PubMed Health⌕ Search

Biomedical subjects

A Buob

Publications and source records attributed to A Buob.

5 recordsLinked to original sources

[Anticoagulation in primary prevention of thromboembolism in advanced left ventricular dysfunction].

BACKGROUND: Patients with heart failure have an increased risk for thromboembolic events. In clinical practice the physician is often confronted with the decision to establish a prophylactic anticoagulation. DATA: The incidence for clinical embolization is 1.5 to 3.5% per year. It seems that patients with a lower peak oxygen uptake and with a lower ejection fraction are at higher risk for embolic events. There is no evidence for a correlation of such events with the clinical classification (NYHA) or with the genesis of heart failure. Concerning a prophylactic anticoagulation, the results of the published studies and meta-analyses are inhomogenous with a benefit in some, no difference in others and a significant disadvantage for the patients with anticoagulation in a part of them compared to a non-treated control group. None of these data is established by a prospective, randomized, controlled study with the primary endpoint thromboembolic event in patients with or without anticoagulation. The incidence for a hemorrhage under anticoagulation is 0.6-5.3% per year for life-threatening and 0.04-0.64% for fatal bleeding. CONCLUSION: Because of similar incidences for thromboembolic events and for the bleeding complication of anticoagulation, there is no evidence for a general indication for anticoagulation of patients with heart failure, persistent sinus rhythm and lack of risk factors. In patients with high-grade heart failure (e.g. VO2max < 14 ml/min/kg body weight or left ventricular ejection fraction < 20-30%), who belong to a high-risk population, anticoagulation should be considered and may be acceptable in individual cases.

Anticoagulants↗

[Morphological changes in correlation with so-called idiopathic ventricular tachycardias from the right ventricular outflow tract].

"Idiopathic" ventricular tachycardia is an exclusion diagnosis. The underlying reasons and mechanisms of "idiopathic" ventricular tachycardias are still not completely understood. Recent investigations showed a high prevalence of morphological abnormalities in the right ventricle of patients with "idiopathic" ventricular tachycardia out of the right ventricular outflow tract, which could often be correlated with the origin of the ventricular tachycardia. These described abnormalities were not uniform. Here we report about a patient suffering from drug-refractory "idiopathic" ventricular tachycardia for 10 years. This is the first report in which the origin of an "idiopathic" ventricular tachycardia could be localized by right-ventricular angiography, magnetic resonance tomography and electrophysiological study in the area of an interventricular septal thickening of the right ventricular outflow tract and cured by radiofrequency catheter ablation.

Catheter Ablation↗

[Atrial defibrillators].

The promising results achieved with low-energy, internal atrial cardioversion have stimulated the development of an implantable atrial defibrillator. Initial clinical experience with the Metrix system in a group of highly selected patients with refractory atrial fibrillation (AF) suggests that atrial defibrillation can be performed effectively and safely by using a stand-alone device. The extension of this therapy will depend on the results of further prospective studies comparing this new therapeutic option with other new non-pharmacological methods to treat AF. Internal atrial cardioversion is feasible at low energies with current endocardial transvenous lead configurations primarily designed for ventricular defibrillation. As AF is a frequent arrhythmia in implantable cardioverter defibrillator recipients, the capability for atrial defibrillation has recently been incorporated in a newly designed dual chamber defibrillator (Jewel AF system). Initial clinical experience with this device that combines both detection and treatment in the atrium as well as in the ventricle indicates a significant improvement in the management of patients with both supraventricular and ventricular tachyarrhythmias.

Adult↗

Changes in pulmonary calcitonin gene-related peptide and protein gene product 9.5 innervation in rats infected with Mycoplasma pulmonis.

Changes in the expression of calcitonin gene-related peptide (CGRP) and polyneural protein gene product 9.5 (PGP) in hilar peribronchial innervation was investigated by immunohistochemistry in specific pathogen-free rats chronically infected with Mycoplasma pulmonis. Image analysis of immunostained sections revealed a reduction of approximately 62% in the amount of CGRP- and PGP-immunoreactive innervation of the peribronchial area in the infected animals. The portion of the total bronchial perimeter occupied by bronchus-associated lymphoid tissue was increased six-fold. The decrease in the CGRP-immunoreactive area could be the result either of an enhanced CGRP release or of a loss of nerve fibres. The decrease in the PGP-immunoreactive fibres indicates a degenerative loss of nerves. Increased bronchus-associated lymphoid tissue and decreased bronchial innervation by neurons releasing the immunomodulatory neuropeptide CGRP might both contribute to the pathophysiology and symptoms of mycoplasmosis in the rat.

Animals↗