.     

A His bundle electrocardiographic analysis of cardiac conduction in the pediatric and adolescent patient

Bipolar electrode catheter recordings of His bundle electrograms with three simultaneously recorded surface electrocardiographic leads were obtained from 30 pediatric and adolescent patients (aged 3 to 18 years). In 14 patients, cardiac murmurs were proved to be innocent by cardiac catheterization. The control conduction intervals were compared to those of 13 patients with congenital heart disease, and three with acquired heart disease (myocardiopathy, rheumatic valvular disease, and Friedreich's ataxia).P-R, intra-atrial (P-A), A-V nodal (A-H), and intraventricular (H-V) conduction intervals were measured to the nearest 5 msec. Conduction delays were analyzed in each of the three components of the P-R interval. These delays occurred both in single components of the system as well as in combined conduction delays and were not always demonstrable by surface electrocardiograms. The Wenckebach phenomenon induced by atrial pacing was localized to the A-V node as well as the His-Purkinje system. This technique of intracardiac electrogram recordings is safe, does not significantly prolong cardiac catheterization time, and often yields unique and useful data concerning A-V conduction.     

Efficacy of chronic amiodarone therapy in patients with variant angina pectoris and inhibition of ergonovine coronary constriction

In three patients with vasospastic angina pectoris, chronic amiodarone administered orally at doses of 800 and 1,000 mg/day totally suppressed spontaneous episodes of ischemic chest pain for 8 to 14 months. Before treatment, ergonovine maleate 0.2 to 0.4 mg intravenously provoked chest pain and similar ischemic ECG changes as those occurring spontaneously. During amiodarone treatment ergonovine vasoconstriction was totally or partially inhibited. In addition to calcium-blocking agents, amiodarone is another spasmolytic drug which effects smooth muscle relaxation by different mechanisms and appears to be useful for the chronic treatment and prevention of variant angina. The vasodilator property of amiodarone is achieved by both direct action and noncompetitive alpha receptor antagonism of coronary vasculature.     

Effects of premature depolarization on refractoriness of ischemic canine myocardium

In 25 pentobarbital anesthetized dogs we measured refractory periods (RPs) of regularly driven complexes and premature ventricular depolarizations (PVDs) with a range of coupling intervals or of regularly driven complexes and the complex following the PVD, i.e. the postextrasystolic depolarization (PED). Measurements were made during control periods and during occlusion of a branch of the left anterior descending coronary artery. The difference in control and occlusion RPs was less following some PVDs with short coupling intervals than following other PVDs with longer coupling intervals. Variations in the coupling interval of PVDs had less effect on RPs of the PVDs in ischemic than in nonischemic tissue. RPs of PEDs were prolonged with respect to RPs of regularly driven complexes in both ischemic and nonischemic tissue, but the prolongation in ischemic tissue was significantly greater than that in nonischemic tissue, 8 ± 4 msec and 2 ± 2 msec respectively, p <.001. The difference in effect of PVDs on RPs of ischemic and nonischemic tissue results in greater disparity of refractoriness between ischemic and nonischemic tissue following some long coupling interval PVDs than following some PVDs with shorter coupling intervals. In addition the greater prolongation of RPs of PEDs in ischemic than in nonischemic tissue can result in increased disparity in RPs than the disparity between ischemic and nonischemic tissue present during regular drive.