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Biomedical subjects

F Moleiro

Publications and source records attributed to F Moleiro.

11 recordsLinked to original sources
PubMed1979

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↗
PubMed1978

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↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1975

Atrioventricular block after reciprocating atrioventricular junctional tachycardia.

Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 sec) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the "upper" His bundle, above the site from which the H deflection was recorded.

Atrioventricular Node↗
PubMed1975

Primary cardiomyopathy in identical twins.

Seventeen year old identical twin brothers with no family history of cardiopathy began experiencing palpitations almost simultaneously. In both, examination revealed marked cardiomegaly and hypokinesia of the ventricular walls, and clinical and radiologic signs of progressive cardiac failure developed a few days later. Both boys died suddenly, 49 days and 5 months, respectively, after the initial examination. Electrocardiographic and vectorcardiographic studies revealed a severe intraventricular conduction disturbance that coincided with histologic changes in the myocardial tissue, including profuse interstitial fibrosis, hypertrophy and degeneration of the myocardial fibers, aberrant arrangement of the muscular fibers and considerable alteration of the structure of cardiac tissue. In the absence of hereditary and chromosomal factors, and excluding possible viral intervention during fetal life, it is believed that a teratogenic factor can produce the structural alterations of the tissue and derangement of the fibers observed in these hearts. The irregular contractions of the heart at the level of the net-like meshwork, disarrangement of myocardial fibers, and adaptative mechanisms of the heart inherent in the destruction of the contractile tissue contributed to the functional cardiac disorders that resulted in congestive heart failure and sudden death in these twins.

Adolescent↗
PubMed1975

Electrophysiologic studies in a patient with atrial flutter and 1:1 atrioventricular conduction.

Intracardiac electrophysiologic studies were performed in a patient having paroxysms of atrial flutter with 1:1 atrioventricular (A-V) conduction. Although duration of conduction intervals was normal during sinus rhythm, the atrio-His (A-H) interval did not show the expected increase when the atria were stimulated at progressively higher rates. The results of pacing with the extrastimulus technique also indicated that the refractory periods of the A-H tissues were shorter than normal. Yet, intravenously administered ouabain produced a significant increase in these refractory periods. The findings in the case are compatible with a partial A-V nodal bypass with a shorter refractory period than the A-V node or with an A-V node with unusual capacity for rapid conduction. The response to ouabain therapy was that of A-V nodal tissues.

Adult↗
PubMedDate not supplied

[Gap phenomenon in the bundle of his conduction].

His bundle electrograms recorded during atrial stimulation with the extrastimulus technique permitted the analysis of the so called gaps in bundle branch conduction. Three different types of gaps were identified each with a distinct electrophysiological mechanism. In type I gap a CLBBB pattern disappeared at shorter coupling (A1-A2) intervals because the more premature impulses encountered a greater degree of the delay at the A-V node therefore reaching the left bundle branch after its effective refractory period had ended. During this part of the cycle the H1-H2 were longer and H2-V2 intervals shorter than when CRBBB was present. In type II gap a CRBBB pattern disappeared at shorter coupling intervals because the premature impulses met a greater delay in the proximal portions of the His-Purkinje system. In consequence, they arrived at the right bundle branch when its effective refractory period had expired. When this occurred the H1-H2 interval were shorter and the H2-V2 longer than those at which CRBBB had been present. The patient with type III gap had CLBBB. A-V conduction was possible through the right bundle branch very late in the cycle. However, it could not occur at shorter coupling intervals finally reappearing at even shorter coupling intervals. True supernormal conduction or vagal pulsatile discharges could have been present. Yet, we favor, as the most likely possibility, the existence of 2:1 phase 4 block with latent or abortive escapes not recorded in the surface leads.

Bundle of His↗
PubMedDate not supplied

[Electrophysiology of pacemakers by demand. Critical analysis].

The adequate interpretation of cardiac arrhythmias should be done in context with the clinical facts. In case of arrhythmias induced by pacemakers, it is essential to have detailed information about the characteristics of the electronic instrument. This paper shows, that only with precise information about the electrophysiological facts of a certain instrument, it is possible to diagnose the origin of an arrhythmia, its significance related to normal function or disfunction of the apparatus and the proper measures can be taken for correcting the disorder. Examples of clinical cases have been presented, and undoubtedly a growing improvement in the elaboration of the electronic instruments, will enrich, the already ample field of cardiac arrhythmias. All of it will lead to an undoubtful benefit for patients, medical personnel who are involved in the electric treatment of the disturbances in rhythm and conduction.

Arrhythmias, Cardiac↗