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Biomedical subjects

A Raviele

Publications and source records attributed to A Raviele.

At least 91 records · Page 5Linked to original sources
PubMed1981

Respiratory variation in Frank vectorcardiography and echocardiography in children.

Forty pediatric patients underwent echocardiographic and Frank vectorcardiographic studies during normal respiration. The right ventricular minor axis (RVEDD) increased significantly with inspiration (p less than 0.005), while the left ventricular minor axis did not significantly change. The distance from the anterior chest wall to the center of the left ventricle did significantly increase with inspiration (p less than 0.005). Some vectorcardiographic parameters changed with inspiration, also. Both the maximal spatial vector to the left (MSVL) and the X to the left (X-L) significantly decreased with inspiration. Although the average magnitude of these changes was small (10-15%), there was wide variation. Five of twenty-one patients with left ventricular hypertrophy during expiration had a clearly normal Frank VCG during inspiration. It is suggested that phases of respiration should be monitored when evaluating the Frank VCG in pediatric patients.

Adolescent↗
PubMed1981

["Left bundle branch block" pattern induced by premature right atrial stimulation. Electrogenetic and clinical considerations (author's transl)].

Although in the last years very important knowledges have been obtained in the field of the intraventricular conduction disturbances, many electrocardiographic-vectorcardiographic findings concerning the left bundle branch block (LBBB) and their electrogenesis are still controversial. With the purpose to clarify this problem we have reviewed and analysed 23 cases in whom BCG-VCG patterns of "complete" or "incomplete" LBBB were induced by the premature right atrial stimulation (PRAS) during an electrophysiologic study in man. The analysis of these cases have demonstrated that: 1) the same LBBB pattern can be caused by a slowed conduction or block at different sites of left intraventricular conduction system i.e. not only in the main stem of the left bundle branch (LBB) (tronkular LBBB) but also within the bundle of His (intra-His LBBB) or in all the three fascicles of the LBB distally to its subdivision (divisional LBBB); 2) ECG-VCG are not able to distinguish the anatomical or functional site of slowed conduction or block; 3) the right or left axis deviation in the LBBB is not due to LBBB per se but it represents or a block at two different sites, i.e. a tronkular or intra His LBBB plus a block in the anterior or posterior subdivision of the LBB, or a block at only one side i.e. a tronkular, intra-His or divisional LBBB but with prevalent involvement of one fascicle of the LBB; 4) the ECG-VCG "incomplete" LBBB pattern is similar to that of the left ventricular enlargement; 5) figures of "atypical LBBB" are not specific of myocardial necrosis; 6) the criteria for the diagnosis of "complete" LBBB are not reliable. We conclude that, since LBBB pattern does not always correspond to a slowed conduction or block in the main stem of the LBB, the current terminology of LBBB is inappropriate and could be changed with another which considers the site of delayed activation and not the site of slowed conduction. Therefore we propose the following terminology: 1) generalized left ventricular activation delay instead of LBBB without axis deviation; 2) generalized left ventricular activation delay superiorly predominant instead of LBBB with left axis deviation; 3) generalized left ventricular activation delay inferiorly predominant instead of LBBB with right axis deviation.

Adult↗
PubMed1981

[The right ventricular activation in ventricular activation delays. An endocardial mapping study (author's transl)].

To investigate the right ventricular activation, filtered bipolar recordings (1 cm interelectrode distance) of Apex (RVA), Inflow tract (RVIT) and Outflow tract (RVOT) of the right ventricle were obtained in 4 groups of subjects. 1st group: 25 cases with normal QRS; 2nd group: 7 cases with left ventricular conduction disturbances (4 LBBB and 3 LAH patterns); 3rd group: 20 cases with chronic coronary heart disease (CCHD) and RBBB alone (5 cases) or combined with LAH (15 cases); 4th group: 9 young subjects without heart disease (7 cases) or ostium secundum atrial septal defect (2 cases) and RBBB pattern. The activation times were calculated from the beginning of the QRS in the first endocavitary rapid deflection. The data obtained (average +/- s.d.) for QRS duration (QRSd), RVA, RVIT and RVOT were respectively: 1st group: 97 +/- 9, 23 +/- 9, 36 +/- 9, 39 +/- 8; 2nd group: 133 +/- 43, 20 +/- 14, 25 +/- 9, 42 +/- 6; 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. Activation times as expected were similar in 1st and 2nd groups. Significant differences were noted between 1st and 3rd groups (p less than 0.001) in activation times of RVA, RVIT and RVOT. Between 1st and 4th group significant differences were noted in activation times of RVA and RVIT (p less than 0.001) while no significant differences were observed for RVOT (p greater than 0.05). In 2 cases of the third group (CCHD) and in the 2 cases of atrial septal defect the activation time of RVA was within the normal range suggesting a peripheral block. In the cases of the 3rd group with troncular RBBB activation times of RVIT and RVOT were significantly related to the QRSd (r = 0.79 and 0.65, p less than 0.001 and less than 0.01 respectively), while there was no significant correlation between the activation time of RVA and the QRSd. In accordance with other Authors our study demonstrates that: 1) the RBBB pattern in ASD has a peripheral electrogenesis; 2) the RBBB pattern in CCHD is generally due to a troncular block but our study also suggests the possibility of a distal block in these patients. In contrast with some Authors the RBBB pattern in young people without heart disease was due to a troncular and not to a peripheral block. Finally, the absence of correlation observed in the cases with troncular block of the 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. QRSd and RVIT and RVOT activation times might be explained as follows: 1) in high degree troncular block the RVA activation time is due to the time employed byt the wave front to cross the septum which is probably similar in all the cases; 2) the QRSd depends on the activation time of the peripheral areas which depends on the variable spread of activation of the right ventricle probably due to a variable participation of the specialized conduction system.

Adolescent↗
PubMed1980

The anterior displacement of the QRS loop as a right ventricular conduction disturbance. Electrophysiologic and vectorcardiographic study in man.

Anterior displacement (AD) of the QRS horizontal loop (Frank VCG method) was induced by programmed right atrial stimulation (PRAS) in 15 cases. When AD occurred we noticed changes of the terminal QRS vectors and of the T loop similar to those observed in incomplete right bundle branch block (RBBB). The increasingly anticipated extrastimuli induced progressively the AD and then progressive degrees of RBBB. The anterior shifting of the efferent limb never appeared after the induction of RBBB. A left conduction disturbance never appeared after the AD. In cases of supposed incomplete left bundle branch block (i.e. left ventricular hypertrophy) the QRS duration decreased when the AD was induced. Therefore, the AD induced by PRAS and probably those observed in some clinical cases are due to a right ventricular conduction disturbance.

Adult↗
PubMed1980

[Accelerated idioventricular rhythm wih isorhythmic A-V dissociation. An electrophysiological study (author's transl)].

Three cases of accelerated idioventricular rhythm with isorhythmic A-V dissociation are presented. One case was affected by hypertrophic non obstructive myocardiopathy and two cases were affected by coronary heart disease with previous myocardial infarction. In all the cases of the arrhythmia persisted for days or months. By means of the electrophysiological study we could establish that 1) the focus was not protected by entrance block and 2) it was localized in the main branches of the conduction system. In the first case the focus was localized in the right bundle branch, in the second case, it was localized in the anterior fascicle of the left bundle branch and in the third case in the posterior fascicle of the left bundle branch. These electrophysiological characteristics suggest that the arrhythmia was due to increased firing of normal idioventricular pacemakers. On the basis of this electrogenetic interpretation we outline that in our cases the term of accelerated idioventricular rhythm should be preferred to others used in literature such as slow ventricular tachycardia.

Adult↗
PubMed1979

The role of left ventricular conduction in the electrogenesis of left ventricular hypertrophy. An electrophysiologic study in man.

Various electrocardiographic and vectorcardiographic (ECG-VCG) patterns of ventricular conduction disturbances are inducible by premature right atrial stimulation (PRAS). These patterns are a consequence of different degrees of refractoriness in the specialized ventricular conduction system. We observed that the intermediate phase of left bundle branch block (LBBB) induced by PRAS in 20 subjects with normal basal QRS (complexes) were similar to those of left ventricular hypertrophy (LVH). In 18 patients with basal ECG-VCG signs of LVH, right bundle branch block (RBBB) induced by PRAS produced a progressive disappearance of these signs and the "normalization" of the tracings. The initial maximum QRS vector decreased, disappeared or remained absent in the patients with LBBB induced by PRAS, and appeared (when absent in the basal VCG) and remained unchanged (when present) in patients with RBBB induced by PRAS. In this paper we discuss the electrogenetic implications of these data. The ECG-VCG sings of LVH are probably dependent on a slowed conduction in the left bundle branch system, while anatomical hypertrophy per se probably plays a less important role.

Adult↗
PubMed1977

[Evolutive study of the vectorcardiogram from the 14th day to the 6th month of life on the normal infant].

With the purpose of a better evaluation of the changes of cardiac potentials during the early hemodynamic arrangement of the normal heart, the authors analyze the VCG of 10 normal children periodically recorded from the 14th day to the 6th month from birth. Rotation of QRS, T and P loops in the three planes, direction and voltage of principal planar and spatial vectors were analyzed. The QRS loop showed a balanced distribution between right and left ventricular forces in the second week and developed a leftward orientation from the 4th week to the 3rd month, as demonstrated both by the loss of clockwise rotation of horizontal QRS loop and by the progressive leftward and backward direction of intermediate vectors. The initial vectors were sketched or absent in the 14th day and increased successively until the typical Q loop. The voltage of terminal vectors did not change in the course of time, but the S loop in the horizontal plane lost its original clockwise rotation and shifted to middle posterior line. The T loop progressively shifted backward so that it was always posterior after the 30th day. The P loop in the frontal plane was similar to the adult's one while in the horizontal plane it often presented a figure-of-eight. The semeiological aspects and the electrogenic considerations of these changes were discussed.

Age Factors↗