Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade

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.     

Autonomic blockade and sick sinus syndrome. New concept in the interpretation of electrophysiological and Holter data

Autonomic blockade is commonly employed as a test of sinus nodedysfunction. We compared primary and secondary atrial postpacingpauses and postextrasystolic sino-atrial responses before andafter autonomic blockade in 56 patients with the clinical diagnosisof sick sinus syndrome. Pharmacological autonomic blockade wasachieved by atropine 0.04 mg kg^–1 and propranolol 0.2mg kg^–1 i.v. In a group of patients with a normal intrinsicheart rate the number of positive electrophysiologic variablesassociated with sinus node dysfunction declined after autonomicblockade. In 91% of these patients, sinus node function wascharacterized by a normal intrinsic recovery time, gradual exponentialreturn to the constant sinus cycle length, and biphasic postextrasystolicreturn responses. Three patients in this group had intrinsicSA-block revealed by atrial pacing and verified by Holter monitoring.Besides normal intrinsic pacemaker properties in 53% of patients,rhythm monitoring revealed severe sinus node dysfunction asmanifested by bradycardia and the tachycardia-bradycardia syndrome.SA-block and sinus arrest up to 29120 ms. In the abnormal intrinsicheart rate group, disturbed intrinsic rhythmicity was characterizedin all by a prolonged corrected intrinsic recovery time (2320±2740ms [± SD]), arrhythmia and/or brady-cardia in the secondarypostpacing cycles, chaotic postextrasystolic patterns, or prolongedsinoatrial conduction times. Significantly slow minimal heartrates during sleep significantly prolonged average sinus cyclelengths and positive ECGs for sinoatrial disorders in the wakingperiod were present on the 24-rhythm recording. It is concluded that intrinsic heart rate obtained by autonomicblockade is the best and most simple method for the diagnosisof intrinsic sinus node dysfunction. Combined autonomic blockadeand electro-physiological tests can be of great value in unmaskingthe severity and degree of intrinsic dysfunction and analyzingthe abnormality of secondary pacemaker function. These investigations,however, are rather insensitive and therefore ineffective indetecting autonomic sinus node dysfunction. To assess the roleand significance of the autonomous neurovegetative tone in thegenesis of sinoatrial disorders, rhythm monitoring is required.     

Diagnostic value pharmacological autonomic blockade in patients with suspected sick sinus syndrome

The study comprised 67 subjects, mean age 43.7 years, with suspected sick sinus syndrome, in whom rapid atrial pacing before and after combined atropine and propranolol was performed by Narula's method. Three groups were formed: group I--with normal sinus node recovery time (SNRT) and corrected sinus node recovery time (CNRT) before and after the autonomic blockade; group II--with functional disorders of the sinus node and group III--with intrinsic sinus node dysfunction. After autonomic blockade in groups I and II mean SNRT, CNRT, post-stimulation cycle lengths (except No. 2 and Nos. 5, 6, 10, respectively) shortened, whereas HR rose. In contrast, in group III mean SNRT, CNRT, post-stimulation cycle lengths (Nos. 1, 2, 6, 10) and HR increased. Significant differences in post-stimulation cycle lengths were observed between groups I and III as well as groups II and III. In conclusion, rapid atrial pacing after combined atropine and propranolol helps us to diagnose latent sick sinus syndrome and extrinsic sinus node dysfunction more precisely, and significant differences in post-stimulation cycle lengths between the groups confirm diagnostic value.     

Electrophysiological effects and mechanism of action of oral quinidine in patients with sinus bradycardia and first degree A-V nodal block

The effects of quinidine on sinus nodal and A–V nodalfunction were assessed in 20 patients (age: 60±7 years)with sinus bradycardia and a prolonged A–H interval. Electrophysiologicalstudies were performed twice in each patient. In the first study,the measurements of sinus and A–V node function were evaluatedboth in the basal state and after autonomic blockade (propranolol0.2 mg kg^-1 and atropine 0.04 mg kg^-1). Oral quinidine was administeredfor 3–4 days (1200 mg day^-1) and the study was then repeatedusing the same methods. Comparison of data obtained in the twostudies in the basal state allowed us to evaluate the overalleffect of quinidine. Comparing the results obtained followingautonomic blockade, the direct action of the drug could be assessed.Inthe basal state quinidine did not significantly change the functionof either node. In contrast, after autonomic blockade, significantchanges were noted after quinidine. In 3 patients with sinusrate <50 beats min^-1 and an abnormal intrinsic heart rate,quinidine induced marked depression of sinus automaticity.Thesedata suggest that: (1) in patients with sinus bradycardia andprolongation of the A–H interval, oral quinidine has adirect depressant effect on sinus and A–V nodal function,but this effect is counteracted by autonomically mediated actions;(2) in patients with moderate or severe bradycardia and an abnormalintrinsic heart rate, the drug can induce marked depressionof sinus automaticity.     

Electrophysiological effects and mechanism of action of oral quinidine in patients with sinus bradycardia and first degree A-V nodal block

The effects of quinidine on sinus nodal and A–V nodalfunction were assessed in 20 patients (age: 60±7 years)with sinus bradycardia and a prolonged A–H interval. Electrophysiologicalstudies were performed twice in each patient. In the first study,the measurements of sinus and A–V node function were evaluatedboth in the basal state and after autonomic blockade (propranolol0.2 mg kg^-1 and atropine 0.04 mg kg^-1). Oral quinidine was administeredfor 3–4 days (1200 mg day^-1) and the study was then repeatedusing the same methods. Comparison of data obtained in the twostudies in the basal state allowed us to evaluate the overalleffect of quinidine. Comparing the results obtained followingautonomic blockade, the direct action of the drug could be assessed.Inthe basal state quinidine did not significantly change the functionof either node. In contrast, after autonomic blockade, significantchanges were noted after quinidine. In 3 patients with sinusrate <50 beats min^-1 and an abnormal intrinsic heart rate,quinidine induced marked depression of sinus automaticity.Thesedata suggest that: (1) in patients with sinus bradycardia andprolongation of the A–H interval, oral quinidine has adirect depressant effect on sinus and A–V nodal function,but this effect is counteracted by autonomically mediated actions;(2) in patients with moderate or severe bradycardia and an abnormalintrinsic heart rate, the drug can induce marked depressionof sinus automaticity.     

Variations of normal sinus node function in relation to age: role of autonomic influence

An electrophysiological study of sinus node function, includingmeasurements of resting heart rate, maximal corrected sinusnode recovery time and sinoatrial conduction time, was performedin 30 patients, 12–79 years of age, without any clinical,electro car diographic or electrophy siological evidence ofsinus node disease. To analyse autonomic influences, variables were measured beforeand after sympathetic and parasympathetic blockade. No significantcorrelations were observed between age and electrophysiologicalmeasurements of sinus node function at the control study orafter sympathetic blockade. In contrast, the electrophysiologicalparameters of intrinisic sinus node activity were correlatedwith age and showed a progressive lengthening of mean sinuscycle length, of maximal corrected sinus node recovery timeand of sinoatrial conduction time. In addition, measurements after vagolysis suggest a progressivedecrease of parasympathetic activity with increasing age. These data also indicate that the respective role of the twocomponents of the autonomic nervous system vary with increasingage: parasympathetic activity predominates in younger subjects;sympathetic and parasympathetic tones are equilibrated in oldersubjects. The normal sinus node function represents an equilibrated system:in parallel with ageing of the intrinsic properties of the sinusnode, parasympathetic activity decreases so that basal propertiesremain stable throughout life.     

The sinus node function: normal and pathological

To determine the evolution with age, of extrinsic and intrinsicsinus node electrophysiological parameters and to assess therole of each component of the autonomic nervous system relativeto age in patients with and without sick sinus syndrome, electrophysiologicalstudies of sinus node function were performed in 223 patientssubdivided into four groups according to the results of theirelectrophysiological testings: group I included patients withnormal extrinsic and intrinsic sinus node function, group IIpatients with exclusive extrinsic sinus dysfunction, group IIIpatients with exclusive intrinsic sinus dysfunction and groupIV patients with extrinsic and intrinsic sinus node dysfunction.The electrophysiological study was performed twice: at basalstate and after autonomic blockade. Whatever the sinus node function (normal or abnormal) the extrinsicsinus node electrophysiological variables did not correlatewith age; inversely all the electrophysiological measurementsof the intrinsic sinus node (normal or abnormal) lengthenedprogressively with age, suggesting an ageing phenomenon of theintrinsic sinus node throughout life. Moreover, the study ofthe percentage of chronotropy of the sinus node electrophysiologicalvariables shows a predominance of vagal tone in young subjects,whereas sympathetic activity is most prominent in elderly patientswith and without sick sinus syndrome. The sinus node (normal or pathological) represents an equilibratedsystem: the age-related modification of the autonomic nervoussystem counterbalances the senescence of the intrinsic sinusnode in such a way that the basal electrophysiological characteristicsremain stable throughout life.     

Sinus Node Recovery Time Assessment Revisited: Role of Pharmacologic Blockade of the Autonomic Nervous System

Sinus Node Recovery and Autonomic Blockade. Sinus node recovery time assessment is used to diagnose clinically significant sinus node dysfunction (SND) when Holter has failed to prove a relationship between sinus bradyarrhythmias and symptoms, but consensus has not been reached as to the value of including assessment after pharmacologic blockade of the autonomic nervous system. This issue was addressed in the present study performed on 52 patients with syncope or presyncope/dizziness (n = 48), sinus bradyarrhythmias (n = 45), or both (n = 41). Group 1 consisted of 13 patients with a proven relationship between symptoms and sinus bradyarrhythmias. Group 2 consisted of 39 patients with suspected SND. The protocol included three pacing periods at two pacing rates and was performed at baseline (n = 52), after single doses of atropine and propranolol (0.02 mg/kg and 0.1 mg/kg, respectively) (n = 41), and again after a second dose (n = 29). The sensitivity of prolonged recovery times was 77% in group 1. Among group 2 patients, 56% had prolonged recovery times at baseline (79% when including the results after the first dose of drugs). The second dose did not contribute diagnostic information, but it caused significant adverse reactions in 7 of 29 patients (P < 0.001). These 7 patients were all older than 60 years. Assessment of sinus node recovery time after pharmacologic blockade of the autonomic nervous system thus increases the sensitivity of the method in patients with suspected SND and normal baseline results. However, only 50% of the initially suggested doses of atropine and propranolol is sufficient and eliminates the risk for significant adverse reactions.     

Influence of beta block and autonomic nerve block on the recovery time of the sinus node in sick sinus syndrome and carotid sinus syndrome

In order to evaluate the relative role of the automatic nervus system and of the intrinsic electrophysiologic properties on the sinus node function, we measured the corrected sinus node recovery time before and after autonomic nervous system blockade in 24 patients. Fourteen had a sick sinus syndrome, five had a carotid sinus syncope, two had syncope of unknown origin associated with bradycardia. Beta blockade was obtained by infusing metoprolol intravenously at a dosage of 0.2 mg/kg; complete automatic blockade was achieved by further i.v. administration of atropine at a dosage of 0.04 mg/kg. After beta blockade, the corrected sinus node recovery time increased in patients with sick sinus syndrome and intrinsic slow heart rate, whereas it decreased in patients with carotid sinus syncope or with syncope and bradycardia. In patients with sick sinus syndrome and normal intrinsic heart rate the response was variable. A positive direct correlation was found between the changes of the corrected sinus node recovery time induced by beta blockade and those induced by autonomic blockade; that is, both either prolonged or shortened the corrected sinus node recovery time. The changes of the corrected sinus node recovery time after beta blockade alone were inversely correlated with the intrinsic heart rate. We conclude that patients with intrinsic depression of the sinus node have an increased sympathetic tone.     

Nonpharmacologic Validation of the Intrinsic Heart Rate in Cardiac Transplant Recipients

Background: The maximum sinus rate during exertion in humans is inversely related to age. However, the sinus rate at rest is quite variable. The intrinsic heart (IHR) following pharmacologic blockade of autonomic tone with propranolol and atropine has been proposed as a test of sinus node function and is related to age by the linear regression equation: IHR = 118.1 – (0.57 × age). Whether this relationship exists for transplanted hearts for which the donor sinus node is denervated has not been determined. Methods: The relationship between the resting heart rate and the age of the donor heart was examined in 103 patients 1 year following orthotopic cardiac transplantation in the absence of rejection or intercurrent illness. Patients receiving beta-blockers, calcium blockers, antiarrhythmic drugs, digitalis, theophylline, or with biopsy evidence of rejection or abnormal coronary arteriograms were excluded from analysis. Results: The recipient age, left ventricular ejection fraction, pulmonary capillary pressure, cardiac index, donor heart ischemic time and cardiopulmonary bypass time did not correlate with the rate of the resting donor sinus node. The resting heart rate was inversely related to age of the donor heart by the linear regression equation: HR = 112.0 – (046 × age). Conclusion: The resting rate of the denervated sinus node is related to donor age with a regression equation that is similar, though slightly slower, than that predicted after pharmacologic autonomic blockade.     

Short-term rapid atrial pacing produces electrical remodeling of sinus node function in humans

INTRODUCTION: Depression of sinus node function occurs in dogs and in patients after cessation of atrial flutter and fibrillation. We tested whether transient atrial pacing might produce similar changes in humans. METHODS AND RESULTS: We studied the impact of short-term rapid atrial pacing, simulating atrial tachyarrhythmias, on sinoatrial conduction time (SACT) and corrected sinus node recovery time (CS-NRT) in 10 patients undergoing electrophysiologic study. None had recognizable structural heart disease, history of atrial fibrillation or flutter, autonomic dysfunction, or any tachycardia for at least 24 hours before study. All cardiac drugs were discontinued >5 half-lives prior to study. No patient had significant hypotension during atrial stimulation. SACT and CSNRT were measured at baseline, and sinus node reset zone was determined. Right atrial pacing was performed for 10 to 15 minutes, after which SACT and CSNRT were measured again. Both parameters increased significantly, from 423+/-208 msec to 491+/-214 msec and from 80+/-50 msec to 96+/-53 msec, respectively (P = 0.02 and P < 0.001, respectively). CONCLUSION: Rapid atrial pacing for only 10 to 15 minutes, simulating transient atrial tachyarrhythmias, alters sinus node function in humans. Additional studies are needed to evaluate the mechanism, but the clinical implication is that even transient episodes of atrial tachyarrhythmias can cause sinus node remodeling in patients.     

Differential effects of functional autonomic blockade on the variables of sinus nodal automaticity in sick sinus syndrome

To study the pathophysiologic mechanism of sick sinus syndrome and to establish the relation of intrinsic heart rate, corrected sinus nodal recovery time and sinoatrial conduction time in this syndrome, electrophysiologic studies were conducted in 22 men (mean age 60 ± 12 years) with the clinical diagnosis of sick sinus syndrome. Measurements were determined before and after autonomic blockade with propranolol (0.2 mg/kg body weight) and atropine sulfate (0.04 mg/kg). Fifty-nine percent of patients (Group I) had an abnormal intrinsic heart rate, suggesting intrinsic abnormality of sinus nodal automaticity; 41 percent (Group II) had a normal intrinsic heart rate after autonomic blockade, suggesting disturbed autonomic regulation. One patient with an observed intrinsic heart rate higher than the upper limit of predicted intrinsic heart rate was also included in Group II. The mean corrected sinus nodal recovery time before autonomic blockade was 751 ± 502.8 ms and was abnormal (more than 450 ms) in 10 of the 13 patients in Group I and 2 of the 9 patients in Group II. After autonomic blockade this interval was 694 ± 638.7 ms and was abnormal in 12 of the 13 patients in Group I and in 2 of the 9 patients in Group II. The patients in each group could be further classified into three groups on the basis of normal or abnormal corrected sinus nodal recovery time before or after autonomic blockade. Not all patients with abnormal intrinsic heart rate (Group I) had abnormal corrected sinus nodal recovery time and vice versa. Patients in Group II were younger in age, had a lesser incidence of organic heart disease and were more severely symptomatic.Mean sinoatrial conduction time during control studies was 210.4 ±96.3 ms and decreased significantly (143.2 ± 59.6 ms, p < 0.005) after autonomic blockade. This interval was abnormal in 3 of the 13 patients in Group I and in 6 of the 9 patients in Group II during control studies; after autonomic blockade it remained abnormal in 3 patients in Group I and in 1 patient in Group II.It is concluded that determination of heart rate and corrected sinus nodal recovery time after autonomic blockade increases the sensitivity of electrophysiologic testing and offers some insight into the pathophysiology of sick sinus syndrome. Patients with sick sinus syndrome who have a normal intrinsic heart rate have a greater incidence of abnormal sinoatrial conduction time than do those with an abnormal intrinsic heart rate. Thus, abnormal sinoatrial conduction time is usually due to extrinsic autonomic influences.     

Sick sinus syndrome: comparative study of atrial and ventricular stimulation tests

Subjects with a ventriculo-atrial block and normal sinus function exhibit acceleration of the sinus rhythm during incremental right ventricular pacing; this acceleration is nor observed or is hardly visible in patients with sinus node dysfunction. Incremental right ventricular pacing up to 150/min was performed in 16 patients with ventriculo-atrial block (Group A) referred for investigation of sinus node dysfunction and the results compared with the classical tests of atrial pacing (Strauss'graph, atrio-sino-atrial conduction time, sinus node recovery time). The same tests were carried out in 19 patients without sinus node dysfunction (Group B). In the latter group, sinus rhythm exceeded 80/min during right ventricular pacing at 150/min and the rate increased with respect to the basal rhythm was always greater than 10/min. In Group A premature atrial pacing gave abnormal results in 4 cases, sinus node recovery times were abnormal in 15 cases, and rapid right ventricular pacing abnormal in all cases (sinus rhythm less than 80/min and/or rate increase of less than 10/min). There was no relation between the increased sinus node recovery time and the degree of rate increase during rapid ventricular pacing. Incremental right ventricular pacing, therefore, seems to be a new method of investigating sinus node function but complementary studies are required to determine its limitations, the exact mechanism and to try to widen its application to subjects without ventriculo-atrial block.     

Sinus node recovery time in the elderly.

Measurement of the sinus node recovery time has been proposed as a diagnostic tool for recognition of the sick sinus syndrome. The latter is most frequently encountered in elderly patients with hypertension, coronary heart disease, and atherosclerosis. In order to provide normal values for the sinus node recovery time in this particular population group, atrial pacing studies were carried out in 30 subjects over 50 years of age, all with peripheral vascular disease and some with angina pectoris (10), residua of infarction (6), or hypertension (7). On stimulation, 7 patients maintained a I:I atrioventricular conduction up to the rate of 180/min. Second degree atrioventricular block developed in all other cases. On six occasions, Wenckebach's periods appeared at the relatively slow pacing rate of 120/min. The maximum postoverdrive pause ranged from 680 to 1600 ms with an average of 1100 ms plus or minus 190 (10). For each pacing speed, a correlation was found between the duration of the pause and the control intrinsic cardiac rate, longer pauses being associated with longer resting PP intervals. Beyond 120/min, the duration of the pause was seen to shorten progressively as the driving rate was increased. Finally, the behavior of the sinus node pacemaker following interruption of pacing showed individual variations. After pacing at relatively slow rates, a prompt return to near control values was consistently observed, whereas, after fast rates of driving, a phase of secondary depression developed in about one-half of the studied cases.     

Abnormal sinus node function in clinical arrhythmias

To understand abnormal sinus node function in clinical atrial arrhythmias, it is essential to understand the normal function of the sinus node. Much of our understanding of the sinus node comes from work done in rabbits. In small animals, the node is a thin structure and can be modeled in two dimensions. However, in canines and humans, the node is a more complex structure completely surrounded by myocytes. Recent data suggest that the node may be insulated from the surrounding atrial myocytes, except at a limited number of exit sites. A model of the node with discrete exit sites explains how atrial activation can be initiated from multiple sites simultaneously. Within the node there may exist specialized pathways that explain the complex conduction within the node. Multiple cell types, with different intrinsic rates, combined with the nonuniform distribution of autonomic receptors, provide a basis for understanding the dynamics of heart rate control and the initiation of atrial activation. In addition, this model of the sinus node provides a framework to propose novel mechanisms underlying various atrial arrhythmias, such as atrial premature depolarizations or sinus node reentry.     

Atrial pacing for sick sinus syndrome

Atrial pacing is the most physiological way to pace patients with sinus node disease, as it provides both AV synchrony and a normal ventricular activation pattern. Long-term studies comparing atrial and ventricular pacing imply that atrial pacing results in fewer cardiac complications and, possibly, reduced mortality. Ventricular pacing should thus, if possible, be avoided in patients with sinus node disease. The potential risk of impending high-grade AV block during atrial pacing is low, with an annual incidence around 1% if patients are selected appropriately. Approximately 40-50% of patients with sinus node disease show signs of chronotropic incompetence during physical exercise, and are thus candidates for atrial rate responsive pacing. A preoperative evaluation of candidates for atrial pacing should include long-term Holter/telemetry, exercise test, carotid sinus stimulation, and an electrophysiological study excluding significant AV conduction disturbances.     

The role of the autonomic nervous system on sinus node function in patients with intermittent sinoatrial block

Sinus node (SN) function was analyzed with and without autonomic blockade (AB) in 31 patients (mean age: 57.6 +/- 12.8) with intermittent sinoatrial block. Twenty-one patients had organic heart disease; in the remaining ten signs of underlying heart disease were not present. Nineteen patients had dizziness or syncope. Sinus cycle length, sinus rate, corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After control measurements, AB was produced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of electrophysiological parameters were then repeated. After AB sinus rate and CSRT did not show statistically significant differences, whereas SACT decreased significantly (P less than 0.001). When intrinsic heart rate (IHR) was abnormal (11 cases), intrinsic CSRT was always abnormal, whereas when IHR was normal, intrinsic CSRT was normal in 11 patients and abnormal in nine. In several cases, when sinus rate increased after AB, CSRT decreased and vice-versa. The parameters of intrinsic SN function were normal in 80% of patients with a normal heart and only in 14.2% of patients with organic heart disease. These data indicate that: (1) during the control period SACT is mainly conditioned by the vagal tone; (2) abnormalities in control CSRT are not uniformly abolished after AB in patients with normal IHR; (3) AB has a differential effect on the two variables of SN automaticity; i.e. sinus rate and CSRT; and (4) in patients without underlying heart disease, the SN dysfunction is almost exclusively related to alterations of the autonomic nervous system.     

Evaluation of sinus node automaticity and sinoatrial conduction in children with normal and abnormal sinus node function

Sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) were determined in each of 28 children. Eighteen children (ages 2 to 14 years) had electrocardiographically normal sinus node function and served as controls. Ten children (ages 4 to 13 years) had electrocardiographic evidence of sinus node dysfunction, consisting of inappropriate sinus bradycardia, periods of sinus arrest or sinoatrial exit block. Mean control SNRT was 133% of the sinus cycle length with an upper normal limit of 151% (mean + 2 SD). Control SACTs ranged from 45-105 ms with mean and mean + 2 SD values of 71 ms und 105 ms. In the patients with SND, SNRTs averaged 168% and five patients had abnormally prolonged values of 158 to 256%. Mean SACT was 101 ms with four children having values greater than 105 ms. Seven of the 10 patients with SND had at least one electrophysiologic abnormality. This study defines normal sinoatrial conduction in children and validates the data by demonstrating a close correlation with similar data obtained from adult populations. Although abnormal electrophysiologic data confirms the presence of sinus node dysfunction, normal values for SNRT and SACT do not insure normal sinus node function.     

Rate adaptive pacing in sick sinus syndrome: effects of pacing modes and intrinsic conduction on physiological responses, arrhythmias, symptomatology and quality of life

An atrial-based pacing mode is superior to ventricular constantrate demand pacing (VVI) mode in patients with sick sinus syndrome(SSS) by providing both rate adaptation and atrioventricular(AV) synchrony. The use of a non-atrial sensor to overcome chronotropicincompetence and preserve normal intrinsic AV conduction inpacemaker therapy for SSS was investigated in 15 consecutivepatients (mean age 66±2 years). All had intact AV conduction(antegrade conduction capacity >100 beats. min^–1 andan atrialpaced to intrinsic R interval of 220 ms). DDDR pacemakerscapable of being programmed into atrial rate adaptive (AAIR),dual chamber rate adaptive (DDDR) and ventricular rate adaptive( VVIR) modes were used Beginning with an acute study, arterialpressure was invasively assessed in each pacing mode duringphysiological stresses and low level exercise. In the ambulatoryphase, the incidence of ventricular pacing and arrhythmias (Holierrecording), diurnal blood pressure changes (ambulatory bloodpressure recording), and symptom and quality of life level (questionnairesand interviews) were compared. Despite similar heart rate changes during acute physiologicalstresses, a higher blood pressure was recorded during AAIR orDDDR pacing compared with VVIR pacing. Systolic blood pressureover 24 h was lower in the VVIR mode (122 ± 5 mmHg) thanAAIR/DDDR pacing (129 ± 61128 ± 6 mmHg, P<0.05).VVIR pacing was associated with a higher frequency of atrialand ventricular ectopics, with two patients developing paroxysmalatrial fibrillation. Ventricular pacing was used in a higherpercentage in the DDDR compared with the VVIR mode (64 ±11 and 39 ± 7%, P<0.03). VVIR pacing was associatedwith more palpitations, a lower level of general well beingand depression. Despite the use of a sensor to overcome chronotropic incompetence,VVIR pacing is a less satisfactory pacing mode for SSS. AlthoughAAIRIDDDR pacing may achieve similar haemodynamic and clinicalstatus, in patients with intact A V conduction, AAIR pacingmay be preferable by avoiding an abnormal ventricular activationpattern     

Remodeling of sinus node function after catheter ablation of right atrial flutter

INTRODUCTION: The purpose of this study was to investigate the effect of ablation of right atrial flutter upon sinus node function in humans. METHODS AND RESULTS: This study enrolled 35 patients. Twenty-four patients (16 men and 8 women; age 68 +/- 11 years) were referred for ablation of persistent atrial flutter (duration 8 +/- 11 months). After ablation, there was abnormal sinus node function defined as a corrected sinus node recovery time (CSNRT) > or = 550 msec. The control group consisted of 11 patients who were undergoing pacemaker implantation for sinus node disease but did not have a history of atrial dysrhythmias or ablation. Within 24 hours of ablation or pacemaker implantation, baseline maximal CSNRT was measured through a permanent pacemaker by AAI pacing at six cycle lengths: 600, 550, 500, 450, 400, and 350 msec. CSNRT then was measured in the same manner at 48 hours, 14 days, and 3 months after ablation/pacemaker implantation. P wave amplitude and duration, and percent atrial sensing also were assessed at the same intervals. For patients undergoing atrial flutter ablation, there was progressive temporal recovery of CSNRT (1,204 +/- 671 msec at baseline vs 834 +/- 380 msec at 3 months; P < 0.001) and a significant increase in the percent atrial sensing and P wave amplitude at 3 months compared with baseline (P < 0.001). In control subjects, there was no change in the CSNRT, percent atrial pacing, or P wave amplitude. CONCLUSION: After ablation of persistent atrial flutter, there is temporal recovery of CSNRT and increase in spontaneous atrial activity. These findings suggest that atrial flutter induces reversible changes in sinus node function.