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Biomedical subjects

P Rizzon

Publications and source records attributed to P Rizzon.

At least 271 records · Page 15Linked to original sources

Left posterior hemiblock in acute myocardial infarction.

Fifteen cases of left posterior hemiblock associated with acute myocardial infaction were studied. In 5 cases the left posterior hemiblock was the only intraventricular conduction defect, while in the other 10 cases it was associated with complete right bundle-branch block. Left posterior hemiblock proved to be an early complication, appearing within a few hours from the onset of the acute episode, and an ominous sign, since hospital mortality rate was 87 per cent. Cause of death was mainly pump failure. In most of these cases ther was electrocardiographic evidence of infarction involving both anterior and inferior ventricular walls. Infarction of most or all of the ventricular septum was a common finding in the cases examined anatomically. Histologically, acute changes involving mainly the posterior septal and midseptal fibres were observed in 6 of the 8 cases studied. On the basis of these findings and of other published findings an alternative physiopathological mechanism for so-called left posterior hemiblock is proposed.

Acute Disease↗

[Interatrial block with retrograde activation of the left atrium (author's transl)].

Six cases with P wave abnormalities compatible, according to the criteria of Castillo and Vernant, with the diagnosis of block of the Bachmann's bundle, have been studied by means of intra-atrial and esophageal electrography. In two cases the P wave abnormalities were intermittent. In agreement with the results of Castillo and Vernant right atrial activation appears to be normal and coincides with the initial positive deflection of the P wave in leads II, III, and aVF. Left atrial activation starts at the end of the right atrial activation, coinciding with the terminal negative deflection of the P wave in leads II, III, and aVF and shows an abnormal progression from the lower part to the upper part of the atrium. This pattern of atrial depolarisation can only be explained by a block of the superior interatrial pathways. On the basis of the present findings it is supposed that the block occurs in a specialized type of atrial tissue rather than in the common atrial myocardium. From the clinical point of view it is of some interest to point out that this abnormal pattern of atrial depolarisation does not necessarily prolong the atrial deloparisation and may not determine a terminal negative deflection of the P wave in lead II.

Adult↗

[Electrophysiological bases of the antiarrhythmic activity of amiodarone (author's transl)].

The electrophysiological effects of orally administered Amiodarone (600 mg daily for 8 days) were evaluated using His bundle electrograms, the extrastimulus method and atrial pacing in 16 patients with proved ischemic heart disease. Our results show that Amiodarone: 1) does not affect sinus node activity; 2) considerably prolongs the refractory periods of the atrium; 3) slightly and inconsistently prolongs the refractory periods of the atrio-ventricular node and the intraventricular conduction system; 4) slightly decreases the atrio-ventricular conduction; 5) does not consistently depress the intraventricular conduction. These properties contribute to the explanation of the antiarrhythmic effects of the drug.

Adult↗