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.

A case of narrow complex bigeminy, what is the underlying rhythm?

Narrow complex bigeminy is a common electrocardraphic finding that can be caused by second degree sinoatrial exit block or ectopic atrial bigeminy. These rhythms can be very challenging to distinguish on a 12-lead electrocardiogram. In this case of an elderly woman who presented with narrow complex bigeminy, we review the differentiating features of second degree sinoatrial exit block and ectopic atrial bigeminy.

Long-term effects of frequent maximal breath-holding on the cardiac health of elite freedivers.

Cardiac arrhythmias are commonly reported in freedivers during maximal voluntary breath-holds, but their influence on the cardiological status and their long-term effects on the cardiac health of these athletes have not been investigated. Here we present the results of a study on 32 healthy young men (mean age 32.6 ± 1.3 years) who were divided into two groups of 16 subjects. One group included 16 continuously training freedivers at the "high achievers in sports" level (DIVERS group). The CONTROL group included 16 healthy young men not involved in sports. The subjects were monitored using 24-h electrocardiogram (ECG), and echocardiological study (EchoCG) for all the subjects was performed. The mean heart rate in the DIVERS group was 69.5 ± 1.7 bpm compared with 70.9 ± 1.5 bpm in the CONTROL group. The minimal heart rate was 42.3 ± 1.0 bpm in the DIVERS group and 48.8 ± 1.7 bpm in the CONTROL group (P < 0.005). The maximal heart rate was 132.8 ± 4.6 bpm in the DIVERS group and 132.1 ± 2.9 bpm in the CONTROL group. ECG analysis revealed supraventricular arrhythmias in the DIVERS group: four of the DIVERS (25%) exhibited supraventricular couplets and triplets, three (19%) exhibited transient first- and second-degree AV blocks (Mobitz type 1) at night, and one (6%) exhibited a second-degree sinoatrial block at night. According to the echocardiogram, the DIVERS had slightly larger left ventricles (5.1 ± 1.33, P < 0.05) and left atriums (41.1 ± 12.7) compared with the CONTROL group without exceeding the normal values. The right ventricle volume (3.6 ± 0.69, P < 0.05) was somewhat above the upper normal value (up to 3.5 cm). In conclusion, freediving athletes exhibited changes in their cardiac status, most likely due to the regular exercise, that were not associated with regular maximal voluntary breath-holds. These changes are within the normal physiological values and do not limit their freediving practice.

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.

Use of machine learning and Poincaré density grid in the diagnosis of sinus node dysfunction caused by sinoatrial conduction block in dogs.

BACKGROUND: Sinus node dysfunction because of abnormal impulse generation or sinoatrial conduction block causes bradycardia that can be difficult to differentiate from high parasympathetic/low sympathetic modulation (HP/LSM). HYPOTHESIS: Beat-to-beat relationships of sinus node dysfunction are quantifiably distinguishable by Poincaré plots, machine learning, and 3-dimensional density grid analysis. Moreover, computer modeling establishes sinoatrial conduction block as a mechanism. ANIMALS: Three groups of dogs were studied with a diagnosis of: (1) balanced autonomic modulation (n = 26), (2) HP/LSM (n = 26), and (3) sinus node dysfunction (n = 21). METHODS: Heart rate parameters and Poincaré plot data were determined [median (25%-75%)]. Recordings were randomly assigned to training or testing. Supervised machine learning of the training data was evaluated with the testing data. The computer model included impulse rate, exit block probability, and HP/LSM. RESULTS: Confusion matrices illustrated the effectiveness in diagnosing by both machine learning and Poincaré density grid. Sinus pauses >2 s differentiated (P < .0001) HP/LSM (2340; 583-3947 s) from sinus node dysfunction (8503; 7078-10 050 s), but average heart rate did not. The shortest linear intervals were longer with sinus node dysfunction (315; 278-323 ms) vs HP/LSM (260; 251-292 ms; P = .008), but the longest linear intervals were shorter with sinus node dysfunction (620; 565-698 ms) vs HP/LSM (843; 799-888 ms; P < .0001). CONCLUSIONS: Number and duration of pauses, not heart rate, differentiated sinus node dysfunction from HP/LSM. Machine learning and Poincaré density grid can accurately identify sinus node dysfunction. Computer modeling supports sinoatrial conduction block as a mechanism of sinus node dysfunction.

Prolonged sinoatrial block in an infant with respiratory syncytial viral bronchiolitis.

Complete heart block in children admitted to the pediatric intensive care unit with respiratory syncytial viral (RSV) infections has been described. This report describes a prolonged sinoatrial block exceeding 4 s in an infant with RSV, which, to the authors' knowledge, is the longest such event described in the published literature. This block was followed by shorter episodes within the next 24 h. An extensive workup showed no other known cause of bradycardia or sinoatrial block. The infant was discharged home with 48 h Holter monitoring, which was normal. At this writing, the infant has remained asymptomatic since discharge. Respiratory syncytial viral infections may cause prolonged sinoatrial block in an otherwise healthy child.

Deficient zebrafish ether-à-go-go-related gene channel gating causes short-QT syndrome in zebrafish reggae mutants.

BACKGROUND: Genetic predisposition is believed to be responsible for most clinically significant arrhythmias; however, suitable genetic animal models to study disease mechanisms and evaluate new treatment strategies are largely lacking. METHODS AND RESULTS: In search of suitable arrhythmia models, we isolated the zebrafish mutation reggae (reg), which displays clinical features of the malignant human short-QT syndrome such as accelerated cardiac repolarization accompanied by cardiac fibrillation. By positional cloning, we identified the reg mutation that resides within the voltage sensor of the zebrafish ether-à-go-go-related gene (zERG) potassium channel. The mutation causes premature zERG channel activation and defective inactivation, which results in shortened action potential duration and accelerated cardiac repolarization. Genetic and pharmacological inhibition of zERG rescues recessive reg mutant embryos, which confirms the gain-of-function effect of the reg mutation on zERG channel function in vivo. Accordingly, QT intervals in ECGs from heterozygous and homozygous reg mutant adult zebrafish are considerably shorter than in wild-type zebrafish. CONCLUSIONS: With its molecular and pathophysiological concordance to the human arrhythmia syndrome, zebrafish reg represents the first animal model for human short-QT syndrome.

[Treatment of patients with long nocturnal asystoles and obstructive sleep apnea syndrome by creating continuous positive air pressure in the upper respiratory tract].

AIM: To study prevalence of obstructive sleep apnea syndrome (OSAS) in patients with nocturnal asystoles, and assess therapeutic efficiency of constant positive air pressure (CPAP) applied to upper respiratory tract in this category of patients. METHODS: The study incorporated 37 patients (33 men and 4 women, average age 50+/-11 years) with nocturnal heart beat interruptions of over 3 seconds. Baseline examination revealed grade II-III arterial hypertension in 67.5%, coronary heart disease - in 19%, diabetes mellitus in 8% and no cardiovascular disease - in 5.5% of patients. Sinus rhythm was registered in 30 (81%) of patients, 7 (19%) patients had permanent atrial fibrillation. Causes of deteriorated cardiac conduction were as follows: sinoatrial blocks and sinoatrial arrests (n=18), grade II-III atrio ventricular block (n=10), combination of these forms of bradyarrhythmias (n=2) and block of conduction to ventricles in permanent atrial fibrillation (n=7). According to intra esophageal cardiac pacing, the function of sinus node and atrio ventricular conduction appeared to be undisturbed in all patients with sinus rhythm. All patients have undergone polysomnographic (PSG) examination. For patients with OSAS, an individual selection of therapeutic pressure was carried out using the CPAP apparatuses. CPAP therapy was considered effective against OSAS if normalization of apnea/hypopnea index (AHI) was observed. RESULTS: OSAS was registered in 25 cases (68%) (mean AHI 54.9+/-28.7), 20 patients (80%) had severe grade of the syndrome. CPAP therapy appeared to be effective in all patients. At the background of treatment AHI decreased from 60.7 to 5.5 episodes per hour of sleep, mean oxygen saturation of arterial blood rose from 74 to 90%. Effect of CPAP therapy relative to cardiac conduction abnormalities was attained in all 19 patients with sinus rhythm and only in one patient with permanent atrial fibrillation. CONCLUSION: OSAS was revealed in 68% of patients with nocturnal bradyarrhythmias. Individually selected therapy with constant positive pressure in patients with nocturnal asystoles and OSAS efficiently eliminated in sleep asystoles and made it possible to avoid pacemaker implantation in some patients.

Association of atrial fibrillation in patients with interatrial block over prospectively followed controls with comparable echocardiographic parameters.

Interatrial block (IAB) (P wave >or=110 ms) is a potential risk of atrial fibrillation (AF). However, few investigations have assessed the relevance of echocardiographic parameters, particularly the contribution of its known correlate, left atrial enlargement in this regard. We identified 32 consecutive patients with comparable echocardiographic parameters, such as left atrial dimension and left ventricular ejection fraction. Patients were evaluated for IAB and followed for 15 months for cardiovascular events (heart failure, transient ischemic attacks, and stroke), atrial tachyarrhythmias (AF/atrial flutter), and death. Preexisting AF and IAB (p = 0.02) were significantly associated with future AF events. However, logistic regression analysis indicated that IAB was not an independent predictor of future AF, only preexisting atrial tachyarrhythmias was (hazard ratio 39.5, 95% confidence interval 2.7 to 576.3, p = 0.007). In conclusion, in patients with comparable echocardiographic parameters, such as left atrial size and left ventricular ejection fraction, IAB remained associated with AF after a 15-month follow-up. Additional investigation is needed to confirm the extent of the association.

[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.

Sinoatrial and Atrioventricular Blocks: Who First Described Them and How? [Retrospectroscope].

The relationship among cardiac pacemakers is characterized by the fact that one pacemaker is usually dominant and all the others are subsidiary. The sinoatrial node acts as the dominant pacemaker, and all other potential pacemaker tissues are discharged by a conducted impulse before their respective diastolic depolarizations attain threshold. These pacemakers are called subsidiary to emphasize the fact that, under normal circumstances, they are engaged in conducting impulses, but, under abnormal circumstances, they may become actual pacemakers.

Bradydysrhythmias and atrioventricular conduction blocks.

Bradydysrhythimas include sinus bradycardia, junctional brady-cardia, and idioventricular rhythm, which can be distinguished by examining the tracing for the presence or absence of P waves,noting the morphology of these P waves, and determining the width of the QRS complex. Sinoatrial blocks may occur in either first, second, or third degree varieties. Only second degree sinoatrial block can be detected on the 12-lead ECG. Sinus pause and sinus arrest may mimic second degree sinoatrial block, but their periodicity is irregular. The cyclic variability of sinus arrhythmia is unique; as with the other bradydysrhythmias, it may be innocent or pathologic depending upon clinical circumstances. Atrioventricular blocks may occur, and, similar to sinoatrial blocks, they are also categorized as first-, second-, or third degree. These are of greater clinical relevance than their sinoatrial counterparts.

[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.

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.

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 510 to 900 ms (mean 743 +/- 141) and the longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,018 +/- 168). A long sinus or atrial pause occurring at the termination of tachycardia or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 +/- 1,674), was provoked by the administration of various drugs. These included an intravenous bolus injection of adenosine triphosphate (5 mg; one patient), intravenous bolus injection of verapamil (5 mg; one patient), a combination of a single oral dose of diltiazem (120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient). In five patients, low frequency deflections suggestive of sinus node activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing with a long arrest suggesting suppression of sinus automaticity was also noted in three of these five patients; the longest sinus arrest in these three patients was 4,160, 4,800 and greater than 4,910 ms, respectively. The remaining patient with a pause of 6,840 ms had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome.

Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage. It is concluded that the application of carotid sinus massage in patients with the hypersensitive carotid sinus syndrome produces profound changes in sinoatrial conduction including sinoatrial exit block, as well as shifts in primary pacemaker site and sinus node arrest. These alterations in conduction and automaticity are reversible with atropine and may be secondary to denervation sensitivity to acetylcholine.

Confirmation of the prevalence and importance of a 12-lead investigation for diagnosis of interatrial block [corrected].

We investigated 500 consecutive, unselected electrocardiograms of outpatients for interatrial block (IAB) using all 12 leads rather than the usual recommendation in the literature, which is lead II, sometimes with another lead. IAB had been reported in 2 widely separated large general hospitals in >40% of 1,000 patients in sinus rhythm in each. Because the P waves in IAB (duration > or =110 ms) generally have low amplitude despite their excessive width, we used magnifying graticules and, for greater specificity, a minimal duration of > or =120 ms. Four hundred sixty-nine patients remained after excluding those with atrial arrhythmias or technically poor tracing. Two hundred three of these patients (40.6%) had IAB. Had we used lead II alone, only 110 cases would have been identified, which would have meant overlooking almost 1/2 the cases with this lesion, which is important (1) as a predictor of atrial fibrillation and other arrhythmias, and (2) represents a large, dysfunctional left atrium. Leads V3 and V4 yielded larger numbers of IAB than lead II. (The slightly smaller prevalence than in the 2 cited studies may be due to our using 1/2 the number of patients.) Electrocardiographic interpreters should seek IAB in all 12 leads and consider its anatomic functional and predictive correlates.