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Biomedical subjects

R Cappato

Publications and source records attributed to R Cappato.

64 records · Page 4Linked to original sources
PubMed1987

Prominent anterior QRS forces: clinical, electrocardiographic and prospective study.

Recent data suggest that the prominent anterior QRS forces (R greater than or equal to S in V1 and/or V2 leads), in the absence of posterior myocardial infarction, right ventricular hypertrophy, or WPW syndrome, are related to an intraventricular conduction disturbance, at times rate-dependent. We followed 240 subjects with prominent anterior QRS forces and without the above mentioned diseases (study group), (mean age: 44.6 +/- 16 years, mean follow-up: 8 +/- 2 years) and 240 subjects without the anterior displacement (control group), (mean age: 44.4 +/- 14 years, mean follow-up: 7.9 +/- 1.9 years). The age distribution, sex, prevalence of organic heart disease, and follow-up period did not show significant differences between the two groups. QRS duration, prevalence of left ventricular hypertrophy pattern, S1 S2 S3 morphology, terminal r wave in AVR and s wave in V6 were similar in the two groups. During the follow-up period the incidence of right and left bundle branch block and fascicular block was very similar in the two groups of patients. These data suggest that prominent anterior QRS forces do not appear to be related to an initial involvement of the main bundle branches and fascicles and do not increase the likelihood of appearance of an intraventricular block of more advanced degree. The clinical, ECG and prospective data are not helpful in localizing either the ventricle or the area of the ventricle affected by conduction disturbance responsible for the anterior displacement. Our data suggest that the prominent anterior QRS forces express a normal variant of ventricular depolarization and that this finding does not have, per se, any unfavourable clinical implication.

Adult↗
PubMed1987

Electrophysiological effects and mechanism of action of oral quinidine in patients with sinus bradycardia and first degree A-V nodal block.

The effects of quinidine on sinus nodal and A-V nodal function were assessed in 20 patients (age: 60 +/- 7 years) with sinus bradycardia and a prolonged A-H interval. Electrophysiological studies were performed twice in each patient. In the first study, the measurements of sinus and A-V node function were evaluated both in the basal state and after autonomic blockade (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1). Oral quinidine was administered for 3-4 days (1200 mg day-1) and the study was then repeated using the same methods. Comparison of data obtained in the two studies in the basal state allowed us to evaluate the overall effect of quinidine. Comparing the results obtained following autonomic blockade, the direct action of the drug could be assessed. In the basal state quinidine did not significantly change the function of either node. In contrast, after autonomic blockade, significant changes were noted after quinidine. In 3 patients with sinus rate less than 50 beats min-1 and an abnormal intrinsic heart rate, quinidine induced marked depression of sinus automaticity. These data suggest that: (1) in patients with sinus bradycardia and prolongation of the A-H interval, oral quinidine has a direct depressant effect on sinus and A-V nodal function, but this effect is counteracted by autonomically mediated actions; (2) in patients with moderate or severe bradycardia and an abnormal intrinsic heart rate, the drug can induce marked depression of sinus automaticity.

Aged↗
PubMed1987

[Role of the autonomic nervous system in the genesis of the electrophysiologic pattern of the double nodal pathway].

Thirty-five patients (age: 53 +/- 13 years) with dual A-V nodal pathways pattern were studied following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Six of them had "idionodal" paroxysmal reentrant supraventricular tachycardia. After autonomic blockade the dual A-V nodal pathways pattern remained in 20 patients (57%) and disappeared in 15; however, in the latter, the effective refractory period of the fast pathway decreased significantly and the disappearance of the slow pathway conduction may not have been real since the marked shortening of the fast pathway refractory period may have masked the slow pathway conduction. The longest A2-H2 interval, the effective and functional refractory periods of the fast pathway did not change significantly after autonomic blockade. Even the electrophysiological measures of the slow pathway in the 20 patients in whom they were comparable did not change significantly. The behaviour of the fast and slow pathways measures varied from patient to patient after autonomic blockade. In the 6 patients with idionodal reentrant tachycardia a discrepancy between jump persistence after autonomic blockade and tachycardia induction was observed. These data suggest that: 1) the dual A-V nodal pathways pattern is mainly related to the anatomic structure of the A-V node; 2) the autonomic system affects in a variable way the conduction velocity and the refractoriness of the fast and slow pathways; 3) the dual A-V nodal pathways pattern and the reentry circuit of idional tachycardia imply two different electrophysiological substrata.

Atrioventricular Node↗
PubMed1986

Intrinsic electrophysiologic properties of reentrant supraventricular tachycardia involving bypass tracts.

This study evaluates the effects of autonomic blockade (propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg) in 20 patients with paroxysmal supraventricular tachycardia (SVT). In 8 patients the SVT circuit involved a concealed atrioventricular bypass for retrograde conduction (group I) and in 12 a concealed atrio-His pathway (group II). Autonomic blockade did not significantly change atrial and ventricular refractory periods, whereas it prolonged atrioventricular nodal refractoriness without varying AH interval. The ventriculoatrial interval did not change in any patient. The H2A2 interval was unchanged in all but 2 group II patients. In both groups, the effective refractory period of the concealed bypass was prolonged by autonomic blockade. In the basal state, SVT was induced in all patients; after autonomic blockade, SVT was induced in 7 patients in group I (87%) and in 7 in group II (58%) (p less than 0.05). Cycle length of SVT was prolonged after autonomic blockade in 11 of these 14 patients. The variations were observed only in the anterograde conduction (Ae-H interval), whereas retrograde conduction (H-Ae interval) was unchanged in all patients. These data indicate that the autonomic system appears to facilitate induction of SVT in patients with concealed atrio-His bypass as well as shorten the cycle length of SVT in both groups of patients.

Adult↗
PubMed1986

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.

Adult↗
PubMed1986

Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block.

Thirty-four patients with a prolonged A-H interval (group I) and 26 with A-V nodal Wenckebach block (group II) were studied in the basal state and after autonomic blockade (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1 in order to assess the role of autonomic system in A-V nodal conduction disturbances. In group I, the A-H intervals did not change significantly after autonomic blockade, whereas pacing cycle length for Wenckebach block, effective and functional refractory periods of the A-V node decreased significantly (P less than 0.05). In the 22 patients with organic heart disease these variables did not change significantly after autonomic blockade, whereas in the 12 without underlying heart disease, they decreased in all cases (P less than 0.001). In the former, the variables of intrinsic A-V nodal conduction were normal in only 9% of patients, whereas in the latter they were normal in 66%. Also in group II, the intrinsic A-H intervals were normal in only 6% of patients with cardiac disease but were normal in 63% without underlying heart disease. These data suggest that in the patients with first and second degree A-V nodal block and organic heart disease, the conduction disturbance is predominantly related to intrinsic involvement of A-V node, whereas in the subjects without underlying heart disease the A-V nodal blocks appear mainly related to autonomic alterations.

Adolescent↗
PubMed1986

[Dextrocardia and Wolff-Parkinson-White syndrome. Electrocardiographic diagnosis].

A patient affected by dextrocardia and WPW syndrome with atrio-ventricular bypass connecting the left sided atrium to the left ventricle (located to the right) is described. Signs of organic heart disease were not present. Electrocardiogram showed, in addition to typical features of ventricular pre-excitation, a QS pattern in leads V4-V6. During exercise testing the pre-excitation disappeared and the electrocardiogram recorded with inverted peripheral cables and right precordial leads, did not show alterations. The analysis of this case and of another previously published suggests that a QS pattern in left precordial leads is highly suggestive for dextrocardia, even in presence of ventricular pre-excitation.

Dextrocardia↗
PubMed1986

[Method for differentiating in humans the direct effects of anti-arrhythmic drugs from those mediated by the autonomic nervous system. Effects of quinidine and propafenone].

We have set up a method which investigates the different modes of action of an antiarrhythmic drug in man, in particular the direct effects of the drug and those mediated by the autonomic nervous system (ANS). The electrophysiological study (ES) is performed twice in each patient. In the first study the parameters of sinus and A-V nodal functions are evaluated both in the basal state and after pharmacological autonomic blockade (AB) (propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Subsequently, the antiarrhythmic drug is administered per os until a steady-state has been achieved and the ES is then repeated with the same method. By comparing the data obtained in the two studies in the basal state, before and after drug administration, we can evaluate the overall effect, and by comparing those obtained after pharmacological AB we can assess the direct action of the drug. From the comparison of the percentage changes in the examined parameters in the basal state and following AB we can evaluate whether the drug, besides having a possible direct action, also has another one which is mediated by the ANS. This method can be adapted to the way of administration and to the pharmacodynamics of the drug. If the drug does not induce important hemodynamic effect, it can be studied also after intravenous administration. In this case during the first study we can evaluate the overall effect and during the second study the direct effect. The electrophysiological parameters are then compared with the above mentioned method.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Different electrophysiological modes of action of oral quinidine in man.

The purpose of this study was to evaluate the effects of oral quinidine on the normal sinus node (SN) and A-V node and to determine if the drug exerts in man the same effects observed in cardiac tissue preparations (i.e. both direct and vagolytic action). Electrophysiological studies were performed twice in each of 16 patients (mean age: 57.7 +/- 12 years) with normal resting and intrinsic heart rates and normal A-H intervals. In the first study, the parameters of SN and A-V node were evaluated both in the basal state and following pharmacological autonomic blockade (AB), (propranolol 0.2 mg kg-1 and atropine 0.04 mg kg-1), Oral quinidine was administered for 3-4 days (1200 mg day-1) and the electrophysiological study was then repeated using the same methods. From the comparison of data obtained in the two studies in the basal state the overall effect of quinidine was evaluated, and by comparing those obtained following AB the direct action of the drug was assessed. The overall effect of quinidine on SN and A-V nodal functions was very slight since sinus cycle length, corrected SN recovery time, sino-atrial conduction time, A-H interval, A1-H1 interval at a cycle length of 600 ms and Wenckebach periods did not change significantly after the drug. On the contrary, following AB these measures increased significantly (P less than or equal to 0.01). These results provide evidence of dual effects of oral quinidine in man: a direct depressant action and an autonomically mediated opposing action, very probably vagolytic. The overall effect of the drug is very slight.

Administration, Oral↗