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The sinoatrial node (SAN) is the dominant pacemaker of the heart. Abnormalities in SAN formation and function can cause sinus arrhythmia, including sick sinus syndrome and sudden death. A better understanding of genes and signaling pathways that regulate SAN development and function is essential to develop more effective treatment to sinus arrhythmia, including biological pacemakers. In this review, we briefly summarize the key processes of SAN morphogenesis during development, and focus on the transcriptional network that drives SAN development.

We report here five cases of sinus bigeminy in which comparatively long PP intervals alternated with comparatively short PP intervals, suggesting 'sinus escape-capture bigeminy' or 'sinus extrasystolic bigeminy'. In three of the cases, these two forms of sinus bigeminy were found in the same patient. This is the first study on 'sinus escape-capture bigeminy' alternating with 'sinus extrasystolic bigeminy'. The electrocardiographic findings in these cases suggest the possibility that 'sinus escape' in the sinoatrial junction is not true escape. Attempts are made to explain that apparent sinoatrial junctional escape occurs as a result of markedly slow conduction through the slow sinoatrial pathway, using the concepts of 'dual sinoatrial pathways' and 'double atrial response'.

Summary (2-Chloroethyl)-trimethylammonium chloride (Chlormequat chloride, Chlorocholine chloride, Cycocel, CCC) in single doses of 50 mg./kg. and 100 mg./kg. was administered to rabbits by stomach tube. Electrocardiograms (three standard limb leads) were recorded before and after CCC administration and also after 30 minutes and 1, 2, 3 and 4 hours. Serious disturbances of the heart action as well as failure of respiration appeared after the larger dose which resulted in the death of six out of eight rabbits. The ECG showed initially a depression of the S-T segment and some changes in the T wave amplitude. Later, at the agonal stage, marked sinus bradycardia and sinus arhythmia were noted. It is suggested that the effects observed were due to stimulation by CCC of the parasympathetic nervous system. Zusammenfassung Die Wirkung von 2-Chlorathyl-trimethylammonium auf das Elektrodiagramm des Kaninchens 2-Chlorathyl-trimethylammonium-chlorid (Chlormequat-chlorid, Chlorcholin-chlorid, Cycocel, CCC) wurde Kaninchen in Einzelgaben von 50 und 100 mg/kg mit der Magensonde verabfolgt. Elektrokardigramm (drei Standard-Extremitaten-Ableitungen) wurden unmittelbar vor und nach der Gabe von CCC registriert. Weitere Aufnahmen wurden 1/2, 1, 2, 3 und 4 Stunden nach der Applikation von CCC gemacht. Schwere Storungen der Herztatigkeit und Aufhoren der Atmung waren die Folgen der groseren Dosis, wobei sechs von acht Kaninchen eingingen. Zuerst zeigte das Elektrokardiogramm eine Senkung des ST-Segmentes und Anderungen der Amplitude der T-Zacke. Spater, wahrend der Agonie, wurde eine deutliche Sinusbradykardie und Sinusarrhythmie sichtbar. Vermutlich sind die beobachteten Phanomene die Folgen einer starken Reizung des parasympathischen Nervensystems durch Chlorcholin-chlorid. Resume L'effet du chlorure de 2-chlorethyl-trimethylammonium sur l'electrocardiogramm du lapin On administre a des lapins, a l'aide d'une sonde gastrique, du chlorure de 2-cklor-ethyl-trimethylammonium (chlorure de chlormequate, chlorure de chlorocholine, Cycocel, CCC), a des doses uniques de 50 et 100mg/kg. On enregistre l'electrocardiogramme (trois derivations standardes des extremites) immediatement avant et apres administration de CCC. On procede a d'autre mesures 1/2, 1, 2, 3 et 4 heures apres application de CCC. Comme effet de la dose elevee, on observe de graves troubles de l'activite fonctionelle du coeur et un arret respiratoire, avec issue fatale chez 6 sur 8 lapins. L'electrocardiogramme manifeste en premier lieu une depression du segment ST et des modifications de l'amplitude de l'onde. T. Plus tard, pendant l'agonie, on observe une nette bradycardie et arythmie sinusoidale. Les phenomenes observes sont vraisemblablement les consequences d'une forte excitation du systeme nerveux parasympathique par le chlorure de chlorocholine. Resumen La accion del cloruro de 2-cloroetil-trimetilamonio sobre el electrocardiograma del conejo Con la sonda gastrica en dosis unicas de 50 y 100mg/kg peso vivo se administro cloruro de 2-cloroetil-trimetilamonio (cloruro de clormecuato, cloruro de clorcolina, Cycocel, CCC) a conejos. Los electrocardiogramas (tres derivaciones tipo en extremidades) se registraron inmediatamente antes y despues de aplicar la dosis de CCC. Otros registros se efectuaron a la 1/2, 1, 2, 3 y 4 horas despues de aplicar el CCC. Consecuencias de las dosis mayores eran alteraciones graves en la actividad cardiaca y cese de la respiracion, muriendo seis de ocho conejos. El electrocardiograma mostraba primero un descenso del segmento ST y cambios en la amplitud de la punta T. Mas adelante, durante la agonia, se apreciaban bradicardia y arritmia sinusales claras. Se supone que los fenomenos observados son consecuencia de un estimulo intenso del sistema nervioso parasimpatico por el cloruro de clorcolina.

The risk for complications while providing moderate and deep sedation is greatest when caring for patients already medically compromised. It is reassuring that significant untoward events can generally be prevented by careful preoperative assessment, along with attentive intraoperative monitoring and support. Nevertheless, we must be prepared to manage untoward events should they arise. This continuing education article will review critical aspects of patient management of respiratory and cardiovascular complications.

We report here 2 cases of sinus arrhythmia considered to be a form of nonrespiratory sinus arrhythmia because they did not have variances in the RR interval sequence within the oscillations modulated by respiration. Because the patients had pulsus alternans similar that observed in bigeminy, and because they did not have signs or symptoms of heart failure, we believe the arrhythmias represent intrinsic alterations of the electric activity of the sinus node

Objective:To examine associations between autonomic nervous system and adrenocortical reactivity to laboratory stressors and buccal cell telomere length (BTL) in children.Methods:The study sample comprised 78 children, aged 5 to 6 years, from a longitudinal cohort study of kindergarten social hierar

to conduct a clinical, genetic, and functional analysis of 3 unrelated families with familial sinus bradycardia (FSB).mutations in the hyperpolarization-activated nucleotide-gated channel (HCN4) are known to be associated with FSB.three males of Moroccan Jewish descent were hospitalized: 1 survived an out-of-hospital cardiac arrest and 2 presented with weakness and presyncopal events. All 3 had significant sinus bradycardia, also found in other first-degree relatives, with a segregation suggesting autosomal-dominant inheritance. All had normal response to exercise and normal heart structure. Sequencing of the HCN4 gene in all patients revealed a C to T transition at nucleotide position 1,454, which resulted in an alanine to valine change (A485V) in the ion channel pore found in most of their bradycardiac relatives, but not in 150 controls. Functional expression of the mutated ion channel in Xenopus oocytes and in human embryonic kidney 293 cells revealed profoundly reduced function and synthesis of the mutant channel compared to wild-type.we describe a new mutation in the HCN4 gene causing symptomatic FSB in 3 unrelated individuals of similar ethnic background that may indicate unexplained FSB in this ethnic group. This profound functional defect is consistent with the symptomatic phenotype.

T-wave oversensing poses a clinical challenge often resulting in inappropriate therapies and shocks. T-wave oversensing can often be resolved by certain programmable adjustments while accepting a small risk of undersensing ventricular fibrillation. The following case depicts a girl with LQT whose transvenous defibrillator repeatedly demonstrated T-wave oversensing despite optimizing various programmable features and a separate pace/sense lead. Utilization of an LV epicardial pace/sense lead with stable R-waves affirmed an unusual resolution of T-wave oversensing and avoidance of inappropriate shocks.

Physiological responses (i.e., EEG, heart period, respiratory sinus arrhythmia (RSA)) were monitored in 5-month-old infants during the replacement of an adult's smiling (SF) with a blank face (BF) in a face-to-face setting. Affect, while the infant looked at and away from the adult's face during both conditions, was analyzed. Infants displayed neutral and some positive affect while looking at both SF and BF. RSA was quantified continuously during both conditions. RSA increased during BF relative to SF. EEG was quantified only while the infants were looking at the adult's face during both conditions. An increase in theta over multiple scalp areas (AF3,4; F7,8; FC3; T6) was observed during BF relative to SF. The data suggest that infant attention to BF and SF reflect different psychophysiological processes that can be indexed by RSA and scalp-recorded theta.

We describe a case in which reflection of a palatal flap for removal of a mesiodens is presented as the triggering factor for bradycardia caused by stimulation of the trigeminocardiac reflex. The management of the case, as well as the reflex arc, is discussed.

In this investigation, we sought to further test the hypothesis that parasympathetic deficiency exists among persons with Prader-Willi syndrome, by examining respiratory sinus arrhythmia. The study sample comprised two groups of patients: 14 subjects with Prader-Willi syndrome and 14 age- and sex-matched controls. Each subject's electrocardiogram was recorded in a quiet room and digitized by a personal computer during five 1-minute periods. RR intervals within each 1-minute period were converted to heart rate in 120 successive 0.5-second intervals. The resultant heart rate time series was converted to its underlying frequency composition by a fast Fourier transform and averaged across minutes. Respiratory sinus arrhythmia was defmed as the variability in the time series over a frequency range (0.096 to 0.48 Hz) corresponding to a range of respiratory rates from six to 30 breaths/minute. Analysis revealed significantly less variability in the heart rates of subjects with Prader-Willi syndrome relative to age- and sex-matched controls (group x frequency bin: F = 2.26, P < .05). An analysis of covariance adjusting for body mass index differences between the groups produced identical results. These findings support the existence of a parasympathetic deficiency among subjects with Prader-Willi syndrome independent of their body mass. This is likely due to dysregulation of the central autonomic network. (J Child Neurol 1996;11:121-125).

The chronotropic response during graded, symptom limited exercise was investigated in 32 cardiac transplant recipients a mean of 49 +/- 18 days after transplantation. All patients had systematic evaluation of postoperative donor sinus node (SN) function and the cardioacceleratory response was compared according to the SN function. Twenty-one patients had normal postoperative SN studies (corrected SN recovery time520 msec, group I) while the SN function was impaired postoperatively in the remainder (n = 11, group II; corrected SN recovery time 4,149 +/- 6,283 msec in 5 patients, junctional escape rhythm in 6 patients). All patients had regained sinus rhythm at time of the exercise test. Patients in group II had lower basal sinus rates at the beginning of exercise (91.5 +/- 11 vs 101.4 +/- 7 beats/min, P0.02). This lower chronotropy was maintained over every incremental step (F rate between groups = 30, P = 0.0001, F rate vs workload = 15, P = 0.0001 by two-way ANOVA) and resulted in a significantly lower heart rate at individual peak exercise (108.3 +/- 20 vs 124.2 +/- 13 beats/min, P0.02). A total of 14/16 patients in group I but only 2/16 patients in group II accomplished a peak heart rateor = 120 beats/min (P = 0.009). The workload achieved did not differ between the groups (107 +/- 29 vs 102 +/- 32 watts, P0.5). These data show a lower SN chronotropy during rest and at peak exercise in cardiac transplant recipients with postoperative SN deficiency and apparent normalization of SN function.

Atrial undersensing is a common problem in permanent atrial and dual chamber pacing. The purpose of this study was to evaluate the relationship between transesophageal atrial wave (EsAW) and right atrial endocavitary (RA). Forty-seven patients 72 +/- 9.7 years of age, with symptomatic bradyarrhythmias were studied. The EsAW was filtered with a high pass filter of 10 Hz (Arzco preamplifier-filter), using 1, 2, and 3 cm bipolar transesophageal catheters. Atrial bipolar floating 1, 2, and 3 cm electrograms from the high RA (HRA) and from the mid RA (MRA), as well as unipolar electrograms from the right auricle (RAUR) were recorded 1 day later. Comparison by paired t-test showed no significant differences between EsAW and bipolar sensing in RA, but significant differences between EsAW and RAUR (P = 0.0001). The results of the Spearman correlation coefficient for sensing (mV) for EsAW, HRA, and MRA, respectively, were: 1 cm, 1.8 +/- 0.9, 1.7 +/- 0.9, and 1.9 +/- 0.9 (z3.5; P0.0003); 2 cm, 2.2 +/- 0.9, 1.9 +/- 0.8, and 2.1 +/- 0.9 (z2.3; P0.03); 3 cm, 2.1 +/- 1, 2 +/- 0.9, and 2.2 +/- 1.0 (z2.9; P0.003); and the result for the monopolar RAUR was 3.0 +/- 1.0 (z1.4; P0.17). These findings, if confirmed in more patients, indicate that preoperative EsAW recording could be useful in estimating the quality of bipolar floating electrograms from the RA but not of unipolar RAUR.

Casts of the left atrial appendage, obtained at postmortem examination, show its variable and complex morphology. One left atrial …

In 21 patients with and 31 without junctional escape beats, a comparison of the symptoms, revealed that there were no significant differences (p greater than 0.05) in the symptoms between these two groups manifesting a sick sinus syndrome. Thus, the occurrence of junctional escape beats did not provide the anticipated shortening of the asystolic pauses to prevent the occurrence of symptoms related to the period of electrical silence. In 7 patients with an escape junctional rhythm, the long pause was interrupted by the occurrence of a regular junctional rhythm. The pause was not preceded by a supraventricular tachycardia, ruling out physiologic overdrive suppression of the junctional pacemaker. The period of asystole preceding the junctional rhythm was not multiple of the R-R interval of the junctional rhythm. 4 additional patients demonstrated long periods of asystole, uninterrupted by junctional escape beats and at other times exhibited shorter pauses which were terminated by junctional escape beats. These findings can be explained by the presence of a 'junctional arrest' which is analogous to sinoatrial arrest. The phenomenon of 'junctional arrest' may be one tenable explanation to account for the lack of protection by junctional escape activity against the symptoms associated with the sick sinus syndrome.

Epicardial potentials of the sinus node, the right atrium, and the right ventricle were recorded in dogs during cold potassium-induced cardioplegia. We found that the sinus node fibers were more resistant to the cardioplegia than were the other myocardial fibers. When the cardioplegia rendered the atrial muscle inexcitable, the high frequency atrial potential was delayed and then abolished in the sinus node electrogram, and a smooth tracing similar to the action potential of the sinus node cell appeared. These findings should be pertinent for the cardiac surgeon attempting to avoid surgically-induced sinoatrial arrhythmias.

This paper discusses the problem of prestimulus variability in cardiac activity and its implications for the measurement of evoked cardiac responses (ECRs). Two methods which have been proposed to reduce error arising from respiratory sinus arrhythmis (SA) were reviewed critically. The first approach attempts to control only for the error associated with the sampling of the prestimulus level. This is considered inappropriate since it does not take into account the continuation of SA into the poststimulus period. The second approach reviewed was time series analysis which provides an elegant statistical solution of the problem. Unfortunately, the application of time series analysis has not yet been evaluated for adult cardiac data. A third approach which utilizes an adjustment for SA by employing the actual prestimulus values of an SA cycle was proposed. The application of this technique in the case of a pseudostimulus demonstrated that correction for SA results in significantly smaller 'responses' with less variance than does a conventional procedure which does not take prestimulus variability into account.

In an eight-choice reaction task, the influence of erroneous responses upon the temporary changes in the level of heart rate (HR) was studied. It was shown that after errors there was a short-term deceleration of the HR-level, while after correct responses an accelerating tendency was found. This phenomenon has to be regarded as an additional source of fluctuations of the HR-level. Therefore, it has to be taken into account when suppression of sinus arrhythmia is used for assessing the level of mental load.

Onehundred andseventy-five patients withatrial fibrillation treated forthefirst timewithDC shock weredivided into twogroupsaccording toyearofbirth. GroupIreceived a long-acting quinidine bisulphate preparation, thedosage ofwhich was adjusted togive serumlevels of1-3mg./l. Side-effects wererarewiththis dosage. Group 2received noquinidine. Ofthe88patients ofgroup I,sinus rhythm was restored in75(85%). Whenleaving thehospital 64(73%) still hadsinus rhythm, andafter 3 months 52(59%). Thecorresponding figures forthe87patients ofGroup2 were 73(84%), 54(62%), and30(34%). Thedifference at3 months isstatistically highly significant. Because ofthese results itisconcluded thatelectric conversion ofatrial fibrillation should beperformed forthefirst timewithout quinidine prophylaxis. Ifthere isfailure orearly recurrence,however, a second electric conversion withsubsequent quinidine treatmentshould be considered.

1.1. The P-R interval often shows an inverse relationship to the R-R interval in sinus arrhythmia. 2.2. When this phenomenon was first observed, it was thought possibly to be specific for active rheumatic fever. Further study, however, showed that it occurred in many individuals with normal hearts. 3.3. Four possible explanations for this P-R phenomenon are discussed. 4.4. It is suggested that the Wenckebach phenomenon may be due to a pathologic exaggeration of the fatigability of the conducting tissue frequently found even under normal conditions.

General inspection of an electrocardiogram shows whether a cardiac arrhythmia is benign or serious, but a specific diagnosis requires more thorough analysis. A systematic approach, such as the one described here, will aid the clinician in making an accurate diagnosis.

Marked symptomatic sinus bradycardia was treated by permanent pervenous Bifocal (sequential atrioventricular) demand pacemaker (BFD) implantation in four patients. The specific mode of operation and the complications encountered are analyzed. In the group of implants, six different BFD pulse generators were used; two of these generators underwent premature battery failure, one developed runaway and a fourth, premature circuit instability. Improper position or later displacement of the J-shaped atrial electrode prompted a special problem—ventricular stimulator inhibition. This self-inhibition is unique to this variety of generator and requires repositioning of the atrial electrode. The longterm high drain of energy and the electrical instability of the pulse generator are problems remaining to be solved before this mode of pacing can reach its full potential use.

In one area of Sweden interest has been directed towards the improved detection of patients with symptomatic bradyarrhythmias. Monitoring facilities were increased and indications for monitoring were expanded. In particular, patients with cerebral ischaemic episodes were included, introducing the concept of "cardiogenic neurology". This has resulted in a significantly increased frequency of recognition and treatment of patients requiring permanent pacemakers.

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