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Biomedical subjects

D Monizzi

Publications and source records attributed to D Monizzi.

14 recordsLinked to original sources
PubMed1988

Atrial electrophysiologic properties of patients with asymptomatic Wolff-Parkinson-White syndrome.

To evaluate the existence of a peculiar atrial electrophysiologic substrate, we studied 18 patients with asymptomatic Wolff-Parkinson-White (WPW) syndrome. These patients were compared with 10 age-matched normal subjects (N). Effective and functional refractory periods were determined at two right atrial sites (high and low in the lateral wall), during atrial pacing (100 min-1) and at twice diastolic threshold. Disperson (D) of effective (ERP) and functional (FRP) refractoriness was evaluated as the difference between refractory periods at the two atrial sites. WPW patients showed significantly lower mean values of effective and functional refractoriness at both atrial sites and significantly higher mean values of D-ERP and D-FRP. Moreover, in calculating the highest normal values of D-ERP and D-FRP (as mean values of N plus 2SD) it was observed that WPW with abnormal values of D showed a statistically (chi 2 test) higher incidence (100%) of induced atrial fibrillation (AF). These findings indicate the existence of both an abnormal atrial electrophysiologic substrate and of a higher vulnerability in WPW. Finally, AF was induced generally at the site with the lower refractoriness (i.e. low lateral site). This should be taken into account when considering how atrial fibrillation can be induced more easily.

Adolescent↗
PubMed1988

Effects of propafenone on directly measured sinoatrial conduction time.

Electrophysiologic investigation of the effects of antiarrhythmic drugs on sinoatrial conduction time (SACT) is conditioned by the inadequacies of indirect methods employing premature or asynchronous atrial stimulation. Direct recording of sinus node electrogram (SNE) is unaffected by the limitations of the indirect methods and is particularly useful when the effect of a drug on SACT is to be studied. In the present study the effect of propafenone on SACT directly (D) measured from SNE in 12 patients (7 male and 5 female subjects, 61 +/- 10 years) with normal sinus node function (NSNF) was investigated. DSACT, sinus node cycle length (SCL) and corrected sinus node recovery time (CSNRT) were evaluated before and 20 min after i.v. administration of 1 mg/kg propafenone. The following results (mean +/- SD) were obtained: in control condition SCL was 854 +/- 143 ms; CSNRT 316 +/- 82 ms; DSACT 88 +/- 20 ms. After propafenone SCL was 849 +/- 119 ms; CSNRT 340 +/- 93 ms; DSACT 97 +/- 15 ms (p less than 0.05). DSACT ranged from 60 to 105 ms and from 60 to 120 ms, respectively, before and after propafenone. In conclusion, in patients with NSNF propafenone 1. does not affect sinus node automatism and 2. prolongs significantly DSACT, which, however, remains within the upper normal limit.

Adult↗
PubMed1986

Influence of current strength on excitability and conduction of human atrium and atrioventricular node.

The influence of current strength on excitability and conduction of atrium and atrioventricular node was assessed in 25 patients using different current strengths (2, 3, 4, 5, 7, 10, 15 mA) and introducing extrastimuli (parasinusal zone) after the eighth paced complex of a basic drive (100 beats X min-1). Bipolar stimulation with the distal pole as cathode was performed so that effective and functional refractoriness of atrium and atrioventricular node, and the maximum value of atrial latency (interval between the extrastimulus and the beginning of atrial activity), intra-atrial conduction time, and AH interval could be determined at each current strength. In some patients atrioventricular nodal effective refractoriness could or could not be determined at each current strength, whereas in others the determination was possible only at the highest or the lowest current strengths. Moreover, the increase in current strength induced a progressive parallel reduction in both atrial effective and functional refractoriness; induced a progressive lengthening of intra-atrial conduction time (this was seen only in patients with a history of atrial arrhythmias); allowed the maximum possible lengthening of AH interval; and did not visibly influence atrioventricular nodal refractoriness and atrial latency. By altering atrial refractoriness and intra-atrial conduction time current strength affects the prematurity of the atrial impulse and the time at which it reaches the atrioventricular node. These findings should be taken into account when diagnostic and therapeutic electrophysiological procedures are performed.

Electric Stimulation↗
PubMed1985

Effects of pharmacologic autonomic blockade on atrial electrophysiologic properties in normal subjects and in patients with sinus node disease.

In order to elucidate the influence of autonomic nervous system on atrial electrophysiologic properties, we studied 10 patients with sinus node dysfunction and 10 age-matched normal subjects. In each of them effective and functional refractory periods of the right atrium (near its junction with the superior caval vein) were measured, during atrial pacing (100/min) and using variable current strengths (2, 3, 4, 5, 7, 10, and 15 mA), before and after pharmacologic autonomic blockade (using intravenous propranolol 0.2 mg/kg and atropine 0.04 mg/kg). Mean values of effective and functional refractory periods at each current strength were significantly higher in patients with sinus node disease than in normal subjects both before and after autonomic blockade. Blockade did not significantly modify mean values of effective and functional refractory periods at any current strength, either in patients with sinus node disease or in normal subjects. Furthermore, autonomic blockade did not change the effects of the increase of current strength on atrial refractoriness in either group. We conclude that our data indicate a prolonged refractoriness to be present in patients with sinus node disease even in the absence of influences from the autonomic nervous system. Thus, we can suggest a "primary" involvement of atrial fibers in this pathophysiological condition. Propranolol together with atropine did not induce changes of atrial refractoriness. Indeed, they probably exerted an opposite effect. The effects of the increase of current strength on atrial excitability do not seem to be mediated by autonomic humoral agents.

Aged↗
PubMed1984

Aging and atrial electrophysiologic properties in man.

In order to assess the influence of age on atrial electrophysiologic properties, we studied 17 normal subjects, whose ages were homogeneously distributed between 17 and 78 years, measuring in each of them effective (ERP) and functional (FRP) refractory periods at 3 sites of the right atrium (high, middle and low in the lateral wall) at the same driven frequency (120/min). Twice threshold stimuli of 2 msec duration were applied. Dispersion of atrial refractoriness was measured as the longest minus the shortest refractory period. A significant direct correlation was observed between age and dispersion of atrial refractoriness (of ERP: r = 0.75, P less than 0.001; of FRP: r = 0.82, P less than 0.001). Moreover, age showed a significant direct correlation with refractoriness at high right atrium (ERP: r = 0.66, P less than 0.01; FRP: r = 0.76, P less than 0.001), but did not correlate with that at the other two sites. We suggest that ageing modifies atrial refractoriness in a non-uniform manner inducing a progressive increment of dispersion of atrial refractoriness. The impression is that a slow but continuous process takes place from juvenility to old age.

Adolescent↗
PubMed1984

The effects of atropine on sinoatrial conduction time directly measured from sinus node electrogram. A comparison with results furnished by indirect methods.

The effects of atropine on sinoatrial conduction time (SACT) measured directly (SACTD) from the sinus node electrogram (SNE) were investigated in 15 patients with normal sinus node function. A comparison was undertaken with the results furnished by indirect methods which employ premature (SACTS) and asynchronous atrial stimulation (SACTN) to calculate SACT. In the control state SACTD was 92.5 +/- 16.4 ms, SACTS 78.2 +/- 22 ms, and SACTN 97.9 +/- 32.2 ms. After atropine SACTD was 70.6 +/- 15.6 ms (P less than 0.0005), SACTS 46.7 +/- 14.3 ms (P less than 0.0005) and SACTN 43.1 +/- 12.7 ms (P less than 0.0005). Mean percent decreases of SACTN (51.6 +/- 21) and SACTS (37.4 +/- 18) were statistically greater than that of SACTD (23.5 +/- 13.3) (P less than 0.0005 and P less than 0.01 respectively). While the reduction of SACTS and SACTN was greater than that of sinus cycle length (SCL) (29.2%), SACTD showed a reduction significantly less than that of SCL (P less than 0.005). Thus, SNE recording confirms that atropine induces a shortening of SACT in normal patients, but significantly less than that indicated by indirect methods.

Adult↗
PubMed1984

[Comparison of Narula's technic of direct and estimated sinoatrial conduction at increasing rates in normal subjects].

Twenty eight normal subjects in sinus rhythm underwent direct measurement of sinoatrial conduction time (SACTD) by sinus node potential recordings (SNP) and indirect evaluation by Strauss (SACTS) and Narula's methods (SACTN) using the extrastimulus technique. Stimulation in Narula's method was undertaken at three different rates, 3, 6 and 9 beats per minute faster than the spontaneous rate of the subject (SACTN3, SACTN6, SACTN9). The mean values (+/- SD) were as follows: SACTD 84 +/- 18, SACTN3 85 +/- 29, SACTN6 96 +/- 33, SACTN9 101 +/- 36. The mean value of the SACTD was significantly lower than that of the SACTN9 (p less than 0,01) but there were no significant differences between SACTD and SACTN3 and SACTN6. The three values of the SACTN were closely related to each other but not to the values of the SACTD.

Action Potentials↗
PubMed1984

Clinical electrophysiological effects of chronic administration of verapamil: the phenomenon of overdrive excitation of junctional pacemaker.

The electrophysiological effects of chronic administration of verapamil were studied in 10 patients with normal sinus node function, who received 160 mg of the drug every eight hours for at least two weeks. Uncorrected and corrected sinus node recovery time, sino-atrial conduction time, effective and functional refractory periods were normal in each case. In three patients, at the cessation of atrial pacing, an overdrive excitation of junctional pacemaker with short lasting A-V dissociation was observed.

Electric Stimulation↗
PubMed1984

Effects of atropine on atrial refractoriness and its dispersion in humans.

To evaluate the influence of atropine on atrial refractoriness and its dispersion, we studied ten subjects with sinus bradycardia who were otherwise healthy. Effective and functional refractory periods were measured at three sites of the right atrium (high, middle, and low in the lateral wall), in sinus rhythm and during atrial pacing (120/min), before and after i.v. administration of 0.04 mg/kg of atropine. Both before and after administration, dispersion of atrial refractoriness was determined from the range of refractory periods measured at the three atrial sites as the longest minus the shortest refractory period. Our data indicate that atropine was able to significantly reduce refractoriness and its dispersion. The study protocol allowed us to exclude the possibility that cycle length played a role. The antivagal effect of atropine seemed to explain our findings, even if the possibility that the drug had a direct effect could not be excluded.

Aged↗
PubMed1982

[Atrial refractoriness and its dispersion in different physiopathologic conditions].

Previous studies have demonstrated a prolonged and non-uniform atrial refractoriness in patients with both sinus node dysfunction and supraventricular tachyarrhythmias. However, they have not been able to define separately the influence on atrial electrophysiologic properties of isolated "bradycardia", of sinus node dysfunction and of supraventricular tachyarrhythmias. Therefore we have measured the effective and functional refractory periods at three different sites of the right atrium (high, middle and low lateral wall) in 16 normal subjects (N), in 9 patients with chronic asymptomatic sinus bradycardia (AB), in 9 patients with sinus node dysfunction but without evidence of supraventricular tachyarrhythmias (SSS) and in 10 patients with paroxismal atrial fibrillation (PAF). The study was performed both in sinus rhythm and during atrial pacing (120 beats/min) utilizing twice threshold stimuli. Dispersion of atrial refractoriness (D) was determined from the range of refractory periods measured at the three different atrial sites as the longest minus the shortest refractory period. Refractoriness at the high site of the lateral wall (parasinusal zone), mean values of the refractory periods obtained at the three atrial sites, and dispersion were compared among the three groups. Refractoriness at the two rates (sinus rhythm and 120 beats/min) was also compared. During sinus rhythm SSS, AB and PAF showed a significantly higher refractoriness than N, while only SSS and PAF showed increased D. Atrial pacing reduced refractoriness but not D in all groups. At the same driven frequency refractoriness of SSS and AB, and D of SSS and PAF were still significantly higher than those of N. Finally, it is noteworthy that during paced rhythm, single values of mean refractoriness of SSS did not correspond with those of N. In conclusion, our data suggest that: 1) sinus node dysfunction and supraventricular tachyarrhythmias exert an independent influence on atrial electrophysiologic properties; 2) the presence of a less homogeneous recovery of atrial excitability should be considered as a possible concause in the genesis of atrial fibrillation; 3) chronic isolated sinus bradycardia seems to be characterized by a longer atrial refractoriness and not by an increased D; 4) contrary to results obtained in animal subjects, there does not seem to be a relation between D and cycle length in man.

Adult↗