A case report of sinoatrial arrest caused by temporal lobe epilepsy in subclinical glioblastoma.

BACKGROUND: Atrial fibrillation with symptomatic bradycardia, higher grade atrioventricular block, and sinus node disease are all common indications for permanent pacemaker implantation. The most frequent causes of sinus node disease treated with pacemaker implantation involve degenerative structural changes of the sinus node; less often, extrinsic causes (such as damage due to myocardial infarction or heightened parasympathetic nervous system activity) lead to pacemaker implantation. CASE PRESENTATION: A 50-year-old patient with syncope and documented sinoatrial arrest was referred. Neurologic exams (including CT and EEG) revealed no pathologies, so a pacemaker was implanted. Postoperatively, syncope occurred again due to a focal seizure during which sinus rhythm transitioned to atrial pacing by the device. Further neurologic testing revealed focal epilepsy. Six months later, stage IV glioblastoma was diagnosed and the patient was treated surgically. CONCLUSION: Intracerebral tumors should be considered in the differential diagnosis for patients with unexplained sinoatrial block, as well as in patients with repeat syncope after pacemaker implantation. Cranial MRI could aid the diagnostic workup of such cases.

P-wave pseudonormalization after iatrogenic coronary sinus isolation.

We report a case of a 58 year old gentleman with prior history of catheter ablation for persistent atrial fibrillation (AF). His baseline ECG showed sinus rhythm with a broad and notched P-wave in lead II and biphasic P-wave (positive/negative) in leads III and aVF previously described as advanced interatrial block. A redo ablation procedure was performed due to AF recurrence. An iatrogenic isolation of the coronary sinus (CS) was observed during ablation with marked narrowing and loss of the terminal negative component of the P-wave on the surface ECG.

A protective role of Nox1/NADPH oxidase in a mouse model with hypoxia-induced bradycardia.

Although it has been reported that endotoxin-induced expression of Nox1 in the heart contributes to apoptosis in cardiomyocytes, functional role of Nox1 at the physiological expression level has not been elucidated. The aim of this study was to clarify the role of Nox1 under a hypoxic condition using wild-type (WT, Nox1(+/Y)) and Nox1-deficient (Nox1(-/Y)) mice. ECG recordings from anesthetized mice revealed that Nox1(-/Y) mice were more sensitive to hypoxia, resulting in bradycardia, compared to WT mice. Atrial and ventricular electrocardiograms recorded from Langendorff-perfused hearts revealed that hypoxic perfusion more rapidly decreased heart rate in Nox1(-/Y) hearts compared with WT hearts. Sinus node recovery times measured under a hypoxic condition were prolonged more markedly in the Nox1(-/Y) hearts. Sinoatrial node dysfunction of Nox1(-/Y) hearts during hypoxia was ameriolated by the pre-treatment with the Ca(2+) channel blocker nifedipine or the K(+) channel opener pinacidil. Spontaneous action potentials were recorded from enzymatically-isolated sinoatrial node (SAN) cells under a hypoxic condition. There was no significant difference in the elapsed times from the commencement of hypoxia to asystole between WT and Nox1(-/Y) SAN cells. These findings suggest that Nox1 may have a protective effect against hypoxia-induced SAN dysfunction.

Arrhythmias in children having a single left superior vena cava and minimal structural heart disease.

BACKGROUND: The presence of a single left superior vena cava in the absence of complex congenital heart disease is uncommon, and, in the absence of hemodynamic consequences, it would not be expected to result in cardiovascular signs or symptoms. Single case reports and our anecdotal experience suggested to us that this anomaly is highly associated with cardiac arrhythmias. OBJECTIVE: We sought to describe the clinically important arrhythmias in a population of young patients having this anomaly. METHODS: A retrospective chart review was performed from all patients <20 years old and who were determined by echocardiography over an 11-year-period to have a single left superior vena cava and minor or no coexisting congenital heart defects. The prevalence of nonsinus pacemaker, age-corrected sinus rate percentile, and prevalence of brady- or tachyarrhythmias was compared with a control group of patients having bilateral superior vena cavae. RESULTS: Eight patients having a single left and 55 patients having bilateral superior vena cava(e) were identified. The existence of this anomaly tended to be associated with a lower age-corrected sinus rate percentile (17.5% vs 75%, P = 0.09), and was associated with a higher prevalence of arrhythmias (50% vs 7%, P = 0.014) compared with the control group. In the study group, one patient each had clinically relevant sinus node dysfunction, third-degree AV block, Wolff-Parkinson-White syndrome and atrial fibrillation, and AV nodal reentrant tachycardia. CONCLUSION: Even in the absence of symptoms, patients found to have a single left superior vena cava should be monitored long-term for clinically important arrhythmias.

Intermittent interatrial block after electrical cardioversion for atrial fibrillation.

A 67-year-old woman with persistent atrial fibrillation presented for elective electrical cardioversion. The patient was cardioverted to normal sinus rhythm with a synchronized 150 joules (J) biphasic shock. Varying P-wave morphology suggesting intermittent interatrial block (IAB) was noted after the cardioversion on the rhythm strip. Three minutes later the patient developed early recurrence of atrial fibrillation and a second successful 150 J biphasic shock was delivered; IAB was still evident on a single lead II monitoring. However, the patient remained in sinus rhythm. The patient was discharged in normal sinus rhythm with electrocardiographic evidence of intermittent interatrial block. This case report examines the occurrence of IAB postcardioversion for atrial fibrillation and speculates on its prognostic significance.

[Association between severe obstructive sleep apnea syndrome and sinus dysfunction].

OBJECTIVE: To preliminarily investigate the association between severe obstructive sleep apnea syndrome (OSAS) and sinus dysfunction (SD). METHODS: From March of 2005 to June of 2006, 70 patients with severe OSAS and 36 simple snorers underwent electrocardiography by polysomnography. In order to compare their sinus function and analyse the risk factors of SD, atropine test with simultaneous monitoring of ultramicroelectrocardiogram (UMECG) was performed in those with the lowest heart rate < 40 pbm, or the highest sinus heart rate < 90 bpm, or the longest R-R interval > 2.0 seconds. All data were statistically analyzed with SPSS 13.0 software. RESULTS: Sixteen of the 70 severe OSAS patients were diagnosed as with SD with an incidence of 22.9%, significantly higher than that in the patients with simple snore (2/36, 5.6%, P = 0.025). In 70 patients with severe OSAS (16 patients with SD), single factor analysis indicated that there was a significant difference between those with SD and those without SD in Nadir pulse oxygen saturation, longest apnea duration and incidence of coronary artery disease (T test, P = 0.002; T test, P = 0.029; Fisher's Exact test, P = 0.043), and Logistic regressive analysis showed that the risk factors of SD were the decrease of Nadir pulse oxygen saturation (P = 0.003, OR < 0.001, 95% CI 0.000 - 0.016) and age (P = 0.055, OR = 1.053, 95% CI 1.007 - 1.125). CONCLUSIONS: The incidence of SD in patients with severe OSAS is higher than that in simple snore. Lower Nadir pulse oxygen saturation during sleep was the major risk factor for occurrence of SD in patients with severe OSAS.

[The ECG-phenomenon of ST segment elevation: the reasons for it and its clinical significance].

The authors adduce a detailed analysis of the reasons for ST segment elevation, which is found in patients with various pathologic conditions and in some normal individuals, basing this analysis on their own experience and literature data. The authors pay special attention to differential ECG-diagnostics of ST elevation, which plays the most significant part in practice.

[Dorsal medulla oblongata stroke after a wasp sting]. / Infarctus dorsal du bulbe dans les suites d'une piqûre de guêpe.

INTRODUCTION: Although wasp stings can cause local reactions such as pain, flare, edema, swelling and severe reactions, including anaphylaxis; neurological vascular complications are rare. CASE REPORT: We report a case of a 36-year-old male who developed focal neurological symptoms after a wasp sting. The brain MRI showed an infarct in the left dorsal medulla. The blood test has showed an elevated level of venom-specific IgE antibodies and the skin test with wasp venom was highly positive. Improvement occurred rapidly after treatment with methylprednisone. The postulated mechanisms include vasoconstriction and platelet aggregation secondary to an injection of distinct allergens contained in wasp venom. CONCLUSION: It would thus be important to ask patients about any recent wasp sting, in order to provide appropriate treatment.

Atropine often results in complete atrioventricular block or sinus arrest after cardiac transplantation: an unpredictable and dose-independent phenomenon.

BACKGROUND: A paradoxic response to atropine with development of atrioventricular (AV) block has been described in patients after heart transplantation (HTx). We investigated further the incidence and dose-response relationship of this paradoxic atropine response and explored predictive factors. METHODS: We investigated 25 clinically stable patients (age 55 +/- 2 years) 18 to 126 months after HTx. After endomyocardial biopsy, a temporary pacemaker was introduced and patients were monitored. Atropine was given in ascending doses (0.004 mg/kg body weight initially, total cumulative dose 0.035 mg/kg body weight). Physiologic tests were performed to evaluate the presence of reinnervation. RESULTS: In 20% of the patients (5/25), a paradoxic response to atropine was observed. Four patients exhibited third degree AV block, one of whom also demonstrated sinus arrest. A fifth patient showed sinus arrest only. In all patients but one, there was no ventricular escape rhythm before ventricular pacing was commenced (10 sec after block). The observed adverse effect was not correlated with the applied atropine dosage, and predisposing factors could not be identified, apart from a slightly lower resting heart rate (80 +/- 5 vs. 90 +/- 2 beats/min, P = 0.07). CONCLUSION: A significant proportion of patients respond paradoxically to atropine after HTx, leading to asystole as the result of sinus arrest or AV block. Although a plausible explanation for this effect remains speculative, our data indicate that the use of atropine or other anticholinergic drugs in patients after HTx is contraindicated.

Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression.

BACKGROUND: Homozygous mutant mice with a defect of klotho gene expression (kl/kl) show multiple age-related disorders and premature death from unknown causes. METHODS AND RESULTS: The kl/kl mice subjected to 20-hour restraint stress showed a high rate (20/30) of sudden death, which was associated with sinoatrial node dysfunction (conduction block or arrest). Heart rate and plasma norepinephrine of kl/kl mice, unlike those of wild-type (WT) mice, failed to increase during the stress. Intrinsic heart rate after pharmacological blockade of autonomic nerves in kl/kl mice was significantly lower than that in WT mice (380+/-33 versus 470+/-44 bpm; n=7). The sinus node recovery time after an overdrive pacing (600 bpm, 30 seconds) in kl/kl mice was significantly longer than in WT mice (392+/-37 versus 233+/-24 ms; n=6). In isolated sinoatrial node preparations, the positive chronotropic effect of isoproterenol was significantly less, whereas the negative chronotropic effect of acetylcholine was significantly greater in kl/kl than in WT mice. There was no degenerative structural change in the sinoatrial node of kl/kl mice. The precise localization of klotho was analyzed in newly prepared klotho-null mice with a reporter gene system (kl(-geo)). Homozygous kl(-geo) mice showed characteristic age-associated phenotypes that were almost identical to those of kl/kl mice. In the kl(-geo) mice, klotho expression was recognized exclusively in the sinoatrial node region in the heart in addition to parathyroid, kidney, and choroid plexus. CONCLUSIONS: In the heart, klotho is expressed solely at the sinoatrial node. klotho gene expression is essential for the sinoatrial node to function as a dependable pacemaker under conditions of stress.

Sino-atrial block during anesthesia in a patient with breast cancer being treated with the anticancer drug epirubicin.

IMPLICATIONS: Epirubicin, an anticancer drug, causes cardiotoxicity. We reported a case of sino-atrial block during general anesthesia in a woman with breast cancer who had received epirubicin. Anesthesiologists should be aware of the possible occurrence of sino-atrial block with epirubicin, and planting a pacemaker might be considered even in asymptomatic patients.

Sinus node dysfunction after Fontan modifications--influence of surgical method.

BACKGROUND: Sinus node dysfunction (SND) is reported to be a troublesome complication following various types of Fontan operations. The correlation of post-Fontan SND with surgical methods was evaluated in this study. METHODS: By reviewing the medical records, surface ECGs, and Holter monitoring, the range of heart rate (HR) and the risk of SND at intermediate term after Fontan type operation (follow up: 41.3+/-13.1 months) were analyzed between two age matched groups of patients, consisting of the extracardiac conduit group (EC, n=33) and the lateral tunneling group (LT, n=35). RESULTS: Junctional rhythm was observed in nine out of 35 patients in LT and five out of 33 patients in EC during the follow-up period. Resting HR was faster in EC than that in LT (108+/-15 vs. 82+/-21, P<0.001). Average and maximal HR in Holter monitoring were also faster in EC than those in LT. SND was found in 13 cases (10 in LT, three in EC) during follow-up and one required pacemaker implantation. In the case of situs solitus heart, SND was less frequent in EC than in LT (0/16 vs. 8/26, P=0.01). In the case of heterotaxy syndrome, SND occurred in similar number of cases (3/17 vs. 2/9). The staged approach to Fontan completion did not influence SND. LT repair was the only factor causing sinus node dysfunction according to multivariate logistic regression (P=0.03, OR 5.96). CONCLUSIONS: Lateral tunnel type surgical repair was more likely to lead to the development of sinus node dysfunction than extracardiac conduit operation. In the case of heterotaxy syndrome, surgical method had no significant influence.

Sick sinus syndrome.

Sinus-node dysfunction is common in the elderly and, in most cases, does not cause any symptoms. Despite the high number of laboratory investigations, most diagnoses of sinus-node dysfunction are made by 12-lead electrocardiography, which shows severe sinus bradycardia, sinus arrest, or sinoatrial block. Continuous electrocardiographic monitoring, exercise testing, and electrophysiologic investigations (including pharmacologic interventions to cause complete autonomic blockade) are sometimes useful in detecting transient or latent sinus-node abnormalities. The term sick sinus syndrome should be reserved for patients with symptomatic sinus-node dysfunction. Sick sinus syndrome has a protean presentation with variable degrees of clinical severity. Symptoms are often intermittent, changeable, and unpredictable. Because these symptoms can be observed in several other diseases, none are specific to sick sinus syndrome. Owing to the nonspecific nature of its symptoms, sick sinus syndrome can be diagnosed only when clear electrocardiographic signs corroborate symptoms. In the absence of a demonstrable link between signs and symptoms, a diagnosis can be presumed only when signs of severe sinus dysfunction are present and when every other possible cause of symptoms has been excluded carefully. Sinus-node dysfunction frequently is associated with diseases of the autonomic nervous system, and autonomic reflexes play a major role in the genesis of syncope. Survival does not seem to be affected by sick sinus syndrome. Atrioventricular block, chronic atrial fibrillation, and systemic embolism are major pathologic conditions that affect the outcome of the syndrome. Treatment should be aimed at controlling morbidity and relieving symptoms. Cardiac pacing is the most powerful therapy; physiologic pacing (atrial or dual-chamber) has been shown definitively to be superior to ventricular pacing.

Development of sinus node disease in patients with AV block: implications for single lead VDD pacing.

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.

Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation.

BACKGROUND: Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. METHODS AND RESULTS: Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. CONCLUSIONS: This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.