Biomedical subjects
Publications and source records attributed to F Moleiro.
A case of inferior wall myocardial infarction (IWMI) with left anterior hemiblock (LAH) is presented. The LAH became type 2:1 in the course of the disease. Electrocardiographic signs of LAH in the presence of IWMI are outlined, and the behavior and etiology of the T-wave changes are analyzed.
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.
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.
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.
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In penetrating the heart and developing in it, Trypanosoma cruzi produces an immunoallergic reaction that leads to changes in the histological structure of the myocardium; these changes alter the fundamental properties of the heart, causing fundamental dynamic disorders and morphological changes in the organ.In Chagas' cardiomyopathy, the velocity of impulse propagation diminishes in the auricular and ventricular musculature, altering the activation mechanism, this being shown by changes in the P-wave and in ventricular focal blocks.The functional refractory period (FRP) is shortened in the auricular and ventricular tissue and constitutes, together with changes in conductivity, the physiopathological basis that explains the circus movement-the fundamental factor of the arrhythmias of this stage of the disease. Localization of the inflammation in the A-V conduction system increases the duration of the FRP, producing all types of A-V block.The oedema and the cellular interstitial infiltration seen during this acute phase reduce the distensibility of the fibres; this, in turn, limits their contractility, producing a decrease in systolic volume and an increase in the final diastolic pressure in the chambers of the heart-fundamental factors in reducing kinesia and in increasing the heart's volume.In the chronic phase, destruction of the contractile tissue and fibroblastic proliferation bring into play compensatory mechanisms that maintain the strength of cardiac contractions; the elongation of the fibres and the nature of the dynamic pressure-volume curves explain the dilatation of the chambers of the heart and the dynamic changes seen in this phase of the disease.
Attempts were made to produce myocarditis by Trypanosoma cruzi inoculation in healthy dog puppies 6 to 8 weeks old. Significant electrocardiographic abnormalities were produced, coinciding with interstitial inflammatory processes in the cardiac tissue and with degenerative changes in the myocardial fibres. In puppies showing these changes, profound changes in the excitability and the functional refractory period of the atrial and ventricular muscular tissue were observed. The administration of Peruvosid in doses of 0.0240 to 0.0647 mg./kg. tended to diminish the excitability, previously increased by the inflammatory process, at the same time increasing the functional refractory period duration which had previously been shortened. The fact that Peruvosid corrects these fundamental factors in the genesis of cardiac arrhythmias suggests that the drug may be useful in the treatment of cardiac insufficiency produced by Chagas' myocardiopathy, in which arrhythmias are one of the basic characteristics.
A report is made of a rare case of Wilms' tumour which simulated clinically a syndrome of ;right heart failure', as found in some cases of Ebstein's disease. The clinical, radiological, and electrocardiographic study led to the suspicion of this type of malformation. The cine-angiographic study revealed two important facts: the impossibility of approaching the inferior vena cava with opaque material injected into the azygos vein and a filling defect of the right atrium. The post-mortem study revealed the presence of a Wilms' tumour of the right kidney which extended into the inferior vena cava and into the right atrium without producing metastases. This seems to be the first case of this peculiar course of a Wilm's tumour which has grown into the right atrium, resulting in this bizarre clinical picture.
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.
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.
Few clinical studies have dealth with annihilation, entrainment and modulation of ventricular parasystolic rhythm. Parasystolic modulation was diagnosed in 9 nonmedicated patients because single, 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. In two 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.
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In order to asses the predictive value of serial electrophysiologic studies in the selection of an effective long-term effective antiarrhythmic regimen, we studied 16 patients with recurrent sustained ventricular tachycardia (VT), resistant to conventional medical treatment. (group 1) Eleven patients in this group had chronic chagas myocarditis, and several hospitalizations and cardioversions had been required for therapy of VT. In addition, 35 patients (group 2: control) underwent electrophysiological studies to evaluate rhythm disturbances differences to TV. Ventricular Tachycardia was successfully initiated and terminate with programmed electrical stimulation of the right ventricle only in the group 1. After control studies, the effects of several drugs (ajmalin, amiodarone, carbamazepine, disopyramide, diphenilhydantoin, mexiletine, procainamide, propranolol, quinidine and verapamil on the ability to initiate VT were assessed. A drug was considered effective only if it prevented the initiation of VT and allowed long-term suppression o clinical VT. All the patients of group 1 were placed on chronic oral therapy with the effective agent and were followed for an average period of 16 months (range 5 to 47 months). In all 16 patients we could document complete long-term prophylaxis against VT. This method offers advantage in terms of morbidity, mortality, duration of therapy, and promptness of choosing an effective drug add expense to the patient over traditional empirical methods of drug selection.