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Biomedical subjects

R Pirani

Publications and source records attributed to R Pirani.

At least 19 recordsLinked to original sources

Prevalence of mycobacteria in a swimming pool environment.

A study was performed to evaluate the prevalence of non-tubercular mycobacteria in swimming pool environments. The bacteria in question were found in 88.2% of pool water samples. The most frequent species were Mycobacterium gordonae (73.5% of samples; range 1-840 cfu 100 ml - 1), M. chelonei (38.2% 2-360 cfu 100 ml - 1) and M. fortuitum (35.3% 2-250 cfu 100 ml - 1). The same species were also recovered from the water at the different phases of the treatment cycle, with relative percentages similar to those of the pool water. Shower floors and pool edges also presented high concentrations of the mycobacteria (100% of samples) and M. marinum was isolated from the surfaces of pool edges on two occasions (4.5% of samples). The swimming pool environment provides a suitable habitat for the survival and reproduction of mycobacteria. Although mycobacteria are common in swimming pools, human mycobacterial disease associated with their use is rare. Apart from superficial infections with M. marinum, the risk of more serious diseases in subjects with weakened immune systems should not be underestimated, given the widespread presence of mycobacteria that are possible opportunistic pathogens and the direct contact bathers have with the water and aerosol.

Bacteriological Techniques↗

Long-term effects of theophylline in atrial fibrillation with a slow ventricular response.

In 17 patients (aged 78 +/- 9 years) with symptomatic atrial fibrillation and a slow ventricular response not related to drugs, a resting electrocardiogram and 24-hour Holter recording were obtained before and 5 to 6 days after administration of slow-release theophylline (700 mg/day), and successively every 3 months during the long-term phase. Fourteen patients had organic heart disease, and 13 complained of syncope or presyncope, and 4 of asthenia and easy fatigability. At the steady-state evaluation, theophylline significantly increased resting heart rate (HR) by 42%, mean 24-hour HR by 31% and minimal 24-hour HR by 34%. Cardiac pauses > 2,500 ms disappeared or markedly decreased. The daily number of wide QRS complexes increased. Serum theophylline level was 13 +/- 5 ng/ml. During the follow-up period (20 +/- 18 months), the mean daily theophylline dosage was 450 mg and the mean serum theophylline level 9 ng/ml. Seven patients died: 1 because of heart failure, and 6 because of noncardiac death. One patient complained of a syncopal episode during 1 visit. The drug markedly reduced asthenia and easy fatigability. During the long-term phase, HR increased spontaneously in 3 patients, and the treatment was interrupted. In 2 patients, theophylline had to be discontinued because of gastric intolerance. During long-term therapy, HR was similar to that observed at the steady-state evaluation, despite the reduction in daily dosage. The data suggest that theophylline is an effective therapy in most patients with symptomatic atrial fibrillation and a slow ventricular response.

Aged↗

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↗

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↗

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↗

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↗

[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↗

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.

Adolescent↗

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↗

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.

Adolescent↗

[Effects of the autonomic nervous system on the refractory periods of atrioventricular conduction in man].

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)

Adolescent↗

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)

Adolescent↗

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.

Adult↗

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.

Adult↗

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.

Adolescent↗