Sinus Node Electrogram Research Articles

症例 洞結節電位直接記録法による洞自動能,洞房伝導の評価

症例 洞結節電位直接記録法による洞自動能,洞房伝導の評価

Investigation of Atrial Vulnerability by Analysis of the Sinus Node EG From Atrial Fibrillation Models Using a Phase Synchronization Method

Atrial fibrillation (AF) can result in life-threatening arrhythmia, and a clinically convenient means for detecting vulnerability remains elusive. We investigated atrial vulnerability by analyzing the sinus electrogram (EG) from AF animal models using a phase synchronization method. Using acetylcholine (ACh)-induced acute canine AF models (n= 4), a total of 128 electrical leads were attached to the surface of the anterior and posterior atria, and the pulmonary veins to form an electrocardiological mapping system. ACh was injected at varying concentrations with ladder-type adjustments. Sinus EGs and induced AF EGs that pertain to specific ACh concentrations were recorded.We hypothesize that the atrial vulnerability may be correlated with the Shannon entropy (SE) of the phase difference matrix that is extracted from the sinus EG. Our research suggests that the combination of SE with the synchronization method enables the sinus node EG to be analyzed and used to estimate atrial vulnerability.

Aortic stiffness is increased in acromegaly regardless the method of assessment

acid prevents atrial fibrillation associated with heart failure in a rabbit model. Am J Physiol Heart Circ Physiol 2011;300:H1814–21. [19] Michellucci A, Toso A, Mezzani A, et al. Noninvasive recording of sinus node activity by Pwave triggered SAECG. Validation using direct intra-atrial recording of sinus node electrogram. Am J Noninvasive Cardiol 1993;7:132–7. [20] Ehlert F, Gaur A, Steinberg JS. Correlation of the P-wave signal-averaged electrocardiogram to intra-cardiac atrial conduction. Circulation 1996;94:I-70. [21] Nomura M, Kawano T, Nakayasu K, Nakaya Y. The effects of losartan on signalaveraged P wave in patients with atrial fibrillation. Int J Cardiol 2008;126:21–7. [22] Chen J, Shearer GC, Chen Q, et al. Omega-3 fatty acids prevent pressure overloadinduced cardiac fibrosis through activation of cyclic GMP/protein kinase G signaling in cardiac fibroblasts. Circulation 2011;123:584–93. [23] Ciulla MM, Paliotti R, Esposito A, et al. Effects of antihypertensive treatment on ultrasound measures of myocardial fibrosis in hypertensive patients with left ventricular hypertrophy: results of a randomized trial comparing the angiotensin receptor antagonist, candesartan and the angiotensin-converting enzyme inhibitor, enarapril. J Hypertens 2009;27:626–32.

Role of the Low Amplitude Potential in the Initial P Wave Signal-Averaged Elestrogram in Sick Sinus Syndrome

The cause of abnormally low amplitude of the initial P wave signal-averaged electrocardiogram (P-SAECG) in patients with sick sinus syndrome (SSS) is unknown. Thirteen normal patients (Group C) and 33 with SSS (Group S) were examined. The root mean square amplitude for the initial 30 ms (EP30) and the duration of below-4 microV signals of the filtered P waves (ED4) were measured using the P-SAECG. The interval from an atrial potential on the sinus-node electrogram (SNE) to P wave onset (AS-P), and the interval from the P wave to the atrial potential on the His-bundle-electrogram (P-AH) were measured in the electrophysiological study. The sino-atrial conduction time was measured by a conventional method (indirect sino-atrial conduction time (SACTi)) and using SNE (direct sino-atrial conduction time (SACTd)). The EP30 was significantly lower and the ED4 significantly longer in Group S. The AS-P was significantly longer in Group S (p<0.01), but the P-AH was not different. In Group S, the AS-P was significantly correlated with EP30 and ED4 (p<0.01), but the P-AH was uncorrelated. The SACTi was significantly correlated with EP30 and ED4 (p<0.05), but the SACTd was uncorrelated. The abnormality of the initial portion of the P-SAECG observed in SSS appears to be due to disturbed conduction through the atrial myocardium around the sino-atrial node.

Clinical and Electrophysiological Characteristics of Binodal Disease

Although coexistence of atrioventricular conduction disturbances with sick sinus syndrome (SSS), so-called binodal disease (BND), is a frequently encountered disorder, its clinical significance and electrophysiological characteristics remain unknown. One hundred and seven patients with SSS were divided into BND (n=30) and N-BND groups (n=77). Sinus cycle length, sinus node recovery time (SRT), sino-atrial conduction time (SACT), the number of isolated sinus node electrograms, atrio-His (AH) interval, His-ventricular (HV) interval, intra-atrial conduction time (PA intervals) and QRS width were measured. In addition, the prevalence of bundle-branch block was obtained. The parameters of sino-atrial and intra-atrial conduction were significantly longer in the BND group: SRT (5,070+/-2,628 vs 3,122+/-1,856 ms, p<0.05), SACT (115+/-30 vs 87+/-21 ms, p<0.05), PA intervals (56+/-13 vs 41+/-8 ms, p<0.05). The BND group was more likely to have atrial fibrillation than the N-BND group (83.3% vs 53.2%, p<0.01). HV interval, QRS width and the prevalence of associated bundle-branch block did not differ between the 2 groups. BND patients not only had sino-atrial and atrioventricular node dysfunction, but also widespread atrial conduction disturbances. Thus, in the clinical setting BND should be categorized as severe SSS.

A noninvasive transesophageal signal averaging technique for detection of sinus node electrogram.

We have developed a noninvasive transesophageal signal averaging technique for direct recording of sinus node electrogram. In this study, sinus node electrograms were recorded from 106 of 138 patients (77%), comparable to that (46%) recorded by conventional transesophageal technique, 59 were male and 47 were female ranging in age from 10-74 years (mean 44.2+/-12.4 years). The signals from lead I, surface averaged lead and esophagus averaged lead were amplified (up to 100 microV/cm), filtered (0.1-50 Hz), AD converted to 16-bit accuracy at a sampling rate of 2 KHz and averaged by using the three channel low-noise amplifier. The signal averaged esophageal sinus node potentials are deflections of low-amplitude and low-frequency preceding the P wave. Two morphologies, the domed wave (64 of 106 patients, 60%) and the smooth upstroke slope (42 of 106 patients, 40%), can be seen. The directly recorded sinoatrial conduction time was 82.3 +/-18.6 msec (mean+/-2 SD), ranged from 23-112 msec, amplitude was 3.8-27.7 microV and dv/dt was 0.42-1.92 mV/sec. The sinoatrial conduction time recorded by the transesophageal catheter technique was comparable to that (80.4+/-18. 1 msec) recorded by the transvenous catheter method perfectly. We think that signal averaged sinus node electrogram could be recorded in sinus rhythm in most patients with normal sinus node function and proper filter settings, high amplification and anti-drift technique are important in recording signal averaged esophageal sinus node electrogram.

Electrophysiological testing of sinus node function: diagnostic and prognostic application-including updated information from sinus node electrograms.

Sinus node function, including automaticity, conduction, and refractoriness, can be studied in the human electrophysiology laboratory. This review details the current methods used for such studies and discusses their clinical value. Of special emphasis in this article is the role of sinus node electrography in the clinical laboratory. Included also is an update of the data relating the duration of sinus node depolarization as measure on sinus node electrograms to other parameters that assess sinus node function as well as data supporting the direct relationship between the duration of the sinus node depolarization as the severity of sinus node dysfunction.

A mathematical model of sinus node function: validation by recording of sinus node electrograms.

We have applied a mathematical function to model sinus node recovery after atrial pacing at different cycle lengths in 13 autonomically denervated, anesthetized canines. This model provides "pure" indexes of sinoatrial conduction and of suppression of automaticity. We compared sinoatrial conduction computed from the model (SACTc) with sinoatrial conduction measured directly utilizing a catheter recording the sinus node electrogram (SACTd) to test the validity of the model. We used both the model and the sinus node electrogram to further define events after pacing. There was close agreement between SACTc and SACTd with correlation coefficients at pacing cycle lengths of 20 and 50% below resting of 0.86 (P < 0.0001) and 0.78 (P < 0.0001), respectively. We verified that the conventional sinus node recovery time is due both to suppression of automaticity and prolongation of sinoatrial conduction. Sinoatrial conduction time returned rapidly to normal over 1-3 beats, whereas automaticity recovered exponentially over 20-40 postpacing intervals. The model accurately describes postpacing phenomena and has the potential to provide a useful adjunct to the measurement of the sinus node electrogram for assessment of sinus node function in the experimental laboratory.

Noninvasive Recording of Sinus Node Activity by P-Wave-Triggered Signal-Averaged Electrocardiogram: Validation Using Direct Intra-Atrial Recording of Sinus Node Electrogram

In order to evaluate if sinus node activity can be detected by surface ECG, at least 200 sinus beats of 3 bipolar orthogonal leads (horizontal, vertical, and sagittal position) were averaged in 33 consecutive patients (mean age: 58 ± 19 years). Each lead signal (0.5-300 Hz) was independently averaged triggering P wave by the template-comparing method and then filtered (0.5-25 Hz) and amplified. In 29 patients (88%), amplification revealed the presence of a progressive upstroke slope beginning during the isoelectric line and ending at the earliest observed atrial activation in the 3 nonamplified and nonfiltered leads (mean voltage: 9.3 ± 6.4 pV). Such pre-P signal was always lost with 50-Hz high-pass filtering, and could be present in 1 or more leads; in the latter case, the longest duration was considered. The length of pre-P signal proved to be strictly correlated (r = 0.9932, p < 0.001) with that contemporaneously furnished by the direct intra-atrial recording of sinus node electrogram (0.05-35 Hz, mean of at least 20 measurements). Mean values of noninvasive and invasive pre-P lengths were 76 ± 29 and 74 ± 30 ms, respectively. In conclusion, it seems possible to detect from surface ECG a pre-P activity whose character and timing are well correlated to those obtained by endocavitary recording of sinus node signal. These findings suggest the possibility of a clinical use of noninvasive sinus node activity recording for diagnostic purposes.

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 ± 2.8 s (mean ± SD).Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block.Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to >14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 ± 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 ± 1,686) and was normal in 5 patients and prolonged in 17.Group III consisted of seven patient with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 ± 1, 121).Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.

Postextrasystolic sinoatrial exit block in human sick sinus syndrome: Demonstration by direct recording of sinus node electrograms

Ten patients with sick sinus syndrome having repetitive sinus node electrograms during long postpacing pauses were studied during programmed atrial stimulation. Sinus node activity was recorded using a percutaneous catheter electrode. A sinus node electrogram was recorded before the return atrial beat in seven patients; it was similar to the sinus node electrogram observed during postpacing pauses and is clearly identified because sinoatrial conduction time was markedly prolonged following the atrial extra beat. Complete sinoatrial exit block occurred in four patients. (1) Sinus node electrograms were thus validated both during postpacing pauses and during programmed atrial stimulation in most patients with sick sinus syndrome. (2) Sinoatrial conduction time was markedly prolonged after one extrasystole, accounting for supracompensatory atrial return cycles. (3) If it were cumulative following multiple extrasystoles, this effect could constitute the electrophysiologic link between an abnormal response during programmed atrial stimulation and the complete sinoatrial block recorded during the pauses that follow rapid atrial pacing.

The Relationship Between Sinoatrial Conduction Time and Sinus Cycle Length Revisited

In 1974 we reported an inverse relationship between sinoatrial conduction time (SACT) and sinus cycle length (SCL) during sinus arrhythmia utilizing the indirect atrial premature stimulation technique for estimating SACT, However, this behavior seemed anomalous try analogy with the AV node. Subsequent to 1974, methodological considerations about and limitations of the indirect techniques for estimating SACT became apparent, making us question our former impression. When the capability to directly record sinus node electrograms was developed and established in the 1980s, we had the means to reevaluate the SACT/SCL relationship. This report presents our findings in 40 patients: the SACT/SCL relationship is direct, not inverse. Moreover, we also show that during the phasic fluctuations of sinus arrhythmia, the P‐P alterations are initiated more frequently by changes in sinoatrial conduction time than by changes in sinus cycle length.

The Duration of the Sinus Node Depolarization on Transvenous Sinus Node Electrograms Can Identify Sinus Node Dysfunction and Can Suggest Its Severity

Catheter recorded sinus node electrograms (SNE) allow visualization of sinus node depolarization (SND). The SND on a bipolar SNE is probably a composite reflecting both P cell action potentials and intranodal conduction. Reduced rate of rise, prolonged action potential duration and/or delayed intranodal conduction might each prolong the SND duration. Thus, SND duration might reflect several clinically important sinus node abnormalities and aid in the recognition of sick sinus syndrome. Moreover, the SND duration might be expected to be the most prolonged in patients with the most severe sinus node dysfunction. To test this hypothesis, we determined SND duration in 32 patients and correlated it with the presence or absence of evidence of sinus node dysfunction by ECG and/or electrophysiological (EP) studies. Seven patients had no sinus node dysfunction (group 1); 10 patients had mild sinus node dysfunction (a single abnormality of corrected sinus recovery time, sinoatrial conduction time, PCLp, or ECG) (group 2); and 15 patients had two or more abnormalities electrocardiographically and/or by EP testing (group 3). The SND duration (mean/range) was 129/95-190 msec in group 1, 151/95-225 msec in group 2, and 196/140-260 msec in group 3. In group 3, three patients who had ECG evidence of sick sinus syndrome and abnormalities on all three EP parameters, the SND duration was 230/200-260 msec. Carotid sinus massage (CSM) was found to prolong the SND duration in 5/7 patients in groups 2 and 3 where the SND could be measured both before and during CSM. CSM was necessary to allow visualization of the SND in 3/7 group 1 patients; thus their recorded values may be falsely long. The normal with a SND duration greater than 150 (190 msec) had it measured during CSM. None of the group three patients with SND duration less than msec had a prolonged CSRT or ECG evidence of sick sinus syndrome. Literature review revealed SNE recordings on 18 patients with sick sinus syndrome on which the SND duration could be measured; it was greater than or equal to 200 msec in all. Thus, the SND duration appears to reflect the presence and degree of sinus node dysfunction. Sinus node dysfunction appears unlikely if the SND duration is less than 150 msec and is likely to be severe if the SND duration is greater than 200 msec.

Sinus node electrogram recording in complete atrioventricular block

Surface electrocardiogram (ECG), sinus node electrogram (SNE), His bundle electrogram (HBE), and intracardiac electrogram of high right atrium (HRA) were recorded synchronously in 11 of the 14 consecutive cases with complete atrioventricular block (CAVB). SNE showed the presence of a pre-P wave that preceded in all the P wave on the ECG and had no relationship to QRS complex or TU repolarization. This confirmed that the pre-P wave arose from the sinus node. Direct sinoatrial conduction time (SACTd) in nine cases was within the normal range (<120 msec). SACTd in another two cases was prolonged to 185 msec and 210 msec, respectively, suggesting their abnormal sinus node conduction.

Correlation between directly measured and indirectly estimated sinoatrial conduction time in children

The indirectly estimated sinoatrial conduction time has been widely used in children to assess sinus node (SN) function, but has never been validated in pediatric patients. Using a standard quadripolar catheter with high amplification and low-pass filters, SN electrograms were recorded in 11 of 26 (42%) pediatrie cardiac patients (age range 10 months to 18 years) with normal SN function. The sinoatrial conduction time was measured directly from the SN electrogram and estimated indirectly by the premature stimulation and continuous pacing methods. The direct sinoatrial conduction time (15 to 91 ms) in these 11 patients (ages 1 to 18 years) correlated well with that estimated by the premature stimulation method (r = 0.81, n = 9, p < 0.01). There was a poor correlation between the direct and continuous pacing methods (r = 0.53, n = 8, p = 0.17). It was concluded that SN electrograms can be recorded in children and that there is a good correlation between the directly measured sinoatrial conduction time and the indirectly estimated sinoatrial conduction time by the premature stimulation method.

Comparison of indirect and direct sinuatrial conduction time by synchronous sinus node electrogram

In order to determine whether or not the estimated indirect sinuatrial conduction time represented the real sinuatrial conduction time, we recorded the synchronous sinus node electrogram, on which direct sinuatrial conduction time could be measured during constant atrial pacing, in 21 cases with normal sinus node function. The results show first that the difference between direct and indirect sinuatrial conduction time is statistically significant ( P < 0.05); the correlation of the two is poor ( r = 0.29). Second, the direct sinuatrial conduction time after constant atrial pacing is significantly longer than that before constant atrial pacing, which means constant atrial pacing has resulted in obvious depression of conduction through the sinus node. Our conclusion is that estimated indirect sinuatrial conduction time does not represent real sinuatrial conduction time. The calculation formula using constant atrial pacing has been based on a major unproven assumption.

Sino‐Atrial Dissociation: Evidence by Intracardiac Recordings in Man and by Microelectrode Studies on Isolated Rabbit Atrium

The electrophysiologic mechanisms of sinus dysfunction have recently been determined by direct recordings of the sinus node electrogram. The association of various degrees of abnormalities in the formation of the impulse within the sinus node and of sinoatrial conduction block, represents the pathophysiological substrate of the mechanism of sinus node dysfunction. The purpose of this work is to present clinical and experimental data supporting the concept of sinus node isolation. In our clinical case, the sinus node was probably intact despite aspects of sinus node dysfunction on the surface ECG. Sinus node electrograms were recorded with a sinoatrial conduction time of 100 ms (normal values in our laboratory: 83 ms +/- 38 ms). Atrial mapping demonstrated that the area depolarized by the sinus node involved a 2 cm2 zone surrounding it. This perisinusal activity could not be recorded on the surface ECG. Both exit and entry blocks in the sinus node were demonstrated. Our experimental data showed a total desynchronization between the electrical activity of the sinus node and that of the atrium under hypoxic conditions. Both types of cases demonstrated that an atrial dysrhythmia was coexisting with regular sinus activity. From these data we concluded that a sinus node free from any pathological involvement could be associated with severe symptoms of sinus node dysfunction on the surface ECG.

A simple modified technique for recording sinus node electrogram.

We recommend a technique for recording a sinus node electrogram (SNE) that is quite simple and makes it easy to locate the electrode poles firmly in the place underlying the sinus node (SN); the success rate is 97%.

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

The origins of the sinus node pacemaker complex in man: Demonstration of dominant and subsidiary foci

To test the hypothesis that the human sinus node is capable of demonstrating multiple sites of impulse generation, we assessed spontaneous shifts in the sinus node pacemaker complex, and shifts after overdrive atrial pacing, premature atrial stimulation and carotid sinus massage. A total of 24 patients aged 59 +/- 15 years (mean +/- SD) in whom stable sinus node electrograms were obtained were selected for the study. Ten of the 24 patients had sick sinus syndrome, whereas 14 had no sinus node dysfunction. All 24 patients had atrial pacing at cycle lengths of 1,000 to 300 ms; 9 patients had premature atrial stimulation and 12 had carotid sinus massage. Shifts in the sinus node pacemaker complex occurred spontaneously in 4 (17%) of the 24 patients; after atrial pacing at cycle lengths of 800 to 300 ms (mean 387 +/- 92) in 15 (63%) of 24 patients; after premature atrial stimulation at one or more coupling intervals in 5 (56%) of 9 patients and during carotid sinus massage in 9 (75%) of 12 patients. Shifts in the sinus node pacemaker complex lasted one to six beats and returned to the original site within two to seven beats. Spontaneous shifts in the sinus node pacemaker complex occurred in 3 of 14 patients without sick sinus syndrome and were induced in 6 (60%) of 10 patients with sick sinus syndrome and 11 (79%) of 14 patients without sick sinus syndrome. Shifts in sinus node pacemaker complex were characterized by loss of primary negativity, change in P wave morphology, significant (p less than 0.001) prolongation of sinoatrial interval and sinus cycle length.