Search

The investigation of cardiac dysrhythmias has become increasingly more complex, time consuming, and expensive.’ A complex case requires 5 to 8 hours of physician time. Although automated computer technologies have been applied to dysrhythmia recognition by surface ECG and postcase measurement of electrophysiology data,2 they have not, to our knowledge, been used to perform stimulation protocols or measure stimulated intracardiac intervals automatically during electrophysiologic testing on line. It is the purpose of this article to report the development of a stimulation/measurement system and programs, which automatically measure intracardiac intervals during electrophysiologic study, and to compare these measurements to those obtained in the usual manner.

Until now the selective recording of sinus potentials in man is not yet possible. Therefore, information about the sinus node function can only be obtained by means of indirect methods. One of these methods is the measurement of the so-called sinus node recovery time (Mandel et al., 1971 and Mandel et al., 1972). This method is based upon the known electrophysiological phenomenon of postdrive or overdrive suppression.

The effect of iv digoxin on normal sinus node function was studied after pharmacologic autonomic blockade (AB) in ten patients. Sinus cycle length (SCL), sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) were determined before and after AB with propranolol (0.2 mg/kg body weight) and atropine sulfate (0.04 mg/kg body weight) iv, and 15 min, 30 min, and 45 min after 1 mg iv digoxin. AB resulted in a significant decrease (P less than 0.01) in SCL (916 +/- 158 to 716 +/- 120 ms), in SNRT (1,229 +/- 221 to 871 +/- 190 ms), and in SACT (79 +/- 34 to 44 +/- 10 ms). Fifteen minutes after iv digoxin there was no significant change observed in SCL (716 +/- 120 to 708 +/- 92 ms), in SNRT (871 +/- 190 to 864 +/- 148 ms), or in SACT (44 +/- 10 to 46 +/- 15 ms). Similar results were obtained 30 min after digoxin administration. It is concluded that a single therapeutic dose of digoxin has no direct effect on electrophysiologic parameters of normal intrinsic sinus node function.

Electrophysiological studies were conducted in 13 patients with normal sinus node function and 14 with sinus node dysfunction before and after intravenous lidocaine. Mean +/- SEM sinus cycle length significantly shortened from 810 +/- 34.3 to 774 +/- 34.3 msec in patients with normal sinus node (P less than 0.001) and from 1061 +/- 67.6 to 1016 +/- 64.5 msec in patients with sinus node dysfunction (P less than 0.025) after lidocaine. Mean sinus recovery time was 1027 +/- 49.4 before and 1026 +/- 52.5 msec after lidocaine in patients with normal sinus node (NS) and 1269 +/- 97.7 before and 1170 +/- 73.8 msec after lidocaine in patients with sinus node dysfunction (P less than 0.05). Mean calculated sinoatrial conduction time was 87 +/- 9.5 before and 90 +/- 9.2 msec after lidocaine in patients with normal sinus node (NS) and 80 +/- 10.3 before and 96 +/- 10.2 msec after lidocaine in patients with sinus node dysfunction (P less than 0.001). Mean atrial effective and functional refractory periods were not significantly changed with lidocaine. Thus lidocaine shortened sinus cycle length in both groups, without affecting atrial refractoriness. Lidocaine appeared to depress perinodal tissue only in patients with sinus node dysfunction. The abbreviation of sinus recovery time in patients with sinus node dysfunction could reflect increased sinus automaticity and/or increased perinodal refractoriness, allowing entrance block to occur. This mechanism may explain why sinus arrest has been noted in some patients during lidocaine administration.

We reviewed the values and the limitations of deductive analysis and electrophysiological testing of sinoatrial arrhythmias (SAA). Both methods have a place in the evaluation of SAA and are complementary. Careful analysis of the surface ECG and the response of the sinus node to various tachyarrhythmias and to atrial premature beats can provide important information about the automatically of the sinus node and sinoatrial and atriosinus conduction. Because of the sporadic nature of some SAA, the surface ECG sometimes must be supplemented by ambulatory ECG recording. This approach improves one's ability to analyze the underlying mechanism and it can also clarify the relation between the SAA and the patient's symptoms. Electrophysiological testing can be employed to reproduce certain SAA and to assess the effects of various drugs on sinus node function. This approach is superior to deductive analysis in the identification of some sinoatrial conduction abnormalities and sinus node reentry. Among the disadvantages of electrophysiological testing are its invasive character and the fact that normal electrophysiological results do not exclude sinus node dysfunction. A definitive clarification of the underlying mechanism of SAA requires direct recording of the sinus node electrogram.

Six-hydroxydopamine (6OHDA) was injected directly into the subepicardium of the sinus node area in an attempt to damage sympathetic nerve terminals in the sinus node. The changes in sinus node function were observed for 4 weeks. The predominant rhythm was of sinus origin throughout the observation period. The sinus rate progressively decreased from 145.1 +/- 14.2 to 76.2 +/- 12.1 beats/min during the first week after injection of 6OHDA. The sinus rate remained at this level for 2 weeks, followed by a gradual increase to 89.3 +/- 18.2 beats/min 4 weeks after injection of 6OHDA. These sinus rates were only significantly different from control dogs through the 14th postoperative day. The sinus rate was considerably increased by intravenous atropine injections 5 to 7 days after the injection of 6OHDA into the sinus node area. The sinus node recovery time was much longer in dogs with an injection of 6OHDA than that in the control dogs throughout the observed period. These results suggest that elimination of the sympathetic influences on the sinus node can be achieved by direct injection of 6OHDA into the sinus node area in the dog, and that sinus node function can be depressed by decreasing sympathetic tone alone, in the absence of an intrinsic dysfunction of the sinus node.

The sick sinus syndrome is a descriptive term coined by Lown (1966) and popularized by Ferrer (1968), referring to a constellation of clinical signs, symptoms, and electrocardio-graphic (ECG) criteria defining sinus node dysfunction. The syndrome is characterized by syncope or other manifestations of cerebral dysfunction in association with sinus brady-cardia, sinus arrest, sinoatrial block, alternating bradyarrhythmias and tachyarrhythmias and/or carotid hypersensitivity. Clinical signs and symptoms, however, result from failure of escape pacemaker function not from sinus node malfunction per se (Mandel and Laks, 1974); thus, the sick sinus syndrome may represent a generalized disorder of the conduc- tion system.

Twenty-four hour recording of electrocardiogram was performed in 5 cases, aged from 42 to 75 years, with paroxysmal tachyarrhythmias (paroxysmal supraventricular tachycardia (PSVT) 2 cases and paroxysmal atrial fibrillation (PAf) 3 cases) for the purpose of assessing the effects of digitalis on sinus node function from the chronobiological point of view. All of the pauses following the termination of PSVT or PAf observed during a day were measured in 4 cases as the sinus node recovery time (SNRT). Corrected sinus node recovery time (CSNRT) was determined by subtracting the penultimate P-P cycle length from the SNRT. Both SNRT and CSNRT were prolonged in all cases after digitalis administration. In 1 case observation on the diurnal variation of SNRT and CSNRT showed the most marked prolongation of these values at 6:00 a.m. after digitalis administration. The second degree of SA block was observed in 2 cases in the early morning after digitalis treatment. In the other 2 cases sinoatrial conduction time (SACT) was calculated by the use of premature atrial contraction and corrected by dividing by the basic cycle length before and after digitalis administration. Neither SACT and CSACT showed significant differences between the values before and after the treatment in 2 cases, nor the diurnal variation of SACT and CSACT showed significant differences. Above results suggest that digitalis should be used with caution in patients with paroxysmal tachyarrhythmia because even small amounts of digitalis might provoke sinus node dysfunction. Twenty-four hour recording of electrocardiogram is useful in the earlier recognition of sinus node dysfunction induced by digitalis.

La cryosonde inhibe la fonction sinusale et permet la tachycardie auriculaire induite par l'isoproterenol

During the last decade, propranolol has been used clinically in the management of patients with arrhythmias, angina pectoris and hypertension (1–8). However, in man little data are available pertaining to the electrophysiological effects of propranolol on the normal sinus node function. In most of the previous studies the effect of propranolol has been analyzed regarding only one parameter of sinus node function, i.e. the changes in spontaneous cycle length or rate. Despite isolated reports in man, published data on the effects of propranolol on other parameters of sinus node function are limited (9–15). In view of its extensive clinical use in patients with various types of arrhythmias, especially supraventrl- cular tachycardias (SVT), i.e. atrial fibrillation, atrial flutter, or atrial tachycardia, which inherently produce overdrive suppression of the sinus node, it is of clinical importance to learn the effects of propranolol on various parameters of sinus node function, both in patients with normal and abnormal sinus node function. The purpose of this paper is to present our data on the effects of intravenous propranolol on 3 parameters of sinus node function: 1) spontaneous cycle length, 2) sinoatrial conduction time and 3) sinus node recovery time.

The sick sinus syndrome (German, Sinusknotensyndrom; French, maladie de l’oreillette) encompasses a group of cardiac rhythm disturbances and their corresponding clinical manifestations which, in the last analysis, are a consequence of impaired formation and/or conduction of sinus node impulses [5, 9, 19]. This paper deals with clinical manifestations due to defective sinus node function as well as relevant problems in conjunction with pacemaker therapy. With respect to the latter, it appears reasonable and profitable to present our own findings on the clinical manifestations — which we believe attributable to disturbance of sinus node function — on a group of those of our patients whose illness could only be managed by pacemaker implantation (the mode of patient selection for this topic is presented in more detail under the heading “Discussion”).

Verapamil is the prototype of slow-channel inhibiting drugs which exert their effect mainly on the sinus and atrioventricular node (Bayer et al., 1975; Kohlhardt et al., 1976; Wit and Cranefield, 1974; Zipes and Fischer, 1974). Experimental studies in the isolated sinoatrial preparation have shown that it has a marked depressant effect on sinus node activity (Bayer et al., 1975; Chiba, 1975; Obayashi et al., 1975; Wit and Cranefield, 1974). Verapamil causes a decrease in the amplitude of the action potential and a small decline in the maximal diastolic potential (Wit and Cranefield, 1974). Sinus node discharge is decreased and may be followed by subtreshold oscillations leading to irregular failure of impulse initiation (Bayer et al., 1975; Kohlhardt et al., 1976; Wit and Cranefield, 1974). Selective injections of verapamil into the right coronary artery of the dog also caused a decrease in heart rate with appearance of nodal rhythms which was not the case if it was administered intra- venously (Garvey, 1969). In contrast to the experiments in isolated preparations, studies in the intact animal have failed to demonstrate a depressant effect of verapamil on the sinus node at therapeutic doses (Garvey, 1969; Obayashi et al., 1975). Heart rate increases after iv injection of verapamil (Garvey, 1969). However, after high doses not used in the clinical setting, marked sinus suppression also ensued in the conscious dog (Obayashi et al., 1975).

Sinus node electrograms (SNEs) on atrial overdrive suppression test (AOD) and estimated sinoatrial conduction time (SACT) measurements were recorded. Typical SNE (TSNE), characterized by low-frequency, anatomically localized pre-P wave potentials (Reiffel et al.) were obtained in 12 of 18 patients (pts) with normal sinus node function (group I) and 15 of 26 pts with sick sinus syndrome (SSS) (group II). In 9 of 15 SSS pts but only 2 or 12 in group I “atypical” SNEs (ASNE) with inverted waves at the beginning of P wave were recorded on SNE recordings of the first sinus recovery beat by overdrive atrial pacing (OAP) for either AOD or SACT measurements, or both. On the basis of ASNE following OAP, the 26 SSS pts fell into 3 subgroups: TSNE with the same configuration as recorded before OAP was observed without ASNE throughout the study in 6 pts (IIA). ASNE was observed without TSNE throughout the study in 11 pts (IIB). TSNE before OAP and ASNE following OAP were recorded in 9 pts (IIC). Corrected sinus node recovery time in IIB was significantly longer than in either IIA or IIC (P < 0.0005). Estimated SACT (Narula’s method) for either A, B or C was significantly (P < 0.0005) longer than in group I. There was no significant difference in either estimated SACT or directly measured SACT between IIA and IIC. A significant correlation existed between estimated SACT and directly measured SACT in group I (r = 0.88) and IIA (r = 0.75) (P < 0.01) but not in IIC (r = 0.48). ASNE may result from a pacemaker shift.

The mechanism responsible for spontaneous cardiac rhythmicity has been of interest to physicians since the time of Hippocrates.1From the 17th to the 18th century, a neurogenic theory was attributed to Willis.1However, a different explanation was proposed in 1754 by Haller; he thought that the heart beat originated from intrinsic irritability of myocardial cells.2This concept was further supported by the observation that embryonic myocardial cells beat rhythmically considerably before innervation.3 The presence of a specialized cardiac area responsible for the intrinsic rhythmicity of the mammalian heart was not identified until the late 19th and early 20th centuries. At that time, the pacemaker site was identified as an area between the superior and inferior vena caval insertions into the right atrium. Experiments were performed to confirm this area as the "pacemaker" of the heart by studying (1) the shape of the P wave, (2) the

We have performed an electrophysiologic study (EPS) in 18 subjects (mean age 21 +/- 17 years) with normal sinus node function (group A) and in 15 patients (mean age 43 +/- 26 years) with sinus node dysfunction (group B). Three extrastimulus methods (both Strauss and Kirkorian methods and our modification of the extrastimulus method) were carried out in 31 patients of both groups and sinoatrial conduction times (SACTSTR, SACTKIR,SACTMOD) could be estimated in 27 of them. SACT by the Narula method (SACTNAR) was assessed in 25 patients of both groups. Sinus node electrograms (SNEs) were attempted in 22 patients and were obtained in 17 of them. Among the indirect methods, by comparison with SACTSTR in group A the best correlation was for SACTMOD (r = 0.81) and the weakest for SACTKIR (r = 0.67); there was no significant difference between SACTs estimated by Strauss and other methods. In group B the weakest correlation was also for SACTKIR (r = 0.68), whereas the correlations for both SACTMOD and SACTNAR were similar (r = 0.72 and r = 0.74, respectively); in this group SACT was significantly underestimated only by the Kirkorian method (P less than 0.01; sensitivity of 45%). By our method sensitivity was 82%, similar to both the Strauss and Narula methods (92 and 92%, respectively). By comparison of indirect methods with the direct measurement of SACT we have found similar good correlations for the Strauss, our own, and the Narula methods in group A (r = 0.81, r = 0.75, r = 0.79, respectively) and in group B (r = 0.81, r = 0.86, and r = 0.72, respectively); here too the weakest correlation was, in both groups, for the Kirkorian method (r = 0.67, and r = 0.68, respectively). The SACT in group B was the more significantly underestimated (P less than 0.001). Significant underestimation of SACT occurred also by our method and the Strauss method (P less than 0.01, and P less than 0.001, respectively), whereas the Narula method did not significantly underestimate the directly measured SACT. From the SNEs after atrial pacing we have shown the limitation of the Kirkorian method and observed the conspicuous beat-to-beat variability of SACTdirect' as the possible explanation of chaotic pattern of return cycles by the extrastimulus methods in some patients of group B.(ABSTRACT TRUNCATED AT 400 WORDS)

Although the mechanism responsible for cardiac rhythmicity has been of interest to physicians since the time of Hippocrates it was not until the late 19th and early 20th century that experiments were designed which identified a pacemaker site (493,536). Clinical disorders of sinus node function have, however, only been the subject of reports over the past several decades (75,225,228,757). Studies were then directed toward the catagorization of the clinical manifestations of sinus dysfunction in man. Ferrer, in her initial description, commented on the multifaceted clinical presentations of sinus node dysfunction in man (263). Subsequently, workers have commented on the varied clinical background and subsets of electrocardiographic diagnoses present during the clinical manifestations of sinus dysfunction (264,522,586,670,706).

We have recently described the electrophysiological basis of a new algorithm for the QT (TX) sensing rate responsive pacemaker. By using the new software program running on the standard programmer it has been possible to simulate the new algorithm in ten patients with complete heart block (seven patients had implanted TX units and three were paced with an external TX pacemaker) during routine exercise testing. In this way a single-blind, intra-patient comparison of the pattern of pacing rate change using both the existing and new algorithms was possible. In nine out of the ten cases the time taken to increase the pacing rate from 70 to 80 bpm was reduced significantly when the new algorithm was used (P = 0.037). Additionally, the correlation between the atrial and ventricular rates in those patients with normal sinus node function (seven patients) was determined. In all cases we have observed a significantly improved correlation between the atrial and ventricular paced rates during exercise with the new algorithm (P less than 0.001).

The design of atrial synchronous, ventricular inhibited (VDD) pacemakers has been improved. Physiologic long-term benefit has now been established, although this mode of pacing accounts for approximately one percent of implanted devices. With the ultimate control of pacemaker-mediated tachycardia through atrial refractory programming close at hand or already available, one might expect an increase in VDD pacing in patients with exercise-induced high degree heart block and stable sinus node function.

This study compared a new method to estimate sinoatrial conduction time (SACT) using continuous atrial pacing proposed by Narula et al with the widely used method using premature atrial stimulation originally proposed by Strauss et al. The estimated SACTs by the two methods were obtained in 19 patients with normal sinus node (SN) function (Group A) and 8 patients with abnormal SN function (Group B). Estimate of the SACT by the Narula method was taken as the difference between the first atrial return cycle after pacing and the basic sinus cycle length (BSCL). The Narula method was performed for a train of 8 consecutive beats at three different pacing cycle length (PCL); PCL (1) greater than or equal to BSCL--50, PCL (2) greater than or equal to BSCL--100 and PCL (3) greater than or equal to BSCL--150 msec. In group A, the estimated SACTs by the Strauss method was 185 +/- 49.3 msec, meanwhile the SACTs by the Narula method were 148 +/- 80.7 at PCL (1), 181 +/- 58.7 at PCL (2) and 212 +/- 84.5 msec at PCL (3) (mean +/- SD); the coefficient of correlation between the Strauss method and the Narula method were 0.58, 0.84, and 0.67, respectively. On the other hand, in group B, atrial return cycles by the Narula method were abnormally prolonged (over 215 msec) in 5 of 8 cases (63%) even at PCL (2) and in all of the cases (100%) at PCL (3). By the Strauss method, SACTs in 6 of 8 cases could not be defined; however it was possible to assess the type of SN dysfunction by the pattern of the atrial return cycles. In conclusion, the estimated SACT by the Narula method at PCL (2) corresponded well with the SACT by the Strauss method in patients with normal SN function. However, it was difficult to determine SACT in patients with Sick Sinus Syndrome by both methods.

To compare the effects of ethmozin on sinus node (SN) function in the presence (9 patients) and absence (17 patients) of SN dysfunction, sinus cycle length (SCL), maximal corrected sinus recovery time (CSRT), paced cycle length yielding peak SN suppression, and indirect sinoatrial SA conduction time (SACT) were determined before and after intravenous administration of ethmozin in the dose 2 mg/kg. The mean +/- SD SCL were significantly shortened in patients with normal SN and were not changed in patients with SN dysfunction after ethmozin administration. The mean maximal CSRT was 252 +/- 72 before and 284 +/- 86 ms after ethmozin administration in patients with normal SN function (p less than 0.05). In patients with SN dysfunction (p less than 0.1) the mean maximal CSRT was found to be 1016 +/- 434 before and 2170 +/- 1756 ms after ethmozin administration. The mean SACT was 158 +/- 41 before and 174 +/- 51 ms after drug administration in patients with normal SN (p less than 0.05). Four out of nine patients with SN dysfunction developed second degree SA exit block after ethmozin administration, whereas SACT increased significantly in the remaining group of patients (180 +/- 35 to 210 +/- 32 ms; p less than 0.05). The PR, PA, AH, and HV intervals significantly lengthened and the valves of QRS and QT were not changed after ethmozin administration in either group. The conclusion is drawn that ethmozin should be administered cautiously to patients with SN dysfunction, particularly to patients with SA exit block, sinus pauses, or secondary pauses (in particular, with bradycardia-tachycardia syndrome).

A direct recording of sinus node activity has not yet been accomplished in man. Therefore, indirect methods for estimation of sinus node activity and sino-atrial conduction have been used. In addition to high rate test, programmed atrial stimulation was introduced for assessing sinus node function (Goldreyer and Damato, 1971; Saroff et al., 1971 ; Narula et al., 1972). In 1973 Strauss et al. used this technique for calculation of sino-atrial con- duction time in man. Since then many clinical investigators have published their experi- ences with this method (Seipel et al., 1974; Steinbeck et al., 1974; Dhingra et al., 1975; Goodman et al., 1975; Mandel et al., 1975; Masini et al., 1975; Medvedowsky etal., 1975; Engel et al., 1976; Scheinman et al., 1976; Strauss et al., 1976; Breithardt et al., 1977; Crook et al., 1977; Dhingra et al., 1977; Jordan et al., 1977; Steinbeck and Luderitz, 1977; Ueda et al., 1977). However, experimental and clinical data have shown that this method is burdened by unresolved methodological problems (Miki and Rothberger, 1922; Eccles and Hoff, 1934; Langendorf et al., 1962; Bonke et al., 1969, 1971; Strauss and Bigger, 1972; Fleischman, 1973; Klein et al., 1973; Miller and Strauss, 1974; Reiffel et al., 1974, 1975; Seipel and Breithardt, 1975; Ticzon et al., 1975; Breithardt and Seipel, 1976; Strauss and Wallace, 1976). In addition, the clinical relevance of the method is an unanswered question. Therefore, we performed programmed atrial stimulation in different groups of patients with and without sinus node dysfunction in order to correlate SACT with other clinical data.

Overdrive atrial stimulation was performed in 20 electrophysiologically normal children at the time of routine diagnostic cardiac catheterization, for the determination of the sinus node recovery time (SNRT). Measurements were made at pacing rates of 120, 150, 180, and 200 beats/min. The absolute recovery times demonstrated wide range of values (420-1280 msec). Expressed as a percent of the resting P-P interval, values at pacing rates of 120 and 150 beats/min were 109-166%, with significantly less overdrive suppression (P less than 0.001) occurring at the two faster pacing rates. Atropine diminished the maximum SNRT in all patients tested. This study reports normal values for the SNRT in children. Factors which influence the SNRT are the resting heart rate, the rate of overdrive, and the autonomic tone. In children, the sinus node recovery time should be expressed in terms of the resting sinus interval.

To assess the variability of the currently used electrophysiologic parameters and their possible circadian rhythm, sequential bedside electrophysiologic testing was performed during a 24-hour period, at intervals of 1 to 2 hours, in 12 patients who had normal atrioventricular (AV) conduction times and normal sinus node function. The coefficients of variation during the 24-hour period were: +/- 10.4% for the R-R interval, +/- 10.6% for the sinus node recovery time (SRT) at atrial pacing of 100 bpm, +/- 32.5% for the corrected SRT, +/- 15.1% for the ventriculoatrial (VA) effective refractory period (ERP), +/- 8.3% for the AV nodal ERP, +/- 5.7% for the AH interval, +/- 5.2% for the HV interval, +/- 5.5% for the atrial ERP, +/- 3.3% for the right ventricular ERP, +/- 2.8% for the QT interval, +/- 4% for the VA interval, and +/- 3.4% for the retrograde Kent bundle ERP. Between 12:00 midnight and 7:00 AM, there was significant lengthening of: the sinus node rate (p less than 0.0005), the SRT at atrial paced rates of 100 and 120 bpm (p less than 0.025), the QT interval duration (p less than 0.025), and the ERP of the atria (p less than 0.025), AV node (p less than 0.01), and right ventricle (p less than 0.05). Thus conventional electrophysiologic parameters are subject to daily variability and, like sinus node function, AV nodal and myocardial refractoriness follow a circadian rhythm with an acrophase between 12:00 midnight and 7:00 AM. In addition, prolonged bedside recording of the His bundle potential can be reliably obtained.

Recently, disorders of sinus node function gained clinical importance. Impaired sinus node function in sinoatrial disease, which includes sinus bradycardia, sinus arrest, sinoatrial block, and the bradycardia-tachycardia syndrome [8, 11, 14, 19], cannot easily be assessed, as the recording of electrical activity of sinus node pacemaker cells is not available in man. The analysis of atrial activity in the surface electrogram permits only an overall estimation of sinus node function. This involves the ability to act as an impulse generator and includes the conduction of the impulse from the pacemaker site to the atrium.

The drug management of sick sinus syndrome (SSS.) at the present time is not optimal. Due to this we decided to investigate the effect of Atropine (A) and Glucagon (G) in this syndrome. The effect of Glucagon and A in the sinus (SN) and atrioventricular node (A VN) was compared in 11 patients (pts.), 5 with sick sinus syndrome and 6 with normal sinus node function (N) G shortened the sino-atrial recovery time (SART) in N. by 16.6% (1046 ± 112 to 856 ± 61 msec) P < 0.025 and by 23% in SSS (1408 ± 16 to 1058 msec + 110) P < 0.025 A shortened the SART in N by 19.5% (1046 ± 112 to 832 msec + 77) P < 0.025 and by 26.7% in SSS (1335 ± 193 to 945 msec ± 182) P < 0.10. G increased AVN conduction in N by 12% (165 to 141.6 msec ± 34) P < 0.010 and A by 19% (178 ± 27 to 142 msec ± 21) P < 0.0025. The effects in SSS was similar. G increased the heart rate (HR) by 17% in Nand 26% in SSS (NS). A increased the HR by 26% in Nand SSS. In conclusion G and A have similar effects of shortening the SART and increasing A VN conduction, although pts with SSS are more sensitive to both drugs than N. The effect of G lasted up to 5 minutes while A up to 10 minutes. These electrophysiologic findings show that drugs can be used for the temporary management of patients with SSS.

A simple, inexpensive device capable of measuring the refractory period of the cardiac conducting system has been described. All components used in the device may be purchased for less than $150 and commercial equipment capable of performing similar tasks costs over two-thousand dollars. The undesired features of previous methods have been eliminated and results of using the device in clinical settings have been given.

Already 25 years ago T.C West (1955) described the first microelectrode study of the sinus node. Since then many investigators have been concerned with sinus node function (Brooks and Lu, 1972; Bonke, 1978). Although highly sophisticated techniques have been applied, it looks today that the definite words about the sinus node cannot yet be written. West’s own observations gave already an indication of some of the problems involved. Describing the electrical activity recorded from single nodal cells, he defined “the true pacemaker” as the site which “depolarizes earlier than any other region during any one cardiac cycle”. He established that this “true pacemaker activity” was not confined to a fixed site, he could easily induce shifts of pacemaker dominance by adding drugs like acetylcholine and adrenaline. Those observations indicated that the sinus node is functionally inhomogeneous, at least in its responses to autonomic mediators. Several pacemakers are capable to drive the sinus node and those pacemakers show different responses. Thus, one single pacemaker cell is not representative for the sinus node as a whole. Sinus nodal cells are coupled electrically (Bonke, 1973; Masson-Pevet et al., 1979; Bukauskas et al., 1981), so the configuration of the electrical activity recorded from single cells depends not only on their own activity, but also on changes of the activity of surrounding cells (Bonke, 1978; Mackaay et al., 1980a).

A patient having high grade AV block with intact sinus node function is presented in whom DDDR pacing provided the benefit of preventing 2:1 pacemaker block in response to exercise-induced sinus tachycardia. In paired treadmill tests with the patient blinded as to pacing mode, she was able to exercise longer (7.5 vs 6.6 METS) when programmed in DDDR than in DDDO. This is attributable to circumvention of 2:1 pacemaker block which had resulted in abrupt onset of fatigue and SOB (shortness of breath) when the sinus rate exceeded the maximum tracking rate of 130/min. Outpatient ambulatory electrocardiographic monitoring confirmed this phenomenon during relatively strenuous activity. The theoretic advantages of dual chamber rate modulated pacing compared to the DDDO and VVIR modes are discussed.

The sinus node function was evaluated by rapid atrial pacing in 35 aged patients (mean age 78.2 years) including 10 aged controls, 12 cases with various degrees of AV block, 6 with bradycardia-tachycardia syndrome (BTS), and 7 with sinus bradyarrhythmia (SB). AV block was further divided into A-H block (7 cases) and H-V block (5 cases) by His bundle electrogram which was simultaneously recorded with 3 leads of surface electrocardiogram. Sinus node recovery time (SRT) was measured and its maximum value (SRTmax) was selected from SRTs obtained after pacing with various rates and durations in each patient. SRTmax was also expressed as percentage of the control P-P interval (%SRTmax). For patients in whom the study was repeated 3 to 8 months later, %SRTmax was reproducible in 9 of 14 instances. Prolongation of SRT was not always observed as the rate and/or duration of pacing was increased. SRTmax and %SRTmax were 1,363 +/- 188 msec and 147 +/- 19% (mean +/- SD), respectively, for aged controls, 1,597 +/- 442 msec and 156 +/- 31% for patients with AV block, 2,087 +/- 1,315 msec and 203 +/- 132% for those with BTS, and 3,069 +/- 1,287 msec and 247 +/- 115% for those with SB. SRTmax exceeding the range for aged controls was noted in 4 of 7 cases (57%) with A-H block, 2 of 6 (33%) with BTS, and 5 of 7 (71%) with SB; normal SRT was not infrequently observed in patients with sick sinus syndrome, especially in those with BTS. Analysis of 10 consecutive atrial cycles following cessation of pacing revealed that in 8 cases the first P-P interval (SRT) was followed by longer ones in some occasions (secondary suppression). It was observed almost exclusively in patients with sick sinus syndrome. The possibility of this phenomenon to reflect another feature of sinus node abnormality was discussed.

Although a review article such as this could summarize studies evaluating the effects of a variety of different drugs on sinus node function, we feel that this information is accessible in other articles and ask the interested reader to consult Breithardt et al. (1975, 1976, 1976a, and 1976b), Dhingra et al. (1975, 1976 and 1976a), Dighton (1974, 1975), Engel and Schaal (1973), Goodman et al. (1975), Jose and Taylor (1969), Reiffel et al. (1975), Schamroth (1966), Seides et al. (1974), Steinbeck and Luderitz (1977), Stern and Eisenberg (1969). Instead, we will review the mechanisms underlying drug depression of sinus node function and discuss two variables that may influence the results obtained in any electro- pharmacologic study, namely, the population studied, the experimental protocol and a limitation of the testing procedures.

Pacemaker utilization in the United States has increased at a remarkable rate over the last 15 years. At a time when battery replacements have diminished steadily with the development of lithium power sources, Parsonnet et. al. have still demonstrated a 600516 growth rate in implants over the last 10 years(1). As devices have proliferated they have also become more technologically advanced and more complex with a significantly broader application to both brady and tachyarrhythmias. Although single chambered devices still account for the majority of U.S. implants, it has been estimated that dual-chambered pacemakers will ultimately be responsible for 25–4096 of the pacemaker market(2). Moreover, the continued inadequacy of antiarrhythmic drug therapy in preventing life-threatening arrhythmias and the increased short-term salvage rate for patients who have suffered cardiac arrests both support a rapidly developing role for specialized pacemakers for antiarrhythmic use.

In 35 patients aged 18 to 69 years (mean 48) with clinical, electrocardiographic, or electrophysiological evidence of normal sinus node function, the effect of intravenous propranolol (0.1 mg/kg) was assessed on 3 indices of sinus node function. The drug significantly prolonged sinus node cycle length (12%), slightly prolonged the corrected sinus node recovery time (15%), and slightly but insignificantly lengthened sinuatrial conduction time. Propranolol may be administered safely in patients with normal sinus node function without the fear of producing severe sinus bradycardia, sinuatrial block, sinuatrial pauses, or prolonged sinus asystole, after spontaneous or stimulation-induced conversion of a tachycardia.

The purpose of this study was to find out whether fransesophageal pacing could be utilized for assessment of sinus node function in patients with sick sinus syndrome (SSS). In 17 patients with SSS (study group) we compared the results of sinus node tests obtained both in the basal state and after pharmacological autonomic blockade by endocavitary stimulation and, 24 hours later, by transesophageal pacing. In another group of 17 patients with SSS (control group), we compared the results obtained by two endocavitary studies. In “study group”, sinus cycle length (SCL) and corrected sinus node recovery time (CSRT) did not show significant differences between the two studies both in the basal state and after autonomic blockade, whereas sinoatrial conduction time (SACT) was more prolonged during esophageal pacing (P < 0.01). In “control group”, sinus node measures did not show significant differences between the two studies. In the “study group,” the following coefficients of correlation were obtained in the basal state: SCL, r = 0.65, CSRT, r - 0.57, SACT, r = 0.52 and after autonomic blockade: SCL, r = 0.95, CSRT, r = 0.62 and SACT, r = 0.53. In the basal state, the correlation for SCL and CSRT between the two studies was lower in the “study group” than in the “control group” (P < 0.05), whereas after autonomic blockade the correlation for sinus node measures did not show significant differences between the two groups of patients. These data suggest that transesophageal study influences the autonomic tone regulating the sinus node; however, it is not responsible for important variations in sinus node measures. Thus, this noninvasive method appears useful for assessment of sinus node function in patients with SSS, considering, however, that SACT is more prolonged during pacing fram the esophagus.

We describe an adult with chronic (three years' duration) acquired nonparoxysmal junctional tachycardia, a previously undescribed rhythm. Ambulatory monitoring revealed junctional rates ranging from 75 to 110 beats/min. Electrophysiologic studies demonstrated intact atrioventricular and ventriculoatrial conduction with a normal H-V interval (43 msec) and narrow QRS. Underlying sinus node function appeared to be normal (recovery time of 900 msec). Junctional rate increased with administration of atropine and isoproterenol, suggesting that the junctional pacemaker was located in the proximal His bundle. Electrocardiographic and electrophysiologic observations suggested that this case of chronic nonparoxysmal junctional tachycardia was benign, not necessitating therapy.

To investigate the dynamics and propensity for arrhythmias in intact transgenic hearts comprehensively, optical strategies for panoramic fluorescence imaging of action potential (AP) propagation are essential. In particular, mechanism-oriented molecular studies usually depend on transgenic mouse hearts of only a few millimeters in size. Furthermore, the temporal scales of the mouse heart remain a challenge for panoramic fluorescence imaging with heart rates ranging from 200 min-1 (e.g. depressed sinus node function) to over 1200 min-1 during fast arrhythmias. To meet these challenging demands, we and others developed physiologically relevant mouse models and characterized their hearts with planar AP mapping. Here, we summarize the progress towards panoramic fluorescence imaging and its prospects for the mouse heart. In general, several high-resolution cameras are synchronized and geometrically arranged for panoramic voltage mapping and the surface and blood vessel anatomy documented through image segmentation and 3D heart surface reconstruction. We expect that panoramic voltage imaging will lead to novel insights about molecular arrhythmia mechanisms through quantitative strategies and 3D analysis of intact mouse hearts.

1920;7:353–370. 8. Klein I, Ojamaa K. Thyrotoxicosis and the heart. Endocrinol Metab Clin North Am 1998;27:51–62. 9. Von Olshausen K, Bischoff S, Kahaly G, Mohr-Kahaly S, Erbel R, Beyer J, Meyer J. Cardiac arrhythmias and heart rate in hyperthyroidism. Am J Cardiol 1989;63:930–933. 10. Valcavi R, Menozzi C, Roti E, Zini M, Lolli G, Roti S, Guiducci U, Portioli I. Sinus node function in hyperthyroid patients. J Clin Endocrinol Metab 1992;75:239–242. 11. Colzani RM, Emdin M, Conforti F, Passino C, Scarlattini M, Iervasi G. Hyperthyroidism is associated with lengthening of ventricular repolarization. Clin Endocrinol 2001;55:27–32. 12. Te-Chuan Chou TKK. Electrocardiography in Clinical Practice. 4th ed. Philadelphia: WB Saunders, 1996:535–540. 13. Ee B, Cheah JS. Electrocardiographic changes in thyrotoxic periodic paralysis. J Electrocardiol 1979;12:263–279. 14. McFadzean AJ, Yeung R. Familial occurrence of thyrotoxic periodic paralysis. Br Med J 1969;1:760. 15. Chia BL, Lee KH, Cheah JS. Sino-atrial Wenckebach conduction in thyrotoxic periodic paralysis: a case report. Int J Cardiol 1995;47:285–289.

SEVERE bradycardia has been reported with the use of cimetidine.1 2 3 Bradycardia could have been spurious, but it recurred on rechallenge.1 , 2 Data from animal studies4 , 5 and human right-atrial fibers6 indicate that histamine-enhanced automaticity is antagonized by histamine2 blockers. These observations suggest that histamine2-receptor antagonism by cimetidine could worsen sick-sinus syndrome or blunt the chronotropic response to gastrointestinal hemorrhage. Therefore, we assessed the effect of cimetidine on sinus-node function in patients undergoing electrophysiologic testing. Methods Ten unmedicated patients underwent atrial pacing by use of a quadripolar catheter positioned at the upper portion of the right atrium. Heart rate (average . . .

The effect of amiodarone on sinus node function has been studied in 9 patients with symptomatic sick sinus node as documented by Holter-ECG. All patients had programmable dual-chamber pacemakers. Sinus node activity was assessed by intermittently inhibiting the pacemakers before and after four weeks of oral amiodarone treatment. Sinus node function was not altered by amiodarone in 5 patients but was severely depressed in 4 patients. Thus, it is concluded that amiodarone cannot be used safely in all patients with the tachybrady syndrome for the treatment of symptomatic tachyarrhythmias without concomitant pacing.

Symptomatic sinus bradycardia developed in two patients while they were taking methyldopa and digoxin. In one patient, bradycardia did not occur with either digoxin or methyldopa alone. The other patient, who had never taken methyldopa alone, did not demonstrate bradycardia with digoxin alone. In each patient, normal sinus node function was demonstrated after methyldopa and digoxin therapy was discontinued. Both patients continued to receive digoxin without recurrence of bradycardia. ( JAMA 1981;245:1241-1243)

AUTONOMIC INFLUENCES UPON ELECTROPHYSIOLOGIC PARAMETERS OF SINUS NODE FUNCTION IN IMMATURE PUPPIES: EFFECTS OF CHEMICAL SYMPATHECTOMY