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Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 217 records · Page 12Linked to original sources
PubMed1996

[Sleep apnea as a risk marker in coronary heart disease].

UNLABELLED: Obstructive sleep apnea (OSA) and coronary heart disease (CHD) are both frequent in the middle ages. Both disease share a similar spectrum or risk factors and attendant diseases. The aim of the study was to determine the prevalence of obstructive sleep apnea in patients with coronary heart disease diagnosed by coronary angiography. Furthermore, influence of sleep apnea and attendant diseases and risk factors for coronary heart disease, especially the risk for myocardial infarction and reduced left ventricular ejection fraction, was investigated. We included in this study 143 patients (121 men, 22 women mean age 60 +/- 8 years (35-81) who underwent coronary angiography because of angina pectoris or were suspicious for CHD due to noninvasive investigations. These patients has symptoms of OSA based on a standardized questionnaire. They underwent a four-channel screening with a non-laboratory-monitoring-system (NLMS) for detection of sleep-related breathing disorders. In addition, spectrum of risk factors and concomitant diseases were considered. Sleep apnea was more frequent in patients with CHD (30.6%) in comparison to patients without CHD (21.8%), but did not reach statistical significance. Patients with CHD and OSA had a significantly higher frequency of a history of myocardial infarction and had a significantly lower left ventricular ejection fraction than patients without OSA. IN CONCLUSION: Patients with the combination of OSA and CHD are at higher risk for myocardial infarction and reduced left ventricular ejection fraction. Patients with CHD should be screened for OSA in case of secondary prevention.

Adult↗
PubMed1996

[Persistent dilatation of non-stenosed epicardial arteries in 24- and 48-hour nitroglycerin infusion].

UNLABELLED: It is still a matter of dispute to what extent a direct loss of nitrate mediated vasodilatation (true tolerance) contributes to the development of nitrate tolerance. Aim of this study was to assess to what extent the dilatation of non-obstructed segments of epicardial arteries is attenuated during a continuous 24- and 48-h-infusion of nitroglycerin. In a prospective, randomized and blinded study we investigated 32 patients who underwent diagnostic coronary angiography. All cardiac medication was withdrawn at least for 24 h; patients were randomized to either a 24 h NTG-infusion (group A; 0-24 h saline infusion followed by a 24 h NTG-infusion; n = 16) or a 48 h NTG-infusion (group B; 0-48 h of NTG-infusion; n = 16) in a dosage of 1.5 micrograms/ kg/min. The patients were included if 5 proximal segments of the left coronary artery showed no visible atherosclerosis. A coronary angiography was performed after 24 and 48 h respectively. The lumen diameters were measured by quantitative coronary analysis at baseline and 1 and 3 min after application of 0.2 mg of NTG intracoronarially (i.c.). Blood samples were drawn before and after 24 and 48 h of infusions to measure hematocrit and neurohormones. In group A after 24 h of saline infusion there was a significant increase in lumen diameter from 3.14 +/- 0.17 mm at baseline to 3.51 +/- 0.11 mm (p < 0.001) and 3.60 +/- 0.21 mm (p < 0.001) after 1 and 3 min of NTG i.e. respectively. After 24 h of NTG-infusion there were no significant changes in baseline and values after further NTG i.e. In group B after 24 h of NTG-infusion no significant change in lumen diameter was detectable after NTG i.e. (3.57 +/- 0.23 mm to 3.63 +/- 0.13 mm) and the mean diameter remained unchanged after prolongation of NTG to 48 h (3.58 +/- 0.33 mm). There were no significant differences between the baseline values and the responses to i.e. NTG after 24 and 48 h of NTG infusion. Hematocrit and aldosterone levels decreased significantly after NTG-infusion but not following saline. Renin and norepinephrine remained unchanged throughout the NTG-infusion-periods. IN CONCLUSION: The vasodilatation of non-obstructed segments of epicardial arteries persists during a prolonged infusion period and there is no induction of vascular tolerance between the 24 and 48 h infusion period. These findings further support that there is a different susceptibility of arteries and veins to nitrate tolerance.

Adult↗
PubMed1996

[Driving restrictions for arrhythmia patients--with special reference to the implantable cardioverter/defibrillator].

UNLABELLED: The series "Illness and Vehicular Traffic", published by the German Federal Ministry for Transportation, has set forth the following guidelines on the subject of driving for patients with cardiac rhythm disorders: "Anyone suffering from disorders of cardiac rhythm which might, on occasion, lead to the repeated interruption of oxygen supply to the brain and thus cause disturbances in consciousness or even loss of consciousness, must be considered unsuitable for driving a motor vehicle of any class." While these guidelines are essentially indisputable, it remains unclear how they affect patients with an implantable cardioverter/defibrillator (ICD). The issue is further complicated by the fact that these patients, as a rule, suffer from malignant and life-threatening cardiac rhythm disorders, often owing to a severe cardiac disorder (primarily coronary heart disease and cardiomyopathy). It was the purpose of a recent study to investigate how medical permission to drive in ICD patients is handled in various European countries. A specifically designed questionnaire was addressed to 46 European National Delegates of the Working Groups on Cardiac Pacing in order to determine their present practices and criteria utilized when advising driving restrictions to patients (pts) after ICD implantation. RESULTS: Of the 39 (83%) respondents, 22 (56%) cardiologists advised all pts to abstain from driving. Permanent driving abstinence was advised by 13 (33%) of the responding cardiologists, while temporary driving abstinence for periods of 3 to 18 months (mean 9 +/- 4 months) was recommended by 26 (67%) physicians. Criteria for subsequently advising a longer period of driving abstinence were: presyncope by 15 (38%), syncope by 13 (33%) and multiple shocks by 2 (5%) cardiologists. Despite medical advice not to drive, about one-third of pts resume driving. About half of the pts resumed driving after 6 months, with the vast majority driving 12 months after ICD implantation. Two pts experienced ICD discharges while driving, but no motor vehicle accident occurred. One patient had a motor vehicle collision with a fatal outcome which was not caused by loss of consciousness or ICD discharge. CONCLUSIONS: 1) Fatal accidents of ICD discharges while driving are a rare finding in ICD pts. 2) About half of the physicians always advise their pts to cease driving for a period of 9 +/- 4 months. Despite this medical advice pts resume driving 6 months after ICD implantation. 3) Criteria used in advising driving abstinence are not uniform among physicians. In symptomatic bradyarrhythmias the driving privilege may be reinstated after pacemaker implantation provided that symptoms resulting from the interruption of the oxygen supply to the brain have not recurred.

Accidents, Traffic↗
PubMed1996

[Exogenous adenosine as an anti-arrhythmia agent].

Adenosine has potent cardiac electrophysiologic effects including a negative chronotropic action on the sinus node and a predominant negative dromotropic action on the AV node. The latter property has mainly led to the use of adenosine as antiarrhythmic agent for the acute management of paroxysmal supraventricular tachycardia (PSVT) mediated by a reentrant mechanism involving the AV node. The effects of adenosine are dose-dependent and of very short duration since the half-life is less than 10s. The efficacy rates for termination of AV reentrant tachycardias were found to be 35% with 3 mg, 60-70% with 6 mg, 80% with 9 mg, and 90-95% with 12 mg adenosine. The AV nodal depressant effects of adenosine have also been used for determining the mechanism of wide QRS tachycardias for differentiating supraventricular tachyarrhythmias with aberrant conduction from ventricular tachycardia. Adenosine either terminates or slows almost all types of supraventricular tachyarrhythmias or it leads to unmasking of the underlying mechanism such as atrial flutter with aberrant conduction. One form of ventricular tachycardia, the idiopathic type originating from the right ventricular outflow tract can usually be terminated with adenosine due to its cAMP-mediated mechanism. Adenosine is helpful to detect or to increase preexcitation which is important for planning a catheter ablation procedure since the preexcitation pattern allows to localize the accessory pathway. Since the action of adenosine usually does not alter the accessory pathway conduction it is also useful for control ablation efficacy noninvasively in terms of antegrade conduction and during ventricular pacing for the retrograde conduction. Further evaluation and research is necessary for better understanding of adenosine action on the human atrial electrophysiology since it provokes atrial fibrillation in some patients, and of adenosine action on the different pathways in AV nodal reentrant tachycardias and some accessory pathways with decremental (AV nodal-like) conduction properties.

Adenosine↗
PubMed1996

[Intra-atrial defibrillation--limits and possibilities].

UNLABELLED: External cardioversion has been a remarkably effective and safe method for termination of atrial fibrillation. Originally introduced by Lown and coworkers in 1962, it has been an accepted mode of acute therapy. The disadvantages of this approach are the need for general anaesthesia and the demand for high energies up to 360 J. Intraatrial defibrillation of atrial fibrillation using low energy shocks has been intermittently investigated as an alternative to the external method for over two decades. The following aspects have to be considered during the use of intraatrial defibrillation: the efficacy of this method, the safety, i.e. the potential risk of inducing a proarrhythmic, the patient acceptance during recurrent shock discharges, the phenomenon of the atrial stunning, the risk of a thromboembolism, and the necessity of anticoagulation. Our own experience of 25 patients and the data in the literature indicate that internal atrial defibrillation is a safe and effective method for termination of atrial fibrillation, and is particularly useful in patients who have been refractory to external cardioversion. The mean atrial defibrillation threshold for termination of chronic atrial fibrillation was 9.1 +/- 7.4 J in our patient population, corresponding with a leading edge voltage of 376 +/- 175 V and an impedance of 53 +/- 8 omega. At an energy level of 300 V, 40% of the patients could be effectively converted into sinus rhythm. Apart from the induction of three ventricular depolarizations no other proarrhythmic events could be observed during the delivery of approximately 200 shock discharges, in particular no sustained ventricular tachyarrhythmias. The mean pain score at 60 V was 3.0 +/- 1.1 corresponding with a mild discomfort, and at 140 V 4.6 +/- 0.7 corresponding with a moderate to severe discomfort. Serial multiplane transesophageal echocardiographic examinations demonstrated a reduction of the flow in the left atrial appendage following intraatrial defibrillation. These reduced flows in the left atrial appendage recovered within 7 days. On June 3, 1996 an atrial defibrillator was successfully implanted for the first time in Germany in a patient with symptomatic, drug refractory atrial fibrillation. CONCLUSIONS: Intraatrial defibrillation is a safe and effective method for termination of atrial fibrillation. The electrotherapy with an implantable atrial defibrillator should be considered as an alternative approach in patients with symptomatic, long lasting, and drug refractory episodes of atrial fibrillation.

Atrial Fibrillation↗
PubMed1995

Heart rate to work rate relation throughout peak exercise in normal subjects as a guideline for rate-adaptive pacemaker programming.

We investigated the physiologic heart rate (HR) to work rate (WR) relation throughout peak exercise in normal subjects as a guideline for rate-adaptive pacemaker slope programming. The study group consisted of 41 middle-aged subjects (22 men and 19 women) without evidence of cardiopulmonary disease. Peak-exercise stress tests were performed on a calibrated treadmill by using the symptom-limited "ramping incremental treadmill exercise" (RITE) protocol. The HR response, oxygen uptake, and treadmill workload increments were assessed simultaneously. The HR/WR slope, as determined using linear regression analysis, was 0.37 +/- 0.13 beats/min/W for the entire study group, which indicates an upper range increase of 5 beats/10 W increase of external treadmill work performed, using the mean value +/- 1 SD. Men generated an HR/WR slope of 0.32 +/- 0.09 beats/min/W, and women, 0.43 +/- 0.15 beats/min/W, indicating a significant sex-related difference in the HR/WR relation (p < 0.01). Thus, to achieve an appropriate matching of HR with patient effort, rate-adaptive pacemakers should generate an average increase of approximately 5 beats per increase in 10 W of external treadmill work. The HR/WR relation can easily be determined to provide the clinician with a minimal check system to avoid a hyper- or hypochronotropic paced response to exercise.

Adult↗
PubMed1995

[Nodular pulmonary opacities caused by a severe suppurative bronchitis and bronchiectases].

HISTORY AND CLINICAL FINDINGS: A 67-year-old man with chronic obstructive pulmonary disease (COPD) for many years and a heavy smoker was hospitalized because of increasing dyspnoea and moderately productive cough. His general condition was clearly impaired. He was markedly cyanotic, he had a barrel-shaped chest, and there were wheezing rhonchi throughout the lung. Body temperature was 37.8 degrees C. He had mild ankle oedema. The preliminary diagnosis was exacerbation of the COPD with global respiratory failure. TESTS: There was severe hypoxaemia (pO2 48 mm Hg) with hypercapnia (pCO2 46 mm Hg). Vital capacity was reduced to 1.81, one-second forced expiratory volume 0.91. Chest radiograph revealed multiple nodular opacities, such as seen in bronchial carcinoma with metastases. But computed tomography showed fluid-filled bronchi. Bronchoscopy demonstrated large amounts of dirty-white, sticky secretions as high up as the trachea, confirming the preliminary diagnosis. Klebsiella oxytoca and haemophilus influenzae were cultured from the secretions. TREATMENT AND COURSE: Immediate administration of amoxycillin and clavulanic acid (2.2 g daily) quickly led to clinical improvement. Chest x-ray was normalized after 10 days. But long-term oxygen treatment was instituted because of persisting resting hypoxaemia (pO2 46 mm Hg), after which he was discharged free of dyspnoea. CONCLUSION: To clarify nodular pulmonary opacities in a chest radiograph computed tomography should be performed before bronchoscopy.

Aged↗
PubMed1995

[Catheter ablation as an emergency treatment in Wolff-Parkinson-White syndrome with signs of acute infarct].

A 53-year-old man known to have Wolff-Parkinson-White syndrome suffered an acute posterior-wall myocardial infarction. Despite successful thrombolysis treatment with streptokinase he continued to have attacks of supraventricular tachycardia with angina. The ECG showed a short P-R interval and pre-excitation with positive delta waves in leads V1-6, as well as signs of re-infarction. The tachycardias could not be satisfactorily suppressed by drug treatment. Coronary angiography revealed triple vessel disease. During this investigation ventricular extrasystoles occurred which initiated orthodromic supraventricular tachycardia and angina, as well as monophasic S-T elevations in leads II, III and aVF. This provided the indication for immediate high-frequency catheter ablation left laterally at the mitral anulus after a left-lateral accessory conduction pathway had been identified. Three days later the stenoses of the circumflex and anterior interventricular branches were dilated. The patient has been free of symptoms for 3 months and can exercise up to 150 W. The tachycardias have not recurred.

Angina Pectoris↗
PubMed1995

Prospective study of retrograde coronary venography in patients with posteroseptal and left-sided accessory atrioventricular pathways.

The morphologic features of the coronary vein system was prospectively studied with retrograde venography in 117 patients with left-sided (78 patients) and posteroseptal accessory pathway (39). Findings were compared with accessory pathway localization. A mean of 3.3 +/- 1.5 venous branches draining into the coronary sinus or the great cardiac vein could be visualized. The morphologic condition was described and classified. Incidence, morphologic condition, and distribution did not differ between left-sided and posteroseptal accessory pathway. Venous abnormalities including ectasy, diverticulum, narrowing, angulation, and hypoplasia occurred in 22.2%. Diverticulum and narrowing were present in posteroseptal accessory pathway only and always related to the successful ablation site. In patients with left-sided accessory pathway, ectasy, angulation, and hypoplasia were found. Anomalies were less frequent (9% vs 43.6%, p < 0.001) and had no relation to accessory pathway localization. However, the successful ablation site was in 42.3% located < 5 mm to an angiographically visualized venous branch. In conclusion, posteroseptal accessory pathways are often related to coronary sinus abnormalities. In patients with a left-sided accessory pathway venous malformation is uncommon, whereas a close anatomic relation exists between accessory pathway localization and venous ventricular branches.

Adolescent↗
PubMed1995

Randomized comparison of aspirin and phenprocoumon for prevention of right-sided thromboembolic complications associated with transvenous defibrillation leads.

Death due to pulmonary embolism caused by thrombosis formation along a pacing wire has been reported in patients with antibradycardia pacemakers. The purpose of this prospective and randomized study was to evaluate the effects of prophylactically assigned aspirin (100 mg per day) or phenprocoumon (a coumarin derivative) on the incidence of right-sided thromboembolic complications associated with transvenous defibrillation leads. Multiplane transoesophageal echocardiography and pulmonary scintigraphy were performed in 62 consecutive patients immediately and 6 +/- 2 months after transvenous defibrillator implantation. Aspirin or phenprocoumon was administered to the patients in a randomized and parallel manner. By means of multiplane transoesophageal echocardiography and pulmonary scintigraphy no thromboembolic events were observed immediately after transvenous defibrillator implantation. After 6 +/- 2 months, however, multiplane transoesophageal echocardiography disclosed thrombi on the transvenous leads in 13 of 62 patients (21%) despite antithrombotic therapy. At the same time, pulmonary scintigraphy did not reveal any defects compatible with pulmonary embolism. Although thrombi occurred in only four patients treated with phenprocoumon, but in nine patients receiving aspirin, this difference was statistically insignificant. Other variables associated with the occurrence of thrombosis formation were not identified. One fatal intracranial haemorrhage occurred in the phenprocoumon group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The "low intensity treadmill exercise" protocol for appropriate rate adaptive programming of minute ventilation controlled pacemakers.

The objective of rate adaptive pacemakers that measure minute ventilation by transthoracic impedance is to simulate the physiological relationship of the sensed signal to the sinus node response during exercise, thus achieving an appropriate matching of heart rate with patient effort. The purpose of this study was to determine the physiological relationship between heart rate and minute ventilation (HR/VE) during peak exercise testing in order to develop a database for appropriate rate adaptive slope programming of minute ventilation controlled pacemakers. Due to several clinical limitations of peak exercise testing, it was additionally determined whether the 35-watt "low intensity treadmill exercise" (LITE) protocol can be used as a substitute for peak exercise test using the "ramping incremental treadmill exercise" (RITE) protocol in order to assess the correct HR/VE slope below the anaerobic threshold. The stress tests were performed on a treadmill with the collection of breath-by-breath gas exchange. Linear regression analysis was used to determine the HR/VE slope below and above the anaerobic threshold and during the early, dynamic phase of low intensity exercise with the RITE and LITE protocols, respectively. The results of this testing in 41 healthy subjects demonstrated that the HR/VE relationship throughout treadmill exercise using the RITE protocol was not linear but curvilinear in nature, with a steeper HR/VE slope of 1.54 +/- 0.51 below versus 1.15 +/- 0.37 above the anaerobic threshold (P < 0.005). The HR/VE slope determined during the early, dynamic phase of the LITE protocol (1.58 +/- 0.88) did not differ from the HR/VE slope from rest to anaerobic threshold obtained using the peak exercise RITE test (1.54 +/- 0.51; P = 0.79). Rate adaptive pacing should simulate the curvilinear relationship between heart rate and minute ventilation from rest to peak exercise. The HR/VE slope determined during the early, dynamic phase of low intensity exercise represents the HR/VE slope derived from the RITE protocol below the anaerobic threshold. According to the peak exercise database, the slope above anaerobic threshold can easily be calculated as a percentage of the slope below the anaerobic threshold. The LITE protocol can, therefore, be effectively performed as a substitute for peak exercise stress tests to determine the correct pacemaker rate response factor in order to obtain a physiological heart rate to minute ventilation relationship for the appropriate matching of paced heart rate with patient effort.

Anaerobic Threshold↗
PubMed1995

Incidence of ICD lead related complications during long-term follow-up: comparison of epicardial and endocardial electrode systems.

UNLABELLED: The aim of this study was to evaluate the long-term stability of epicardial and endocardial lead systems for third-generation cardioverter defibrillators (ICDs) and to assess the usefulness of diagnostic tools. One hundred forty patients with 61 epicardial (43.6%) and 79 nonthoracotomy systems (56.4%) were followed for 25 +/- 19 months. A total of 18 (12.9%) lead related complications were documented. Complications of epicardial systems were detected in 10 patients (16.4%) during a follow-up time of 36 +/- 8 months: crinkling of patch electrodes in 6 patients (9.8%), insulation breakage of sensing electrodes in 2 patients (3.3%), and adapter defect in 2 patients (3.3%). Eight of the patients (10.1%) with transvenous-subcutaneous systems had lead related complications during a 13 +/- 6 months follow-up: fracture of the subcutaneous patch lead in 2 patients (2.5%), dislodgement of the right ventricular lead in 2 patients (2.5%), dislodgement of the superior vena cava lead in 2 patients (2.5%), insulation breakage of sensing electrodes in 1 patient (1.3%), and connector defect in 1 patient (1.3%). There was no significant difference in the incidence of lead related complications between epicardial and endocardial systems (P > 0.05). Fractures, dislodgements, and crinklings were documented within the first 8 +/- 5 months by regular chest X ray. Defects of insulation, adapter, or connector were detected 22 +/- 10 months after implantation and were associated with delivery of multiple inappropriate ICD therapies. An operative lead revision was indicated for 4 epicardial (6.6%) and 6 endocardial (7.6%) lead systems. CONCLUSIONS: Endocardial lead systems offer a similar long-term stability as compared to epicardial lead systems. Chest X ray is the most useful tool to detect lead fracture, dislodgment, and patch crinkling. Marker recordings or real-time electrograms have not been helpful in this series to identify patients with suspected lead defects prior to the experience of inappropriate ICD discharges.

Alloys↗
PubMed1995

Changes in the amplitude of endocardial electrograms following defibrillator discharge: comparison of two lead systems.

Changes in the amplitude of endocardial electrograms after an unsuccessful shock attempt have been demonstrated to cause failure of redetection of ventricular fibrillation in patients using an integrated sense-pace defibrillating lead system. Thus, the objective of this study was to compare the effects of defibrillator shocks on the amplitude of endocardial electrograms in 26 patients using two different nonthoracotomy systems, a previous lead (model 0062) or a redesigned version (model 0072). At implant, bipolar endocardial electrograms were obtained before each shock application, during initial detection and redetection of ventricular fibrillation in case the applied shock was unsuccessful, and during intervals of 5, 10, 20, 30, 60, and 120 seconds after each shock delivery. No significant difference was noted in endocardial amplitudes between the lead models 0062 and 0072 during baseline sinus rhythm (12.2 +/- 4.6 mV vs 11.4 +/- 3.8 mV), and during initial ventricular fibrillation (7.0 +/- 2.4 mV vs 7.6 +/- 2.3 mV). During redetection of ventricular fibrillation, however, there was a significant difference (P = 0.0006) in endocardial amplitudes (3.4 +/- 1.9 mV vs 6.6 +/- 2.3 mV) between both leads tested. Comparing lead models 0062 and 0072, marked differences were found in endocardial amplitudes during sinus rhythm 5, 10, and 20 seconds after successful arrhythmia termination: 2.8 +/- 1.9 mV vs 8.6 +/- 2.9 mV (P < 0.0001), 4.6 +/- 2.9 mV vs 9.2 +/- 3.2 mV (P = 0.0007), and 6.4 +/- 4.0 mV vs 10.5 +/- 3.6 mV (P = 0.01). At predischarge testing, failure of redetection of ventricular fibrillation was documented in two patients with the lead model 0062 requiring external defibrillation to restore sinus rhythm. These findings demonstrate a significant less postshock attenuation of the endocardial electrogram amplitudes during persistent ventricular fibrillation after an unsuccessful shock attempt as well as during sinus rhythm immediately following an effective shock delivery using the redesigned lead system model 0072 compared to the electrogram amplitudes obtained in patients using the previous lead model 0062.

Adult↗
PubMed1995

Intravenous adenosine during atrioventricular reentrant tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway.

Adenosine is considered to be a safe agent for termination of orthodromic atrioventricular reentrant tachycardia in patients with accessory pathways. A case with initially successful accessory pathway ablation and without preexcitation during sinus rhythm is presented, in which intravenous adenosine (6 mg) during orthodromic tachycardia was followed by atrial fibrillation and sudden onset of preexcitation with subsequent rapid ventricular response with moderate hemodynamic compromise.

Adenosine↗