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S Kacet

Publications and source records attributed to S Kacet.

92 records · Page 6Linked to original sources

[Is programmed ventricular stimulation still up to date in the medicinal evaluation of ventricular tachycardia?].

Despite considerable advances in the understanding of cardiac arrhythmia mechanisms, death in relation to ventricular tachyarrhythmias remains an important public health problem, and management of ventricular arrhythmias remains a perpetual challenge in clinical cardiology. In the last decade, the development and refinement of implantable cardioverter defibrillators and the progress in techniques of radiofrequency electrode catheter ablation and antiarrhythmic surgery have been revolutionary in the management of ventricular tachycardia. On the other hand, there have been major changes in the use of drug therapy since the publication of the results of the CAST study. Inclusion of mortality as an endpoint in clinical trials highlights the fact that some antiarrhythmic drugs may have the proclivity to exert fatal proarrhythmic reactions while also having the potential to control recurrences of ventricular tachycardia. All these changes that now need to be integrated into global approaches for ventricular arrhythmia control led us to wonder whether serial testing is still up to date in the management of ventricular tachycardia. After more than 20 years of clinical use, there is much concern about the use of serial drug testing to guide antiarrhythmic drug therapy for the management of life-threatening sustained ventricular tachyarrhythmias in light of recent advances in the management of cardiac arrhythmias. The purpose of this article is to discuss, within a relatively brief compass, the cumulative data from different lines of investigations, results of randomized clinical trials, recently acquired beliefs and meta-analytic findings concerning the present place of serial electrophysiologic drug testing in the management of ventricular tachycardia.

Anti-Arrhythmia Agents↗

[Protein C deficiency and vascular thromboses. Apropos of 2 cases and a review of the literature].

Protein C, a physiological inhibitor of coagulation, acts by inactivating coagulation factors V and VIII. It was identified 20 years ago and purified 10 years later. Its anticoagulant properties have been confirmed by the demonstration of thromboembolic diseases associated with constitutional protein C deficiency. Deficiency is defined as a less than 65 p. 100 level of the protein. There is no correlation between protein C level and clinical severity. Constitutional protein C deficiency is transmitted as an autosomal dominant trait. The protein C level observed in homozygous deficiency is about 50 p. 100, more often quantitative (type I) than qualitative (type II), the other coagulation factors being present at normal levels. Protein C deficiency is responsible for recurrent and familial thromboembolic necrosis and for cutaneous necrosis during treatment with antivitamin K drugs. Protein C assays must now be part of the aetiological evaluation of thromboembolic disease. Physiological variations in protein C levels have been encountered in neonates and pregnant women as well as in some pathological conditions, after surgery or under certain treatments. Familial inquiries are essential to detect asymptomatic protein C deficient subjects. Treatment rests on anticoagulants: antivitamin K drugs after effective heparinization in thromboembolic accidents, prevention of accidents by heparin in protein C deficient subjects and when a risk of thromboembolic disease is present. We report here one case of venous thrombosis and one case of arterial thrombosis, both being characterized by the finding of protein C deficiency during full evaluation of haemostasis factors.

Adult↗