Sleep apnea syndrome in patients with cardiac pacemaker.
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BACKGROUND: Heart rhythm disturbances are cardiac side effects in patients with sleep-disordered breathing (SDB), which in itself is considered to be a risk factor for bradycardic rhythm disturbances. OBJECTIVE: We analyzed the prevalence and degree of SDB in patients who received a cardiac pacemaker due to bradycardic rhythm disturbances and investigated the relationship between the severity of an underlying SDB and the type of heart rhythm disturbance. METHODS AND RESULTS: 192 patients (100 males, 92 females, mean age 62.2 +/-12.2 years) were studied using the portable screening device MESAM IV. The respiratory disturbance index (RDI) was calculated visually. The mean RDI in all patients was 9.13+/-11. 09/h, 11.7+/-13.15/h in males and 6.33+/-7.42/h in females. The prevalence ratio of SDB between men and women was 1.7:1, with significant differences in the respective severity (p<0.05). The screening showed a prevalence of SDB (RDI >10/h) of 32.3%. The highest prevalence was found in the group of patients with atrial fibrillation and bradycardia. However, there were no significant differences compared to other types of rhythm disturbances. The RDI in the population studied depended on age and body mass index, but not on the existence or type of rhythm disturbance and not on concomitant diseases. CONCLUSION: The prevalence of SDB in cardiac pacemaker patients is similar to that in patients of comparable age without a pacemaker. A heart rhythm disturbance does not seem to be an independent risk factor for development of SDB. Nevertheless, the differential diagnosis of bradycardic rhythm disturbances in this age group should include a screening for sleep apnea. (+info)
Effect of pulmonary C-fibre afferent stimulation on cardiac vagal neurones in the nucleus ambiguus in anaesthetized cats.
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It has been demonstrated previously that the vagal bradycardia evoked by activation of pulmonary C-fibres is not respiratory modulated. Experiments were carried out in alpha-chloralose anaesthetized cats to determine if these cardiac vagal preganglionic neurones (CVPNs) in the nucleus ambiguus (NA), which have respiratory modulated activity, can be activated when pulmonary C-fibre afferents are stimulated by right atrial injections of phenylbiguanide (PBG). Eleven CVPNs with B-fibre axons in the right cardiac vagal branches were identified and found to be localized within or ventrolateral to the nucleus ambiguus. Ionophoretic application of a high current of dl-homocysteic acid (DLH) induced a vagally mediated bradycardia and hypotension in six of eight sites from which CVPNs were recorded. The activity of B-fibre CVPNs, whether spontaneous (n = 4) or induced by ionophoresis of DLH (n = 7) was respiratory modulated, firing perferentially during post-inspiration and stage 2 expiration. This activity also correlated with the rising phase of the arterial blood pressure wave consistent with these CVPNs receiving an arterial baroreceptor input. Right atrial injections of PBG excited nine of eleven CVPNs tested. In eight of these activated neurones the onset latency of the excitation was within the pulmonary circulation time, consistent with being activated only by pulmonary C-fibre afferents. In two neurones the PBG-evoked excitation still occurred when central inspiratory drive was inhibited, as indicated by the disappearance of phrenic nerve activity. In conclusion, B-fibre respiratory modulated CVPNs can be activated following stimulation of pulmonary C-fibre afferents. (+info)
Brady-tachycardia syndrome after radiotherapy for lung cancer. Assessment by computed tomography and carbon-11 methionine positron emission tomography.
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A 74-year-old male who had received radiotherapy (total 54 Gy) for right lung cancer 7 months earlier developed a symptomatic brady-tachycardia syndrome requiring the implantation of a permanent pacemaker. Chest CT showed a pulmonary tumor of 2-cm diameter in the right lower lobe with direct extension into the surrounding tissue, suggesting the possibility of cardiac invasion. Carbon-11 methionine positron emission tomography (PET) indicated the absence of visible invasion of the heart with lung cancer. The bradytachycardia syndrome, therefore, was considered to be associated with sinus node injury due to radiation. Carbon-11 methionine PET metabolic imaging might play an important role in evaluating noninvasively the cause of the arrhythmia in this patient. (+info)
Cannabinoids cause central sympathoexcitation and bradycardia in rabbits.
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Systemically administered cannabinoids elicit marked cardiovascular effects, and the role of the central and the peripheral nervous system in these effects is not clarified. The aim of this study was to characterize the actions of cannabinoids on cardiovascular regulatory centers in conscious rabbits. A catheter for administration of drugs into the cisterna cerebellomedullaris and an electrode for recording renal sympathetic nerve activity were implanted under halothane anesthesia. Experiments were carried out later in conscious animals. Two cannabinoid receptor agonists were injected intracisternally: the aminoalkylindole WIN55212-2 (0.1, 1, and 10 microg kg(-1)) and the bicyclic Delta(9)-tetrahydrocannabinol analog CP55940 (0.1, 1, and 10 microg kg(-1)). WIN55212-2 and CP55940 dose dependently increased renal sympathetic nerve activity and the plasma noradrenaline concentration and also lowered the heart rate. The highest doses of WIN55212-2 and CP55940 increased blood pressure. In contrast, intracisternal injection of WIN55212-3 (0.1, 1, and 10 microg kg(-1)), an enantiomer of WIN55212-2 with very low affinity for cannabinoid binding sites, had no effects. The CB(1) cannabinoid receptor antagonist SR141716A (0.5 mg kg(-1), i.v. ) attenuated the effects of intracisternally administered WIN55212-2 (0.1, 1, and 10 microg kg(-1)). The results indicate that cannabinoids, acting directly on cardiovascular regulatory centers, elicit sympathoactivation and bradycardia. These effects were likely mediated by CB(1) cannabinoid receptors, because they were elicited by two cannabinoid agonists belonging to different chemical classes (WIN55212-2 and CP55940), but not by the inactive enantiomer WIN55212-3, and because they were attenuated by the CB(1) cannabinoid receptor antagonist SR141716A. (+info)
Incidence of atrial flutter and atrial fibrillation in patients with implanted physiological pacemakers.
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Atrial flutter (AF) is a troublesome arrhythmia for patients with an implanted pacemaker. Although it has recently become possible to eliminate AF by radiofrequency catheter ablation (RF-CA), the incidence of AF before and after pacemaker implantation has not been clarified. The present study was conducted with 123 consecutive patients (69.3+/-11.6 (SD) years old) implanted with pacemakers, excluding patients who had chronic atrial fibrillation (AFib) when the pacemaker was implanted; 69 patients with atrioventricular (AV) block and 54 patients with sick sinus syndrome (including 29 patients with bradycardia-tachycardia syndrome). All patients were implanted with physiological pacemakers. The follow-up period was 4.7+/-1.9 years. In 11 of the 123 patients (8.9%), AF was observed before pacemaker implantation and the incidence was significantly higher in patients with sick sinus syndrome than in those with AV block (16.7 vs 2.9%, p<0.01). Nine of the 29 patients with bradycardia-tachycardia syndrome (31%) had AF. After physiological pacemaker implantation, AF recurred in 9 of the 11 patients, and AF was newly observed in 1 patient. Thus, 10 of the 123 patients (8.1%) had AF after physiological pacemaker implantation. Recurrence of AF was not suppressed by physiological pacing. Thirty of the 123 patients had AFib before implantation of a pacemaker and its occurrence was reduced by physiological pacing (from 24.4% to 12.2%, p<0.05). The incidence of AFib in patients with AF was significantly higher than in those without AF (90.0 vs 5.3%, p<0.001). In conclusion, the recurrence of AF is not prevented by physiological pacing and is closely related to the occurrence of AFib. RF-CA should be considered in patients who have AF before pacemaker implantation. (+info)
Circulatory effects of acute bradycardia in the human fetus as studied by Doppler ultrasound.
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OBJECTIVE: To report on flow changes in fetal arterial, venous and coronary vessels during bradycardia following cordocentesis. Changes in the fetal circulation in response to acute challenges are incompletely understood. METHODS: Fetal blood sampling was performed at 29 + 4 weeks for chromosome analysis in a fetus with multiple malformations including a complete atrioventricular septal defect with competent atrioventricular valve. The procedure was complicated by a 12-min bradycardia of 57 beats/min. 'Heart sparing' (sudden visualization of coronary blood flow) and 'brain sparing' (increased diastolic velocities in the middle cerebral artery) were demonstrated by Doppler examination despite marked circulatory compromise (regurgitation of atrioventricular valve, increased reverse flow in precordial veins and pulsatile umbilical vein flow pattern) which persisted after normalization of the fetal heart rate. The findings had resolved completely at a full cardiovascular examination 6 h after the bradycardia. Pregnancy termination was subsequently performed for partial monosomy 13q. CONCLUSION: Protective fetal changes producing 'heart sparing' and 'brain sparing' and may be operational during episodes of acute fetal bradycardia. (+info)
Inhibition of baroreflex vagal bradycardia by activation of the rostral ventrolateral medulla in rats.
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In stressful conditions, baroreflex vagal bradycardia (BVB) is often suppressed while blood pressure is increased. To address the role of the rostral ventrolateral medulla (RVL), a principal source of sympathetic tone, in inhibition of BVB, we microinjected DL-homocysteic acid (DLH, 6 nmol) into the RVL of chloralose-urethan-anesthetized, sinoaortic-denervated rats to examine the effect on BVB. The BVB was provoked by electrical stimulation of the aortic depressor nerve ipsilateral to the injection sites. DLH microinjection was found to suppress BVB while increasing blood pressure. The inhibition of BVB was observed even during the early phase in which DLH transiently suppressed central inspiratory activity. The inhibition was not affected either by upper spinal cord transection or suprapontine decerebration. Similar results were obtained by microinjection of bicuculline methiodide (160 pmol), a GABA antagonist, into the RVL of carotid sinus nerve-preserved rats due to withdrawal of a tonic GABA-mediated, inhibitory influence including the input from arterial baroreceptors. In conclusion, activation of the RVL inhibits BVB at brain stem level independently of central inspiratory drive. (+info)
Reduction of QTc interval dispersion. Potential mechanism of cardiac protection of pyridostigmine bromide.
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OBJECTIVE: Parasympathetic dysfunction is an independent risk factor in individuals with coronary artery disease, and cholinergic stimulation is a potential therapeutical option. We determined the effects of pyridostigmine bromide, a reversible anticholinesterase agent, on electrocardiographic variables of healthy individuals. METHODS: We carried out a cross-sectional, double blind, randomized, placebo-controlled study. We obtained electrocardiographic tracings in 12 simultaneous leads of 10 healthy young individuals at rest before and after oral administration of 45 mg of pyridostigmine or placebo. RESULTS: Pyridostigmine increased RR intervals (before: 886+/-27 ms vs. after: 1054+/-37 ms) and decreased QTc dispersion (before: 72+/-9 ms vs. after: 45+/-3 ms), without changing other electrocardiographic variables (PR segment, QT interval, QTc, and QT dispersion). CONCLUSION: Bradycardia and the reduction in QTc dispersion induced by pyridostigmine may effectively represent a protective mechanism if these results can be reproduced in individuals with cardiovascular diseases. (+info)