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.
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.
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.
Clinical electrocardiographic evaluation and complete non-invasive assessment including nuclear magnetic resonance (NMR) are reported for 7 subjects with cardiac arrest (CA), 6 due to ventricular ...fibrillation (VF) and 1 to ventricular tachycardia (VT). Two more subjects, one with and one without a family history of non-resuscitated sudden death (NRSD), were included. All 9 subjects showed the typical pattern of the Brugada's syndrome (BS), characterized by incomplete right bundle branch block, ST T elevation in V1 V3. We globally evaluated 64 subjects belonging to the 9 families examined, 5 of whom were identified in Bologna, 3 in Florence and one in Parma. BS is characterized in the experience described in the present paper by a family distribution of the ECG pattern in different members. Furthermore, a family distribution of NRSD, even at a young age, was observed. Electrocardiographic features were consistent with variable degrees and aspects of the intraventricular conduction delay (ICD) and of the ST T elevation pattern. NMR has been performed so far in 23 out of 64 members examined by echo, and was normal in 17/23, with only 6 showing pathological aspects such as mild dilatation of the right ventricle, reduced thickness of the right free wall, isolated dilatation of the right ventricular infundibulum and other minor pathological aspects. Preliminary genetic screening (GS), performed on 20 members of three families, was negative for the typical genetic patterns of right ventricular dysplasia (ARVD). In six families, GS is still ongoing. Genetic screening of sodium channel pathology is in progress in the same families. In conclusion, BS has been documented in the present paper as a hereditary syndrome, both for clinical and ECG aspects, associated with CA due to VF, which required an AICD implantation, at least in symptomatic subjects. There may exist a CONGENITAL form of BS due to pathology of sodium channels, without a demonstrable structural heart disease and an ACQUIRED form of BS secondary to an initial ARVD. From the clinical point of view, a complete evaluation, including serial ECG, pharmacological testing and programmed electrical stimulation of other subjects in the families, may be important in preventing sudden death, mainly in symptomatic subjects who always require an implantable cardioverter defibrillator.
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.
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.
