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Introduction Swallow syncope is a neurally mediated syncope. Multiple causes have been described in literature. A rare cause is arrhythmias. Only a limited amount of cases present the association of swallow syncope and third degree AV-block. Case presentation A 39-year-old man presented with episodes of presyncope while eating. Further medical history, physical examination, resting 12-lead ECG, cyclo-ergometry, transthoracic echocardiography and MRI of the heart were normal. 24 h Holter monitoring demonstrated high-grade third-degree atrioventricular (AV) block. The patient was scheduled for pacemaker implantation. Discussion Arrhythmia is a rare cause of swallow syncope. Reported arrhythmic causes are sinus bradycardia, sinoatrial block, atrioventricular block and complete atrial and ventricular asystole. Essential to the diagnosis is that (pre)syncope is preceded by swallowing and documentation of AV block on 24 h Holter monitoring. Treatment is guided by ESC guidelines which state that reflex syncope has a grade IIa recommendation for pacing, while current evidence suggests that asymptomatic vagally mediated AV block should not be treated until symptomatic.

Although drug-induced short QT syndrome (SQTS) has been recognized, we currently report the first acquired SQTS case induced by bufotalinin (toad, an antineoplastic drug), which is a traditional Chinese folk prescription. It has cross reaction with digoxin and affects the Na+ -K+ -ATPase, the SR Ca2+ release from ryanodine receptor-2 (RyR2), the reactive oxygen species (ROS) production from the mitochondria. The case presented with bradycardia, extreme QT shortening, and sinoatrial block that were resolved after gastric lavage, rehydration, electrolyte (hyperkalemia, hyponatremia, hypocalcemia) correction, and atropine injection. Clinicians should recognize a potential association between toad poisoning and SQTS from this case.

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.

Aims Prior reports using pacing manoeuvres, demonstrated an up to 42% prevalence of residual pulmonary vein to left atrium (PV–LA) exit conduction after apparent LA–PV entry block. We aimed to determine in a two-centre study the prevalence of residual PV–LA exit conduction in the presence of unambiguously proven entry block and without pacing manoeuvres. Methods and results Of 378 patients, 132 (35%) exhibited spontaneous pulmonary vein (PV) potentials following circumferential PV isolation guided by three-dimensional mapping and a circular mapping catheter. Pulmonary vein automaticity was regarded as unambiguous proof of LA–PV entry block. We determined the prevalence of spontaneous exit conduction of the spontaneous PV potentials toward the LA. Pulmonary vein automaticity was observed in 171 PVs: 61 right superior PV, 33 right inferior PV, 47 left superior PV, and 30 left inferior PV. Cycle length of the PV automaticity was >1000 ms in all cases. Spontaneous PV–LA exit conduction was observed in one of 171 PVs (0.6%). In a subset of 69 PVs, pacing from within the PV invariably confirmed PVLA exit block. Conclusion Unidirectional block at the LA–PV junction is unusual (0.6%). This observation is supportive of LA–PV entry block as a sufficient electrophysiological endpoint for PV isolation.

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'.

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.

A retrospective study covering all admissions during a 6-year period revealed 128 patients with sinus node dysfunction (SND). The patients were grouped according to the ECG criteria chosen: group I 33 patients with sinus bradycardia, group II 37 with sinoatrial block/sinus arrest, group III 58 with brady-tachy syndrome. Additional heart disease, predominantly ischaemic, was found in 56%. The frequency and severity of symptoms increased from group I to group III. Pacemaker treatment was given to 40% of the cases, while medical treatment alone was successful in 17%. A follow-up including 104 patients was carried out after a mean observation period of approximately three years. Sixteen patients had died. The cause of death may have been SND per se in only one case. Five patients died of apoplectic insults or complications to such. In total, nine possible or proven systemic embolic events were found--all occurring in patients with brady-tachy syndrome. A progression of the ECG abnormality from a lower to a higher group took place in nine patients during the observation period. It is concluded that SND is a condition with a broad clinical spectrum and a stationary or slowly progressive course. In general, it carries a good prognosis. A substantial number of deaths of disabilities in patients with brady-tachy syndrome may be ascribed to systemic embolism. Long-term anticoagulant therapy is proposed in this subgroup of patients with SND.

Fifty patients with SA block have been treated with permanent pacing and followed up for 1-14 years. Survival after one, two, five and eight years was calculated to 94, 85, 64 and 48%, respectively. These figures indicate an excess yearly mortality in the first five years of 4-5% compared with a population of the same age and sex. Analysis of the survival curves shows that the excess mortality is caused by coexisting diseases, primarily coronary heart disease with previous myocardial infarction and valvular heart disease.

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.

In a retrospective study of patients admitted for acute myocardial infarction (AMI) during six years, sinus node dysfunction (SND) was detected in 20 (1.04%). Twelve had persistent sinus bradycardia, 11 sinotrial block or sinus arrest and six bradytachy syndrome. Symptoms occurred in 17 patients, 12 of whom required temporary pacing for periods up to three weeks. A permanent cardiac pacemaker was implanted in three patients with brady-tachy syndrome. Three patients died during the primary admission and six during the observation period. Follow-up after a mean observation period of 34 months showed continuous signs of SND in 11 out of 19 patients. The arrhythmia caused symptoms in five patients, two of whom had a cardiac pacemaker and two received medical treatment. It is concluded that SND appearing during an AMI persists in a high number of these patients.

Atrioventricular (AV) conduction disturbances in 30 patients with ankylosing spondylitis (Mb. Bechterew) have been examined. Nine patients had AV block I with intermittent AV block II (Wenchebach block), 3 had complete heart block, 1 patient had atrial fibrillation and another had intermittent sinoatrial (SA) block. Thus, 14 (48%) patients had conduction defects. Electrophysiological investigations in 5 patients with AV block and in 1 patient with SA block revealed that the site of the block was proximal to the bundle of His. Two additional patients had prolonged sinus node recovery time implying dysfunction of the sinus node. An association between aortic valvular insufficiency and conduction disturbances was found, but AV block occurred also in patients without signs of valvular regurgitation. Four patients were treated with a permanent pacemaker and 5 with a temporary pacemaker in connection with aortic valvular surgery.

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 symptomatic sick sinus syndrome presents a classic indication for the implantation of a dual-chamber pacemaker according to the current national and international guidelines. However, in cases where dizziness and near syncope due to a sinus node dysfunction are found together with clinical characteristics of a sleep apnea-hypopnea syndrome (SAHS), screening for sleep apnea would be prudent before deciding for a pacemaker. The case report presented herein describes a patient with symptomatic sinus bradycardia and second-degree SA block with a Wenckebach periodicity, in whom the primary decision to implant a pacemaker was altered in favor of treatment with nCPAP (nasal continuous positive airway pressure) because after a careful and thorough evaluation of the patient’s history and symptoms, a severe mixed SAHS was diagnosed. On diagnosing SAHS with an obstructive component in patients with symptomatic bradycardia and SA block, there is no primary need for a pacemaker, but rather for implementing treatment with nCPAP. Thus, a pacemaker should only be considered in patients with intolerance or bad compliance regarding nCPAP, or in those in whom no significant reduction of bradyarrhythmia is achieved.

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.

Introduction: The high posterolateral right atrium (RA) is considered the “sinus node area,” but we lack information on endocardial atrial activation in sinus rhythm. We studied RA and left atrial (LA) endocardial activation in the electrophysiology laboratory. Methods and Results: Thirty-five patients (21 men) aged 47 ± 16.4 years (mean ± SD) underwent RA mapping (22.2 ± 3.8 points). In 21 patients, LA activation was mapped (11.1 ± 3.9 points) through the coronary sinus (CS), right pulmonary artery, and/or a patent oval foramen. Fourteen patients had atrial arrhythmias, and 3 an ECG pattern of Bachmann's bundle block. Endocardial RA activation preceded P wave in 5 (–14 ± 4.2 ms), coincided in 11, and followed P onset in 18 (16.7 ± 6.6 ms). Location of the zero point varied from the superior vena cava to the low RA and from lateral to paraseptal RA. In 19 patients, activation started simultaneously in 2 to 5 points located ≥1 cm apart. RA activation was descending in most, but in 3 with low onset there was collision in the anterior and septal walls. In 15 of 21 patients, descending LA activation dominated, ending in the mid CS in 12, proximal CS in 1, and simultaneously throughout the CS in 2. In 3 with Bachmann's bundle block, CS activation was ascending and in 2 double potentials were recorded from the LA roof. Conclusion: During stable sinus rhythm, RA activation can start in different areas or simultaneously over large areas resulting in different activation patterns, both in the RA and the LA. LA activation is predominantly descending, but in Bachmann's bundle block it becomes ascending, and double potentials suggest a location of block in the LA roof. (J Cardiovasc Electrophysiol, Vol. 15, pp. 524-531, May 2004)

OBJECTIVE: Clinical success of atrial fibrillation (AF) ablation depends on persistent block of electrical conduction across the ablation lines. The fate of ablations performed with temperature-controlled bipolar radiofrequency (RF) is unknown. The purpose of this study was to validate the electrophysiological (EP) efficacy of these lesions, recording pulmonary vein isolation (PVI) after open chest ablation, in the human being. METHODS: Ten consecutive mitral patients (mean age: 53 +/- 12 years) with concomitant AF were treated with the Cobra Revolution (Estech, San Ramon, CA, USA) bipolar RF device were enrolled for EP assessment. During surgery, pairs of additional temporary wires were positioned on the right PVs (RPV) and on the roof of the left atrium (RLA), before ablation. Pacing thresholds (PTs) were assessed before, after a single encircling ablation and at chest's closure. EP study was repeated before discharge and at 3 weeks. RLA wires served as control. RESULTS: Baseline PTs were 0.83 +/- 0.81 mA (range 0.2-3 mA) from RPV and 1.13 +/- 0.78 mA (range 0.3-3 mA) from RLA. PVI was reached in all patients acutely, and was maintained at 1 week. At 3 weeks, the PTs were 14.3 +/- 4.3 mA from RPV (range 7-20 mA) and 3.1 +/- 1.3 mA (range 1.5-7 mA) from RLA. All patients were discharged in sinus rhythm. CONCLUSIONS: Cobra Revolution temperature-controlled bipolar RF provides complete PVI after a single ablation up to 1 week. This notwithstanding, only 30% of patients were completely isolated (exit block validation) at 3 weeks. OBJECTIVE: Clinical success of atrial fibrillation (AF) ablation depends on persistent block of electrical conduction across the ablation lines. The fate of ablations performed with temperature-controlled bipolar radiofrequency (RF) is unknown. The purpose of this study was to validate the electrophysiological (EP) efficacy of these lesions, recording pulmonary vein isolation (PVI) after open chest ablation, in the human being. METHODS: Ten consecutive mitral patients (mean age: 53 ± 12 years) with concomitant AF were treated with the Cobra Revolution (Estech, San Ramon, CA, USA) bipolar RF device were enrolled for EP assessment. During surgery, pairs of additional temporary wires were positioned on the right PVs (RPV) and on the roof of the left atrium (RLA), before ablation. Pacing thresholds (PTs) were assessed before, after a single encircling ablation and at chest's closure. EP study was repeated before discharge and at 3 weeks. RLA wires served as control. RESULTS: Baseline PTs were 0.83 ± 0.81 mA (range 0.2-3 mA) from RPV and 1.13 ± 0.78 mA (range 0.3-3 mA) from RLA. PVI was reached in all patients acutely, and was maintained at 1 week. At 3 weeks, the PTs were 14.3 ± 4.3 mA from RPV (range 7-20 mA) and 3.1 ± 1.3 mA (range 1.5-7 mA) from RLA. All patients were discharged in sinus rhythm. CONCLUSIONS: Cobra Revolution temperature-controlled bipolar RF provides complete PVI after a single ablation up to 1 week. This notwithstanding, only 30% of patients were completely isolated (exit block validation) at 3 weeks.

Aims This study assessed survival, morbidity and impact of pacemaker (PM) therapy in children with Congenital Complete Atrioventricular Block (CCAVB). Methods and Results Data of 32 children, diagnosed as showing CCAVB at a median age of 0·4 years (range foetal–10 years), were retrospectively analysed. For comparison of clinical data patients were separated into two groups: CCAVB without structural heart disease (group 1; n=23) and with structural heart disease (group 2; n=9). Median follow-up time was 10·2 years. Pacemakers (PM) were implanted in 17 group 1 and all group 2 children. Frequency of PM therapy, age and symptoms before PM implantation did not differ significantly between the groups. Indications for PM implantation were bradycardia in 15, decreased exercise tolerance in 6, syncope in 3 and heart failure in 2 children. PM system related complications occurred in 11/26 (42%) children. Although 1 child died due to PM exit block no further CCAVB related symptoms were recorded in children with PM. Conclusion PM therapy reduces mortality and morbidity in children with CCAVB when compared with natural history data. Although children with PM are free from CCAVB related symptoms limited morbidity remains due to PM system related complications.

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.

Aims To determine the clinical significance of the sinoatrial block II° of the Wenckebach type (block W) identified during Holter monitoring. Methods and results The study included 300 patients (mean age 54 ± 17 years; 130 women) with symptoms suggestive of arrhythmia who underwent Holter monitoring. Block W was identified by a dedicated computer program and subsequently confirmed by a cardiologist. Block W was diagnosed in 88 patients (29%). It occurred only during sleep in 37 (12%) patients and during both daytime activity and sleep in 51 (17%) patients. Block W only during sleep happened predominately in young patients aged between 20 and 30 years, whereas episodes that occurred during both daytime and sleep were found mainly in patients between 60 and 70 years of age. Prospective observation time averaged 41 ± 11 months, and the time to the diagnosis of sinus node disease was 26 ± 10 months. Cox multivariate analyses showed that block W during both daytime and sleep is an independent predictor for the future diagnosis of sinus node disease [hazard ratio—13.6 (5.2–35.5); P < 0.0001]. Age-specific analyses confined this effect to the patients ≥50 years of age. The results also suggest that in patients ≥50 years of age block W during both daytime and sleep may be related to a significant improvement in survival [hazard ratio—0.03 (0.007–0.16); P < 0.0001]. Conclusion Block W during daytime activity in patients with symptoms suggestive of arrhythmia indicates an increased likelihood of the future diagnosis of sinus node disease.

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

GRAUX, P., et al.: Contribution of a Pacemaker Bradycardia Detection Algorithm in the Study of Patients with Carotid Sinus Syndrome. While carotid sinus syndrome (CSS) is often suspected as a cause of syncope in the elderly, whether it represents an indication for cardiac pacing may remain uncertain. Bradycardia algorithms included in pacemakers are now able to establish a precise relationship between spontaneous asystole and occurrence of symptoms and strengthen the indication for permanent pacing. This study included seven men and three women (70.5 ± 7.3 years of age) who, over an average period of 54.1 ± 17 months, had suffered from syncope (12.6 episodes/patient) and presyncope (11.2 episodes/patient) attributed to pure cardioinhibition (2 patients) or mixed CSS (8 patients). Other sources of symptoms were excluded by thorough clinical evaluations, including Holter monitoring, echocardiography, and electrophysiological testing. All patients received a CHORUS 6234 pacemaker, the memory of which includes a dedicated bradycardia detection algorithm capable of storing atrial and ventricular chains, and date and time of the last ten pauses and/or bradycardic events. After a initial period of 14.7 ± 8 months, during which symptoms were suppressed, the bradycardia algorithm was activated. From then on, a cumulative increase in the number of patients presenting with diurnal pauses was measured (1 month, n = 0; 3 months, n = 6; 9 months, n = 7; 2 years, n = 8). Fourteen episodes of diurnal asystole were recorded. The mean duration of the longest episodes of spontaneous ventricular standstill was 6,319 ± 1,615 ms and was due to sinoatrial block (n = 7), atrioventricular block (n = 5), and a combination of both (n = 2). In conclusion, activation of the CHORUS bradycardia algorithm allowed confirmation of the appropriateness of permanent pacing in a majority of patients suffering from CSS.

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.

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

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.

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.

The influence of ethanol on the actions of cocaine and ethylcocaine on rat sinoatrial preparations was studied. Ethanol did not modify the depressant effect of cocaine or ethylcocaine on sinoatrial rate (SR) in preparations with spontaneous activity. Cocaine produced sinoatrial block only in the presence of ethanol, and the latter accentuated the sinoatrial block produced by ethylcocaine. Ethanol did not modify the depressant effect of cocaine or ethylcocaine on membrane potentials of atrial fibers in preparations driven at a constant rate. In conclusion, ethanol, in a concentration that did not by itself affect SR or produce sinoatrial block, accentuated the effects of cocaine and ethylcocaine on sinoatrial conduction, without modifying the effects on SR. It is proposed that the accentuation of the block was the consequence of the combination of a depressant action on the fast sodium system and a deterioration of the cell-to-cell coupling.

The sinoatrial (SA) node is the cardiac pacemaker and changes in its adrenergic-muscarinic phenotype have been postulated as a determinant of age-associated modifications in heart rate variability. To address this question, right atria were microdissected, the SA node area was identified by acetylcholinesterase staining, and, using a RT-PCR method, the accumulation of mRNA molecules encoding beta1- and beta2-adrenergic (beta1- and beta2-AR) and muscarinic (M2-R) receptor was quantified to define the proportion between beta-AR and M2-R mRNAs within the sinoatrial area of adult (3 months) and senescent (24 months) individual rat hearts. In adult hearts, the highest M2-R/beta-AR mRNA ratio was observed within the sinoatrial area compared with adjacent atrial myocardium, while in the senescent hearts, no difference was observed between sinoatrial and adjacent areas. This change was specific of the sinoatrial area since adult and senescent whole atrial or ventricular myocardium did not differ in their M2-R/beta-AR mRNA ratio, and was associated with a fragmentation of acetylcholinesterase staining of the senescent SA node. Quantitative changes in the expression of genes encoding proteins involved in heart rate regulation specifically affect the sinoatrial area of the senescent heart.

Spontaneous electrical activity and indo 1 fluorescence ratios were recorded simultaneously in cultured pacemaker cells isolated from the rabbit sinoatrial node. Ryanodine (10 μM) reduced the amplitude of action potential-induced intracellular Ca2+([Formula: see text]) transients by 19 ± 3%, increased the time constant for their decay by 51 ± 5%, and slowed spontaneous firing by 32 ± 3%. 1,2-Bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid (BAPTA)-acetoxymethyl ester (AM; 25 μM) inhibited the [Formula: see text] transients and slowed spontaneous firing by 28 ± 4%. Ryanodine did not alter hyperpolarization-activated or time-independent inward current, but it reduced the sum of L- and T-type Ca2+ currents ( I Ca,L and I Ca,T) in both the presence and absence of BAPTA-AM. In contrast, I Ca,L was unchanged by ryanodine. Slow inward current tails, presumed to be Na/Ca exchange current ( I Na/Ca), were abolished by BAPTA or ryanodine. The results suggest that a decrement of I Ca,T, due to reduction of the intracellular Ca2+ concentration or a direct effect of ryanodine on T-type Ca2+channels, contributes to the negative chronotropic effect. Another possibility, based primarily on theory and results in other preparations, is that a reduction of I Na/Ca, as a consequence of the smaller action potential-induced[Formula: see text] transients, contributes to the effect of ryanodine.

The aim of this study was to investigate the effect of battery capacity, internal current drain, and stimulation energy on pulse generators longevity, and if battery impedance measurements can reliably predict pulse generators end-of-life. For this purpose, the records of 577 patients with a mean age of 65 +/- 14 years who had undergone implantation of two different dual chamber pulse generators (PG1: 409; PG2: 168) were retrospectively reviewed. Battery capacity were 2.3 Ah (PG1) and 3.0 Ah (PG2) while current drain at comparable nominal settings was 20 microA (PG1) and 30 microA (PG2) indicating a higher internal current drain of PG2. After a mean follow-up of 46 +/- 23 months, stimulation energy at reprogrammed output settings was significantly higher in PG1 as compared to PG2 (17.1 +/- 0.14) vs 15.5 +/- 0.24 J). Three PG1 (0.7%) and 12 PG2 (7.1%) (P < 0.01) had to be exchanged after a mean of 77.3 +/- 5.3 months (PG1) and 75 +/- 13.5 months (PG2) (P = NS) due to end-of-life being reached. The difference in battery impedances of PG1 and PG2 gained statistical significance 5 years after implantation (1.0 k omega vs 2.4 +/- 6.7 k omega) preceding the significant difference in PG survival after 6 years (98.7 +/- 1.3% vs 90.7 +/- 4.8%). These results indicate that internal current drain is the most important determinant of the pulse generators longevity and that battery impedance can reliably predict end-of-life. Therefore, the essential information about internal current drain should be available for each pacemaker, since it is required for adequate pulse generator selection. Diagnostic functions of dual chamber pulse generators should include measurements of battery impedance.

Objectives. This study sought to assess the efficacy of oral sotalol for various arrhythmias in pediatric patients and to evaluate the incidence of proarrhythmia and systemic side effects. Background. Sotalol is a beta-adrenergic blocking agent with additional class III antiarrhythmic properties. Experience in pediatric patients is limited. Data concerning the incidence of proarrhythmia in children are lacking. Methods. Seventy-one pediatric patients (mean age 7.3 years) with various supraventricular and ventricular tachyarrhythmias were treated with oral sotalol. All the patients were admitted to the hospital for initiation of sotalol therapy. Antiarrhythmic and proarrhythmic effects of sotalol were assessed by daily surface electrocardiograms (ECGs) during the in-hospital phase and by serial Holter monitoring. Results. Sotalol was either completely (27 [66%] of 41 patients) or partially effective (11 [27%] of 41) in 38 (93%) of 41 patients with supraventricular reentrant tachycardias. In patients with atrial flutter predominantly after operation for congenital heart disease, sotalol was effective in 84% of patients (completely in 9 of 19 and partially in 7 of 19). Ventricular tachycardia was completely (3 of 11) or partially (4 of 11) controlled in 64% of children. Proarrhythmia occurred in seven patients (10%) and consisted of symptomatic bradycardia from sinoatrial block and high grade atrioventricular (AV) block, respectively, in two children; asymptomatic high grade AV block in one; torsade de pointes in one; and relevant increased ventricular ectopic activity in three. Proarrhythmia required drug discontinuation in four patients. Mean duration of treatment for all patients was 18 months (range 1 to 40). Conclusions. Sotalol was an effective antiarrhythmic drug for a wide range of pediatric tachyarrhythmias. The considerable number of patients with proarrhythmic effects indicates the need for initiation of treatment on an inpatient basis and close monitoring by serial Holter electrocardiography.

This study sought to define contemporary trends in permanent pacemaker use by analyzing a large national database.The Medicare National Coverage Determination for permanent pacemaker, which emphasized single-chamber pacing, has not changed significantly since 1985. We sought to define contemporary trends in permanent pacemaker use by analyzing a large national database.We queried the Nationwide Inpatient Sample to identify permanent pacemaker implants between 1993 and 2009 using the International Classification of Diseases-Ninth Revision-Clinical Modification procedure codes for dual-chamber (DDD), single-ventricular (VVI), single-atrial (AAI), or biventricular (BiV) devices. Annual permanent pacemaker implantation rates and patient demographics were analyzed.Between 1993 and 2009, 2.9 million patients received permanent pacemakers in the United States. Overall use increased by 55.6%. By 2009, DDD use increased from 62% to 82% (p0.001), whereas single-chamber ventricular pacemaker use fell from 36% to 14% (p = 0.01). Use of DDD devices was higher in urban, nonteaching hospitals (79%) compared with urban teaching hospitals (76%) and rural hospitals (72%). Patients with private insurance (83%) more commonly received DDD devices than Medicaid (79%) or Medicare (75%) recipients (p0.001). Patient age and Charlson comorbidity index increased over time. Hospital charges ($2011) increased 45.3%, driven by the increased cost of DDD devices.There is a steady growth in the use of permanent pacemakers in the United States. Although DDD device use is increasing, whereas single-chamber ventricular pacemaker use is decreasing. Patients are becoming older and have more medical comorbidities. These trends have important health care policy implications.

"OBJECTVIS: Clinical success of atrial fibrillation (AF) ablation depends on persistent blocking of electrical conduction across the ablation lines. Epicor high-intensity focused ultrasound (HIFU) ablation has been credited with a variable clinical efficacy. The aim of this work is to ascertain the electrophysiological (EP) efficacy of such lesions, by assessing pulmonary vein isolation (PVI) after open chest HIFU ablation, in the clinical setting.. METHODS:. Ten consecutive mitral patients (mean age: 57±10 years) with paroxysmal AF undergoing concomitant ablation with the Epicor ablation system (St. Jude Inc.®, Minneapolis, MN, USA) were enrolled for EP assessment. During surgery, pairs of additional temporary wires were positioned on the right PVs (RPVs) and on the roof of the left atrium (RLA), before epicardial ablation. Exit block (no capture during PV pacing) of RPV and of RLA was assessed before, after ablating and immediately after closure of the chest, in order to check the correct positioning of the wires. EP assessment was repeated before discharge and at 3 weeks.. RESULTS:. Baseline RPV pacing threshold (PT) was 3.5±2 mA (range 1.5-8), of RLA 1.73±1.1 mA (range 0.7-4.3 mA). PVI was not reached any time after HIFU ablation. At the pre-discharge EP study, the absence of isolation was observed in all cases. At 3 weeks, the PTs were 6.8±5.8 mA on RPV (range 2-16) and 6.4±5.3 mA (range 1-19) on RLA. All patients were discharged in sinus rhythm.. CONCLUSIONS:. PVI was not achieved after Epicor HIFU ablations, up to 3 weeks after surgery."

Al though differences in exercise performance have been observed between different rate adaptive modes, the relative impact of atrioventricular (AV) synchrony and rate adaptation on quality of life (QOL) have not been determined. Thirty-three patients with either sinoatrial disease (18) or complete atrioventricular (AV) block (15) received DDDR pacemakers (16 minute ventilation sensing, 17 activity sensing). There were 11 males and 22 females, with a mean age of 66 ± 1 (range 39–78) years. The study was a double-blind, triple cross-over study comparing DDDR, DDD, and VVIR modes. At the end of each 8-week study period in each mode, QOL was assessed by a questionnaire evaluating patients' functional class (Classes I-IV), physical malaise inventory (41 items), illness perception (43 items), and overall QOL rating based on a 48 items measure covering different aspects of the patients' daily life adjustment. Two patients required early crossover from VVIR mode during the study. Patients experienced significantly fewer physi cal malaise such as temperature intolerance, dyspnea, and palpitations in the DDDR mode, compared with either DDD or VVIR pacing. DDDR pacing reduced the perception of illness in 5 of 43 items compared to VVIR pacing, and improved stamina and appetite compared to DDD pacing. The overall QOL score was 102 ± 2, 105 ± 2, 113 ± 2 in the DDDR, DDD, and VVIR modes, respectively, with a higher score indicating a poorer QOL (DDDR/DDD vs VVIR, P < 0.02). There was no change in functional classes between the three pacing modes. In conclusion, VVIR pacing has a lower QOL compared with DDD pacing, which can be further enhanced with rate augmentation.

We performed ambulatory 24-hour esophagus ECG in nine patients with dual chamber pacemakers suspect of transient arrhythmias in order to achieve correct and reliable P wave identification during daily life activities. In all patients episodes were observed with varying atrial artifact to left atrial depolarization sequences. These episodes probably reflected presence of atrial fusion systole, an ECG phenomenon which should be taken into account when analyzing ambulatory esophagus ECG. Thus, the ambulatory esophagus ECG revealed its ability to detect spontaneous atrial depolarization in the presence of pacemaker artifact in patients with DDD(R) pacemakers.

Background— The origin of 40% of syncope cases remains unknown even after a complete diagnostic workup. Previous studies have suggested that ATP testing has value in selecting successful therapy. This patient-blinded, multicenter, randomized superiority trial tested whether, in patients with syncope of unknown origin, selecting cardiac pacing in those with a positive ATP test leads to fewer recurrences than those who do not receive pacing. Methods and Results— From 2000 to 2005, 80 consenting patients (mean age, 75.9±7.7 years; 81% women; 56% without diagnosed structural heart disease) with syncope of unknown origin and atrioventricular or sinoatrial block lasting >10 seconds (average, 17.9±6.8 seconds) under ATP administration (20-mg IV bolus) were recruited from 10 hospitals, implanted with programmable pacemakers, and randomized to either active pacing (dual-chamber pacing at 70 bpm) or backup pacing (atrial pacing at 30 bpm). Patients were followed up regularly for up to 5 years for any syncope recurrence, the primary outcome. Mean follow-up was 16 months. Syncope recurred in 8 of 39 patients (21%) randomized to active pacing and in 27 of 41 (66%) randomized to backup pacing (control), yielding a hazard ratio of 0.25 (95% confidence interval, 0.12–0.56). After recurrence, the 27 recurrent control patients were reprogrammed to active pacing, and only 1 reported subsequent syncope. Conclusion— This study suggests that, in elderly patients with syncope of unknown origin and positive ATP tests, active dual-chamber pacing reduces syncope recurrence risk by 75% (95% confidence interval, 44–88). Clinical Trial Registration— URL: http://www.controlled-trials.com/ISRCTN00029383 . Unique identifier: ISRCTN00029383.

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.

A 22-year-old athlete with nocturnal asymptomatic episodes of transient sinus arrest/sinoatrial block up to 7.3 s and recurrent inappropriate sinus tachycardias which had been incidentally found during Holter electrocardiography diagnostics is presented. In spite of extensive diagnostic work-up including invasive procedures like coronary angiography and electrophysiological study, no causal etiology was found. Based on the normal findings and the lack of symptoms, we decided not to implant a permanent pacemaker. After 14 months, the patient is still asymptomatic. Howerver, the 24-h Holter electrocardiography shows unchanged frequency of nocturnal transient sinus arrest episodes.

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.

Background Although the most frequent extra-pulmonary manifestations of respiratory syncytial virus (RSV) infection involve the cardiovascular system, no data regarding heart function in infants with bronchiolitis associated with RSV infection have yet been systematically collected. The aim of this study was to verify the real frequency of heart involvement in patients with bronchiolitis associated with RSV infection, and whether infants with mild or moderate disease also risk heart malfunction. Methods A total of 69 otherwise healthy infants aged 1-12 months with bronchiolitis hospitalised in standard wards were enrolled. Pernasal flocked swabs were performed to collect specimens for the detection of RSV by real-time polymerase chain reaction, and a blood sample was drawn to assess troponin I concentrations. On the day of admission, all of the infants underwent 24-hour Holter ECG monitoring and a complete heart evaluation with echocardiography. Patients were re-evaluated by investigators blinded to the etiological and cardiac findings four weeks after enrolment. Results Regardless of their clinical presentation, sinoatrial blocks were identified in 26/34 RSV-positive patients (76.5%) and 1/35 RSV-negative patients (2.9%) (p < 0.0001). The blocks recurred more than three times over 24 hours in 25/26 RSV-positive patients (96.2%) and none of the RSV-negative infants. Mean and maximum heart rates were significantly higher in the RSV-positive infants (p < 0.05), as was low-frequency power and the low and high-frequency power ratio (p < 0.05). The blocks were significantly more frequent in the children with an RSV load of ≥100,000 copies/mL than in those with a lower viral load (p < 0.0001). Holter ECG after 28 ± 3 days showed the complete regression of the heart abnormalities. Conclusions RSV seems associated with sinoatrial blocks and transient rhythm alterations even when the related respiratory problems are mild or moderate. Further studies are needed to clarify the mechanisms of these rhythm problems and whether they remain asymptomatic and transient even in presence of severe respiratory involvement or chronic underlying disease.