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A 59-year-old male patient was admitted for possible reflex syncope following loss of consciousness during urination. During the visit, a malaise with unconsciousness occurred. Holter ECG at that time showed increasing sinus bradycardia with transition to a junctional escape rhythm (30/min); in addition, there were several sinus pauses > 2.0 s (the longest almost 10 s). This malaise occurred again during routine EEG, when a focal epileptic seizure on the right fronto-temporal with sinus bradycardia after 15 s was documented. Thus, the diagnosis of ictal asystole was made, anticonvulsant therapy was started, and a cardiac pacemaker was implanted., (© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Restlessness and Syncopes in a Patient from a Home for Elderly Abstract. A broad differential diagnosis should be considered when faced with syncopes. Most common causes are cardiovascular and neurological causes. If there is evidence of epilepsy with sudden loss of tone, look for ictal-triggered arrhythmias. Ictal bradycardias and asystoles are usually benign and self-limiting. In contrast, bradycardias and asystoles in the context of SUDEP are usually fatal and are the result of ictally induced cerebral hypoxemia.

Bradyarrhythmias cause symptoms such as syncope, dizziness, or exercise intolerance and lead to the implantation of > 100 000 pacemakers in Germany annually. They are caused either by sinus node dysfunction (sinus bradycardia, sinoatrial block, sinusarrest, preautomatic pauses in paroxysmal atrial fibrillation, chronotropic incompetence) or by atrioventricular (AV) conduction abnormalities (AV block, complex bundle branch block). Optimal therapy of bradycardia crucially depends on ECG documentation which frequently requires Holter monitoring in the case of intermittent bradycardia. The differential diagnosis of the ECG can sometimes be demanding, for instance in distinguishing sinus bradycardia or AV block from blocked supraventricular premature beats, in understanding chronotropic sinus node incompetence, 2:1 AV block, complete AV block in atrial fibrillation, bifascicular and imminent trifascicular bundle branch block or vagally induced bradycardia. This review presents the ECG in bradycardia and provides tips for a confident interpretation., (© Georg Thieme Verlag KG Stuttgart · New York.)

Bradycardic arrhythmias are classified into disorders of impulse formation and conduction. Impulse formation disorders are diseases of the sinus node. Conduction disturbances are the sinoatrial (SA), atrioventricular (AV) block and bundle branch block. The conduction disturbances are also subdivided in different grades (grade I to III). Clinical manifestations of bradycardic arrhythmias are usually syncope, Morgagni-Adam-Stokes seizures, dizziness, palpitations, or heart failure. The investigation of syncope as the most visible clinical manifestation of bradycardic arrhythmias, is performed in three steps with the goal of risk stratification for sudden cardiac death or major adverse cardiac events. If symptomatic bradycardia is present, there is usually an indication for pacemaker implantation. Prior to a definitive pacemaker implantation reversible or preventable causes must be investigated and treated., (© Georg Thieme Verlag KG Stuttgart · New York.)

In DDD pacing, the left-ventricular electromechanical latency period defines the duration between premature ventricular stimulation and the prematurely ending left-atrial contribution to left-ventricular filling. It has to be considered in diastolic AV delay optimization. Individual duration of this parameter seemed to reflect the ventricular function. Therefore, we compared the left-ventricular electromechanical latency period due to right ventricular stimulus with the documented ejection fraction of two groups, 33 congestive heart failure patients carrying biventricular systems and 13 right ventricular paced bradycardia patients. A mean latency period of 168+/-26 ms was found in the heart failure patients (ejection fraction: 25+/-5%) which was significantly longer (p=0.0039) compared to the bradycardia patients (ejection fraction: 51+/-12%) with a mean latency of 119+/-13 ms. Thus, an increasing latency period during right ventricular DDD pacing therapy indicates decreasing ejection fraction. A cut-off interval of 135 ms allowed the discrimination of 93% of our patients as having an individual ejection fraction of either up to 35% or above. Thus, the left ventricular electromechanical latency period can be used as an additional parameter indicating the necessity to upgrade from right to biventricular DDD pacing.

History and Admission Findings: A 59-year-old man was referred to the hospital for psychiatric reasons. To control hypertension and chronic heart failure he had been treated with 5 mg ramipril and 12.5 mg hydrochlorothiazide. In addition, he received 25 mg spironolactone. A prostate disease was diagnosed two months ago., Investigations: Laboratory analysis revealed a severe hyperkalemia (9.3 mmol/l) as well as an increase in creatinine (24.3 mg/dl) and urea nitrogen (349.0 mg/dl). The ECG showed a bradycardia with increased T-wave amplitudes. Abdominal sonography revealed a full urinary bladder., Treatment and Course: Administration of terbutaline, sodium bicarbonate, and glucoseinfusion lowered potassium level to 6.3 mmol/l before hemodialysis was started. Hyperplasia of the prostate gland was found to be the reason for acute renal failure. Dialysis treatment was only temporarily necessary; afterwards, the patient was transferred to the urology department for subsequent therapy., Conclusion: Hyperkalemia is a life-threatening emergency that requires immediate therapy. Conservative treatment allows to partially correct water-electrolyte imbalance until hemodialysis can be performed. Hyperkalemia often results from the administration of combination therapy with ACE-inhibitors/AT (1)-antaganonists and antikaliuretic diuretics (spironolactone) in renal failure.

Aim: The aim of this study was to investigate the usefulness in providing diagnostic information about syncope by implantation of a loop recorder (ILR)., Methods and Results: The study population consisted of 48 consecutive patients (23 male, 25 female, mean age 42 +/- 17) with unexplained syncope who presented between 1998 and 2002 and underwent extensive cardiological screening and were followed with an implantable loop recorder (Reveal or Reveal Plus). The mean follow-up duration was 9 +/- 6 months. During this follow-up in 17 (35%) patients syncope recurred. Arrhythmia correlating with syncope was documented in 15 (88%) of these patients, in 2 (12%) patients an arrhythmia could be excluded. Of these 15 patients with arrhythmogenic cause of syncope 5 (33%) patients revealed higher degree AV-Block, 7 (47%) patients sinus bradycardia or sinus pauses, 4 (27%) due to sick sinus syndrome and 3 (20%) due to neurally mediated syncope, 3 (20%) patients had atrial tachycardias or atrial fibrillation with rapid AV-conduction. As a result of ILR findings 12 pacemakers were implanted and 2 radiofrequency ablations were performed., Conclusion: The ILR is a valuable and effective tool to establish an arrhythmic cause for unexplained syncope. In these cases they have an impact on subsequent clinical decision making. ILR can also be useful in ruling out arrhythmias as cause of syncope and presyncope.

A 63-year-old male patient diagnosed with chronic schizophrenia and characterized by formal disorders of thought with neologism and paranoid ideation, especially grandiose delusions and feelings of being influenced by radiation, is presented. At admission to psychiatric hospital, the patient reported attacks of weakness and dizziness, which he attributed to his feelings of alien influence. The diagnosis of cardiac disease with severe bradycardia could already be established by basic physical examination. Further diagnostic procedures (e.g., ECG) revealed symptomatic atrioventricular conduction defects (atrioventricular block III). After implantation of a cardiac pacemaker, the somatic symptoms vanished and the patient recovered completely in terms of physical condition.

History and Clinical Findings: A cardiac pacemaker was to be implanted in a 74-year-old man, known for many years to have cardiac arrhythmias. Lown type IVb, because of the onset of severe bradycardic episodes. After appropriate preoperative preparation the patient's anticoagulant medication was changed over 5 days from phenprocoumon (Marcumar) to heparin. The procedure and the immediate postoperative period were without complication. But two days later he had to be admitted to the intensive care unit because of cardiac failure and bleeding into the operation site., Laboratory Findings: One week after starting heparin the platelet count had fallen from 154 x 10(9)/l preoperatively to 92 x 10(9)/l. Haemoglobin concentration was 8.9 g/dl, haematocrit 26.7%. The Quick value of 51%, partial thromboplastin time of 54.1 s, thrombin time of 17.6 s and plasma antithrombin level of 61% provided no further diagnostic pointers. An HIPA test and a PF4/heparin immunoassay, performed as heparin-induced type II thrombocytopenia was suspected, subsequently confirmed the diagnosis., Treatment and Course: After the cardiac status had stabilized the operative wound was explored, but no bleeding site found. Other causes having been excluded (liver failure, disseminated intravascular coagulopathy, septicemia, dilution thrombocytopenia), heparin was discontinued 2 days later. Recombinant hirudin infusion, 0.025 mg/kg per hour, was begun. After 4 days the platelet count had improved, the other clotting parameters were stable within the therapeutic anticoagulant range and the diffuse bleeding had stopped., Conclusion: When changing from phenprocoumon to heparin preoperatively one must be aware of the rare risk of acquired heparin-induced thrombocytopenia. Intravenous recombinant hirudin proved to be a safe treatment until oral anticoagulation had been established, quickly normalizing the platelet count.

Bradyarrhythmias are the cause of syncope in 3 to 10% of cases. Marked bradycardia or asystole can be due to impaired function of the sinus node (sick sinus syndrome), high degree AV block or neurocardiogenic disorders (carotid sinus syndrome, vasovagal syncope). A precise history, ECG and 24-h. Holter recordings are the most helpful tools in diagnosis of bradyarrhythmia-induced syncope. An association between symptoms and documented ECG is essential for proper diagnosis. Sometimes an event-recorder may be helpful for this purpose. If a patient has normal physical examination, ECG, Holter, stress test, tilt-table test and echocardiography, no further electrophysiological investigation is needed. If the noninvasive tests show pathologic results that do not clearly explain the cause of syncope (sinus bradycardia, first-degree AV block, fascicular block, structural heart disease), then electrophysiological studies are recommended, which will also rule out ventricular tachyarrythmias in the differential diagnosis. If all diagnostic tests in a patient with syncope are normal, the prognosis is fairly good despite 30% recurrence rate. Treatment for symptomatic bradyarrhythmias is implantation of a pacemaker. The selection of an appropriate pacemaker system is very important. Dual-chamber systems (DDD) provide physiological stimulation by maintaining AV synchrony; thus, they should be preferred whenever possible.

Implantable cardioverter/ defibrillators (ICD) represent in many patients with ventricular tachyarrhythmias the first line treatment. Up to 15% of the patients requiring an ICD need concomitant permanent cardiac pacing for bradyarrhythmias resulting in the need of simultaneous ICD- and antibradycardic pacemaker-therapy. We present four patients with successful implantation of a transvenous ICD-system (Medtronic Jewel 7220 and Micro Jewel 7221; electrode: Medtronic 6939), all of which had an antibradycardic pacemaker (2 unipolar, 2 bipolar) implanted prior to ICD-implantation. Meticulous intraoperative testing in order to avoid adverse interactions between the two systems has been carried out successfully in all cases. Possible adverse interactions comprise oversensing of pacemaker signals by the ICD with subsequent inadequate therapy, inhibition of defibrillation therapy during ventricular fibrillation caused by false detection of pacemaker spikes by the ICD as well as reprogramming of the pacemaker after shock delivery. A review of the published literature yielded 91 reported cases of combined ICD- and pacemaker-therapy. In 16% of the patients, one or more of the mentioned complications have been observed. Those occurred more frequently with unipolar than with bipolar pacemaker-systems. Thus, combined therapy with antibradycardic pacemaker and transvenous ICD-systems can be performed safely.

The as yet unanswered question, whether patients with sleep apnoea and apnoea-associated bradyarrhythmias have a higher morbidity and mortality rate, was retrospectively investigated in 132 men with sleep apnoea (apnoea index > 10/h). Sleep-associated bradycardic arrhythmias were recorded in 71 (mean age 50.1 years; group 1). For comparison served 61 men with sleep apnoea but no bradyarrhythmias (mean age 51.4 years; group 2), matched for age and weight. There was no significant difference between the two groups as to diagnosis and initial findings on ergometry, lung function tests and blood gas analysis. The apnoea index of 48.1 +/- 23.9/h in group 1 was significantly higher than that of 31.9 +/- 20.1/h in group 2 (P < 0.001). During a follow-up period of a mean of 41.1 (19-66) months, two patients in group 1 died (of myocardial infarction), while one died (of bronchial carcinoma) in group 2 (follow-up period of 29.6 [18-54] months). The two deaths in group 1 were in a subgroup of 16 patients who had declined treatment or had used it irregularly. There was no death among those who had been treated (n = 54), by nasal continuous positive airway pressure, operation or pacemaker implantation. However, no causal relationship could be established from these data between increased mortality rate and apnoea-associated arrhythmias.

Bradyarrhythmias, depending on the patient population, are the cause of syncope in 3 to 10%. Marked bradycardia or asystole can be due to impaired function of the sinus node (sinus node syndrome) or high-grade AV-conduction block as well as carotid sinus syndrome and pathologic vasodepressor reactions. In particular, in the presence of high-grade AV-block, the diagnosis of bradyarrhythmia-induced syncope can frequently be established on the basis of a standard ECG. One of the most common causes of syncope is functional impairment of the sinus node, in particular, an inadequate permanent sinus bradycardia, sinus node arrest or SA-block and paroxysmal atrial tachycardia alternating with atrial bradycardia. The method of choice for detecting suspected paroxysmal arrthythmias is ambulatory ECG monitoring but interpretation may be encumbered by the absence of concomitant symptoms during the registration. Frequently, the use of non-invasive methods alone, such as detailed history, ambulatory ECG and ECG exercise testing, will not render confirmatory findings to document the cause of syncope, that is, > 3 s pause in sinus rhythm or high-grade AV-block. In this situation, the question arises which patients should undergo electrophysiologic examination. Several studies have shown that in patients with a pathologic resting ECG (first degree AV-block, bundle branch block, inadequate sinus bradycardia) and cardiac disease, electrophysiologic studies will document a cause of syncope in more than 30%.(ABSTRACT TRUNCATED AT 250 WORDS)

Indications for electrical pacing were present in 58 of 665 patients with acute myocardial infarction (8.7%). Posterior-wall infarction had occurred in 34, anterior-wall infarction in 20, while two had combined infarction and in a further two precise localisation was not possible. There were 16 deaths (27.6%), six of them with posterior-wall and nine with anterior-wall infarction. Bradycardic arrhythmias with A-V block predominated among posterior-wall infarctions, hemiblocks and bifascicular block in anterior-wall infarctions. Permanent pacing was practised in 14 patients, 11 with posterior and three with anterior-wall infarctions, i.e. permanent pacing was four times as common after posterior than anterior-wall infarctions, the proportion being 2:1 for temporary pacing, largely due to a higher mortality-rate after anterior-wall infarction. Old anterior-wall scars were present in nine of eleven patients with permanent pacing. Because of the danger of late bradycardia or A-V block patients with posterior-wall infarction should be carefully followed in the late phase (from about the third week onwards), especially if it is known that they have an old anterior-wall infarct.

In a 68-year-old female patient glossopharyngeal neuralgia of unknown origin occurred accompained by cardiac arrhythmias (bradycardia to asystole) and loss of consciousness. Subcutaneous atropine injections improved bradycardia but did not influence attacks of pain. Complete and permanent freedom from symptoms was established only after treatment with carbamazepine (Tegretal) 200 mg t.d.s.

106 episodes of ventricular fibrillation were observed in 11 patients, 9 of whom had acute myocardial infarctions. The heart rate before the onset of ventricular fibrillation was below 50 in two episodes, 60 to 100 in 63, and above 100 in 41. 83 attacks of ventricular fibrillation were preceded by fewer than five ventricular premature beats, 23 by more than five, 19 by more than ten. Multifocal ventricular premature beats occurred ten times, runs of ventricular premature beats 11 times, with only three falling into the vulnerable period. Left bundle branch block was present in three patients, right bundle branch block with left anterior hemiblock in two, isolated left anterior hemiblock in two, left posterior hemiblock in one. 85 episodes of ventricular fibrillation occurred during antiarrhythmic treatment, 72 during lidocaine administration. Antiarrhythmic drugs were effective only in reducing the number of ventricular premature beats. The only successful treatment of recurrent episodes of ventricular fibrillation was repeated electrical countershocks.

Twenty-six patients with open-angle glaucoma were investigated to see if and to what extent topical treatment with timolol 0.5% produced systemic effects. All of the patient had contraindications to the systemic use of beta-blockers such as bradycardia, cardiac insufficiency and chronic obstructive pulmonary disease. In some patients the treatment had marked cardiovascular or pulmonary effects, especially in the group with chronic obstructive pulmonary disease.

Two children with exercise-induced syncopes are described. There was no evidence for congenital or acquired cardiac defects, cardiomyopathy or myocarditis in either of them. Both had sinus bradycardia and a consistently normal QT-interval at rest. In both, exercise induced regularly a multiform ventricular tachycardia, additionally in one on occasion a bidirectional, in the other a supraventricular tachycardia. Beta receptor blocking agents prevented tachyarrhythmias in both. Under treatment with beta receptor blocking agents, one child remained without syncopes, the other died suddenly. These cases underline the possiblility that exercise-induced syncopes may be caused by tachyarrhythmias even if the QT-interval of the resting Ecg is normal. In suspicious cases an exercise-Ecg is indicated.

Between 1964 and 1978 twenty patients suffering from acute mesenteric vascular occlusion were treated in the surgical department (University of Münster). The average duration of the anamnesis until their hospitalization was 3.1 days and the actual operation was performed 11.35 hours later on the average. In only 15% of the cases had a correct preoperative diagnosis been given. As regards the frequency of causation, 60% of the mesenteric vascular occlusions were caused by a mesenteric arterioembolism, 20% by a mesenteric venous embolism, 10% by a mesenteric arterial thrombosis and 10% by a non-obstructive occlusion. In a post cardiac infarction condition was the predisposing factor in 50% of all cases, valvular defect in 33.5% and tachyarrhythmia in 16.6%. The causes found for the mesenteric venous tbrombosis were insufficiency of the right heart, absolute bradyarrhythmia, recurrent venous thrombosis of the leg, and myeloproliferative syndromes.

The long-term effect of pacemakers in the management of bradycardic heart failure with or without syncope was tested on 337 patients. The cumulative survival rate of patients with Adams-Stokes attacks without heart failure (group I) was 91% at the end of one year, 73% at the end of three and 35% at the end of eight years. Among patients with Adams-Stokes attacks and accompanying heart failure (group II) 81% survived one year, 64% three and 46% five years, but only 25% eight years. Among patients in whom heart failure was the only indication for pacemaker implantation (group III), 70% were still alive after one year, 56% after three and 17% after five years. Related to the severity of heart failure before and after pacemaker implantation, most of the patients of group II (mild or moderately severe failure) had definite improvement, while of those in group III (mainly severe failure) only about half had less cardiac failure. In patients with severe heart failure and bradycardia (without syncope) long-term results are not likely to be very good, as regards both duration of survival and physical capacity.

The frequency and distribution of risk factors of arteriosclerosis were determined in 405 patients with implanted cardiac pacemakers and compared with the corresponding results of patients with cardiac infarction. The most frequent risk factors were smoking (43,5%), hypertension (35,2%), and diabetes (34,3%) in males, hypertension (52,3%) and diabetes (49,7%) in females. The frequency of cardiac infarction was in average 19,5%. In the infarction group diabetes was lower in both sexes (23,5% and 35,8%), respectively), hyperlipoproteinemia and smoking were more frequent. From the different distribution of risk factors it is suggested, that coronary arteriosclerosis is not the most important etiologic factor in the development of bradycardic dysrhythmias. The higher percentage of diabetes in the pacemaker group could point to metabolic disturbances or specific diabetic vascular disease as harmful factors to the conduction system.