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Biomedical subjects

C A Castillo

Publications and source records attributed to C A Castillo.

At least 19 recordsLinked to original sources

Concealment of manifest, and exposure of concealed, ventricular parasystole produced by isoproterenol.

Few studies have dealt with the effects of isoproterenol on ventricular parasystole. Intravenous isoproterenol (2 to 4 micrograms/min) was administered to 11 nonmedicated patients with ventricular parasystole. At the onset of the drip infusion, 8 patients had continuous parasystole, 2 had intermittent parasystole, and 1 patient (in whom intermittent parasystole was documented 2 to 5 days earlier) showed no manifest parasystolic activity. In all patients, whose control parasystolic cycle length varied between 960 and 2,530 ms, isoproterenol caused a decrease of the parasystolic cycle lengths ranging from 12 to 36%. Therefore, isoproterenol produced a consistent increase of the parasystolic rate. In 4 patients, parasystolic activity ceased to be manifest when the concomitantly enhanced (by isoproterenol) sinus cycle lengths became shorter than 430 ms. This phenomenon reflected a tachycardia-dependent parasystolic concealment, presumably as a result of interference in the parasystolic-ventricular junction. In every case, the arrhythmia reappeared at its initial rate upon stopping the drip infusion. In no patient did parasystolic ventricular tachycardia develop. In the patient without manifest parasystolic beats, isoproterenol unmasked the intermittent parasystole that previously had been intrinsically manifest. The latter effect reflected a true exposure, or unmasking of a latent, rate-independent concealed, parasystolic focus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Electronic pacemaker models of parasystole. With special reference to artificial intermittent parasystole with phase 3 and phase 4 protection and to parasystolic modulation.

This study deals with a method of analysis of artificial pacemaker function which can be used to understand the electrocardiographic manifestations of some spontaneous rhythms. The modes of operation of 11 normally-functioning QRS-inhibited (VVI) pacemakers resembled those of spontaneous automatic nonprotected (nonparasystolic) rhythms. The function of 11 continuous asynchronous (fixed rate or VOO) pacemakers was similar to that of continuous-parasystolic rhythms. In 12 patients with malfunctioning QRS-inhibited (VVI) pacemakers, an abnormally-prolonged pacemaker refractory period was equivalent to intermittent parasystole with phase 3 protection; and non-sensing during the terminal portions of the cycle was the iatrogenic counterpart of intermittent parasystole with phase 4 protection. Premature beats occurring within the periods of phase 3 and phase 4 protection were "encompassed" by ectopic intervals equalling the ectopic cycle length, or twice the ectopic cycle length. Therefore, they were manifested differently from the "decelerating" and "accelerating" phases of modulation since premature beats occurring during the letter phases may be encompassed by ectopic intervals which are longer and shorter, respectively, than the ectopic cycle length. Because in previous reports the search for these phenomena was based on premises established "a priori," future studies should be designed to analyze tracings of "group beating" where no previous conclusions have been reached.

Arrhythmias, Cardiac↗

His bundle recordings in diagnosis of impulse formation in Kent and Mahaim tracts.

His bundle electrograms were recorded in 2 patients with ectopic beats arising in accessory atrioventricular tracts. Case 1 had Wolff-Parkinson-White (WPW) type A and a left-sided Kent tract with a short effective refractory period. Though ectopic impulse formation most probably occurred within the Kent tract itself, a vulnerability-related origin in the ventricular muscle close to the distal end of the Kent tract could not be excluded. In Case 2, with a Mahaim tract extending from His bundle to ventricles, there were three types of QRS morphologies resulting from : (a) atrioventricular conduction exclusively through the normal pathways; (b) atrioventricular conduction through both, normal pathway, and Mahaim tract; and (c) ectopic impulse formation in the Mahim tract. Specialized electrophysiological studies were essential to diagnose these unusual arrhythmias.

Adult↗

Bipolar catheter electrograms for study of retrograde atrial activation pattern in patients without pre-excitation syndromes.

The sequence of retrograde atrial activation of premature ventricular beats was studied in 12 patients without pre-excitation syndrome. Forward and retrograde AV nodal conduction times were within normal limits. The septal low right atrial (LRA2) deflection was inscribed 25 to 55 ms (ave: 37.9 ms) before the low left atrial (LLA2) electrogram and 35 to 75 ms (ave: 53.7 ms) ahead of the high right atrial (HRA2) deflection. LLA2 preceded HRA2 in 8 patients, more or less coincided with HRA2 in 3 cases, and was inscribed 10 ms ahead in 1 patient. In all cases a decrease in the coupling (St1-St2) interval resulted in a proportional increase of the septal LRA1-LRA2, LLA1-LLA2, and HRA1-HRA2 intervals. Atrial echoes occurring in 3 cases had a sequence of arrival of excitation at the recording sites which was similar to the ones shown by the same patients during ventricular pacing. This is in keeping with the existence of an upper common pathway located above the area where functional longitudinal dissociation occurred. Thus, it is concluded that impulses emerging from the AV node in a retrograde direction reach the septal low right atrium before they activate the explored low left atrial sites, regardless as to whether they arise in the ventricles or in the atria.

Arrhythmias, Cardiac↗