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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.

Lyme carditis is typically associated with AV nodal conduction abnormalities. We describe the case of a 66 year old female patient, who experienced a series of syncopal attacks after several tick bites two weeks earlier. ECG monitoring revealed recurrent sinus arrest with a maximum pause duration of 8 seconds. After institution of antibiotic therapy for Lyme carditis, sinus node dysfunction resolved rapidly and the patient had no further syncopes. Pacemaker implantation was not necessary. We therefore have to assume that in this patient Lyme carditis was the cause of symptomatic sinus node dysfunction.

Amiodarone has been shown to improve survival in patients with impaired left ventricular function and ventricular trachyarrhythmias. The clinical applicability, however, is limited by numerous often serious adverse effects. 70 patients receiving the treatment with amiodarone for ventricular tacharrhythmias were investigated regarding the development of symptomatic bradycardia. Group 1 consisted of 25 patients with preexisting conduction disorders, 5 had first degree heart block, 10 had right bundle branch block, and 7 had left bundle branch block on electrocardiographic examination. The 3 remaining patients showed asymptomatic sinus node dysfunction defined as sinus arrest or sinuatrial block. Amiodarone caused symptomatic bradycardia in 6 of the group 1 patients (II degrees-III degrees AV block in 3 patients with preexisting I degree AV block or right bundle branch block; intermittent sinus arrest or SA block in the 3 cases with previous sinus node dysfunction). 45 patients had no conduction disorders before the administration of amiodarone (group II). None of these patients developed symptomatic bradycardia. The difference to group I was significant (p0.0005). Thus, patients with preexisting conduction disorders have a substantial risk of developing symptomatic bradycardia under amiodarone therapy, with an incidence of 24% in group I patients of our collective.

A pacemaker syndrome manifested as transient sensoric aphasia in a 68-year-old woman with a VVI-pace-maker implanted after SA-block. The attack occurred during long-term blood pressure recording and Holter monitoring. Borderline hypotension was documented during ventricular pacing which induced a retrograde excitation of the atrium. Clinical investigations excluded any intracranial abnormality, any source of embolism or stenosis of extra- and intracranial cerebral arteries. Cerebral blood flow measurements revealed a significant increase during pacing at elevated heart rate. Therefore, a device for AV-sequential pacing was implanted and basic pacing rate was elevated. The present case report indicates that focal and not only global cerebral ischemia can be produced by an impairment of systemic hemodynamics due to hypotension and a pacemaker syndrome. Improvement of cerebral blood flow during pacing is an unexpected finding contrasting with the concept of autoregulation. In addition, pacemaker implantation should be discussed in patients with transient cerebral perfusion deficits if an improvement of cerebral blood flow is documented along with rising heart rate.

Before operation as well as over a mean postoperative period of 8.9 years 222 adults with atrial septal defects underwent a follow-up examination concerning frequency and clinical significance of supraventricular dysrhythmias. Thereby disturbances of the formation of stimuli were found before the operative procedure in 60 patients and after the correction in 115 patients. Disturbances of the sinoatrial and atrioventricular conduction were registered preoperatively in 53 cases and postoperatively in 81 cases. Within these statistically significant increases in particular the significant forms of dysrhythmia elevated after the atrial septal defect closure. Thus the tachycardiac atrial dysrhythmias increased from 7 to 28%, complex arrhythmias even from 2 to 16%. Of dysrhythmias to be taken seriously patients with IAVC and supraventricular defect are significantly more frequently affected than those with interatrial septal defects. Size of the defect, shunt volume and pressure of the pulmonary artery did not show any connections with the frequency of dysrhythmia. On the other hand, when accompanying cardiac anomalies, symptoms of a manifest heart insufficiency were present and at an operation age over 40 years arrhythmias were proved more frequently. The complaints of the patients did not correlate with the endangering, but are imprinted by the haemodynamics and its postoperative normalization. By the established profile of complaints and a decrease of frequency from 76% pre- to only 40% postoperative the patient with atrial septal defect cannot estimate his individual risk and needs an adapted long-term concept for his cardiological care.

In the conventional postmortem coronary angiogram and vessels are illustrated by a "compact" filling with contrast medium. In the case of the double contrast technique, a thin film of contrast medium is brought about the inner surface of the arteries. Gas injected under controlled pressures into the vessels acts as a further control against the surrounding media. The method is suitable for a more precise illustration of the subepicardial and large intramural coronary arteries. Of particular advantage is the high transparency of the x-ray pictures and the possibility to make the coronary ostia visible. The evaluation of x-ray pictures produced at different controlled pressures permits conclusions about pressure-volume relations of defined vessel sections, which then can be analysed histologically.

A comparative investigation of the electrophysiological properties of the sino-atrial node, the right atrium, the AV-node, and the intraventricular conduction system was performed in 37 patients. 18 patients had a sino-atrial block, 8 a persistent bradycardia and 11 a brady-tachy syndrome. There are the following conclusions: 1. The greatest dysfunction of the sino-atrial node was observed in the group of patients with sino-atrial block. This can be derived from the determination of the sinus node recovery time and from the occurrence of secondary pauses. 2. The vulnerability of the right atrium, investigated by the extra-stimulus-technique, is enhanced in the brady-tachy syndrome. Measuring the duration of the P-wave and the PA-interval does not give any information about the atrial dysfunction. 3. Patients with a sino-atrial block often have a disturbed AV-node conduction. In most patients it is latent only and easily can be detected by atrial incremental pacing. 4. A hemiblock or bundle branch block is found more often in patients with sino-atrial block and sinus bradycardia than in patients with the brady-tachy syndrome. By the registration of a His-bundle-electrogram a trifascicular block can be uncovered in half of these patients. 5. In the sick sinus syndrome, there is always the possibility of additional dysfunctions in the conduction distal to the sino-atrial node. With special regard to therapeutic measures, a complete evaluation can only be made by of both endocardial recording and stimulation methods.

Atrial pacing up to 250 bpm was performed in 88 patients with suspected sick sinus syndrome or syncopes of unknown origin. Measurements were done on the first five return cycles. According to cSNRTmax they were divided in 3 groups (group 1 less than 525 ms, group 2 greater than or equal to 525 ms less than 1000 ms, group 3 greater than or equal to 1000 ms). The return cycle pattern (PSM) was calculated (mean + standard deviation of PSI 1-PS15 at each pacing rate). A "normal" PSM with long PSI1 and gradual shortening of the subsequent cycles was found only at low pacing rates in group 1 and group 2. At higher rates, the PSI1 shortened and PSI2 lengthened, resulting in frequent secondary pauses (SP). Atrial pacing up to 400 bpm was performed in 20 open chest dogs. SP were frequently obtained at pacing rates above 300 bpm. Intravenous application of propranolol and atropine did not diminish SP, neither did bilateral vagotomy. Additional subthreshold stimuli, as well as stimulation with large interpolar distance did not influence the PSM of SP at high frequencies. Simultaneous stimulation of right atrium and right ventricle had no significant effects on SP. Pacemaker shifts occurring frequently after high rate pacing were not necessarily accompanied by SP. The velocity of activation spread over the sinoatrial region was significantly slower in cases of postpacing beats preceding a SP. It was concluded that the PSM of SP provoked by high rate atrial pacing is neither caused by local release of neurotransmitters nor by pacing induced changes of the autonomic tone nor by pacemaker shifts.(ABSTRACT TRUNCATED AT 250 WORDS)

Five patients with second degree intraatrial block are presented. The first three cases had a sick sinus syndrome with sinus bradycardia, broad P waves and episodes of atrial flutter or fibrillation. In these patients a Wenckebach phenomenon could bei elicited by atrial stimulation at a critical driving rate between the stimulated site and the recording electrode. In the first patient this conduction disturbance was obtained at several right atrial stimulation sites. The block could be elicited in the other two patients only in a limited area of the right atrium respectively only by left atrial pacing. In the remaining two patients an atrial tachycardia with block was observed. The intraatrial conduction disturbance was manifested as an exit block around the ectopic pacemaker. In one patient the tachycardia was induced by digitalis intoxication. In the other patient no etiologic factor of the tachycardia could be found. While the first three patients presented intraatrial conduction disturbances already in sinus rhythm, the last two cases showed after recovery from the atrial tachycardia P waves of normal duration and configuration.

The influence of the autonomic nervous system on sinus node automatism was assessed in 61 patients with suspect sinus node dysfunction. Cardiac frequency and corrected sinus node recovery time (CSNRT) were determined before and after functional autonomic blockade with intravenously administered propranolol (0,2 mg/kg) and atropine (0,04 mg/kg). A pathologic CSNRT was found in 59% of patients before and in 54% after autonomic blockade. In 44% pathologic CSNRT occurred during both conditions. In these patients intrinsic sinus node disease can be assumed. In 15% of patients an initially pathologic CSNRT became normal after blockade. In these patients sinus node dysfunction is caused by autonomic dysregulation. In 10% of patients pathologic CSNRT was seen for the first time after blockade. In such patients an altered autonomic balance seems to camouflage the primary intrinsic sinus node disease. Abnormal intrinsic cardiac frequency (cardiac frequency after autonomic blockade) was observed in pathologic prolongation of CSNRT after blockade, however not in normal CSNRT. On the other hand only 39% of patients with prolonged CSNRT after blockade had at the same time an abnormal intrinsic cardiac frequency. Autonomic blockade improves the diagnosis of the sick sinus node syndrome. Demonstration of abnormal intrinsic cardiac frequency is highly specific of intrinsic sinus node disease. Normal intrinsic cardiac frequency does, however, not exclude intrinsic sinus node disease.

The effect of beta-adrenergic receptor stimulation on sinus node function in patients with sick-sinus syndrome was investigated. Electrophysiological studies were performed in 14 patients (5 males and 9 females) aged 18-81 years before and after intravenous administration of 50 micrograms Prenalterol per kilogram body wt. Prenalterol decreased spontaneous cycle length by 26% (p less than 0.01), which corresponded to an increase in heart rate of 21 beats/min. The corrected sinus node recovery time was shortened by 23% (n.s.) in 10 patients, and was abnormal in 12 patients before and in 10 patients after Prenalterol. Secondary pauses occurred in 8 patients at control and in 9 patients after drug administration, in 2 of them for the first time after Prenalterol. In the sick-sinus syndrome the pronounced chronotropic response to beta-adrenergic receptor stimulation with Prenalterol doses not indicate improvement of impaired sinus node function.

By means of atrial stimulation methods for the establishment of the sinus node recovery time and for the indirect calculation of the so-called sinuatrial conduction time under certain methodical conditions disturbances of the sinus node automatism and of the sinuatrial conduction may be differentiated and moreover latent dysfunctions of the sinus node may be unmasked. Methodical problems in the recognition of the sinus node recovery time by higher-frequent atrial stimulation and the calculation of the sinuatrial conduction time by programmed atrial single or double manifold stimulation result above all on that account, since the various factors which determine the reaction of the sinus node in atrial stimulation are not to be surveyed in the individual case. Since there are no obligatory and reliable criteria for the judgment of the function of the sinus node a statement on sensitivity and specificity of the diagnostic stimulation methods is scarcely possible. With regard to a therapeutic decision aid a higher-frequent stimulation for the determination of the sinus node recovery time is of greater importance than the calculation of the sinuatrial conduction time. For the identification of a disturbed function of the sinus node the two parameters make a diagnostic contribution of approximately the same value.

Clinical cases are presented on the general theme of cardiovascular syncope. A case is cited to illustrate the clinical picture of idiopathic hypertrophic obstructive cardiomyopathy, a frequently disguised and misinterpreted cause of syncope. Chief attention is focused on the concept of fascicular heart block causing syncope. In the light of 3 patients, the various possibilities with respect to etiology, evolution, clinical picture and prognosis of fascicular heart block are outlined. In this context the diagnostic, prognostic and therapeutic significance of His bundle electrocardiography is discussed. Finally, 2 cases are cited to illustrate the sick sinus syndrome as a major cause of syncope. The diagnostic procedure in patients with suspected lazy sinus node is discussed and the results are presented of 16 personally observed cases with this disorder.

External chest wall stimulation was performed in 87 patients in order to overdrive and thereby suppress the implanted pacemaker. The impossibility to inactivate the implanted pacer suggested a disturbed "sensing" function in 12 patients. Marked changes of the escape rhythm were found in 77 patients with suppressable pacemaker when compared with the tracings before pacemaker implantation. Increasing degree of A-V block or marked changes in heart rate were observed in 14 of 35 cases with advanced A-V block. Minor alterations were noted in cases with sick sinus syndrome and atrial fibrillation. Overdrive suppression is a helpful method for the selection of pacemaker dependent patients.

This report demonstrates the results of five observation of the Pacemaker's-twiddler-syndrome, which will not necessarily end in the complete malfunction of the pacemaker unit. Therefore we classify the Pacemaker's-twiddler-syndrome as a partial and a complete form. The partial form is characterized by still effective cardiac stimulation, whereas the complete form can not stimulate the heart muscle because of the retracted electrode. Also methods of early detection and prevention of the Pacemaker's-twiddler-syndrome are discussed.

Bradyarrhythmias are due to disturbance of impulse formation and conduction in the heart. The sick sinus syndrome consists of both forms, sinusbradycardia being the most common type of arrhythmia, followed by sinus arrest and sinuatrial block. There is a wide range of the reported frequency of concomitant intermittent supraventricular tachycardia. Most patients have additional atrioventricular conduction disturbances. Diagnostic methods include measurement of the sinus node recovery time and sinoatrial conduction time, but therapy, i.e. pacemaker implantation depends largely on documentation of significant reduction of heart rate with clinical symptoms. The largest group of bradycardias is due to high degree atrioventricular block. As the prognosis of Mobitz Type II block is unfavorable in regard to development of complete distal av-block, differentiation between type I and II is of clinical importance, particularly in patients with additional fascicular block. Although exact localization of conduction disturbance with the Hisbundle-electrogram is possible, proof or exclusion of block distal to the Hisbundle including high frequency testing with atrial stimulation does not give the sole indication for therapeutic measures as follow up studies of patients with intraventricular conduction disturbances with and without distal block have demonstrated, that progression to complete av-block is difficult to predict.

A day vs. night comparison of type and frequency of cardiac arrhythmias documented by long-term ECG was done in 30 patients with nocturnal respiratory disorders in the form of the sleep apnoea syndrome. The commonest nocturnal arrhythmia was pronounced sinus arrhythmia during the apnoeic phases with variations of cardiac frequency between 40 and 120/min. Supraventricular and ventricular extrasystoles occurred significantly more frequently during the night than during the day. In three patients bradycardiac arrhythmias presenting as sinoauricular and atrioventricular blockades of the 3rd degree with node or ventricular substitute rhythm were seen during the sleep apnoea which could not be demonstrated during the day. Predominantly nightly occurrence of cardiac arrhythmias should lead to differential diagnostic consideration of the sleep apnoea syndrome.

Physiological stimulation can be achieved by either bifocal or rate responsive pacing. The latter pacemakers adapt the heart rate to physical activity by biological signals. Of many possible approaches only three pacemaker systems for rate responsive pacing are available: the QT pacemaker (Tx or Quintech), the respiratory Biorate pacemaker and the activity detecting Activitrax. First our own experiences (8 QT, 6 Biorate, 8 Activitrax pacemakers) and a survey of 95 QT- and 37 Biorate pacemakers from 11 centers are reported. The Biorate pacemaker functions without any problems, its present disadvantage is limited programmability. With the Tx pacemaker failing frequency adaptation (26%) was found more often in the early series, mostly due to voltage polarisation at the tip of the electrode. The Activitrax pacemaker gives satisfactory frequency adaptation, largely depending on the activity of the muscles of the shoulder and pectoral region.

The "specific" investigations for sinus node syndrome (SNS) in 22 patients are analyzed. SNS was defined as sinusbradycardia below 40/min and sinus-standstill over 2 sec. Atropin (1 mg i.v.), exercise test and carotid pressure were of little help in establishing the diagnosis, while Holter monitoring and sinus-node recovery time were significantly abnormal in all patients investigated.

Frequency and importance of secondary pauses (SP) following termination of high rate artrial pacing were evaluated in 64 patients. The maximal values of the first 10 post-pacing cycles, resulting from series of pacing between 70/min--160/min, were compared with the normal post-pacing values of Benditt. SP were present in 1 case (4%) of 23 patients without electrocardiographic signs of sinus node dysfunction (SDF), but in 21 cases (51%) of 41 patients with SDF (p less than 0.01). SP were more frequent in patients with SA-Block and/or sinus pauses (64%) and with bradycardia-tachycardia-syndrome (60%), whereas were more rare (35%) in patients with sinus bradycardia only. Patients with SDF and SP did not significantly differ from patients with SDF without SP concerning absolute and corrected sinus node recovery time, basal heart rate, reduction of cycle length after atropine, abnormal reactions to carotid sinus pressure and frequency of syncopes. In 1 patient SP, present in basal conditions, were not evident after atropine. SP could be interpreted as indication of SDF and should always be searched for because it may be the only evidence of SDF after atrial pacing; therefore SP may reduce the frequency of false negative tests after rapid atrial pacing. Possibly, vagal mechanisms are involved.

18 pigs in which venous catheters were positioned for long-term use were injected with nicotine in physiological saline: group 1: 1 mg without anaesthesia; group 2: 1 mg/animal, Hypnodil-anaesthesia; group 3: 0.0143 mg/kg body weight, Hypnodil-anaesthesia. The dose of 1 mg is corresponding to that amount of nicotine contained in the main smoke of a commercially used cigarette. The dose of 0.143 mg/kg body weight is calculated per 1 kg body weight assuming that a man of 70 kg body weight resorbes the total amount of nicotine (1 mg) after maximum inhalation. Application of 1 mg induced the following alterations: sino-auricular block, AV-block of first and second degree, asystolia up to 2 seconds, short decrease in blood pressure and bradycardia as well as flattening and/or inversion and biphasic reaction of T. A longer lasting increase in blood pressure was observed in non-anaesthesized animals. Animals treated with 0.0143 mg/kg body weight showed AV-block of first degree with subsequent extrasystoles. Blood pressure, heart rate and T-wave showed no alterations. Decisive for the induction and extent of acute disturbances seems to be the dose of nicotine. Therefore, a decrease of the nicotine content seems to be indicated toward a "less harmful cigarette".

Sinoatrial (SA) conduction can be tested in man by premature atrial stimuli. The difference between the post-extrasystolic pause and the spontaneous sinus cycle is a sign of the sinoatrial delay. Extern atrial stimuli provoked over the esophagus showed analogous results to intracardiac tests. The sinoatrial conduction time estimated by the esophagus method is about 20 ms higher. In 30 normal persons it was 95 +/- 36 ms (x +/- 2 SX). 7 patients with sick sinus syndrome showed aberrations as in the intracardiac test. Different types of sinoatrial block should be distinguished. Type I measured by the esophagus method had a "SAE time" over 130 ms. Type II always had compensating postextrasystolic pauses due to higher SA delay. Type III of other authors could not be observed; there are doubts about the rightness of this type. In 2 patients SA blocks over several sinus cysles could be induced by premature stimuli. This feature osberved for the first time has been declared as type IV. In 28 patients with different diseases of the heart type I could be found 12 times and type II 6 times; SA block was not known previously. The calculation of the SA time by atrial stimuli via the esophagus offers a riskless and simple method for the further differential diagnosis of disturbances of the cardiac rhythm.

In view of the unsatisfying drug treatment of bradycardias in most cases, clinical studies with new compounds seem to be urgent. A report is given on experiences with a derivative of atropine (gen. Ipratropiumpromid) in 34 cases suffering from various types of bradycardias. Comparing heart rate following intravenous injections of 0.5 to 1.0 mg, the new drug proved to be definitely more effective than atropine sulfate. Side effects were limited to diminution of salivary glands function.