Search

In 1899, Karel Frederik Wenckebach described a cardiac arrhythmia with periodic dropped beats now referred to as a Wenckebach sequence. This was later shown to be due to a block in the atrioventricular node, but today, we identify Wenckebach sequences throughout the heart with most being recognised on the surface electrocardiograph as characteristic footprints. This manuscript will revisit Wenckebach atrioventricular block, the typical features of which only occur in about 15% of cases, with the remainder atypical. Earlier reports regarded Wenckebach atrioventricular sequences as rare as they are only occasionally seen on the surface 12-lead electrocardiograph. Today, however, with the increased use of ambulatory Holter monitoring, Wenckebach atrioventricular sequences occur in 4-6% of all traces and are particularly common at night in the young. Most, but not all cases are benign and the clinical spectrum will be reviewed. Atypical Wenckebach atrioventricular sequences are a complex group which will be analysed in detail with a broad range of illustrations. Outside the atrioventricular conducting system, such as in the sinus node, Wenckebach sequences may not be obvious as they are partially hidden from the electrocardiographic tracing. However, by understanding the sequence footprints, clues are available in interpreting tracing with periodic pauses. Dual chamber paced rhythms may show Wenckebach sequences due to electronic control of the atrioventricular delay. Rarely exit blocks at the cellular level in the atrium, ventricle or at the pacing electrode-tissue interface can demonstrate Wenckebach sequences recognised on the surface electrocardiograph.

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

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.

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.

The sick sinus syndrome includes symptoms and signs related to sinus node dysfunction. This can be caused by intrinsic abnormal impulse formation and/or propagation from the sinus node or, in some cases, by extrinsic reversible causes. Careful evaluation of symptoms and of the electrocardiogram is of crucial importance, because diagnosis is mainly based on these 2 elements. In some cases, the pathophysiologic mechanism that induces sinus node dysfunction also favors the onset of atrial arrhythmias, which results in a more complex clinical condition, known as "bradycardia-tachycardia syndrome."

Adenosine stress testing in conjunction with radionuclide myocardial perfusion imaging has become a common approach for the detection of coronary artery diseases in patients who are unable to perform adequate levels of exercise. However, specific electrocardiographic alterations during the test have been rarely described. Using a Chinese population, the aim of the present study was to provide a detailed electrocardiographic profile of adenosine stress testing. The study population included 1,168 consecutive outpatients who had undergone adenosine-induced stress myocardial perfusion imaging. Electrocardiographic data during and immediately following the adenosine infusion were collected, and the corresponding myocardial perfusion images were assessed. During adenosine infusion, 174 transient and 47 persistent arrhythmic events occurred in 110 patients (9.42%). Furthermore, frequent premature atrial contractions occurred in 65 individuals and frequent premature ventricular contractions were observed in 73 individuals. Atrioventricular block (AVB) occurred in 75 patients [first degree (I°) AVB, 16; second degree (II°) AVB, 58; third degree AVB, 1), while sinoatrial block occurred in eight patients. ST depression emerged in 69 patients. Patients with a baseline I° AVB had an increased risk of a II° AVB, and patients exhibiting baseline ST depression were more likely to have a further depressed ST segment during the stress test (odds ratio, 28.68 and 5.01, respectively; both P

Objectives This study sought to test the hypothesis that inducing an autoimmune response against the cardiac sodium channel (NaV1.5) induces arrhythmias. Background Sporadic evidence supports the concept that autoantibodies may cause cardiac arrhythmias but substantial experimental investigations using in vivo models have been lacking to date. The NaV1.5 is essential for cardiac impulse propagation and its dysfunction has been linked to conduction disease. Methods Rats were immunized with a peptide sequence derived from the third extracellular loop of the first domain of NaV1.5. After 28 days, we evaluated in vivo both the electrical and mechanical parameters of cardiac function. Histopathology, myocardial gene and protein expression were assessed. Whole-cell patch-clamp was used to measure sodium current (INa) density in isolated cardiomyocytes. Results NaV1.5-immunized rats had high titers of autoantibodies against NaV1.5. On ECG recording, NaV1.5-immunized animals showed significantly prolonged PR-intervals. During Holter ECG-monitoring we observed repeated prolonged episodes of third-degree atrioventricular and sinoatrial block in every NaV1.5-immunized animal, but not in controls. Immunization had no effect on cardiac function. In comparison to controls, myocardial NaV1.5 mRNA and protein levels were decreased in immunized rats. INa density was reduced in cardiomyocytes incubated with sera from NaV1.5-immunized rats and from patients with idiopathic atrioventricular block (AVB) in comparison to sera from respective controls. In patients with idiopathic AVB, we observed autoantibodies against NaV1.5 that were absent in sera from healthy controls. Conclusions Provocation of an autoimmune response against NaV1.5 induces conductance defects probably caused by a reduced expression level and an inhibition of NaV1.5 by autoantibodies, resulting in decreased INa.

Background: Ozone (O3) is a well-documented respiratory oxidant, but increasing epidemiological evidence points to extrapulmonary effects, including positive associations between ambient O3 concentrations and cardiovascular morbidity and mortality. Objective: With preliminary reports linking O3 exposure with changes in heart rate (HR), we investigated the hypothesis that a single inhalation exposure to O3 will cause concentration-dependent autonomic modulation of cardiac function in rats. Methods: Rats implanted with telemeters to monitor HR and cardiac electrophysiology [electrocardiography (ECG)] were exposed once by whole-body inhalation for 4 hr to 0.2 or 0.8 ppm O3 or filtered air. A separate cohort was tested for vulnerability to aconitine-induced arrhythmia 24 hr after exposure. Results: Exposure to 0.8 ppm O3 caused bradycardia, PR prolongation, ST depression, and substantial increases in atrial premature beats, sinoatrial block, and atrioventricular block, accompanied by concurrent increases in several HR variability parameters that were suggestive of increased parasympathetic tone. Low-O3 exposure failed to elicit any overt changes in autonomic tone, heart rhythm, or ECG. However, both 0.2 and 0.8 ppm O3 increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O3-induced alteration in myocardial excitability. Conclusions: O3 exposure causes several alterations in cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low O3 concentrations may cause subclinical effects that manifest only when triggered by a stressor, suggesting that the adverse health effects of ambient levels of air pollutants may be insidious and potentially underestimated.

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'.

Abstract : Historically, milestones in science are usually associated with methodological breakthroughs. Likewise, the advent of electrocardiography, microelectrode recordings and more recently optical mapping have ushered in new periods of significance of advancement in elucidating basic mechanisms in cardiac electrophysiology. As with any novel technique, however, data interpretation is challenging and should be approached with caution, as it cannot be simply extrapolated from previously used methodologies and with experience and time eventually becomes validated. A good example of this is the use of optical mapping in the sinoatrial node (SAN): when microelectrode and optical recordings are obtained from the same site in myocardium, significantly different results may be noted with respect to signal morphology and as a result have to be interpreted by a different set of principles. Given the rapid spread of the use of optical mapping, careful evaluation must be made in terms of methodology with respect to interpretation of data gathered by optical sensors from fluorescent potential-sensitive dyes. Different interpretations of experimental data may lead to different mechanistic conclusions. This review attempts to address the origin and interpretation of the “double component” morphology in the optical action potentials obtained from the SAN region. One view is that these 2 components represent distinctive signals from the SAN and atrial cells and can be fully separated with signal processing. A second view is that the first component preceding the phase 0 activation represents the membrane currents and intracellular calcium transients induced diastolic depolarization from the SAN. Although the consensus from both groups is that ionic mechanisms, namely the joint action of the membrane and calcium automaticity, are important in the SAN function, it is unresolved whether the double-component originates from the recording methodology or represents the underlying physiology. This overview aims to advance a common understanding of the basic principles of optical mapping in complex 3D anatomic structures.

Clinical and electrophysiological characteristics have been investigated in a group of 30 patients with a sick sinus syndrome. No predictable response to exercise or drugs was observed, although a poor response of the sinus rate to atropine was present. Distal conduction abnormalities were found in seven of 14 patients, in whom detailed electrophysiological measurements were made, and sinus node recovery time was abnormal in all except one. Treatment with permanent pacing not only relieved syncope and dizziness, but made drug treatment of associated tachyarrhythmias feasible. The elusive and intermittent nature of the syndrome is stressed. The pathological findings in one case are described at length.

Electrophysiological investigations were performed in 30 patients with symptomatic sinus node disease (SND) to assess the extent and distribution of associated functional disturbances in the conduction system. The tests were performed before and after inhibition of autonomous tone with propranolol, 0.1 mg/kg, and atropine, 0.02 mg/kg. Surface ECG had shown bundle branch blocks (BBB) in 5 patients and fascicular blocks in 2. AV block I had been recorded in 4 patients, while none had shown high-degree AV block. Malfunction was most often detected in the AV junction, 17 patients showing a prolonged conduction time or an abnormal effective AV node refractory period. Intraventricular conduction delay was present in 7 patients, with a prolonged HV interval in 3 and a complete permanent BBB in the others. Rate-dependent BBBs were demonstrated in a further 4 patients. Long cardiac arrests following interruption of atrial pacing, suggesting impaired automaticity also of subsidiary escape pacemakers, were seen in 11 patients. Only 6 patients, 20%, showed no signs of associated malfunction of the conduction system. Thus, detailed electrophysiological assessment demonstrated associated conduction abnormalities in the majority of these SND patients. The results agree with histopathological studies and show that sinus node malfunction is often the clinically apparent manifestation of a widespread degenerative process in the cardiac conduction system.

Cardiac syncopes appeared in four heavily trained male patients without a history of cerebral or heart disease. Three were young athletes participating in competitive sport, one had trained intensively for years after poliomyelitis complicated by paraplegia. On admission all patients had sinus bradycardia; one had second degree atrioventricular (AV) block at rest, and one had transient sinoatrial (SA) block. His bundle studies demonstrated prolonged recovery time of the SA node (SAN) in two, prolonged atrio-His interval in three, and appearance of second degree AV block at abnormally low pacing rates in two. Refractory periods of the AV node (AVN), determined in three, tended to reach the upper limit of the normal range. The dysfunction of SAN and AVN was temporarily abolished in all patients by 1 mg of atropine i.v., and disappeared during exercise test, which was done by the three young athletes. The patient with paraplegia and one of the young athletes, who had second degree AV block at rest, were given atropine, 0.5 mg six times a day, and all three active sportsmen reduced training activity considerably. After 6--12 months all patients were re-examined. None had cerebral symptoms or other complaints. They were in regular sinus rhythm and in excellent physical condition.

The value of long-term electrocardiographic (ECG) monitoring was assessed in 14 patients (8 males, 6 females; mean age 21 [17-30] years) with the idiopathic long QT syndrome (LQTS), 14 healthy subjects of the same age serving as controls. Twelve patients had the typical history of syncopes or sudden cardiac death among family members; seven patients had a history of syncope, while four patients had been successfully resuscitated. None had associated cardiac disease. Among the group with LQTS the rate-corrected QT interval at rest was 498 + 56 ms, in the control group 412 +/- 30 ms (P < 0.005). Resting and maximal heart rates on exercise were similar in the two groups. The rate-corrected QT interval on exercise was significantly longer in the LQTS patients (P < 0.001). In the control group the maximal heart rate in the long-term ECG was significantly higher (144 +/- 28/min) than in the LQTS patients (128 +/- 17/min; P < 0.01). The long-term ECG recorded abnormal findings in five patients: torsade-de-pointes tachycardia in two, T-wave alternans in two, and bradycardia resulting from intermittent sinoatrial block in one. No abnormal findings were recorded in the control group (P < 0.03).

BACKGROUND While P-wave duration (P-dur) and dispersion (P-disp) could both reflect fractionated and inhomogeneous propagation of sinus cardiac impulses, and may therefore be associated with each other, a clear relationship has not been extensively studied. We studied these markers as well as the significance of P-wave terminal force in lead V1 (PTFV1) in relation to the P-wave axis (P-axis). METHODS We appraised our previously studied sample of 500 consecutively numbered, otherwise unselected, electrocardiograms (ECGs) of outpatients from the University of Massachusetts, Worcester, Massachusetts, for the foregoing P-wave characteristics. P-disp, defined as the difference of the duration between the widest and narrowest P wave, and the greatest P-dur after a 12-lead ECG search, was measured manually to the nearest 10 ms. PTFV1 was considered positive when > or = 40 mm2 terminal deflection was present on biphasic P waves on lead V1. Normal P-axis was considered 0 degrees to +75 degrees by manually constructing the mean frontal plane electrical P-axis from standard limb leads. RESULTS After excluding those with atrial arrhythmias, paced rhythms, errors in lead placement, P waves with low amplitude or overall technically poor tracing, 428 ECGs formed our final sample. P-dur was strongly associated with P-disp (P < 0.0001), but the correlation remained weak (r = 0.42). Overall, P-dur was not significantly associated with P-axis but when divided into tertiles and quintiles, the significance was evident within the range of the normal P-axis, particularly 0 degrees to +60 degrees (P < 0.0001). In a subanalysis of 380 ECGs that had appreciable biphasic P waves on lead V1, PTFV1 was noted on 178 (47%) ECGs and was significantly associated with P-dur (P < 0.0001), P-disp (P < 0.0001), and P-axis (P = 002). When considering P-axis in tertiles and quintiles, P-dur was greater in patients with a positive PTFV1 and significant within the normal range of the P-axis, especially from 0 degrees to +60 degrees . CONCLUSION P-dur, P-disp, and PTFV1 appear to share a significant tripartite association in relation to the normal P-axis, particularly when P-axis ranges 0 degrees to +60 degrees . Therefore, for optimal clinical assessment, these markers should be evaluated in relation to the normal P-axis.

Interatrial block (P wavesor = 110 ms) is thought to be associated with underlying myocardial ischemia during exercise but has not been extensively investigated in patients with suboptimal or borderline exercise tolerance tests (3 min exercise). We utilized coronary angiography to assess the relationship of both, the resting baseline and exercise induced increase in P-wave duration with coronary artery disease among patients who had undergone such tests.We prospectively identified 51 consecutive patients with interatrial block who had coronary artery disease and hypertension but not atrioventricular valvular heart disease, and had undergone coronary angiography to evaluate myocardial ischemia after a suboptimal exercise tolerance test. A control group of 64 consecutive exercise tolerance test patients with similar preliminary characteristics but without interatrial block at rest was used for comparison. Patients from both groups were then appraised for significant obstructive lesions (70%) on coronary angiography that were suggestive of myocardial ischemia.Obstructive coronary artery lesions suggestive of myocardial ischemia were more frequent among interatrial block patients but this was not statistically significant (p=0.25). However, change in P-wave duration of20 ms occurred more frequently in interatrial block patients in the presence of a positive exercise tolerance test. Among patients without interatrial block at baseline, more patients who developed new interatrial block had significant disease on coronary angiography.The utility of using interatrial block toward predicting myocardial ischemia among patients with suboptimal exercise tolerance tests is limited. However, further investigation on the early change in P-wave duration in patients with interatrial block and the development of new interatrial block during exercise could be helpful in optimizing exercise tolerance tests, particularly when borderline or suboptimal.

Introduction Interatrial block (P-wave ≥ 110 ms) is clinically associated with left atrial enlargement and electromechanical dysfunction as well as atrial tachyarrhythmias. We prospectively evaluated the incidence of such arrhythmias, especially atrial fibrillation among patients with interatrial block over the course of 1 year. Methods 118 patients (aged 48 to 104 years; female 56.6%) who had been hospitalized between December 15, 2004 and January 14, 2005 were identified and divided into 3 groups based on their respective baseline electrocardiogram (interatrial block = 41 patients, sinus non-interatrial block = 51 patients and atrial tachyarrhythmia = 24 patients). Patients were subsequently followed for 12 months for pertinent cardiovascular events (heart failure, peripheral embolism, transient ischemic attacks and stroke), atrial tachyarrhythmias (atrial fibrillation and atrial flutter) and death as endpoints. Results 19 patients (17.9%) had atrial fibrillation during the 12-month follow-up (sinus non-interatrial block group = 4 [9.1%], interatrial block group = 12 [29.3%] and atrial tachyarrhythmia group = 3 [14.3%]). Coronary artery disease, hypertension, pre-existing atrial fibrillation history, dilated cardiomyopathy, atrioventricular valvular disease and interatrial block (age- and sex-adjusted hazard ratio = 4.2; 95% confidence interval 1.2–14.4; p = 0.02) were significantly associated with future events of atrial fibrillation. However, logistic regression analysis indicated that interatrial block was not an independent predictor of future atrial fibrillation whereas only history of pre-existing atrial tachyarrhythmias was (hazard ratio = 23.6; 95% confidence interval 4.5–121.7; p = 0.0002). Conclusion Interatrial block may be associated with atrial fibrillation but in a 12-month period, does not appear to be an independent predictor of future atrial fibrillation. Continued prospective investigation of such a relationship is certainly warranted given its already known consequences.

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 27-year-old woman with atrial bigeminy is reported in whom long PP intervals alternate with short PP intervals. All P waves are negative in lead II and all PR intervals measure 0.12 s. In the 12-lead electrocardiogram, however, these P waves were definitely different in configuration from each other, and were divided into two groups. Namely, these negative P waves are divided into those of dominant atrial rhythm J1 with 2:1 exit block, and those of atrial escape J2. Long J1-J2 intervals alternate with short J2-J1 intervals. These electrocardiographic findings show the presence of atrial escape-capture bigeminy. Such atrial escape-capture bigeminy in dominant atrial rhythm with 2:1 exit block has never been reported before.

Although cardiac complications are well known in myotonic dystrophy (DM), patients rarely manifest symptoms of cardiac disease, and if so they most often show conduction abnormalities or arrhythmia. In this study, specific cardiac findings were reviewed in 79 patients with DM. No correlation was found between the cardiac assessments and the CTG expansion. Thus, for a single patient the cardiac involvement in the disease can not be predicted from the findings of the genetic investigation. On the other hand, a clear positive relationship of the PR interval with the QRS duration was revealed, as well as a positive correlation between the age of the DM patient and the QRS duration, which increases with 0,54 ms/year. Systolic dysfunction, evaluated by transthoracic echocardiography, seems to be quite uncommon. In 32 % of the patients with a normal ECG, the 24 h Holter monitoring showed arrhythmias and conduction abnormalities. Based on these findings we recommend a follow up of DM patients not only based on the ECG, but also through 24 h Holter monitoring.

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.

By arbitrary definition, a bradycardia is a heart rate of

ee t as, 2 At the atrial level, no P waves can be identified indicating complete sinoatrial block. 2. The first 3 QRS complexes have the same R-R interval (950 ms) and are narrow compatible with an atrioventricular (AV) junctional origin. QRS complexes 5 and 9 have the same QRS configuration. 3. Of interest are the wider QRS complexes occurring after a shorter R-R interval (complexes 4, 6, 8, and 10). QRS complex 4 is 80 ms wide and shows an incomplete right bundle branch block and a pattern of left axis duration. It could have its origin in the AV junction with aberration, with delay in the right bundle branch and the left anterior fascicle owing to premature activation of the His bundle. It could also have an origin shortly after the takeoff of the

Sinoatrial Block After RFC Modification of Sinus Node. Inappropriate sinus tachycardia is a nonparoxysmal tachycardia characterized by high resting heart rates and a disproportionate response to activity. Sinus node modification with radiofrequency current has been used successfully as treatment for this arrhythmia. However, the electrophysiologic mechanisms leading to successful modification are not yet fully elucidated. We report a case of a patient with drug-resistant inappropriate sinus tachycardia in whom successful treatment of the arrhythmia was achieved by documented sinoatrial exit block induced by radiofrequency current applications.

In our previous patients, apparent bradycardia-dependent block has been shown in the atrioventricular (AV) junction and in the accessory pathway. It was suggested that these previous cases were not of true bradycardia-dependent block; namely, that, as a result of periodic increases in vagal tone associated with respiration, conductivity in the AV junction or in the accessory pathway was depressed to a greater degree than automaticity in the sinus node. In the present article, 3 patients with frequent sinoatrial (SA) block were reported. In 1 patient, sinus escape-capture bigeminy caused by SA block was found. In these present patients, when the sinus cycle lengthened, SA block occurred. The purpose of the present article is to show that the patients have apparent bradycardia-dependent SA block, namely, not true bradycardia-dependent SA block. In all patients, the respiration curve was recorded simultaneously with the electrocardiogram. In all patients, during inspiration, the sinus cycle gradually shortened; on the other hand, during expiration, the sinus cycle gradually lengthened, and then a sinus impulse was blocked in the SA junction. These findings suggested that increased vagal tone during expiration depressed conductivity in the SA junction to a greater degree than automaticity in the sinus node.

This paper presents a simulation of the sino-atrial (SA) node by a two-dimensional pacemaker cells array model, based on phase response curve (PRC) interaction. This simple model of the cardiac pacemaker cells, involves only the most basic functional properties, which play a direct role in the determination of the SA node rhythm. The two most relevant functional properties of the pacemaker cells are: the intrinsic cycle length, an "internal" feature of each pacemaker cell, and the PRC, an "overall collective" function. The PRC contains the "information" about the type of interactions of each pacemaker cell with the outside world (i.e., interaction with neighboring cells, external stimulus, etc.), and "strength" of the interaction (strong, weak, etc.). The authors' studied the spatial interaction among a large number of pacemaker cells (15/spl times/15), as a function of the regional variation of cells properties, the "electrical" coupling between cells (the PRC), and the appearance of regions with abnormal cycle lengths. The authors investigated the influence of those parameters on the mutual interaction between the pacemaker cells, on the activation pattern and conduction time of the array, and on a pseudo-electrocardiogram (ECG) signal. This study demonstrates that by representing the pacemaker cells in the SA node by only two fundamental features, and by applying a simple physical-mathematical model, one can create a global picture of the SA node system. This enables one to explore physiological phenomena related to the genesis and maintenance of the SA node activity, and to gain insight into the conditions which predispose the SA node instability, and conduction disturbances.

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.

Sinoatrial block (SAB) is often difficult to identify in the presence of bradycardic rhythms. This study demonstrates several manifestations of so-called escape capture bigeminy in 14 patients. Although periods of 1:1 sinoatrial conduction can aid in the analysis of SAB, the electrocardiographic pattern of bigeminal rhythm may be the only electrocardiographic clue of SAB. In one case, both sinoatrial entrance and exit block were identified. In eight instances, digitalis or digitalis plus a beta or calcium blocking agent could be partially implicated as the cause of SAB. In 6 of 14 patients, a permanent pacemaker was required to correct the bradycardia, in spite of discontinuation of aggravating antiarrhythmic agents or electrolyte derangement.

Interatrial block (IAB) (P waveor=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.

Two women with atrial escape-capture bigeminy were reported in whom sinus P waves and escape P waves alternated with each other. Their electrocardiographic findings showed that, during the bigeminal rhythm, 2:1 exit block of sinus impulses associated with entrance block of escape impulses occurred in the sinoatrial junction. Three phenomena are suggested to explain the observations. (1) Seeming bradycardia-dependent sinoatrial exit block may have occurred, probably as a result of phasic changes in vagal tone due to respiration, with decreased vagal tone depressing conductivity in the sinoatrial junction to a greater degree than automaticity in the sinus node. (2) In case 1, type II second-degree entrance block in the sinoatrial junction may have occurred, reflecting the presence of sinus parasystole with incomplete entrance block. (3) Sinus escape also may have occurred, especially in case 2. These phenomena have never been reported before.

A 59 year old woman presented with acute onset of fever, chills, diaphoresis, vague chest discomfort, and was found to be hypotensive and tachypnoeic. An electrocardiogram demonstrated sinoatrial block with a junctional rhythm between 50 and 80 beats/min. All cultures were negative and imaging studies unrevealing. Her urine tested positive for Legionella pneumophila antigen serotype 1 and she improved with antibiotic therapy.

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.

Congenital sick sinus syndrome has been described sporadically. The syndrome may comprise various components of sinus bradycardia, atrial fibrillation, and right atrial inexcitability.1–7 In the current case, detailed electrophysiological evaluation was undertaken with electroanatomic mapping of the right atrium and coronary sinus (CS) and of associated supraventricular arrhythmias. ### Case A 37-year-old asymptomatic male physician from Mexico without any previous medical problems was referred after routine physical examination for evaluation of atrial fibrillation with a slow ventricular rate. Arrhythmia duration was unknown. He stated that bradycardia had been consistently noted on previous clinical examinations and had been attributed to competitive long-distance running since childhood. Heart rates in the “40s” had been noted since age 10 to 11 years when he had been informed of a “heart murmur.” Subsequent echocardiographic examination had been normal. The patient denied any family history of sudden death or arrhythmias. He had no siblings and no children. His prior records (and those of his parents) were unavailable. Physical examination was normal except for a regular bradycardia of 45 beats/min. Twelve-lead ECG showed fixed R-R intervals. No clear P-wave activity was identified. However, there was small-amplitude baseline electric activity of debatable origin, interpreted variously by experienced electrocardiographers as standstill, artifact, or atrial fibrillation waves (Figure 1A). A transthoracic echocardiogram showed normal ventricular volume and function (left ventricular end-diastolic diameter, 52 mm; left ventricle end-systolic diameter, 34 mm) and mild tricuspid regurgitation with estimated pulmonary artery systolic pressure of 40 mm Hg. Both atria were severely enlarged (left atrial volume index, 58 mL; right atrial area, 41 cm2). Doppler echocardiographic examination of both tricuspid and mitral atrioventricular (AV) inflow showed complete absence of A waves, indicating lack of left and right atrial contractile activity (Figure 2). A transesophageal echocardiogram did not reveal any evidence of …

Atrial fibrillation (AF) is the most frequently diagnosed cardiac arrhythmia. Anti-arrhythmic drugs may be used to suppress ectopic foci and interrupt reentry circuits, but are often insufficient to treat recurrent AF and have a number of adverse effects. Alternative therapies, such as catheter and surgical ablation, have been explored. This investigation examines the importance of assessing exit block when performing surgical ablation during beating-heart treatment of AF.This was an evaluation of pooled data from multicenter prospective results obtained in AF patients who received ablation with a new, irrigated, vacuum-integrated device that creates linear lesions during beating-heart/open-chest or minimally invasive, port-access procedures. Electrocardiogram or Holter data were collected intra-operatively and at 1, 3, 6, and 12 months. Outcomes were also evaluated for patients who were or 'were not' tested for exit block following the ablation procedure.A total of 93 patients were treated (61 open-chest surgeries, 32 port-access procedures). There were no device-related complications and no operative mortality. At 341 days' average follow-up, 71/86 (83%) patients were free from AF, 66/86 (77%) were in sinus rhythm, and 60/86 (70%) were free from AF and off Class I and III anti-arrhythmic drugs (AADs). At 12 months, 23/23 (100%) patients with exit block confirmed were AF free compared with 13/21 (62%) patients with exit block not tested (p≤0.01, Fisher's exact test); 20/23 (87%) were in sinus rhythm compared with 12/21 (57%) patients with exit block not tested (p≤0.05, Fisher's exact test); and 20/23 (87%) were AF free without Class I and III AADs compared with 10/21 (48%) patients with exit block not tested (p≤0.01, Fisher's exact test). Both open-chest and port-access procedures yielded decreases in left-atrial size from baseline to 6 months' follow-up. Patients undergoing port-access procedures also observed an increase in left-ventricular ejection fraction, which was also significant at 6 months.Patients in whom exit block was confirmed following an ablation procedure were more likely to have successful clinical outcomes. Since testing for exit block must be performed on a beating heart, total epicardial beating-heart ablation may provide an important treatment for AF, providing intra-operative feedback indicative of long-term outcomes.

Five electrocardiogram (ECG) analyzing systems were tested with a microcomputer-based ECG signal generator to assess the accuracy of the systems in interpreting Wenckebach periodicity. Although normal sinus rhythm with normal PR intervals and sinus rhythms with first-degree atrioventricular (AV) block were diagnosed by all five systems, second-degree AV block with classic Wenckebach periodicity was routinely misdiagnosed by four of the five systems. No system recognized the atypical Wenckebach periods in a total of 200 trials, misinterpreting the phenomenon as atrial fibrillation, supraventricular rhythm, sinoatrial block, and other rhythm disturbances. In advanced AV block and a variety of ventricular arrhythmias, none of the five systems diagnosed second-degree AV block with Wenckebach periods. Marked unsatisfactory performance with regard to the diagnosis of Wenckebach periodicity indicates the urgent need for accelerated and comprehensive testing of ECG diagnostic equipment. The present generating device was seen as an effective troubleshooter in optimizing the diagnostic competency of computerized ECG systems.