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By arbitrary definition, a bradycardia is a heart rate of

OBJECTIVE—To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. DESIGN—441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. RESULTS—Cumulative incidence of sinus node disease was 0.65% per year without differences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. CONCLUSIONS—In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients. Keywords: dual chamber pacing; sinus node disease; atrial fibrillation

In the early days of sleep research it was thought that heart block (second and third degree atrioventricular block), sinus arrest, or sinoatrial block were frequent findings in patients with sleep apnoea. Tilkian and co-workers1 reported that more than 50% of patients with sleep apnoea develop episodes of heart block during sleep. In 400 patients studied by Guilleminault et al 2 bradycardic arrhythmias were reported in almost 18% of the patients and later studies found heart block in 9–13% of patients with sleep apnoea.3 4 Due to ventricular asystoles of up to 13 seconds in duration it was hypothesised that heart block might lead to an increased mortality risk in these patients.2 A recent publication challenged previous results in that no increased prevalence of bradycardic arrhythmias was seen in patients with sleep apnoea compared with those without sleep apnoea.5 To examine these seemingly discrepant results further we performed Holter monitoring in 239 consecutive patients diagnosed as having sleep apnoea (apnoea/hypopnoea index >10/h) using a validated ambulatory recording device based on the measurement of heart rate, Sao 2, snoring sound, and body position. Episodes of second and third degree atrioventricular (AV) block and/or sinus arrest of more than two seconds in duration occurred in 17 of the 239 patients.6 There was no significant difference in age between patients with and without heart block (mean (SD) 50.7 (12.8) versus 52.1 (9.8) years), but those with heart block were significantly more obese (38.7 (7.3) versus 30.7 (4.6)). Twelve of the 17 patients (70.6%) had arterial hypertension, seven (41.1%) suffered from heart failure (NYHA II–III), and four (23.5%) had pulmonary hypertension. None of the patients reported a myocardial infarction in their medical history, and in only one (5.9%) exercise testing showed signs of coronary heart disease. Ten …

In February 2013, two sisters, aged 18 and 24, presented with a history of episodes of loss of consciousness (ELCOs) occurring since childhood. In the past 2 years, the ELCOs increased to an average of 10/year, preceded by migraines and lasting at least 10 min, with loss of postural control and slow recovery. The sisters also reported, brief lapses of consciousness. In 2010 and 2012, sleep-deprived EEG, during-sleep EEG, ambulatory EEG and a brain MRI, were all inconclusive for epilepsy. A nitrate-stimulated tilt test was followed by a brief ELCO in both girls, reflecting an uncertain diagnosis of vasovagal syncope, as the patients presented with pretest orthostatic hypotension.1 The finding of sinoatrial node arrest with ELCOs on Holter monitoring in the younger sister (figure 1) and on loop recording in the elder sister (figure 2) supported dual-chamber pacemaker implantation, in July 2012 and January 2013, respectively. Nevertheless, the ELCOs did not cease, and a neurological workup was again inconclusive. In May 2013, a patients’ relative documented a seizure episode in …

Objectives To analyse of the complications caused by permanent pacemaker implantation Methods The number of all patients receiving a permanent pacemaker in the inclusive period January 1995 to July 2011 were 297 in our hospital. These patients with an age range of 31–85 years (The mean age of patients was 60±10.5 years.) were paced. Of these 205 were males (age range 52–95 years). Of these 91 were wenmen. In 287 brady arrhythmias ( bradyarrhythmia ) patients, there were 174 patients with sick sinus syndrome (sinus bradycardia, sinus pause, sinoatrial block, bradycardia-tachycardia syndrome), 108 patients with Atrioventricular block (complete heart block, Mobitz type 2 block), 15 patients with three branch block and 71 patients with binodal disease. There were 10 patients with heart failure for Dilated cardiomyopathy, three patients with vessel pneumogastric syncope, one patients with Carotid sinus syndrome and one patients with long Q-T syndrome. The method of permanent pacemaker implantation followed WANG-fangzheng introduction. Electrode values request: atrial pacing threshold low 1.0 V, P wave amplitude high 2.5 mV ventricular pacing threshold low 1.0 V, R wave amplitude high 2.5 mV, The range of impedance is 300–1000 Ω. VVI pacemakers were implanted in 173 patients, AAI pacemakers were implanted in 28 patients, DDD pacemakers were implanted in 81 patients, DDDR pacemakers were implanted in two patients, CRT pacemakers were implanted in two patients. Results All operations of implanting permanent pacemaker succeeded and the bradycardia symptom of all patients disappeared. In this study, pacing threshold is 0.2–1.3 V (the mean was 0.45±0.10 V), The impedance was 350–1280 Ω (the mean was 690±103 Ω), P wave amplitude was 3.9–8.5 mV (the mean was 5.0±3.0 mV), R wave amplitude was 5.6±14.5 mV (the mean was 8.5±3.6 mV). There were four patients with haematoma of the pocket of pacemaker. By the treatment of pumping, squeezing and treading with sandbag, the haematoma disappeared. The Skin incision of one patient did not healed after 1 month due to a suture. After the suture was taken out, the Skin incision healed and did not find infection of the pocket of pacemaker. There was one patients with prolapse of the pocket of pacemaker, one patients with long-dated diabrosis. Adams-Stokes syndrome occurred in one patient9s operation, the patient highly depended on pacemaker. Electrocardiograph recorded sinus pause when the patient occurred twitched. After Cardiopulmonary resuscitation, heartbeat of the patient returned. Pacemaker syndrome occurred in two patients with VVI Pacemaker. The related symptom disappeared after turning pacing frequency to 50 hpm. Electrode of in one patient9 heart right ear dislocated and Back to normal by banning activities of the sufferer. Pacing threshold in one patient increased, the related symptom disappeared after adjusting output voltage. Muscles in left breast area of one patient jumped, the related symptom disappeared after adjusting output voltage. one patient happened sudden death when working due to unexplained reason. There were no reported incidences of haemothorax, pneumothorax, Arteriovenous fistula, infection of the pocket of pacemaker, electrode fracture, Electrode shift and death in this study. Conclusions Skilled operation method can obviously reduced incidences of complications of permanent pacemaker. Permanent pacemaker insertion can be effective and safe, and the rate of complications was low.

The British Pacing and Electrophysiology Group guidelines for pacemaker prescription recommend single chamber atrial pacing as the most appropriate pacing mode for sinus node disease in the absence of atrioventricular conduction disturbance.1 As such it offers a rare combination of maximum clinical effectiveness for the minimum cost and a good training opportunity. However, it seems that this message has yet to be translated into pacing practice in the UK. In this issue of Heart , Clarke et al retrospectively analyses the pacing activity for sinus node disease in a tertiary pacing centre over five years.2 They conclude that in their centre £103 000 per year could have been saved by more judicious use of AAI pacing, largely by reducing the DDD implant rate. It seems likely that these potential savings are equally applicable to the rest of the UK. Current pacemaker prescribing for sinus node disease is frequently illogical, ignores current evidence, and misses out on training opportunities for junior staff. The evidence to support atrial based pacing for sinus node disease, rather than single chamber ventricular pacing, is very strong. Numerous retrospective studies have demonstrated that mortality and morbidity are greater in ventricular only paced patients,3-5 and that the progression to chronic atrial fibrillation (AF) is less common in patients with atrial based pacing.3-10 Although these data may be criticised for the potential biases inherent in retrospective studies, since 1994 data have been available from the first prospective randomised study.11 Andersen et al were able to demonstrate a reduction in the frequency of AF and incidence of thromboembolism (5% v 18%) with atrial pacing after three years of follow up. The most recent analysis of this study (at 5.5 years of follow up) has also shown a significant reduction in all cause mortality (35.5% v …

Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs.

The symptoms of 100 patients with chronic cardiac sinoatrial disorder were analysed. The most common presenting features were syncope in 34 cases and dizziness in 22 cases. Over three-quarters of the patients had cerebral ischaemic symptoms at some stage of the disease. Diagnostic difficulties are often encountered and are illustrated by two case histories. Although sinoatrial disorder has been described in association with neuromuscular diseases, only one such example was found in this series. The patient had a limb girdle dystrophy with cardiomyopathy and diffuse disease of the cardiac conducting system. Muscle biopsy samples taken from 11 patients with idiopathic sinoatrial disorder were normal showing no evidence of subclinical muscular disease.

In an unselected population of 2030 newborn infants studied by electrocardiography (ECG) between April 1975 and April 1977, 35 were found to have arrhythmias or other cardiac conduction abnormalities. Further investigation by means of 24-hour ECG monitoring showed that apparently serious tachyarrhythmias, such as ventricular tachycardia and slow heart rates associated with sinoatrial block, may be present without clinical disturbance in some newborn babies. Six infants had both bradycardia and tachycardia in the 24-hour recording, although the screening ECG had shown only one of these abnormalities. The alarming ECG appearance of some of the arrhythmias suggested a possible aetiological link with some unexplained sudden infant deaths: a multicentre study could determine this more readily and is therefore recommended.

Six patients with symptoms due to sinoatrial block are described in whom no relief or improvement in block occurred when they were treated with isoprenaline or ephedrine. All six patients were treated by ventricular cardiac pacing with complete relief of symptoms. Despite the theoretical disadvantages of parasystole and loss of accrochage in treating these patients by ventricular pacing they have survived for periods of 18 months to over five years.