Antonio Masoni

Effects of amiodarone on supraventricular tachycardia involving bypass tracts

This study evaluates whether the electrophysiologic effects of i.v. amiodarone in patients with reentrant supraventricular tachycardia (SVT) can predict the efficacy of long-term oral therapy with this drug. The effects of oral and i.v. amiodarone were studied in 27 patients with SVT. In 14 the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (Group I), and in 13 a concealed atrio-His bypass (Group II). Intravenous amiodarone induced significant prolongation of the AH interval, the refractory periods of the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium. The ventriculoatrial interval was slightly prolonged in Group I patients and did not change in Group II patients after i.v. administration of the drug. In both groups, the effective refractory period (ERP) of the concealed bypass was prolonged by i.v. amiodarone. During control state, SVT could be induced in all patients; after i.v. administration of the drug, SVT was presented in 6 patients in Group I and in 8 patients in Group II. In all cases, in which i.v. amiodarone prolonged the ERP of the concealed bypass to more than 350 ms, the drug always prevented SVT even when given orally. All but 2 patients--1 from Group I and 1 from Group II--remained asymptomatic after oral amiodarone. In the patient from Group I, SVT had been prevented by i.v. amiodarone, whereas in the patient from Group II SVT could not be induced by ventricular stimulation during the control state, but appeared after i.v. administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Reproducibility of electrophysiological parameters of sinus node following autonomic blockade

We investigated the reproducibility of sinus node cycle length (SCL), corrected sinus node recovery time (CSRT) and sino-atrial conduction time (SACT) during the control state and following autonomic blockade in 25 patients (mean age: 56.9 +/- 13.8 years). Autonomic blockade was induced by i.v. administration of propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). The electrophysiological study was repeated after 24 hr and the results were compared. The patients were divided into two groups: Group 1 (15) with normal and Group 2 (10) with abnormal intrinsic sinus node function. Following autonomic blockade in Group 1 the daily variations in SCL, CSRT and SACT were very slight whereas in Group 2 there was far greater variability in these parameters. However, in the latter group there were no patients who changed their status from prolonged to normal intrinsic CSRT on the second study, whereas SACT changed its status in 2 patients. In Group 1 the daily variations in sinus node parameters were much slighter following autonomic blockade than during the control state. In Group 2 the variations were very similar during control and following autonomic blockade. These data suggest that: (1) following autonomic blockade the reproducibility of sinus node parameters is very good in Group 1, whereas in Group 2 several patients show marked daily variations in sinus node parameters; (2) following autonomic blockade the sinus node electrophysiological parameters are meaningful in diagnosing an involvement of intrinsic sinus node function; and (3) in patients with abnormal sinus node parameters during control state, but with normal intrinsic sinus node function, the daily variations are mainly due to change in autonomic tone, whereas when the intrinsic sinus node function is abnormal, the day to day variations during control state appear due predominantly to intrinsic sinus node abnormalities.

Effects of autonomic blockade on dual atrioventricular nodal pathways pattern

Fifteen patients (age: 57.6 +/- 14 years) showing dual A-V nodal pathways pattern during basal electrophysiological testing were studied following pharmacological autonomic blockade (iv propranolol 0.2 mg/Kg and iv atropine 0.04 mg/Kg). After induction of the autonomic blockade, the dual A-V nodal pathways pattern was not present in four patients due to disappearance of the slow pathway; the pattern remained in 11 (73%). The longest A2-H2 interval, the effective and functional refractory periods of the fast pathway did not change significantly following autonomic blockade. Even the electrophysiological measures of the slow pathway, in the 11 patients in whom they were comparable, did not change significantly after autonomic blockade. These data suggest that: the dual A-V nodal pathways pattern is mainly related to the intrinsic structure of the A-V node; the autonomic nervous system only affects in a variable way the refractoriness and the conduction velocity in the two pathways.

The role of the autonomic nervous system on sinus node function in patients with intermittent sinoatrial block

Sinus node (SN) function was analyzed with and without autonomic blockade (AB) in 31 patients (mean age: 57.6 +/- 12.8) with intermittent sinoatrial block. Twenty-one patients had organic heart disease; in the remaining ten signs of underlying heart disease were not present. Nineteen patients had dizziness or syncope. Sinus cycle length, sinus rate, corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After control measurements, AB was produced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of electrophysiological parameters were then repeated. After AB sinus rate and CSRT did not show statistically significant differences, whereas SACT decreased significantly (P less than 0.001). When intrinsic heart rate (IHR) was abnormal (11 cases), intrinsic CSRT was always abnormal, whereas when IHR was normal, intrinsic CSRT was normal in 11 patients and abnormal in nine. In several cases, when sinus rate increased after AB, CSRT decreased and vice-versa. The parameters of intrinsic SN function were normal in 80% of patients with a normal heart and only in 14.2% of patients with organic heart disease. These data indicate that: (1) during the control period SACT is mainly conditioned by the vagal tone; (2) abnormalities in control CSRT are not uniformly abolished after AB in patients with normal IHR; (3) AB has a differential effect on the two variables of SN automaticity; i.e. sinus rate and CSRT; and (4) in patients without underlying heart disease, the SN dysfunction is almost exclusively related to alterations of the autonomic nervous system.

Latent abnormalities of sinus node function in patients with organic heart disease and normal sinus node on clinical basis

Sinus node (SN) function was analyzed in 22 patients (mean age: 46.2 +/- 12.9 years) with organic heart disease and normal SN on clinical basis (group I) and in 20 normal subjects (mean age: 43.9 +/- 15.6 years), (control group). Sinus cycle length (SCL), corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After the control study, autonomic blockade (AB) was induced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of SCL, CSRT and SACT were then repeated. The mean SCL values were very similar in the two groups during the control state and after AB. There were no significant differences in SACTs between the two groups during the control state or after AB. On the contrary, the CSRT of group I was significantly longer than that of control group during the control state (344.8 +/- 78.9 versus 262.2 +/- 46.3 msec, P less than 0.001) and after AB (238.9 +/- 72.8 versus 166.8 +/- 39.3 msec, P less than 0.001). The analysis of real depression of SN automaticity (CSRT minus SACT) in the two groups shows that prolongation of CSRT in group I during the control study and after AB is related to an intrinsic abnormality of SN automaticity; on the contrary, no dysfunctions of the autonomic nervous system appear. These data indicate that the intrinsic abnormality of SN automaticity represents the earliest involvement of the SN in subjects with organic heart disease and normal SN on clinical basis, although this conclusion is speculative and requires experimental verification.

Left bifascicular block with normally conducting middle fascicle.

A case of aortic insufficiency showing an ECG pattern of left ventricular hypertrophy and strain has been followed over time. One year after the initial observation, the ECG and VCG recordings showed the appearance of a left bifascicular block, due to involvement of the anterior and posterior fascicles, with normal septal activation. It is suggested that the normally functioning middle fascicle activates the inferior two-thirds of the septum. This hypothesis is discussed in light of recent experimental data.

Right precordial q waves due to anterior fascicular block. Clinical and vectorcardiographic study

Summary The ECG and clinical data of 1008 patients with anterior fascicular block (AFB) were analysed. The patients were divided into two groups: group 1, those showing no q waves in precordial leads V 2 V 3 ; and group 2, 139 patients (13.78%), showing qrS pattern in V 2 , V 3 leads with small, narrow and not-slurred q waves. In the first group, 35 patients had no clinically manifest cardiac disease and 19 patients had congenital heart disease. There were patients in this group in all decades of life. No patient in group 2 was in the first three decades of life and all had some form of acquired heart disease. Vectorcardiograms (VCG) of 35 control patients with normal electrocardiograms (ECG), 32 patients with AFB without q waves, and 30 patients with AFB and q waves were analysed and compared. The 10 and 20 msec vectors in patients with AFB, as compared to normal patients, showed a more inferior (P

Physiopathological and diagnostic hypotheses in peripheral block

Delays and conduction blocks may occur in Purkinje fibers, junctions and muscular cells. Since such blocks may take place everywhere in the ventricles and not only in the free walls, we prefer to use the term peripheral instead of parietal block. The electrophysiologic problems connected with such blocks are discussed. The localization of the ventricle affected by the block is usually simple using VCG recording and is based on the orientation of terminal vectors. It is more difficult to recognize the ventricular walls affected by the block, the intraparietal localization and the source of the block: Purkinje fibers, junctions or muscular fibers. We maintain the concept that peripheral blocks alter not only the terminal phases of ventricular depolarization, but sometimes also the initial ones, in that the Purkinje-junction-muscular fibers system can be damaged in the septum with the major conduction pathways remaining intact. Several discrepancies found between the prescence of electric patterns of septal necrosis and autopsy data may be explained by peripheral blocks localized in the left septum.

A method for evaluating different modes of action of an antiarrhythmic drug in man. The effects of propafenone on sinus nodal functions

In vitro experiments have shown that the antiarrhythmic effects of propafenone are due to a direct depressant action and to a beta-blocking activity. In this study a method was used to evaluate the direct effect and the autonomically mediated actions of an antiarrhythmic agent in a clinical setting. An electrophysiological study was performed twice, at an interval of 24 hr, in 17 patients (age: 52 +/- 17 years) with normal resting and intrinsic heart rate. In the first study the overall effect of intravenous propafenone (1.5-2 mg/kg) was evaluated by comparing the sinus node parameters obtained during the basal state and after drug administration. In the second study the direct depressant effect of the drug was evaluated by comparing the electrophysiological variables obtained following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg) and after propafenone. In the first study there was no significant change in the sinus cycle length and corrected sinus node recovery time and only a small (9.1%) increase in sinuatrial conduction time, whereas in the second study these variables increased significantly. The degree of increase in sinus cycle length and corrected sinus node recovery time was significantly higher in the second study than in the first one. These data suggest that: (1) propafenone has direct depressant effect on sinus automaticity but this effect is counteracted by autonomically mediated actions (most likely of vagolytic type); (2) the beta-blocking effect of the drug demonstrated in isolated atria is not seen in a clinical setting.

Left ventricular parietal block: Diagnostic and clinical study

Fifty-five patients with widened QRS complexes due to the presence of slurred S waves or of terminal slurrings on R waves, in more than three leads, with no infarction or bundle branch and fascicular blocks, were studied with the usual clinical examinations as well as vectorcardiographic recording. A parietal block of the left ventricle was diagnosed when, in the presence of a normal development of ventricular depolarization in the initial and middle phases, the terminal QRS loop was delayed, sometimes irregular and displaced leftward and posteriorly. When this delay was directed to the right, the ventricular localization was puzzling. The comparison of the electrocardiographic (ECG) and vectorcardiographic (VCG) data on the terminal part of ventricular depolarization showed some discrepancies and revealed the greater importance of VCG investigation for the study and the localization of parietal blocks. The pathogenesis of such minor conduction disturbances is not yet clear, since the experimental data on the anatomical-functional structures are different: the Purkinje network, Purkinje fiber-muscle junction or common myocardium. In some cases we think it is possible to localize the structure concerned; in any case we can always localize it at the level of the free ventricular wall.