Bedside evaluation of sinus bradycardia: usefulness of atropine test in discriminating organic from autonomic involvement of sinus automaticity.

In 55 patients with persistent sinus bradycardia who underwent an electrophysiologic study of sinus node, both in the basal state and after autonomic blockade (propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg), an atropine test (0.02 mg/kg) was performed the following day. The 49 patients in whom sinus rate could be evaluated after atropine were subdivided into two groups--group I, 24 patients (age: 54 +/- 13 years) with normal intrinsic sinus automaticity (normal intrinsic heart rate and intrinsic corrected sinus node recovery time) and group II, 25 patients (age: 62 +/- 9 years) with abnormal intrinsic sinus automaticity. In group I, atropine increased sinus rate from 53.7 +/- 4 to 87.9 +/- 17 bpm (delta %: 65.5 +/- 33) and in group II from 51.6 +/- 5 to 73.9 +/- 14 bpm (delta %: 43.1 +/- 26). The discriminant threshold of sinus rate after atropine and its percent increase, obtained by discriminant analysis, was 80 bpm and +52%, respectively, with a misleading classification of 32% and 36%, respectively. The overall predictive accuracy of sinus rate after atropine was higher than the percent change in sinus rate (73% and 65%, respectively). These data evidence that the atropine test is not very helpful in discriminating between an organic and an autonomic involvement of sinus automaticity in patients with sinus bradycardia.

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.

The hemodynamic response of the conscious pregnant guinea pig to nicotine.

The hemodynamic response to continuous intravenous infusion of nicotine, at 4.5 and 18 micrograms/min, was measured using radiolabeled microspheres in nine chronically catheterized pregnant guinea pigs. These gave serum nicotine levels of 72.3 +/- 6.6 ng/ml and 315 +/- 32 ng/ml (mean +/- SEM), respectively. During low-dose nicotine infusion there was no significant change in cardiac output, its distribution, or uteroplacental blood flow. During high-dose nicotine infusion, cardiac output fell from 257.8 +/- 30.9 ml/min to 212.7 +/- 19.3 ml/min (p less than 0.05) and uteroplacental blood flow fell from 31.2 +/- 3.1 ml/min to 22.3 +/- 2.4 ml/min (p less than 0.05). During control, low-dose, and high-dose periods, serum epinephrine levels rose from control value of 60.2 +/- 2.6 to 98.9 +/- 35 and 1200 +/- 295 pg/ml (p less than 0.05 low dose versus high dose) and serum norepinephrine levels did not change significantly during nicotine infusion. Hence at nicotine levels 20 times but not at two to five times those seen in smokers, modest reductions in cardiac output and uteroplacental blood flow were observed.

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.

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.

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.

[Familial arrhythmogenic dysplasia of the right ventricle. Observation of 3 cases]. / Displasia aritmogena del ventricolo destro ad incidenza familiare. Osservazioni di tre casi.

A family with "arrhythmogenic right ventricular dysplasia (ARVD)" is described. ARVD is pathologically characterised by a partial or total degeneration of the right ventricular myocardium, replaced by fatty and fibrous tissue. This causes dangerous ventricular arrhythmias or congestive heart failure in infancy. About the three described patients, a sixteen-year-old subject died suddenly, and his anatomical and histopathological reports have been presented. Familiarity, rarely treated in literature, and the presence, in the died subject, of a damage of the left ventricle too, are the peculiar characteristic of these "ARVD" cases. The importance about instrumental non-invasive studies has been underlined in order to know early "ARVD", which can be deceptive clinically. The authors suppose there is surely, at the beginning of "dysplasia", a genetic alteration of the right cardiac musculature, but acquired noxae could insert afterwards, on this genetic basis.

[Dextrocardia and Wolff-Parkinson-White syndrome. Electrocardiographic diagnosis]. / Destrocardia e sindrome di Wolff-Parkinson-White. Diagnosi elettrocardiografica.

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.

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.

Transmission of neonatal listeriosis in a delivery room.

Two cases of neonatal listeriosis occurred in a hospital within a two-week period. Both infants were infected with the same organism, Listeria monocytogenes, type 1a, bacteriophage type 6 (lysotype 1652). Both infants were born in the same delivery room, 17 hours apart. The index patient became septic shortly after birth and died after 48 hours despite antibiotic therapy. The mother of the index patient was febrile and had chorioamnionitis. The second infant became ill with meningitis at 13 days of age. Neither infants nor mothers were attended by the same medical or nursing staff nor were they in the same labor or postpartum areas or nurseries. However, both infants were resuscitated in the same delivery room after birth by means of laryngoscope, suction catheter, and emergency resuscitation (Ambu) bag. Although it was hospital policy to clean and sterilize resuscitation equipment after use, the equipment had only been wiped with alcohol between patients in this instance, since sterile replacement equipment was not available during the early-morning hours when the index birth occurred. Therefore, we believe the contaminated resuscitation equipment was the source of infection in the second infant. This episode emphasizes the importance of appropriate disinfection of respiratory resuscitation equipment to prevent nosocomial infection due to L monocytogenes, an unusual but important pathogen in neonates.

Electrophysiology of normal anterograde atrio-ventricular conduction with and without autonomic blockade.

The electrophysiological measures of atrio-ventricular (A-V) conduction were investigated in 20 normal subjects (mean age: 43.9 +/- 15.7 years) both during basal state and after pharmacological autonomic blockade. In the basal state A-H and H-V intervals and H wave duration ranged from 55-110 ms (mean 83 +/- 15.9), 35-45 ms (mean 39.5 +/- 3.9) and 10-20 ms (mean 17 +/- 4.1), respectively. The lowest atrial rate inducing Wenckebach periods ranged from 150-200 beats min-1 (mean 176.5 +/- 13.8). The effective refractory period (ERP) and the functional refractory period from FRP) of the atrium ranged from 160-260 ms (mean 211 +/- 26.7) and 210-280 ms (mean 252.5 +/- 21.2), respectively. The ERP and the FRP of the A-V node were in the ranges 230-310 ms (mean 269.3 +/- 27.2) and 330-450 ms (mean 395 +/- 41.2), respectively. After autonomic blockade the H-V interval and the H wave duration did not change in any subject. The A-H interval was in the range 55-105 ms (mean 82.5 +/- 15) and the lowest atrial rate inducing Wenckebach periods 150-220 beats min-1 (mean 179.5 +/- 13.5). The ERP and the FRP of the atrium ranged from 170-270 ms (mean 215.5 +/- 28.3) and 210-300 ms (mean 254 +/- 27.2), respectively. The ERP and the FRP of the A-V node were in the ranges 220-320 ms (mean 260.8 +/- 32) and 330-440 ms (mean 383.3 +/- 43.7), respectively. The A-V node variables did not change significantly following autonomic blockade. These data indicate that: the definition of normal values of A-V node measurements after autonomic blockade allow us to evaluate the role of the autonomic nervous system in the patients with A-V node conduction disturbances; in the basal state the normal values of A-V conduction variables we obtained, of refractory periods in particular, are shorter than those previously reported; this appears to be related to the strict criteria we used in subject selection.

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.

Single ultrasonic estimation of fetal weight in utero compared with birth weight.

A single ultrasonic determination of fetal weight in utero was made in 270 singleton pregnancies. Infants were divided by birth weights into two groups, less than and greater than the 50th percentile. Ultrasonically determined fetal weight correlated with birth weight (R2 greater than or equal to 0.52) beyond 33 weeks' gestation. Mean fetal weights measured by ultrasound at various stages of gestation correlated well with published values.

[Effects of the autonomic nervous system on the refractory periods of atrioventricular conduction in man]. / Effetti del sistema neurovegetativo sui periodi refrattari della conduzione atrio-ventricolare nell'uomo.

The purpose of the work is to evaluate in clinical setting the effects of autonomic nervous system on the refractory periods of atrio-ventricular (A-V) conduction. Electrophysiological study was carried out, both during basal state and after autonomic blockade induced by i.v. administration of propranolol 0.2 mg/Kg and atropine 0.04 mg/Kg, in 21 subjects with normal atrio-ventricular node conduction (A-H less than or equal to 120 msec) and normal sinus rate (mean age: 54.3 +/- 16.3 years). Following autonomic blockade the sinus cycle length decreased significantly (P less than 0.01), whereas A-H interval, A1-H1 interval at cycle length of 460 msec and the longest atrial pacing cycle length inducing Wenckebach block did not change significantly. Effective and functional refractory periods of the A-V node did not show significant variations after autonomic blockade (342.2 +/- 41 versus 337.2 +/- 54.2 msec and 435.9 +/- 58.9 versus 430 +/- 60.9 msec, respectively); however, these refractory periods changed variably from subject to subject; in some patients they increased and in others there was a marked decrease. There were no significant variations of atrial effective and functional refractory periods after autonomic blockade (249.5 +/- 29.6 versus 256.6 +/- 31.9 msec and 276.4 +/- 27.1 versus 287.7 +/- 33.4 msec, respectively); they too showed a variable response from subject to subject. The relative refractory period of His-Purkinje system, evaluated in 3 patients, increased in all after autonomic blockade (420 +/- 20 versus 463.3 +/- 15.2 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade.

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through 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.

Slight middle slurring in V1-V2 without bundle branch block. An electrocardiographic and follow-up study.

A slight middle slurring in V1 and/or V2 with rS morphology (R less than S) in these leads, without right or left bundle branch block is a nearly ignored electrocardiographic finding. The purpose of this work is to provide a prospective and electrocardiographic analysis of this finding. We followed 200 subjects with middle slurring in V1 and/or V2, in the absence of bundle branch block (study group), (age: 41.5 +/- 19 years, follow-up period: 5.7 +/- 2.5 years) and 200 subjects with rS morphology in V1-V2 without the middle slurring (control group), (age: 39.8 +/- 20 years, follow-up period: 5.2 +/- 2 years). The age, sex, prevalence of organic heart disease, QRS duration and follow-up period did not show significant differences between the two group. In the study group there was a higher prevalence of vertical axis (P less than 0.001), of S1S2S3 morphology (P less than 0.001) and of terminal r wave in a VR (P less than 0.05) compared to control group. During the follow-up period, a right bundle branch block appeared in 19 subjects of study group (incomplete in 15 and complete in 4) and in 2 (complete) of control group (P less than 0.001). A left bundle branch block appeared only in one patient of study group and in one of control group. We conclude that the isolated slight middle slurring in V1-V2 expresses an initial involvement of the right bundle branch system and increases the likelihood of appearance of right bundle branch block.