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The objective of the study is to generate and simulate various abnormal ECG signals, by extracting their geometrical features using MATLAB. The resulting signal is reasonably close approximate to that of the real ECG signal. The goal is to enable a constructive tool to analyse ECG signals for the academic use, thus eliminating the complex task of signal processing.

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.

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.

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.

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.

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.

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

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.

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.

In the early days of sleep research it was thought that heart block (second and third degree atrioventricular block), sinus arrest, or sinoatrial block were frequent findings in patients with sleep apnoea. Tilkian and co-workers1 reported that more than 50% of patients with sleep apnoea develop episodes of heart block during sleep. In 400 patients studied by Guilleminault et al 2 bradycardic arrhythmias were reported in almost 18% of the patients and later studies found heart block in 9–13% of patients with sleep apnoea.3 4 Due to ventricular asystoles of up to 13 seconds in duration it was hypothesised that heart block might lead to an increased mortality risk in these patients.2 A recent publication challenged previous results in that no increased prevalence of bradycardic arrhythmias was seen in patients with sleep apnoea compared with those without sleep apnoea.5 To examine these seemingly discrepant results further we performed Holter monitoring in 239 consecutive patients diagnosed as having sleep apnoea (apnoea/hypopnoea index >10/h) using a validated ambulatory recording device based on the measurement of heart rate, Sao 2, snoring sound, and body position. Episodes of second and third degree atrioventricular (AV) block and/or sinus arrest of more than two seconds in duration occurred in 17 of the 239 patients.6 There was no significant difference in age between patients with and without heart block (mean (SD) 50.7 (12.8) versus 52.1 (9.8) years), but those with heart block were significantly more obese (38.7 (7.3) versus 30.7 (4.6)). Twelve of the 17 patients (70.6%) had arterial hypertension, seven (41.1%) suffered from heart failure (NYHA II–III), and four (23.5%) had pulmonary hypertension. None of the patients reported a myocardial infarction in their medical history, and in only one (5.9%) exercise testing showed signs of coronary heart disease. Ten …

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.

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.

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.

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.

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.

SummaryThe subepicardial injection of 0.1 cc of digitalis or of a strophanthin preparation, as well as of other substances, over the sinus area leads to the immediate but transient appearance of sinoauricular block. This phenomenon is attributed to a reflex inhibition of the sinus node centers caused by the mechanical stimulus and not to a specific effect of the injected substances. In some instances the centers of the auriculo-ventricular node are also inhibited.

Sinoatrial block of two types has been described; (1) with progressive prolongation of sinoatrial conduction time leading to a dropped beat; and (2) dropped beats without such preceding conduction changes. These are strictly analogous to the Wenckebach and the Mobitz types of atrioventricular block. The literature on this subject has been surveyed, together with available information on the postulated anatomic and functional pathways of inter- and intra-atrial conduction. We have postulated that, in the present case, both varieties of sinoatrial block coexist, thus explaining the variable distance between the two types of P waves. Such a hypothesis also requires the assumption of functional pathways between the S-A node and the two atria, with dissociation of the two atria, and with partial dissimilar block between each atrium and the S-A node. Although interatrial dissociation, both partial and complete, and each variety of sinoatrial block have been previously described, so far as we have been able to learn, their coexistence has not been previously noted.

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.

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

Introduction: Serious cardiac toxicity due to lithium toxicity is uncommon and generally only occurs in individuals with underlying heart disease. Cardiac impairment may result in dysrhythmias, including sinus bradycardia, sinoatrial block, and first-degree atrioventricular block. This paper describes a patient with complete AV block in the course of chronic lithium treatment. Case report: Fifty-seven year-old female was brought into the emergency department (ED) due to altered mental status and malaise by ambulance from hospice. She had hypertension, type-II diabetes mellitus, and depression. The caregivers told that she had been fine yesterday, had taken regular medications (lysinopril, furosemid, acetyl salicylic acid, oral antidiabetic tablets and lithium (300 mg tb/day)). Her vital signs were; blood pressure: 70/45 mmHg, pulse: 37 bpm, respiratory rate: 22 bpm, and oxygen saturation 86%. She was confused and unresponsive to verbal stimulation. Her EKG revealed total atrioventricular block. Initial biochemical results were unremarkable except for a lithium level of 2.2 mmol/l (therapeutic range 0.5-0.8 mmol/l) and an increased creatinine of 2.11 mg/dl. A transvenous pacing electrode was introduced into the right ventricle, which allowed rapid restoration of haemodynamic and neurological status. Her neurologic examination was completely normal in the follow-up period and she was discharged without sequelae. Conclusion: In conclusion, emergency physicians should bear in mind that complete AV block can ensue in the course of lithium toxicity and it is an entity that should be included in the differential diagnosis. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

A logic error in the software of Cosmos II results in apparent malsensing of atrial signals at high rather than low sensitivity settings. The paradoxical function was found in 54 out of 87 units tested (= 62%) if the atrial sensitivity was increased and in 54 out of 87 units tested (= 62%) if the atrial sensitivity was increased and the ventricular refractory period was lengthened beyond critical limits that could be defined individually. The problem inherent in both unipolar (66%) and bipolar systems (54%) is attributed to a summation of a physiological signal and internal noise, which has to be detected at the atrial level within a specific timing window to disable atrial sensing for the next pacing cycle. The malfunction virtually disappears if the ventricular refractory period does not exceed 210 msec. It is recommended, therefore, that Cosmos II pacemakers be left at their nominal ventricular refractory value (200 msec).

Atrioventricular (AV) nodal reentry requires intact retrograde ventriculoatrial (VA) conduction. The purpose of this study was to assess the contribution of various pacing and pharmacologic techniques to uncover VA conduction during apparent unidirectional VA block, and to evaluate the role of several biologic and electrophysiologic factors in concealment of retrograde conduction. Forty healthy dogs underwent catheter-electrophysiologic studies of AV and VA conduction. Group I (20 animals) had intact VA conduction. Group II (six animals) had VA dissociation with ventricular pacing initiated during sinus rhythm, but the presence of VA conduction was confirmed by isoproterenol infusion or by premature ventricular stimulation. In group III (14 animals), the above techniques failed to uncover VA conduction. Eight of 14 group III animals underwent thoracotomy and crushing or freezing of the sinoatrial (SA) node. Ventricular pacing initiated during sinus standstill was associated with 1:1 VA conduction in each experiment. VA conduction time and retrograde Wenckebach cycle length, both in the baseline state and during isoproterenol infusion, were significantly longer in the eight animals in group III than in those in group I. Age, gender, weight, breed, sinus cycle length, and anterograde AV conduction properties were not significantly different between groups I, II, and III. The data suggest that (1) in normal dogs, complete unidirectional VA block probably does not exist; (2) in the presence of anterograde input to the AV node, even sophisticated pacing and pharmacologic maneuvers may fail to uncover the presence of VA conduction; (3) although anterograde input is essential for concealment of VA conduction, the phenomenon is more closely associated with depressed retrograde than with anterograde AV nodal characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Patients with sinus node disease (SND) who are unable to achieve an adequate increase in heart rate during exercise are candidates for atrial rate-responsive pacing (AAI-R). We have implanted 40 AAI-R systems in SND patients with an average follow-up of 12.5 +/- 8 (range 3-30) months. All the patients received an activity-sensing pulse generator (Activitrax, Medtronic or Sensolog, Siemens-Pacesetter) with a single atrial lead. Only patients with an intraoperative AV nodal block cycle-length above 100 beats min-1 were included. During follow-up, one patient was observed to have transient asymptomatic 2:1 AV-block during sleep. No patient developed persistent AV-block or chronic atrial fibrillation. Twelve patients with persistent chronotropic incompetence were assigned for a randomized double-blind crossover study, comparing exercise treadmill capacity in AAI-R with conventional atrial inhibited pacing (AAI). During AAI-R pacing the maximum heart rate during exercise was 120 +/- 1 beats min-1 compared with 97 +/- 21 beats min-1 during AAI pacing (P less than 0.01). The average exercise time increased from 11.2 +/- 2 min during AAI-pacing to 13.4 +/- 3 min during AAI-R pacing (P less than 0.01). AAI pacing should be considered for patients with SND and chronotropic incompetence.

SummaryAbout two consecutive cases of acute intoxication by trichlorethylene, the authors want to point out the possible occurrence of serious disturbances in cardiac conduction which are less frequently described in the literature than disturbances in myocardial excitability.

A 4-year-old girl with post-surgical complete atrioventricular block received an epicardial dual chamber pacemaker system. During further growth intermittent exit block occurred, first misinterpreted as neurological seizures. The epicardial lead was replaced using a transvenous approach, and a pacemaker with an integrated home monitoring facility was implanted. After her discharge, a rise in the pacing threshold automatically initiated an event message. On the basis of this information, the patient was called in and imminent dislodgement of the ventricular lead was diagnosed by x-ray. The lead was repositioned and was found stable over 1-year follow-up.

The ionic basis of automaticity in the sinoatrial node and His-Purkinje system, the primary and secondary cardiac pacemaking regions, is discussed. Consideration is given to potential targets for pharmacologic or genetic therapies of rhythm disorders. An ideal target would be an ion channel that functions only during diastole, so that action potential repolarization is not affected, and one that exhibits regional differences in expression and/or function so that the primary and secondary pacemakers can be selectively targeted. The so-called pacemaker current, If, generated by the HCN gene family, best fits these criteria. The biophysical and molecular characteristics of this current are reviewed, and progress to date in developing selective pharmacologic agents targeting If and in using gene and cell-based therapies to modulate the current are reviewed.

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

We identified a family with 10 affected members in four generations suffering from adult-onset progressive sinoatrial and atrioventricular conduction disease, sudden death due to ventricular tachyarrhythmia, dilated cardiomyopathy, and a unique type of brachydactyly with mild hand involvement (short distal, middle, proximal phalanges and clinodactyly) and more severe foot involvement (short distal, proximal phalanges and metatarsal bones, short or absent middle phalanges, terminal symphalangism, duplication of the bases of the second metatarsals, extra ossicles, and syndactyly). The phenotype differences from other reported genetic abnormalities and linkage exclusion of Holt-Oram syndrome, ulnar-mammary syndrome, brachydactyly type B or Robinow syndrome, and cardiac conduction disease or Brugada syndrome loci suggest that we report on a new hereditary heart-hand syndrome.

Myocardial contractility is regulated by adrenergic stimulation, the strength-length relationship and the force-frequency relationship or Bowditch effect. The latter mechanism was clearly demonstrated in muscle strips, in the isolated heart as well as in in-vivo experiments. The aim of this study was to further investigate the role of the force-frequency effect on the contractile response to exercise or isoproterenol infusion in conditions of restricted increases in heart rate i.e., AV-block, sinus node block and beta-adrenoceptor block.Nineteen dogs were instrumented with a left ventricular miniature pressure gauge, catheters in the aorta, pulmonary artery and left atrium and pacing leads on the left atrium and left ventricle. In order to control the chronotropic response during sympathetic stimulation, permanent AV-block was induced in nine dogs, sinus node block using UL-FS 49 and beta-adrenoceptor block using propranolol was studied in ten dogs.Adrenergic stimulation (isoproterenol 0.4 micro g/kg or exercise) after total AV-block failed to increase LVdP/dt. However, increasing LV pacing rate (from 50 up to 200 bpm) prior to adrenergic stimulation elicited a significant increase in LVdP/dt (4762 +/- 166 mmHg/s vs. 6485 +/- 381 mmHg/s, p0.05). In dogs in sinus rhythm, heart rate and LVdP/dt response to isoproterenol and exercise following pre-treatment with UL-FS 49 is significantly reduced, with heart rate increasing from 103 +/- 7 up to 154 +/- 5 bpm and LV dP/dt(max) from 2925 +/- 171 mmHg/s to 6249 +/- 400 mmHg/s compared to the response in control conditions (HR 220 +/- 3 bpm and LV dP/dt(max) 7473 +/- 616 mmHg/s) (p0.05). When heart rate is matched using atrial pacing, the LVdP/dt(max) response reached comparable values as observed in control conditions (7310 +/- 550 mmHg/s). Similar responses were obtained during exercise. Beta-adrenoceptor blockade attenuates considerably the heart rate and LVdP/dt response to sympathetic stimulation. Adjusting heart rate with atrial pacing restores only partially LVdP/dt(max).During sympathetic stimulation, the chronotropic response plays a major role for the concomitant full expression of the inotropic response. In conditions where increases in heart rate are absent or severely restricted such as in permanent AV-block, sinus node block and beta-adrenoceptor block, the inotropic response will also be impaired.