Reversible cardiomyopathy following chronic supraventricular tachycardia.
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Biomedical subjects
Publications and source records attributed to A Michelucci.
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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.
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.
Two cases are described where atropine induced the disappearance of reset zone as response to premature atrial stimulation for blocked retrograde atrial conduction. Because of this, sinuatrial conduction time could not be estimated. The sinus node electrogram allowed the direct measurement of sinuatrial conduction and showed a facilitated anterograde conduction through the perinodal fibers after administration of the drug.
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.
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.
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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.
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.
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.
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.
In a case of a 2:1 second degree A-V block during sinus rhythm, PR intervals of two different durations occur, either separately or alternating beat-by-beat. The longer intervals are not caused by concealed conduction in the A-V junction of the preceding blocked impulses and the shorter ones are not due to supernormal conduction induced by the blocked impulses. This primary PR interval alternans is alternating from a pathophysiological point of view; it only concerns every other impulse alternately traveling along the faster and slower A-V junctional pathway.
ECGs and left ventricular systolic time intervals were studied in 26 patients suffering from major depressive disorder treated with clomipramine. ECGs did not show, with one exception, drug-induced changes. The ratio of pre-ejection period to left ventricular ejection time, both corrected for heart rate (PEPc/LVETc), presented no significant changes, as compared with initial findings, in the group of patients considered as a whole. 27% of patients, however, showed individual percent changes greater than 8%, both increases and decreases having been observed. Cardiac findings were in no way related to clomipramine plasma levels.
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A method of recording the sinus node potential (SNP) has recently been introduced in clinical electrophysiology. The sinoatrial conduction time can now be measured directly (SACTD) as the interval between the onset of the SNP and the onset of atrial activation. We measured the SACTD in 16 normal subjects and in 7 patients with sinus node dysfunction. These values were compared with those obtained by the indirect methods of Strauss et al (SACTS) and Narula et al (SACTN). In normal subjects the SACTD ranged from 50 to 130 ms (average 84,4 +/- 22,35); the SACTS, from 55 to 160 ms (92,9 +/- 29,3), and the SACTN from 70 to 175 ms (113,2 +/- 28,8). In patients with sinus node dysfunction the SACTD ranged from 200 to 290 ms (227 +/- 32,5), the SACTS, from 52 to 198 ms (111,8 +/- 59,3) and the SACTN from 89 to 251 ms (142,3 +/- 63). No significant difference was observed between normal and pathological subjects using the indirect methods of evaluation. However, the SACTD method showed a very significant difference between the two groups (p less than 0,0005) with no overlap. No correlations were observed between the values obtained by the indirect and direct methods of measuring SACT.
The purpose of our study was to investigate the effects of old age on sinoatrial function. We analyzed data obtained from 35 normal adults who were divided into 3 Groups: A (20-40 years, n=11), B (41-61 yrs, n=12). We evaluated: mean sinus node cycle length, sinus node recovery time, corrected sinus node recovery time, effective and functional refractory periods (EARP and FARP) and sinoatrial conduction time. EARP and FARP in Group C were significantly longer than in Group A (P less than 0.0025 and P less than 0.0005, respectively) and in Group B (P less than 0.005 and P less than 0.025, respectively). The differences were significant also when the values were expressed in percent of SCL (Group A vs Group C: P less than 0.005 for EARP, and P less than 0.005 for FARP; Group B vs Group C: P less than 0.025 for EARP and P less than 0.025 for FARP). These were the only significant differences observed between the three groups. Our data indicate that in normal adults the aging process does not affect sinus node automatism and impulse spread to the atrium, while atrial refractoriness is lengthened significantly.
Atrial refractoriness and vulnerability were studied in 10 patients with paroxysmal atrial fibrillation (PAF) and in 12 age-matched normal subjects (N). Effective and functional refractory periods were measured at three sites of the right atrium: high, middle and low in the lateral wall, both in sinus rhythm and during atrial pacing (120/min). Twice threshold stimuli were applied. Dispersion of refractoriness (D) was measured as the longest minus the shortest refractory period. Atrial fibrillation (AF) was induced in 5 of the PAF; in each of these 5 only one atrial site proved vulnerable (middle in one case, low in the other 4). In every case the shortest refractory period was located at the vulnerable atrial site. In vulnerable patients coupling intervals only slightly different from those which induced AF determined an abrupt change in the atrial electrogram recorded at the vulnerable site, suggesting a modified and in some way abnormal behaviour of the atrial activation wave. At the same time the interval between the beginning of the electrogram at the vulnerable site and of that obtained by the electrode positioned near the A-V node lengthened, suggesting a lower conduction velocity of the atrial activation wave. PAF evidenced significantly higher refractoriness and D than did N during sinus rhythm. Atrial pacing significantly reduced refractoriness but not D, which remained significantly higher than that of N at the same driven frequency. In conclusion, lower cycle length (paced rhythm), a short refractory period and the possibility of delivering extrastimulus at shorter coupling intervals seem conditions favourable to the induction of irregular activation of atrial myocardium. The increased D might be connected to the particular pathophysiological condition of our patients.
Sinus node electrogram is characterized by a smooth, low-frequency upstroke slope beginning before P wave and followed by a rapid deflection that results from initial atrial activity. Sinoatrial conduction time (SACT) can be measured directly (SACTD) from the sinus node electrogram as the interval from the onset of the upstroke slope to the onset of atrial activation. In our laboratory the values found in 20 patients with normal sinus node function ranged between 50 and 130 msec (mean 86.5 +/- 21.3). We compared SACTDs with those obtained by three indirect methods using the atrial premature stimulation technique (Strauss method) or the asynchronous pacing (Narula/Raviele method). In this part of the study were included 15 patients presenting A3A4 = A1A1 (i.e. without a depression of the sinus node) in the zone of reset and A2A3 greater than A1A1 (i.e. positive SACTs) when Narula/Raviele method was employed. No correlation was observed between directly measured and indirectly estimated SACTs. On this last point opposite conclusions have been drawn by the few papers published until now. The discrepancy may be explained by the different incidence on the study populations a) of the various factors determining the return cycle length b) of the measurement errors in SACTD.