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Biomedical subjects

F Moleiro

Publications and source records attributed to F Moleiro.

At least 37 records · Page 2Linked to original sources

Sustained ventricular tachycardia in chronic chagasic myocarditis: electrophysiologic and pharmacologic characteristics.

Sustained ventricular tachycardia (VT) develops in many patients with chronic Chagasic myocarditis. Programmed stimulation was used to study the electrophysiologic characteristics of VT in 15 patients with Chagas' cardiomyopathy. Nine patients were in New York Heart Association functional class I, 5 were in class II and 1 patient was in class III. The average ejection fraction was 56 +/- 7%, which is somewhat better than that reported in patients with VT owing to idiopathic cardiomyopathy. In 11 patients VT could be reproducibly initiated and terminated by programmed stimulation. Intravenous mexilitene prevented induction of VT in 7 of 8 patients; amiodarone did not prevent induction in 3 of 4 patients. Our data indicate that the mechanism of VT is likely to be reentrant in many patients, and therefore VT can be produced by extrastimuli. Electrophysiologic study is therefore useful for establishing the diagnosis of sustained VT and may be useful for guiding initial therapy in selected cases of Chagas' disease.

Adolescent↗

Annihilation, entrainment and modulation of ventricular parasystolic rhythms.

Annihilation and one-to-one entrainment of modulated parasystolic rhythms in humans has not been previously discussed. In 9 nonmedicated patients, it was possible to measure the intrinsic, parasystolic ectopic cycle length given by the intervals between 2 consecutive parasystolic beats without any interposed nonparasystolic beat. The corresponding values varied between 960 and 2,350 ms (corresponding to rates between 62 and 26 beats/min). In addition, modulation could be determined, because nonparasystolic beats falling during the initial 59% of the cycle prolonged the parasystolic cycle length (by 12 to 37.5%), whereas those that fell later in the cycle shortened it (by 9 to 25%). Plotting this prolongation or shortening as a function of the temporal position of the nonparasystolic beats in the cycle yielded biphasic response curves, of which 7 were symmetric and 2 asymmetric. In 2 patients, episodes of concealed one-to-one entrainment were initiated by late nonparasystolic (sinus) beats and, later on, terminated by early ventricular extrasystoles. In 2 other patients (and in 2 separate occasions) nonparasystolic beats, falling in part of the cycle located in between those of maximal delay and acceleration, produced pacemaker annihilation (cessation of automatic activity for the remaining monitoring time). Parasystolic annihilation and concealed entrainment may be one of the causes that can explain the large, spontaneous, day-to-day variability in the incidence of ectopic ventricular beats reported in Holter recordings. Nevertheless, future prospective studies performing interventions that can change the sinus and ectopic rates are required to corroborate our finding.

Arrhythmias, Cardiac↗

Multiple electrophysiologic manifestations and clinical implications of vagally mediated AV block.

Clinical, surface ECG, and intracardiac findings were analyzed in 20 patients with spontaneous conduction disturbances in whom vagally mediated AV block could be induced by carotid sinus pressure during electrophysiologic evaluation. The latter demonstrated that the surface ECG pattern attributed to bradycardia-dependent (phase 4), and paroxysmal block within the His bundle and bundle branches could reflect vagally mediated, bradycardia-associated (rather than bradycardia-dependent), and paroxysmal AV nodal (AH) block. The decision regarding the use of pacemakers was not based on QRS duration or on patterns (or site) of block but on the underlying clinical settings and the correlation of symptoms with maximal ventricular (R-R) pauses. However, more studies are required to extend our findings, especially to other subgroups of patients (or normal individuals) in whom vagally mediated block occurs.

Aged↗

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↗

Effects of lignocaine on bidirectional tachycardia and on digitalis-induced atrial tachycardia with block.

Most recent studies discussing tachycardias with alternating QRS polarity have referred to those known as torsade de pointes. This report, in contrast, deals with bidirectional tachycardia and the effects of lignocaine on 10 patients with this arrhythmia. Three of the patients also had digitalis-induced atrial tachycardia with block. In one patient, a single bolus of lignocaine was followed (five minutes later) by ventricular fibrillation, but the other nine patients received two boluses of 75 mg followed by a drip infusion of 3 mg/min. The drug terminated the episodes of atrial tachycardia with block and bidirectional tachycardia in all patients thus treated. Whereas the abolition of the bidirectional tachycardia was permanent in the seven patients with digitalis intoxication, it recurred after stopping the drip infusion in the two patients without digitalis toxicity. It is concluded that lignocaine can be useful in the treatment of digitalis-induced bidirectional tachycardia and atrial tachycardia with block. From this study no conclusions can be drawn, however, as to whether lignocaine is superior to other class I or class IV agents.

Adult↗

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of Wolff-Parkinson-White Syndrome.

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-"distal" His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the "proximal" His bundle was stimulated. In these two patients, having as "common denominators" short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possible due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the "slow" nodal pathway.

Adolescent↗

Preliminary studies with an implantable multimodal A-V pacemaker for reciprocating atrioventricular tachycardias.

The efficacy of a recently developed programmable implantable pacemaker which can be used in the management of supraventricular tachycardias (with, or without, associated bradyarrhythmias) was evaluated in the cardiovascular laboratory and at the bedside in the coronary care unit. Although this pacemaker functions primarily in a DVI-DVO mode, it was also made (iatrogenically) to operate in a DOO mode. The study was performed in six patients with reciprocating atrioventricular tachycardias (four of the long P-R--short R-P type and two of the short P-R--long R-P type). Both DVI-DVO and DOO pacing abolished all episodes of tachycardia in five of the patients. However, DOO pacing was also capable of initiating episodes of tachycardia in two of the six patients. The events observed in two of the patients raise the possibility that (reversed) ventriculoatrial sequential pacing may be required in some tachycardias of the short P-R--long R-P type. This preliminary study suggests that programmability of pacing modes, rates, and intervals is a desirable feature that pacemakers used to manage drug-resistant tachycardias should have.

Adult↗

Programmed simultaneous biventricular stimulation in man, with special reference to its use in the evaluation of intraventricular reentry.

Programmed stimulation was alternatively performed exclusively from the right ventricular endocardium, exclusively from the left ventricular epicardium and simultaneously from both ventricles in 8 patients who did not have coronary artery disease or bundle branch block. A specially constructed QRS triggered pacemaker, (with a refractory period of 260 msec and an escape interval of 800 msec) connected to the right ventricular and left ventricular electrodes, was used to perform simultaneous biventricular stimulation. The latter had no untoward effects and was not more dangerous than exclusive right ventricular, or exclusive left ventricular, stimulation. In 3 patients, pacemaker-induced repetitive firing occurred during right and left ventricular pacing. Persistence of this phenomenon (in these 3 patients) during simultaneous biventricular stimulation is in keeping either with a microreentry occurring in the vicinity of the electrodes or with a macroreentry involving the bundle branches. A more precise evaluation of the reentry circuit requires that left ventricular pacing be performed from an endocardial (rather than from an epicardial) site. This study suggests that the pulse generator described in the present communication can be used to produce simultaneous atrial and ventricular activation (or pacing) by connecting one pole to an atrial electrode and the other pole to a ventricular electrode. This modality of stimulation can be effective in preventing or abolishing some types of reciprocating atrioventricular tachycardias.

Aged↗

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.

Bundle of His↗

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.

Adult↗

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.

Cardiac Catheterization↗

Effects of the pacing site on A-H conduction and refractoriness in patients with short P-R intervals.

His bundle recordings were studied in four patients with short P-R and A-H intervals, and narrow QRS complexes, who had experienced several episodes of supraventricular tachyarrhythmias. The heart was paced from the high right atrium (HRA) and the coronary sinus (CS). In three patients the A-H Wenckebach phenomenon occurred at higher rates (greater than 200 pacing beats/min) when the CS was paced than when pacing was performed from the HRA. Moreover, CS stimulation produced smaller increments in the A-H interval than did pacing from HRA. The extrastimulus method of testing was done. In cases 1 and 2 the functional refractory period of the A-H tissues was 15 to 25 msec shorter during CS pacing than when pacing from the HRA. In case 3, the low right atrium (LRA) as well as the other two sites were paced. A type 1 gap was seen from HRA, a type 2 gap from CS, and both types appeared when the LRA was paced. Case 4, in which the mid-right atrium (MRA) was also stimulated, had a double pathway from HRA and CS with conduction through the accessory pathway late in the cycle and through the A-V node earlier in the cycle. However, the A-V node could not be penetrated during MRA stimulation. It appeared that the pacing site influenced the A-H conduction pattern and refractoriness, possibly by changing the site and/or mode of entry of the stimulus into the pathways that are responsible for this syndrome.

Atrioventricular Node↗