Search PubMed⌕ Search

Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 163 records · Page 9Linked to original sources
PubMed1998

Left atrial appendage function after internal atrial defibrillation.

To determine the value of echocardiographic parameters for predicting maintenance of sinus rhythm after internal atrial defibrillation (IAD), transthoracic and transesophageal echocardiography were performed in 38 patients with atrial fibrillation (AF) before IAD. In addition, serial echocardiographic examinations were performed at 1, 7, and 28 days after IAD in 20 patients to assess the effect of IAD on echocardiographic markers of thromboembolic risk. AF had recurred in 49% of patients within 6 months following IAD. Left atrial chamber and appendage size and ejection fraction were not predictive of recurrence of atrial fibrillation. However, peak emptying velocities of the left atrial appendage were significantly lower in patients with recurrence of atrial fibrillation as compared with patients who had maintained sinus rhythm (0.26 +/- 0.1 m/sec vs 0.49 +/- 0.17 m/sec; P = 0.001). A peak emptying velocity < 0.36 m/sec had a sensitivity of 82% and specificity of 83% for predicting the recurrence of AF. Peak A wave velocities increased gradually after cardioversion from 0.47 +/- 0.16 m/sec at 24 hours to 0.61 +/- 0.13 m/sec after 7 days (P < 0.05). One patient developed a new thrombus in the left atrial appendage and another patient suffered a thromboembolic event after IAD. Assessment of left atrial appendage function adds information regarding the probability of maintaining sinus rhythm after the procedure and the need for anticoagulation therapy with IAD.

Anticoagulants↗
PubMed1998

Radiofrequency ablation of atrial flutter.

Atrial flutter can be understood as atrial tachycardia due to a single intra-atrial macroreentrant circuit that is determined by fixed or functional boundaries. In various types of atrial flutter, radiofrequency ablation has become an established curative therapy. During the course of an ablation procedure, five steps can be distinguished: (1) determination of the reentrant circuit; (2) identification of the boundaries; (3) proof of the participation of an isthmus between the boundaries in the reentrant circuit; (4) connection of the barriers by a linear lesion; and (5) proof that the line of block is complete. After establishing these five steps, the acute and long-term results of atrial flutter ablation are comparable to those of other supraventricular tachycardias. In this review, we discuss these principles of atrial flutter ablation with an emphasis on typical atrial flutter.

Atrial Flutter↗
PubMed1998

Quality of life in patients with atrial fibrillation.

INTRODUCTION: The efficacy of a treatment is based primarily on objective criteria such as mortality and morbidity. Besides these criteria, the interest in measuring quality of life in relation to health care has increased in recent years. METHODS AND RESULTS: Although the concept of quality of life inherently is subjective and definitions vary, it generally is agreed that quality of life is a multidimensional construct. The impact of atrial fibrillation (AF) on quality of life has not been evaluated widely using validated methods. Therefore, an international prospective study was designed to assess quality of life over time in patients with AF using validated generic measures and specific conducted disease scales. In addition to a standard demographic questionnaire, patients will complete two predictive scales at baseline and four outcome scales at baseline, and 3-, 6-, and 12-month follow-up. An AF severity score based on subjective and physician-recorded assessments will be used to classify the patient's burden of AF as mild, moderate, or severe. CONCLUSION: Rigorous yet practical approaches are needed to allow for a comprehensive understanding of quality of life in patients with AF. The international study design outlined in this review article represents an attempt to systematically address quality of life in patients with AF and may serve as an example of the types of measures that may be useful in assessing quality of life in patients with AF.

Animals↗
PubMed1998

Specific considerations with the automatic implantable atrial defibrillator.

INTRODUCTION: Internal atrial defibrillation has been evaluated as an alternative approach to the external technique for more than two decades. Previous studies in animals and humans have shown that internal atrial defibrillation is feasible with relatively low energies. The promising results achieved with internal atrial defibrillation have facilitated the development of an implantable atrial defibrillator (IAD). METHODS AND RESULTS: For any new therapy, it is imperative to demonstrate safety, efficacy, tolerability with improvement in quality of life, and cost-effectiveness compared with therapeutic options already available. Maintenance of sinus rhythm or prolonged duration in arrhythmia-free intervals should be demonstrated clearly with an IAD. Initial clinical experience with the Metrix system indicates stable atrial defibrillation thresholds, appropriate R wave synchronization markers, no shock-induced ventricular proarrhythmia, and excellent detection of atrial fibrillation (AF) with a specificity of 100%. Ventricular proarrhythmia has not been reported for correctly R wave synchronized low-energy shocks when closely coupled to RR intervals, and long-short cycles are avoided. CONCLUSION: Preliminary experience with the Metrix system suggests that the IAD may offer a therapeutic alternative for a subgroup of patients with drug-refractory, symptomatic, long-lasting, and infrequent episodes of AF. Further efforts must be undertaken to reduce the patient discomfort associated with internal atrial defibrillation in an attempt to make this new therapy acceptable to a larger patient population with AF.

Algorithms↗
PubMed1997

[Catheter ablation and implantable atrial defibrillators in supraventricular cardiac arrhythmias].

Non-pharmacological tools for treatment of supraventricular tachycardias include radiofrequency catheter ablation, antiarrhythmic surgery, and electrical therapies. Radiofrequency catheter ablation is the first choice in the treatment of symptomatic patients with AV nodal reentrant tachycardias and atrioventricular reentrant tachycardias because of its high success rate and its low complication rate. Furthermore, transvenous radiofrequency catheter ablation may be considered as a curative approach in patients with atrial flutter and in patients with ectopic atrial tachycardias. Whereas the application of radiofrequency catheter ablation for the curative treatment of atrial fibrillation is still experimental, palliative therapy modalities such as AV nodal modification or AV nodal ablation may be performed in patients with drug refractory atrial fibrillation with rapid ventricular response. The recurrence rate of atrial fibrillation is in the range of 40 to 60% within a year despite antiarrhythmic drug treatment. Internal atrial fibrillation is a safe and effective method for acute termination of atrial fibrillation, especially after unsuccessful external cardioversion. The electrotherapy with the implantable atrial defibrillator should be considered as an alternative approach in patients with symptomatic, long lasting, and drug refractory episodes of atrial fibrillation. This innovative electrotherapeutic tool is currently under clinical evaluation. For the selection of the most appropriate therapy, the risk-benefit-ratio has to be taken into account in each individual patient.

Catheter Ablation↗
PubMed1997

[Septic myocardial aneurysm in mitral valve endocarditis. Clinical and pathological-anatomical findings].

HISTORY AND CLINICAL FINDINGS: A 68-year-old woman was hospitalized because of fever and tiredness for 3 months. Her general condition was clearly impaired. She had a mild fever of 38.5 degrees C and on auscultation a 3/6 systolic murmur, maximal parasternally in the 3rd intercostal space, transmitted to the apex. There were distant râles over both lungs, the neck veins were distended and there was ankle oedema. INVESTIGATIONS: C-reactive protein was raised to 17.3 mg/dl (normal up to 0.9 mg/dl), WBC count 19,300/microliter. beta-haemolysing streptococcus (S. agalactiae) was grown in the blood culture. The ECG showed sinus tachycardia (rate of 98/min) and transthoracic echocardiography demonstrated a small pericardial, enlarged ventricles, marked mitral regurgitation and a large vegetation on the posterior mitral leaflet, as well as a 3 x 4 cm mass in the posterior wall of the ventricle, originating from the posterior mitral valve ring and communicating with the vegetation on the mitral valve. The posterior mitral leaflet was perforated. TREATMENT AND COURSE: As endocarditis of the mitral valve with a complicated course was suspected-abscess of the posterior mitral valve ring and septic myocardial aneurysm with associated pericarditis and haemodynamically insignificant effusion-she was transferred to the intensive care unit where she died suddenly of circulatory arrest only 30 min after transfer. Autopsy confirmed the echocardiographic findings. CONCLUSION: Paravalvular abscess in the course of mitral valve endocarditis is rare, but should be looked for at transthoracic echocardiography so that any necessary surgical intervention can be undertaken early.

Aged↗
PubMed1997

N-acetylcysteine attenuates nitroglycerin tolerance in patients with angina pectoris and normal left ventricular function.

The aim of this study was to assess whether N-acetylcysteine (NAC) is able to prevent tolerance to a 48-hour infusion of nitroglycerin (NTG) in the setting of normal left ventricular function. In 16 patients, the hemodynamic response to 0.8 mg sublingual (s.l.) NTG was assessed by measuring mean arterial, pulmonary artery, pulmonary capillary wedge and right atrial pressures, cardiac output, and calculation of the systemic and pulmonary vascular resistances. The parameters were obtained at baseline and 1 to 10 minutes after the s.l. NTG application (day 1). NTG was started at 1.5 microg/kg/min; concomitantly, a bolus of 2,000 mg of NAC was administered, followed by an infusion of 5 mg/kg/hour. Both infusions were continued for 48 hours, and the hemodynamic study was repeated (day 3). The same measurements were obtained in a matched control group of 15 patients with NTG infusion alone. Plasma renin activity, aldosterone, and norepinephrine were measured before and after the infusion period. The first s.l. NTG infusion (day 1) caused a significant decrease in mean arterial (p <0.01), pulmonary artery (p <0.001), and right atrial pressures (p <0.001), and in systemic (p <0.01) and pulmonary vascular resistances (p <0.001) in both groups. After the 48-hour infusion (day 3), there was a total loss of nitrate-mediated vasodilation (pressure values and vascular resistances day 3 > day 1) in 5 of 16 patients (NAC nonresponders), whereas in the other 11 of 16 patients (NAC responders), there was significant vasodilation throughout the infusion period. Tolerance had developed in 14 of 15 patients with NTG infusion alone. The same difference (responder vs nonresponder vs NTG alone) held true regarding the response to the second s.l. NTG infusion after 48 hours. The neurohormonal counter-regulation and intravascular volume expansion (increase in plasma renin activity, p <0.001, and norepinephrine, p <0.05; decrease in aldosterone, p <0.01) did not differ between responders and nonresponders. We conclude that NAC attenuates tolerance development to a continuous NTG infusion in a specific patient subgroup and that this occurs despite the same amount of neurohormonal counter-regulation and intravascular volume expansion compared with patients with tolerance development.

Acetylcysteine↗
PubMed1997

Association between hemodynamic parameters and the degeneration of sustained ventricular tachycardias into ventricular fibrillation in rats.

UNLABELLED: Sustained ventricular tachycardias (VT) often degenerate into ventricular fibrillation (VF). In the present study, the impact of VT on mean arterial blood pressure (MAP), myocardial blood flow (MBF), and myocardial oxygen consumption (MVCO2) was assessed. In addition, the degeneration of sustained VT into VF was analysed with respect to MAP. MBF was measured in 48 anesthetized rats with colored microspheres; arterial catecholamine levels were measured by HPLC in 16 additional rats during control conditions and VT. MBF (4. 66+/-1.29 ml/g/min; mean+/-s.d.) did not change with the onset of VT (5.37+/-1.92 ml/g/min, n.s.). Epinephrine (0.22+/-0.13 ng/ml) and norepinephrine (0.37+/-0.12 ng/ml) increased during VT (3.55+/-2.68 ng/ml, P<0.01; 0.88+/-0.44 ng/ml, P<0.05), respectively. VF was more frequent when MAP remained normal (MAP>80 mmHg: 26%) than with hypotension (MAP<80 mmHg: 2%, P<0.05). Mechanical failure was observed in 10% of rats with severe hypotension (MAP<60 mmHg), and 2% with moderate hypotension (MAP 60-80 mmHg). The endo-epicardial MBF ratio in the VF group was significantly lower than that in the non-VF group (0.94+/-0.17 v 1.11+/-0.24, P<0.05). CONCLUSIONS: severe hypotension predisposes to the occurrence of acute mechanical failure during VT; moderate hypotension during VT, however, serves as a protective mechanism against VF in structurally normal hearts. Subendocardial hypoperfusion in the presence of an increased energy demand during VT is suggested to be responsible for the initiation of VF.

Animals↗
PubMed1997

[Effect of magnesium on sustained ventricular tachycardia].

Intravenous application of magnesium was suggested for the management of persistent ventricular tachycardia. In patients with torsade de pointes tachycardia the injection of magnesium controlled the life threatening arrhythmias reliably, thus magnesium became the treatment of choice in this setting. The results in patients with persistent monomorphic ventricular tachycardia are controversial. In one study, ventricular tachycardias could be controlled in 8 of 10 patients by 2,000 mg magnesium sulfate. In a randomized trial with 43 patients, termination of the ventricular tachycardia could be accomplished in 6 of 20 patients under the influence of 4,000 mg magnesium sulfate, whereas 3 of 24 patients exhibited termination of the tachycardia following placebo; the difference did not reach statistical significance. In our study 4 patients with torsade de pointes tachycardia could be controlled by the application of magnesium glutamate (2 x 1,000 mg intravenously). Of 25 patients with persistent monomorphic ventricular tachycardia, the arrhythmia ended in 8 patients under the influence of magnesium. No significant change of the RR intervals and the QRS duration during ventricular tachycardia could be demonstrated following magnesium injection. Cardiac index during ventricular tachycardia increased from 2.0 +/- 0.6 l/min x m2 to 2.5 +/- 0.1 l/min x m2 (p < 0.05). In a further investigation the dose of magnesium was increased to 2 x 9 mmol. To detect possible interactions with antiarrhythmic agent, 10 patients under chronic antiarrhythmic therapy with class-III-agents were compared with 10 patients without such treatment. Plasma levels of magnesium increased from 0.79 +/- 0.1 mmol/l to 1.87 +/- 0.5 mmol/l. In 5 of the 20 patients ventricular tachycardia ended under the influence of magnesium: 2 patients were on chronic antiarrhythmic agents, whereas 3 had no chronic therapy. There were no significant differences in the RR intervals and the duration of the monophasic action potentials during the ventricular tachycardia under the influence of magnesium. These data indicate that the bolus therapy of magnesium controls persistent monomorphic ventricular tachycardia in a minority of patients only. Therefore, magnesium injection cannot be recommended for treatment of monomorphic ventricular tachycardia in the emergency setting. On the other hand, magnesium application can be considered the therapy of choice for patients with torsade de pointes tachycardia.

Dose-Response Relationship, Drug↗
PubMed1997

[Progressive cerebral parenchyma damage caused by recurrent arterial hypotension].

To date clinical and experimental investigations have focused on acute strokes and complete infarctions. Histological and immunological staining in animal experiments and improved imaging techniques in patients suggest that selective or incomplete infarction is a common pathomechanism. Incomplete infarction can manifest as laminar necrosis at autopsy and as leukoaraiosis in imaging studies. An important mechanism in the genesis of leukoaraiosis is vascular pathology of the long penetrating arteries of the deep white matter combined with episodes of decreased perfusion pressure or hypotension. We demonstrate that the cumulative effect of repetitive, moderate hypotensive episodes on cognitive performance or cerebral tissue has not been adequately studied and appreciated.

Animals↗
PubMed1997

[10 years radiofrequency ablation of accessory conduction pathways].

Catheter ablation of the preexcitation syndrome is a curative treatment. Accessory pathways between structures of the specific conduction system or working myocardium are morphologic prerequisites for orthodromic or antidromic reentrant tachycardia of various frequency, duration, and rate. Detection of mechanisms of tachyarrhythmias and understanding the role of accessory pathways in tachycardia, mapping of accessory connections, function of nodal conduction system, and additional accessory pathways are necessary for successful catheter ablation. Anomalies of the tricuspid valve and coronary sinus and concomitant disease of the heart should be investigated prior to catheter ablation using echocardiography and contrast injection. Different variations of the preexcitation syndrome and the results of catheter ablation in 300 patients are demonstrated. Catheter ablation is indicated in refractory tachyarrhythmias on the basis of accessory pathways. The treatment is performed in a catheterization laboratory by two highly experienced cardiologists in the field of electrophysiology after training in 100 procedures. The investigators need experience in interventional treatment of coronary artery disease, in transseptal puncture, and in the management of complications (coronary and valvular problems, thromboemboly, and pericardial drainage). Catheterization needs careful protection of radiation. An ablation is possible at an atrial or ventricular insertion site of the accessory pathway or in between. Ablation is done during sinus rhythm, atrial stimulation, antidromic reentry, or atrial fibrillation or during ventricular pacing and orthodromic tachycardia. The procedure should end with bidirectional block of the accessory pathway in 90-95% of the patients. Complications occur in 2-4% of procedures. Recovery of accessory conduction is observed in 8%. Catheter ablation of the accessory pathway is the treatment of first choice in symptomatic patients with the pre-excitation syndrome. The procedure has limited risks and a high success rate.

Cardiac Pacing, Artificial↗
PubMed1997

[Decreased apoptosis as a pathogenic factor in intimal hyperplasia of human arteriosclerosis lesions].

Restenosis remains a persistent problem following intravascular reconstruction. Smooth muscle cell proliferation, extracellular matrix production and remodeling are accepted mechanisms of restenotic lesion formation. Decreased programmed cell death (apoptosis) may also contribute to restenosis by prolonging the life span of intimal cells, with their subsequent accumulation and development of hyperplastic lesions. The objectives of the present study were as follows: i) to identify cell death, ii) to distinguish and quantify apoptosis from necrosis, and iii) to compare restenotic with primary lesions. To this end, human atherectomy specimens from 25 primary and 14 restenotic coronary and peripheral lesions were studied by TUNEL test (TdT-mediated dUTP Nick End Labeling; detection of cell death by the presence of fragmented DNA), transmission electron microscopy and morphometric analysis. Intimal hyperplasia was more consistent with restenosis than with primary lesion origin, and was mainly attributed to increased smooth muscle cell density (649 vs. 219 cells/mm2; p < 0.001). The main finding of the present study is that hypercellular restenotic tissue contains fewer TUNEL+ cells than hypocellular plaques (14% vs. 27%; p < 0.05). Most importantly, ultrastructural evaluation revealed a markedly reduced portion of intimal plaque cells, especially smooth muscle cells exhibiting distinct morphologic signs of apoptosis (3% vs. 13%; p < 0.001). In contrast, incidence of necroses did not differ between both lesion types (0.13 vs. 0.12 necroses/ cell; p = 0.49). Thus, our data indicate apoptosis and not necrosis to be the crucial cell death form to account for the apparent discrepancy found in both lesion types with reduced apoptosis in cell-rich restenoses. The findings of the present study suggest that decreased apoptosis is an important regulatory mechanism ultimately leading to intimal hyperplasia as commonly found in human restenosis post angioplasty.

Aged↗