[Differential diagnosis of idiopathic ventricular fibrillation].
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Biomedical subjects
Publications and source records attributed to S Siaplaouras.
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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.
"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.
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.
This study was designed to assess the effect of neutrophil inhibitory factor (NIF), a novel specific inhibitor of CD11b/CD18 on hepatic leukocyte trafficking by intravital microscopy 5 h after hemorrhagic shock. Anesthetized rats were instrumented for invasive hemodynamical monitoring. Hemorrhagic shock was induced for 60 min by withdrawal of arterial blood (mean arterial blood pressure = 40 mmHg). Rats were adequately resuscitated for 5 h to achieve a mean arterial blood pressure > 100 mmHg and were randomly assigned to blinded treatment with NIF or placebo control protein administered as a single intravenous bolus (10 mg/kg) at the time of resuscitation. Intrahepatic leukocyte adhesion was evaluated by in vivo fluorescence microscopy. There were no significant differences observed in hemodynamic parameters between the shock groups throughout the study, however, NIF significantly reduced firm leukocyte adhesion in liver sinusoids. The results suggest that NIF may be beneficial in the attenuation of the pathological shock-induced leukocyte adhesion.