Sinoatrial Conduction Time Research Articles

High-Dose Remifentanil Suppresses Sinoatrial Conduction and Sinus Node Automaticity in Pediatric Patients Under Propofol-Based Anesthesia

We sought to determine the effect of remifentanil on sinus node function and the atrial-His (AH) interval in pediatric patients undergoing radiofrequency catheter ablation. Sixty pediatric patients with Wolff-Parkinson-White syndrome were prospectively enrolled in this study. General anesthesia was induced and maintained with a continuous infusion of propofol. We recorded the calculated sinoatrial conduction time (CSACT), corrected sinus node recovery time (CSNRT), and AH interval when the patients were in a stable anesthetic state and compared the values before and during remifentanil administration at a moderate dose (0.2 μg · kg(-1) · min(-1)) or a high dose (0.4 μg · kg(-1) · min(-1)). Data are expressed as mean (95% confidence interval). At the moderate dose, remifentanil prolonged CSNRT (from 177 [117-237] milliseconds to 245 [167-322] milliseconds after administration; P=0.016), but had no effect on either CSACT (P=0.59) or AH interval (P=0.11). However, high-dose remifentanil prolonged both CSNRT (from 201 [144-260] milliseconds to 307 [232-382] milliseconds after administration; P=0.019) and CSACT (from 48 [31-65] milliseconds to 78 [59-96] milliseconds after administration; P=0.038), but had no effect on the AH interval (P=0.058). The interaction in CSNRT between remifentanil administration and its dose was not different (P=0.44). Remifentanil may inhibit both intraatrial conduction and sinus node automaticity, but it has no effect on conduction through the atrioventricular node. Dose dependency was not observed within the range of 0.2 to 0.4 μg · kg(-1) · min(-1) of remifentanil.

Electrophysiological features in patients with sinus node dysfunction and vasovagal syncope

IntroductionSyncope is a common presentation of sinus node dysfunction (SND). Some patients who receive a permanent pacemaker due to SND do not benefit from it and further diagnostic workup leads to the diagnosis of vasovagal syncope (VVS). The aim of the study was to identify electrophysiological criteria that can be used for identification of patients with SND and concurrent VVS.Material and methodsTransoesophageal atrial pacing (TAP) was performed in 100 patients divided into four groups depending on symptoms and TAP results. Standard electrophysiological parameters of sinus node function and their variability were obtained in the basal state and after pharmacological autonomic blockade (AB).ResultsPatients with concurrent SND and VVS had a greater variability of sinoatrial conduction time assessed by Strauss’ method than patients without incidents of syncope (83.2 ±53.9 vs. 34.1 ±19.6, 47.8 ±33.6 and 32.1 ±22.99). Apart from abnormal sinus node recovery time and second pause, patients with SND had bigger basal state variability of these parameters. In patients with SND and concurrent vasovagal syncope the variability of sinus node recovery time (SNRT), corrected SNRT (cSNRT) and second pause (IIP) decreased after autonomic blockade.ConclusionsPatients with concurrent SND and VVS have distinct electrophysiological features – greater sinoatrial conduction time (SACT) variability and the decrease of SNRT, cSNRT and IIP variability after AB. However, further studies in larger study groups are needed to validate our findings. Transoesophageal atrial pacing is a useful procedure in patients with syncope, especially when the coexistence of more than one cardiac cause is suspected.

Mechanisms of sinoatrial node dysfunction in a canine model of pacing-induced atrial fibrillation

The mechanism of sinoatrial node (SAN) dysfunction in atrial fibrillation (AF) is unclear. The purpose of this study was to test the hypothesis that defective spontaneous sarcoplasmic reticulum (SR) Ca(2+) release (Ca(2+) clock) is in part responsible for SAN dysfunction in AF. Arrhythmic events and SAN function were evaluated in pacing-induced AF dogs (n = 7) and in normal dogs (n = 19) with simultaneous intracellular calcium (Ca(i)) and membrane potential recording. AF dogs had frequent sinus pauses during Holter monitoring. Isolated right atrium (RA) from AF dogs showed slower heart rate (P = .001), longer SAN recovery time (P = .001), and longer sinoatrial conduction time (P = .003) than normal. In normal RAs, isoproterenol 0.3 and 1 mumol/L increased heart rate by 96% and 105%, respectively. In contrast, in RAs from AF dogs, isoproterenol increased heart rate by only 60% and 72%, respectively. Isoproterenol induced late diastolic Ca(i) elevation (LDCAE) at superior SAN in all 19 normal RAs but in only 3 of 7 AF RAs (P = .002). In AF RAs without LDCAE (n = 4), heart rate increased by the acceleration of ectopic foci. Caffeine (20 mmol/L) injection increased heart rate with LDCAE in all 6 normal RAs but did not result in LDCAE in any of the 5 AF RAs (P = .002). Type 2 ryanodine receptor (RyR2) in the superior SAN of AF dogs was decreased to 33% of normal (P = .02). SAN dysfunction in AF is associated with Ca(2+) clock malfunction, characterized by unresponsiveness to isoproterenol and caffeine and down-regulation of RyR2 in SAN.

Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model

Remifentanil has been implicated as causing intraoperative bradyarrhythmias, but little information is available regarding its cardiac electrophysiological effects. Thus, we evaluated the cardiac electrophysiological properties before and after remifentanil in a closed-chest porcine model. Eighteen Landrace-Large pigs were premedicated with ketamine and anaesthetized with propofol (4.5 mg kg(-1) bolus followed by 13 mg kg(-1) h(-1)). After instrumentation, an electrophysiological evaluation was performed under propofol and repeated after remifentanil (bolus of 1 microg kg(-1), followed by an infusion of 0.5 microg kg(-1) min(-1)). We evaluated sinus node function [sinus node recovery time (SNRT) and sinoatrial conduction time (SACT)], atrioventricular (AV) nodal function [AH intervals during sinus rhythm (SR) and atrial pacing, Wenckebach cycle length (WCL), and effective refractory periods (ERP)], atrial, His-Purkinje, and ventricular conduction and refractoriness. Significant changes between 'propofol protocol' and 'propofol+remifentanil protocol' were evaluated. Remifentanil caused a significant increase in sinus cycle length (21%, P=0.001) and a significant prolongation of SNRT (43%, P=0.001), corrected SNRT (136%, P=0.003), SACT (40%, P=0.005), AH interval during SR (17%, P=0.02), AH interval during atrial pacing (25%, P=0.01), and ventricular ERP (12%, P=0.004). There was a tendency towards a prolongation of WCL and AV nodal refractoriness. Similar significant changes were observed in a reference group of seven animals in which sevoflurane was used instead of propofol. No significant changes were observed in atrial parameters, His-Purkinje function, parameters of intraventricular conduction, and QT intervals. Remifentanil depresses sinus node function and most parameters of AV nodal function. This contributes to an explanation for clinical observations of remifentanil-related severe bradyarrhythmias.

Fentanyl Added to Propofol Anesthesia Elongates Sinus Node Recovery Time in Pediatric Patients with Paroxysmal Supraventricular Tachycardia

In some types of pediatric supraventricular tachycardia, reentrant mechanisms are sensitive to enhanced vagal tone. Propofol is a feasible anesthetic for pediatric electrophysiological study and radiofrequency catheter ablation. Although fentanyl and propofol infusions both enhance cardiac vagal tone, it is unclear whether the combination of propofol and fentanyl has a potential to enhance it. In this study, we evaluated the hypothesis that fentanyl combined with propofol could alter cardiac electrophysiological activities in pediatric patients undergoing electrophysiological study and radiofrequency catheter ablation. Twenty-seven pediatric patients (9 Wolff-Parkinson-White syndrome, 7 concealed accessory pathway and 11 atrioventricular nodal reentry tachycardia) were enrolled in this study. Anesthesia was induced with propofol 2.0 mg/kg and was maintained with a continuous infusion of propofol at a rate of 100-167 microg x kg(-1) x min(-1). During a stable anesthetic state, the calculated sinoatrial conduction time and corrected sinus node recovery time (CSNRT) were measured before and after fentanyl administration. The fentanyl dose consisted of an initial 2.0 microg/kg IV bolus and subsequent continuous infusion of 0.075 microg x kg(-1) x min(-1). Bispectral Index scores and systemic blood pressure remained unchanged throughout the examinations. Fentanyl administration significantly prolonged CSNRT (P = 0.005) but not calculated sinoatrial conduction time (P = 0.35). Since an enhanced cardiac vagal tone is one of the causative factors for prolonged CSNRT, our findings greatly support the hypothesis that fentanyl combined with propofol has a potential to enhance cardiac vagal tone.

Effect of Qiangxin Fumai Granule (强心复脉颗粒) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion of the right coronary artery in rabbits

To study the effect of the Chinese medicine Qiangxin Fumai Granule (, QFG) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion (IR) of the right coronary artery in rabbits. The right coronary artery IR model in rabbits was adopted. The modeled rabbits were randomly divided into 4 groups: the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, with 8 animals in each group. In addition, twelve rabbits were selected for the sham-operative group. The drugs were administered once via duodenal perfusion after modeling had been stabilized for 10 min. The changes in AA interval, the sinoatrial conduction time (SACT), the sinus node recovery time (SNRT), the corrected sinus node recovery time (CSNRT) and the index of sinus node recovery time (ISNRT) at different time points during ischemia and reperfusion were measured. The AA interval was prolonged for more than 40 ms in the model group during ischemia. Compared with the model group, the four electrophysiological parameters abovementioned in the high-dose QFG group and the low-dose QFG group were decreased to different extents at each time point (P<0.01 or P<0.05), and no statistically significant differences were found between the QFG groups and the atropine group (P>0.05). QFG is beneficial for accelerating the recovery of sinus node autorhythmicity and conduction function, so as to protect electrophysiological functions of the sinoatrial node. Accelerating the recovery of autorhythmicity and conduction function in the sinus node is considered its electrophysiological mechanism in the treatment of sinoatrial node injury induced by ischemia.

Association of Sinus Node Dysfunction, Atrioventricular Node Conduction Abnormality and Ventricular Arrhythmia in Patients With Kawasaki Disease and Coronary Involvement

This study was performed to investigate the incidence of arrhythmias in patients with Kawasaki disease (KD). Electrophysiologic studies (EPS) were performed in 40 patients (mean age: 10.3+/-5.1 years; 30 males, 10 females) with KD who had severe to moderate coronary artery disease. Clinical arrhythmias were documented in 4 patients (premature ventricular contractions, ventricular tachycardia, atrioventricular block, and ventricular fibrillation). Dual atrioventricular nodal pathways were demonstrated in 3 patients. Nonsustained atrial fibrillation was induced in 1 patient. The AH interval was prolonged in 2 patients. The Wenckebach rate was 164+/-37 beats/min, and 4 of the patients had a decreased Wenckebach rate. The maximum and corrected sinus node recovery times were 997+/-257 ms and 281+/-130 ms, respectively, and 7 patients were thought to be abnormal. The sino-atrial conduction time was 108+/-64 ms, and 2 patients had prolonged conduction times. Although there was no relationship between coronary stenosis or obstruction and the EPS parameters, the incidence of abnormal sinus node and atrioventricular node function is apparently higher in KD patients than in the normal population. These functional abnormalities may possibly be caused by myocarditis or an abnormal microcirculation in the sinus node and atrioventricular node artery. In some patients, myocardial ischemia may provoke malignant ventricular arrhythmia.

The comparative studies of the influences of Urapidil and Nicardipine on sino-atrial node function, atrio-ventricular node function and hemodynamics

Objective To investigate the influences of urapidil and nicardipine on rabbit sinus function, atrio-ventricular node function and hemodynamics. Methods Thirty-two Angora's rabbits were selected and randomly divided into four groups. U1 group:urapidil 0.25 mg/kg; U2 group:urapidil 0.5 mg/kg; N1 group:nicardipine 10 μg/kg; N2 group: nicardipine 20 μg/kg. All these medicine were administrated within 30 seconds. Measurements were taken before and after the administration of urapidil or nicardipine for the following data: mean blood pressure(MAP), heart rate(HR), sino-atrial conduction time(SACT), maximal sinoatrial recovery time(SNRTmax) corrected sinus node recovery time(CSNRT), index of sinus node recovery time(SNRTI), Wenckebach A-V conduction frequency (WB), and P-R interval. Results Significant MAP and HR changes were identified in all of the four groups before and after administration of both urapidil and nicardipine. No significant changes could be found in the rest of the parameters. Intergroup analysis showed that SACT and CSNRT of N1 and N2 groups were shorter than those of the U2 group(P < 0.01); the MAP decreased(P < 0.01) and the HR increased drastically(P < 0.01). Conclusions Neither urapidil(0.25 mg/kg, 0.5 mg/kg) nor nicardipine(10 μg/kg, 20 μg/kg) has any significant influence on rabbit sinus function or rabbit atrio-ventricular node function. Nicardipine could be a better choice than urapidil for parafunctional sinus node patients.

Altered expression of gap junction connexin proteins may partly underlie heart rhythm disturbances in the streptozotocin-induced diabetic rat heart

Previous studies in isolated perfused heart and in atrial preparations have demonstrated significant reductions in beating rate in STZ-induced diabetic rats, which suggests that sinus arrhythmias in diabetes mellitus may be partly caused by intrinsic alteration of sino-atrial node (SAN) function. The effects of diabetes on electrical activity and expression levels of mRNA for gap junction proteins in the SAN have been investigated. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg) administered to young male Wistar rats (200-250 g). Experiments were performed 8-10 weeks after treatment. Conduction time and pacemaker cycle length were measured in sino-atrial node preparations with extracellular electrodes. Expression levels of mRNA for Gja5 (Cx40), Gja1 (Cx43) and Gja7 (Cx45) were measured in SAN and compared with right atrium and right ventricle with real-time quantitative reverse transcription-polymerase chain reaction. Diabetes was confirmed by a significant elevation of blood glucose (356+/-21 mg/dl) compared to age-matched controls (66+/-2 mg/dl). Pacemaker cycle length was significantly prolonged in diabetic heart (415+/-43 ms, n=6) compared to controls (255+/-7 ms, n=6). Sino-atrial conduction time was also significantly prolonged in diabetic hearts (12+/-2 ms) compared to controls (7+/-1 ms). Expression levels of mRNA for Gja5 (Cx40) and Gja1 (Cx43) were moderately increased and for Gja7 (Cx45) was significantly increased in SAN from diabetic heart compared to controls. Expression levels for gap junction connexin proteins were not significantly altered in right atrium or right ventricle from diabetic heart compared to controls. Structural remodelling of gap junction connexin proteins may partly underlie electrophysiological defects in STZ-induced diabetic rat SAN.

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.

Developmental Changes in Sinus Node Function in Growing Children: An Updated Analysis

Sinus node dysfunction (SAND) may be congenital or acquired following injury or surgery for congenital heart lesions. Sinus node function is evaluated by electrophysiological (EP) parameters of corrected sinus node recovery time (CSNRT) and sinoatrial conduction time (SACT). The aim of this study was to determine age- and gender-specific values for CSNRT and SACT in pediatric patients without structural congenital heart disease. Data were collected on 152 patients who underwent an EP study for evaluation of supraventricular tachycardia between 1997 and 2002. All patients received midazolam and propofol and/or isoflurane for sedation and anesthesia, which are known to not affect EP parameters. The age of transition at which CSNRT changed significantly was 14 years (241.5 +/- 102.0 msec in patients younger than 14 years old and 285.6 +/- 144.3 msec in those older than 14 years, p < 0.05). The upper limits of normal CSNRT (mean + 2 SD) were significantly higher (445 vs 275 msec) and the upper limits of normal SACT values were lower (120 vs 200 msec) than the currently used norms in the younger age group. CSNRT values and atrial refractory period values were significantly longer in males compared to age-matched females [278.5 +/- 15.3 VS : 236.4 +/- 13.6 msec (p < 0.05) and 269.0 +/- 4.9 VS: 244.7 +/- 6.8 msec (p < 0.005), respectively]. The new age- and gender-specific values of EP parameters, which reflect sinus node function, may enable more precise recognition of SAND.

Monophasic Action Potential Duration at the Crista Terminalis in Patients With Sinus Node Disease

The repolarization properties of the crista terminalis (CT) cells have not been elucidated in patients with sinus node disease (SND). In the present study a new technique of recording the monophasic action potential (MAP) at the CT was used to examine the repolarization of the right atrium (RA) in SND patients. Symptomatic SND (n=13) patients and age-, sex-matched control patients (n=13) were tested. The MAP duration (MAPD) at a basic cycle length of 600 ms was recorded at the CT in the superior vena cava - RA junction and at the middle - anterior RA with the effective refractory period (ERP) at the high RA. In 6 controls and 4 SND patients, the effect of adenosine triphosphate on the MAPD was examined. The MAPD at the CT exceeded that at the middle - anterior RA in both groups. The MAPD at the CT in the SND group was significantly prolonged compared with the control group (CT: 358+/-39 ms vs 289+/-43 ms). Between the SND and control groups, the MAPD at the middle - anterior RA (278+/-36 ms vs 265+/-39 ms) and ERP (294+/-42 ms vs 266+/-41 ms) did not differ. Both the corrected-sinus node recovery time and sinoatrial conduction time were better correlated with the MAPD at the CT than the MAPD at the middle - anterior RA and ERP. Adenosine triphosphate shortened the MAPD, which was augmented at the CT in the SND patients. A novel method of estimating the MAP at the CT revealed the characteristics of atrial repolarization in SND patients.

Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve.

Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of sinus node function. Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26+/-5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic sinus cycle length, corrected sinus node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the sinus node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of the intrinsic sinus cycle length (P=0.005), prolongation of CSNRT (P<0.0001), caudal localization of sinus activity both during sinus rhythm (P=0.03) and after pacing (P=0.002), prolongation of sinoatrial conduction time (P=0.02), greater number (P<0.0001) and duration (P<0.0001) of fractionated electrograms or double potentials along the crista terminalis, loss of voltage amplitude along the crista terminalis (P=0.02), and abnormal and circuitous propagation of the sinus impulse. This study demonstrates that patients with CHF have significant sinus node remodeling characterized by anatomic and structural changes along the crista terminalis with a reduction in functional sinus node reserve. This finding may have implications for the development of clinical bradycardia in CHF and for the use of negatively chronotropic agents and pacing in this condition.

Sinus node function in patients with Brugada-type ECG.

Some studies have shown that patients with Brugada syndrome (BS) have atrioventricular conduction disturbance, but their sinus node function has not been evaluated. The patients group consisted of 59 male patients and 1 female patient with BS. Supraventricular and ventricular programmed electrical stimulation (PES) was performed. Ventricular fibrillation (VF) or sustained polymorphic ventricular tachycardia was induced by ventricular PES in 26 patients with BS (VF group), but was not induced in the other 34 patients (non-VF group). Sinus node function and conduction of the atrioventricular (AV) node in the control group, non-VF group and VF group were evaluated. Sinus node function was attenuated and the His - ventricle interval was prolonged in the VF group (corrected sinus node recovery time: 452+/-126 ms (VF group), 324+/-146 ms (non-VF group), Sino-atrial conduction time: 179+/-60 ms (VF group), 127+/-60 ms (non-VF group), His-ventricle interval: 41+/-9 ms (VF group), 35+/-8 ms (non-VF group)). The function of both the sinus node and AV node are attenuated in patients with PES-induced VF.

Acute effects of zatebradine on cardiac conduction and repolarization.

Zatebradine, a potent bradycardic agent, is believed to act selectively at the sinoatrial node. The selectivity of such a property relative to various electrophysiologic classes of action is not well defined. To characterize the electrophysiologic properties of zatebradine, the corrected sinus node recovery time, sinoatrial conduction time, conduction intervals, atrial effective refractory period and monophasic action potential duration in the ventricle were measured before and after incremental doses of zatebradine (0.1-1.5 mg/kg) in 15 anesthetized dogs. The electrophysiologic effects of zatebradine developed immediately after a single i.v. bolus dose, reaching steady-steady-state at 15 minutes with the maximum effect evident at 0.75 mg/kg. The IC(50) was 0.23 mg/kg. There was no significant effect on the sinus node recovery time. The PR interval on the electrocardiogram was significantly increased when the dose was higher than 0.25 mg/kg. The duration of the P wave and the PA interval were not changed. Zatebridine greatly increased the AH (from 135 to 178 milliseconds) without changing the HH and HV intervals in His bundle recordings. The EC(50) of this effect was 0.58 mg/kg. The QRS interval was not changed. The QTc was significantly increased from 0.43 to 0.56 s(1/2) (P < 0.05). The action potential duration was significantly increased by high dose zatebradine (> 0.5 mg/kg), the EC(50) for this effect was 0.76 mg/kg. The atrium effective refractory period was significantly increased (31%) with an EC(50) 0.69 mg/kg. These results indicate that zatebradine selectively inhibits sinus node automaticity at low doses. The inhibition of the AV nodal conduction and the lengthening of the refractory period and repolarization in the atria and the ventricles occur at higher dose.

Intrinsic changes on automatism, conduction, and refractoriness by exercise in isolated rabbit heart.

We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger (P < 0.05) in trained vs. untrained animals: R-R interval (365 +/- 49 vs. 286 +/- 60 ms), WCL (177 +/- 20 vs. 146 +/- 32 ms), and functional refractory period of the left ventricle (172 +/- 27 vs. 141 +/- 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.

Sinus node function after mitral valve surgery using the superior septal approach

Background. Sinus node function after the superior septal approach (SSA) in mitral valve surgery is controversial. We assessed sinus node function after this approach based on electrophysiological examinations and electrocardiographic change. Methods. Forty-six patients underwent successful mitral valve surgery via the SSA. Preoperatively, 25 patients were in atrial fibrillation (AF), 20 were in normal sinus rhythm (SR), and 1 patient was paced. Thirteen patients who demonstrated no sinus node dysfunction preoperatively underwent postoperative electrophysiological studies. Peripostoperative cardiac rhythm was monitored using a portable four-lead electrocardiograph, and late cardiac rhythm was examined using standard 12-lead electrocardiography in the outpatient clinic. Results. Twelve of 20 patients with preoperative SR experienced early postoperative supraventricular arrhythmias, but all spontaneously recovered SR. Electrophysiological studies revealed a basic cycle length of 767 ± 74 ms, sinoatrial conduction time of 72 ± 34 ms, sinus node recovery time of 1,119 ± 139 ms, and corrected sinus node recovery time of 349 ± 114 ms, thus demonstrating a lack of sinus node dysfunction. During the postoperative period (34 ± 24 months), 2 of the 20 patients with preoperative SR developed persistent AF, and 3 of the 25 patients with preoperative AF achieved normal SR. Conclusions. The SSA does not appear to cause long-term adverse effects on sinus node function, although temporary effects may occur.

Heart transplantation: Influence of the surgical technique on sinus function

This study analyzes the influence of the surgical technique on the development of sinus dysfunction. Cycle length, corrected sinus node recovery time, and sinoatrial conduction time were determined in 4 groups of dogs under the following conditions: group 1, controls; group 2, subjected to heterotopic heart transplantation with conservation of atrial anatomy; group 3, subjected to orthotopic heart transplantation by using a standard technique; and group 4, treated as in group3, but with an ischemic time of 24 hours. The cycle length was prolonged in all the treated groups when compared with the controls ( P < .01), an effect attributed to the disconnection of the autonomic nervous system during the transplantation procedure. The corrected sinus node recovery time and sinoatrial conduction time were significantly longer in all the animals in groups 3 and 4 when compared with those of groups 1 and 2 ( P < .01); however, there were no significant differences between groups 3 and 4 or between groups 1 and 2. These results suggest that the atrial anatomy play a more relevant role than the ischemic time in the origin of sinus dysfunction occurring after orthotopic heart transplantation.

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.