Sinoatrial Conduction Time Research Articles

Electrophysiological effects of intravenous rilmenidine in man

Ten patients (44 y), 6 with the Wolff-Parkinson-White syndrome, and none with hypertensive disease, underwent electrophysiological studies before and after intravenous infusion of a single dose of 1 mg rilmenidine administered over 15 min. The regimen produced a mean plasma rilmenidine concentration of 3.16 ng.ml-1 at the end of the infusion. There was no significant change in sinus cycle length, PR interval, QRS, QT duration or in PA, AH and HV intervals. Estimated sinoatrial conduction time and corrected sinus node recovery time did not significantly change. In one patient, however, an abnormal pause was noted after termination of rapid atrial pacing. The right atrial effective refractory period decreased from 209 to 194 ms. There was no significant change in the anterograde and retrograde block cycle length or in the refractoriness of the nodal, ventricular and accessory pathways. The cycle length of induced reciprocating tachycardia decreased slightly from 374 to 351 ms. No patient exhibited an abnormal response to the carotid sinus massage. The findings indicate that intravenous administration of 1 mg rilmenidine exerts modest effects on the electrophysiological parameters of the human heart.

Age-related changes in the clinical and electrophysiologic characteristics of patients with Wolff-Parkinson-White syndrome: Comparative study between young and elderly patients

The natural history of patients with Wolff-Parkinson-White (WPW) syndrome remains an intriguing question with respect to clinical decision-making, since serial electrophysiologic data spread over several decades in the same patient are not avaliable in the literature. To study the age-related changes in WPW syndrome, we compared two separate groups of patients referred to this Medical Center for electrophysiologic studies because of a clinical presentation with significant arrhythmias. An elderly group of 42 patients aged 50 years or more were compared with a younger group of 51 patients aged 15 to 30 years. The groups were comparable in terms of clinical presentation, including the number of patients who had reported syncopal eplsodes and those requiring cardioversion of their tachyarrhythmias. Baseline electrophysiologic variables such as sinus rate; sinoatrial conduction time; corrected sinus node recovery time; AH interval; and effective refractory periods of the right atrium, atrioventricular (AV) node, and right ventricular muscie, were significantly greater in the elderly group. Similarly, the anterograde effective refractory period of the bypass tract, the shortest atrial pacing cycle length with 1:1 anterograde conduction via the bypass tract, retrograde effective refractory period of the bypass tract, the shortest ventricular pacing cycle length with 1:1 retrograde conduction via the bypass tract, the shortest consecutive preexcited R-R interval during atrial fibrillation, and the cycle length of orthodromic atrial ventricular reciprocating tachycardia were significantly greater in the elderly group. Although such an electrophysiologic milleu in the elderly group could be interpreted as more berign compared with the younger group of patients and thus conductive to less malignant tachyarrhythmias on a theoretical basis, both groups in fact had a comparable clinical profile including frequency of syncope and direct-current cardiovaerslon. This could in part be due to the fact that the difference in the effective refractory period between the AV node and the bypass tract were comparable between the groups. Thus it is concluded that the management of WPW syndrome in symptomatic elderly patients should be as aggressive as in the younger patients, and radiofrequency or surgical ablation may have to be considered as the initial management option in these elderly patients.

The Conduction System of the Swine Heart

Although the pig has been used as an experimental model for ischemic heart disease and sudden death, relatively little is known about the anatomy of the conduction system (CS) of this animal. We attempted to correlate electrophysiologic and anatomic differences between the pig and human CS. Invasive electrophysiologic studies were performed in five healthy anesthetized pigs. In contrast to the adult human, the pig has sinus tachycardia, shortened PR and H-V intervals, and a relatively short sinoatrial conduction time. Compared with the human CS, serial sections of the CS of pig hearts showed the following differences: (1) the atrioventricular node is located more to the right of the summit of the ventricular septum; (2) the penetrating bundle is very short, and the bifurcation of the bundle into bundle branches occurs more proximally; (3) there is more connective tissue and less elastic tissue; and (4) there is a copious amount of nerve fibers (about 50 percent throughout the CS). The presence of the abundant neural tissue implies that there is an important neurogenic component to conduction in the pig. Because of the above differences from the human, the pig should be used with caution as an experimental model in ischemic heart disease and sudden death where arrhythmias are studied.

Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction

This study was undertaken to evaluate a possible role of sinus node (SN) artery disease in the pathogenesis of sick sinus syndrome (SSS) in patients with an inferior wall acute myocardial infarction (AMI). Coronary angiography and electrophysiologic studies of the SN, both in the basal state and after pharmacologic autonomic blockade, were performed in 23 study patients (mean age 60 years) with SSS and a previous inferior wall AMII and in another 23 control patients (mean age 57 years) with normal sinus rate and a previous inferior AMI. Stenosis of the SN artery (or that proximal to its origin) >50% was present in 13 study patients (56%) and in 8 control patients (34%) (p <0.05). In the study group, the intrinsic heart rate was abnormal in 5 of the 6 patients (83%) with severe SN artery stenosis (≥75% narrowing), in 3 of the 7 (43%) with moderate stenosis (50 to 75% narrowing) and in 3 of the 10 (30%) with insignificant stenosis (<50% narrowing). In the study group, the correlation between the SN measures (heart rate, corrected SN recovery time and sinoatrial conduction time) and the severity of SN artery stenosis was good after autonomic blockade (r between 0.59 and 0.64) and poor in the basal state. These data provide evidence for a role of SN artery disease in the pathogenesis of SSS in patients with an inferior wall AMI.

Sinus nodal dysfunction in young patients with long QT syndrome

Although sinus bradycardia and low heart rate with exercise have been found in some patients with long QT syndrome, systematic evaluation, including intracardiac electrophysiologic (EPS) tests of sinus node function, has not been reported. Records were reviewed of 14 children and adolescents (age 3 to 16 years) with long QT wyndrome (mean QT c 0.51 second) who underwent noninvasive testing and intracardiac EPS because of syncope or cardiac arrest. The resting electrocardiographic (ECG) sinus heart rate was low for age in only 1 of 13 patients, while the lowest Holter-monitored sinus heart rate was abnormal in 4 of 12. The maximum exercise heart rate was abnormally low in 6 of the 12 who underwent exercise testing. For the EPS tests, the corrected sinus node recovery time (CSNRT) was long in 8 of 14 and the sinoatrial conduction time (SACT) was long in six of the nine in whom it was calculable. When both noninvasive and EPS indices are considered, 13 of the 14 patients had some type of sinus node dysfunction.

Electrophysiologic effects of oral diltiazem before and after beta blockade

We conducted electrophysiologic (EP) studies and estimated the sinus node function and atrioventricular (AV) conduction in 10 patients with suspected coronary arterial disease (age range 35-55 years) before and during diltiazem therapy (60 mg thrice daily for 5-7 days). The effect of beta blockade (0.1 mg/kg of intravenous propranolol) was evaluated in both EP studies. The mean spontaneous sinus cycle length (SCL) and the AV nodal Wenckebach cycle lengths (AVWB) were significantly higher (p less than 0.05) after propranolol alone (913 +/- 131 and 504 +/- 197 ms, respectively) compared with baseline values (SCL: 827 +/- 149 ms, AVWB: 439 +/- 173 ms). Diltiazem alone failed to influence the SCL and AVWB significantly. Following the combination (diltiazem + propranolol), SCL (945 +/- 147 ms) and AVWB (533 +/- 148 ms) were significantly higher (p less than 0.05) than baseline and post diltiazem values (SCL: 840 +/- 150 ms; AVWB 457 +/- 103 ms). None of the other parameters (sinoatrial conduction time, corrected sinus node recovery time, AH and HV intervals, AV nodal and atrial effective refractory periods) were significantly influenced by propranolol, diltiazem, or the combination. No patient developed AV block, sinus arrest/sinoatrial exit block, or symptomatic sinus bradycardia following beta blockade after diltiazem administration. Oral diltiazem therapy alone and after beta blockade does not appear to adversely influence the sinus node function and AV conduction in patients below the age of 55 years. The combination of diltiazem and beta blocker thus appears safe in selected patients with coronary arterial disease.

Ｐｉｒｍｅｎｏｌ単回経口投与の電気生理学的効果と心血行動態に及ぼす影響

The electrophysiologic and hemodynamic effects and the pharmacokinetics of a single oral administration of pirmenol were evaluated in 20 patients with supraventricular tachycardia (SVT). Pirmenol, at 1hr after administration, significantly shortened sinus cycle length and sinoatrial conduction time. HV interval (46±10msec to 54±11msec, P<0.01), refractory period of the right atrium and the right ventricle were significantly prolonged. Furthermore, anterograde refractory period of accessory pathway and retrograde refractory period of AV node and accessory pathway were prolonged. Hemodynamic study revealed increased systemic and pulmonary vascular resistance and decreased stroke volume index. Induction of SVT was suppressed in 11 out of 16 patients. Among 5 patients who were not suppressed at 1hr, 2 patients resulted in noninducible at 2hr after administration. Plasma concentration of pirmenol at 1hr after administration was 1.0±0.4μg/ml in effective cases and was 0.4±0.5μg/ml in failed cases (P<0.05). Pharmacokinetics of single oral pirmenol were, tmax of 2.9hr, Cmax of 1.4μg/ml, t1/2 of 6.8hr and AUC of 18.7μg·hr/ml. In conclusion, a single oral administration of pirmenol was highly effective in suppression of induction of SVT with sufficient hemodynamic tolerance.

Electrophysiologic findings after Fontan repair of functional single ventricle

Cardiac arrhythmias are well recognized sequelae of the Fontan operation for complex congenital anomalies. In this study the electrophysiologic effects of the Fontan procedure were evaluated in 30 patients who underwent cardiac catheterization with electrophysiologic study 1.9 ± 1.3 years (mean ± SD) after modified Fontan repair for functional single ventricle. Abnormalities of sinus node or ectopic pacemaker automaticity were detected in 50% (15 patients) by determination of a prolonged corrected sinus node or pacemaker recovery time. Total sinoatrial conduction time was prolonged in 50% of the patients with normal sinus rhythm. Sinus noue or ectopic atrial pacemaker function was entirely normal in only 43% of patients. The predominant atrial rhythm was normal sinus in 70% and ectopic atrial or junctional in 30%. Abnormalities of atrial effective and functional refractory periods were noted in 43% of patients and were most pronounced at faster paced cycle lengths. Atrial endocardial catheter mapping revealed intraatrial conduction delays between adjacent sites in 76% of the patients tested and in eight of nine patients with inducible intraatrial reentry.Programmed atrial simulation induced nonsustained supraventricular arrhythmias in 10% of the 30 patients and sustained arrhythmias in 27%. Intraatrial reentry was the most common inducible arrhythmia and was present in seven of the eight patients with sustained and two of the three patients with nonsustained atrial arrhythmias. Atrioventricular conduction abnormalities were noted in 10% (three patients). No patient had inducible ventricular arrhythmias with programmed ventricular stimulation.The electrophysiologic findings after Fontan repair include abnormal sinus node function, prolonged atrial refractoriness, delayed intraatrial conduction and inducible atrial arrhythmias. The predictive value of electrophysiologic testing in this group of patients is unknown. Further study and continued clinical follow-up are essential to determine which patients will be at risk for the development of late life-threatening arrhythmias.

Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade–B. Marcus Et Al.: Postoperative intrinsic sinus node evaluation

Sinus node dysfunction is a recognized problem following surgery for congenital heart disease. Seven postoperative patients with sinus node dysfunction (5 Mustard, 1 tetralogy of Fallot, 1 Fontan) underwent electrophysiology study of sinus node function during combined autonomic blockade (CAB) utilizing propranolol 0.2 mg/kg i.v. and atropine 0.04 mg/kg i.v. to evaluate intrinsic sinus node function isolated from autonomic control. During CAB, intrinsic heart rate, intrinsic corrected sinus node recovery time, and intrinsic sinoatrial recovery time were measured. These results were compared with age-matched normal intrinsic data from our lab [normal (n = 7, mean age 9 years) IHR 128 +/- 24, intrinsic corrected sinus node recovery time 135 +/- 40 ms, intrinsic sinoatrial conduction time 86 +/- 19 ms]. Among postoperative Mustard patients (n = 5, mean age 13 years, mean years postoperative 11) 2 of 5 had clearly abnormal intrinsic sinus node function with nonsinus rhythm during CAB; 3 of 5 had sinus rhythm during CAB with normal or mildly abnormal intrinsic sinus node function. The postoperative case of tetralogy of Fallot (age 20 years, postoperative 14 years) had mildly abnormal intrinsic sinus node electrophysiology study. The postoperative case of Fontan (age 16 years, postoperative 1.5 years) had sinus rhythm at rest but left atrial rhythm during CAB. Different aspects of sinus node dysfunction may be expressed during resting electrophysiology study vs. electrophysiology study utilizing CAB. The pathophysiology of sinus node dysfunction among postoperative pediatric patients is not homogeneous with regard to the contribution of intrinsic sinus node dysfunction. In those patients with normal or mildly abnormal intrinsic sinus node function, an important pathophysiologic influence of the autonomic nervous system is implicated.

Assessment of sinus node function in patients with congenital long QT syndrome.

Sinus node function was evaluated in 4 patients with congenital long QT syndrome suffering from recurrent episodes of syncope and ventricular arrhythymias. Three of the 4 patients had bradycardia at rest on a 24-hour ECG. Sinus node function was examined by the atrial overdrive suppression test and the atrial premature stimulation test. Corrected sinus node recovery time (CSNRT) was prolonged in all patients. Total sinoatrial conduction time was also prolonged in 2 of the 4 patients. In all patients with abnormally high values, these values returned to normal after atropine administration, except in one patient. His prolonged CSNRT remained high after atropine administration, indicating abnormal automaticity such as that seen in sick sinus syndrome. These results show that sinus node function in congenital long QT syndrome is often associated with autonomic dysfunction, and sometimes with intrinsic disturbances of sinoatrial conduction.

Diagnostic Value of Carotid Sinus Hypersensitivity

In order to evaluate the diagnostic value of carotid sinus hypersensitivity (CSH) we have investigated 163 asymptomatic patients (88 male, 75 female, mean age 57.9 +/- 22.7 years) and 210 symptomatic patients (108 males, 102 females, mean age 61.1 +/- 28.1 years) with syncopes or dizziness. Thirty two of the 163 asymptomatic patients (20%) and 87 of the 210 symptomatic patients (41%) showed CSH (asystole greater than or equal to 3 sec during carotid sinus pressure). Male patients had a higher number of CSH than female (28% vs 10% in the asymptomatic group, 48% vs 34% in the symptomatic group). Electrophysiological investigations were performed in all 210 symptomatic patients. Normal electrophysiological results had 94 of the 210 patients. Thirty seven of these 94 patients showed CSH (39%). Prolonged sinus node recovery time (SNRT) and/or prolonged sinoatrial conduction time (SACT) were evaluated in 38 patients. Seventeen of the 38 patients had CSH (45%). Disorders of atrioventricular (AV) conduction were evaluated in 43 patients. Seventeen of the 43 patients showed CSH (40%). Thirty-five patients had both AV conduction disorders and prolonged SNRT or SACT. Sixteen of these 35 patients showed CSH (46%). In conclusion, no significant difference was found between patients with and without pathological electrophysiological results. The CSH is without value for predicting sinus node dysfunction and AV conduction disorder.

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.

Olea europaea L. and oleuropein: Effects on excito‐conduction and on monophasic action potential in anaesthetized dogs

AbstractThe effects of a glyceroethanolic macerate of the leaves of Olea europaea L. and of oleuropein on excito‐conduction and on the right atrial and ventricular monophasic action potential (MAP) have been studied in anaesthetized dogs using the technique of endocavitary recording. At the higher doses tested, a slight increase in the sinusal cycle of the sinoatrial conduction time and of the sinus node recovery time, together with a prolongation of the atrioventricular and intraventricular conduction and an increase of the atrial and ventricular MAP duration were observed. This may be due to a decrease in the repolarization phase 3. These electrophysiological effects indicate an inhibitory action both on the swift influx of sodium and on the slow influx of calcium, as well as a decrease in potassium conductance.

Electrophysiology of heterotopic heart transplant: Experimental study in dogs

Electrophysiological properties were studied in a heterotopic heart transplant model developed in 44 dogs (Group I). Cycle length was 359.5 +/- 55.2 ms in the recipient heart and 500.9 +/- 77.9 ms in the donor heart (P less than 0.001). Sinoatrial conduction time was 38.6 +/- 13.6 ms in the recipient heart and 38.6 +/- 10.4 ms in that of the donor (not significant). The Wenckebach point was 175.4 +/- 31.1 ms in the recipient organ and 214.3 +/- 42.6 ms in the donor heart (P less than 0.001). The retrograde block point was 271.6 +/- 48.0 ms in the recipient heart and 353.6 +/- 47.3 ms in that of the donor (P less than 0.01). The effective antegrade refractory period was 133.4 +/- 28.7 ms in the recipient heart and 167.3 +/- 46.3 ms in the donor organ (P less than 0.001). An epicardial atrial cartography was performed at 44 preset points in both hearts, revealing a normal activation sequence and delays of 36-98 ms (mean 58 ms) in the recipient heart and from 39 to 59 ms (mean 50 ms) in the donor heart (not significant). In another 11 dogs (Group II), the same electrophysiological study was carried out under basal conditions and after pharmacological blockade of the autonomic nervous system with atropine (0.04 mg (kg body weight)-1) and propranolol (0.2 mg (kg body weight)-1). No significant differences were found in any of the parameters studied upon comparison of Group II animals in basal conditions with Group I recipients, and Group II dogs after blockade with Group I donors. These results demonstrate that the differences in automatism, conduction and refractoriness between the donor and recipient hearts are not attributable to differences in the haemodynamic situation or in the anaesthetic technique, but to denervation.

Evidence for central site of action to explain the negative chronotropic effect atropine: Studies on the human transplanted heart

The chronotropic response to atropine is biphasic; low doses cause slowing of the sinus rate and high doses cause acceleration. Although it is accepted that atropine functions as a competitive antagonist at high doses, the mechanism of the negative chronotropic response at low doses is controversial. Specifically, it is unclear whether the effect is mediated centrally or peripherally. Since at the time of cardiac replacement all central nervous system connections to the heart are severed, the transplanted heart is a unique model for separating these effects.Graded doses of atropine sulfate (0.5, 1.0, 2.0, 4.0, 8.0 and 40.0 μg/kg body weight) were administered to 12 human heart transplant recipients to test the hypothesis that the bradycardiac effect of low dose atropine is centrally mediated. The baseline sinus cycle lengths of the decentralized donor and innervated native sinus nodes were 694 ± 20 and 733 ± 27 ms, respectively. At the 0.5 and 1.0 μg/kg doses, the cycle lengths of the native sinus node increased by 29.1 ± 13.5 and 23.1 ± 14.2 ms, respectively. At the 2.0 μg/kg dose the sinus cycle length again shortened to control. At the maximal dose of atropine the sinus cycle length shortened by 138.3 ± 29.7 ms compared with control. In contrast, the decentralized donor sinus node exhibited a flat dose response to atropine. High dose atropine (40 μg/kg) caused no change in the donor heart's atrial effective refractory period, corrected sinus node recovery time, or sinoatrial conduction time measured by either the Strauss or the Narula method.In summary, low dose atropine had no effect on the cycle length of the decentralized donor sinus node, but it lengthened the cycle length of the innervated native sinus node. High dose atropine similarly had no effect on the cycle length of the decentralized donor sinus node, but it shortened the cycle length of the innervated native sinus node. High dose atropine also had no effect on atrial refractoriness, sinus node recovery time or sinoatrial conduction time in the decentralized donor heart. Thus, the results suggest that in humans a central site of action is sufficient to explain the transient bradycardia caused by low dose atropine and that the effect depends on intact central neural connections. The data also confirm that high dose atropine has no direct or indirect effect on the human transplanted heart. Although atropine may have central and peripheral cardiac effects, central effects are probably of greater importance.

Exercise Correlates of Electrophysiologic Assessment of Sinus Node Function in Young Individuals.

This study evaluated prospective exercise correlates of sinus node function in young individuals. Subjects for this study were 25 children and young adults who required cardiac catheterization for a symptomatic arrhythmia. Measurements of sinus node function at elechophysiological catheterization were the sinus node recovery time (SNRT) and sinoatrial conduction time (SACT). Maximal exercise testing was performed using a Bruce treadmill protocol the day prior to cardiac catheterization. Exercise measurements included resting heart rate, peak heart rate, cardiac acceleration from rest to 3 minutes, from rest to 6 minutes, from rest to peak, and from 3 to 6 minutes, cardiac deceleration from peak to 1 minute postexercise, deceleration for each minute of recovery, recovery heart rates for each of 5 minutes postexercise, heart rate at which respiratory exchange ratio >1.0 and slope of the heart rate - VO2 curve. Exercise testing did not predict intracardiac measures of sinus node function either as a group ("normal" vs. "abnormal" groups) or individually.

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.

Electrophysiological evaluation of the sinus node in patients with atrioventricular and/or intraventricular conduction defects

The authors evaluated retrospectively sinoatrial conduction time (SACT), sinus node recovery time (SNRT), and corrected sinus node recovery time (CSNRT) in 272 patients with atrioventricular and/or intraventricular conduction defects without evidence of overt sinus node dysfunction. The study was designed to determine the prevalence of electrophysiologic sinus node abnormalities in patients with overt atrioventricular and/or intraventricular conduction defects. One or more sinus node electrophysiological abnormalities were observed in 133 cases (48.9%). There was a significant prevalence of electrophysiologic sinus node abnormalities only in patients older than 71 years of age. The data suggest that the involvement of the specialized conduction system is much more diffuse than one might expect simply observing the single recorded ECG defect and that the prevalence of associated defects of the conduction system increases with increasing age of patients.

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.

The effect of Alinidine on sinus node function and sinoatrial conduction time studied by atrial epicardial maps and EPS

The effect of Alinidine on sinus node function and sinoatrial conduction time studied by atrial epicardial maps and EPS