Background-The tachycardia detection interval (TDI) in implantable cardioverter/defibrillators (ICDs) is conventionally programmed according to the slowest documented ventricular tachycardia (VT), with a safety margin of 30 to 60 ms. With this margin, VTs above the TDI may occur. However, longer TDIs are associated with an increased risk of inappropriate therapy. We hypothesized that patients with slow VTs (Ͻ200 bpm) may benefit from a long TDI and a dual-chamber detection algorithm compared with a conventionally programmed single-chamber ICD. Methods and Results-Patients with VTs Ͻ200 bpm were implanted with a dual-chamber ICD that was randomly programmed to a dual-chamber algorithm and a TDI of Ն469 ms or to a single-chamber algorithm with a TDI 30 to 60 ms above the slowest documented VT cycle length and the enhancement criteria of cycle length variation and acceleration. The primary combined end point was the number of all inappropriate therapies, VTs above the TDI, and VTs with significant therapy delay (Ͼ2 minutes). After 6 months, a crossover analysis was performed. Total follow-up was 1 year. One hundred two patients were included in the study. The programmed TDI was 500Ϯ36 ms during the dual-chamber phase and 424Ϯ63 ms during the single-chamber phase. For the primary end point (inappropriate therapies, VTs above the TDI, or VTs with detection delay), a moderate superiority of the dual-chamber mode was found: Mann-Whitney estimatorϭ0.6661; 95% CI, 0.5565 to 0.7758; Pϭ0.0040. Conclusions-Dual-chamber detection with a longer TDI improves VT detection and does not increase the rate of inappropriate therapies despite a considerable increase in tachycardia burden.
IN A REVIEW of the current concepts of metabolism of anaesthetic agents by Greene, it is conspicuous that many of these drugs depend on the integrity of liver function for their detoxifieation. 1 For this reason, multiple hepatic enzyme systems have been repeatedly studied with each agent as it is introduced into experimental and clinical practice.Conney and his co-workers 2-~ have shown that "pretreatment" of rats with phenobarbital shortened the sleeping time produced by thiopental, hexobarbital, and pentobarbital. Other anaesthetic drugs which have been studied include morphine, meperidine HC1, urethane, codeine, gluthetimide, nitrous oxide, methoxyflurane, and carbromal.By direct methods, a quantitative increase in the liver microsomal enzyme activity has been demonstrated to be the responsible accelerating factor of the drugs' disposition. 8,5,6 Conversely, a prolonged effect can be attained by the previous adminislzation of compounds that would have an inhibiting action on the same enzyme systems. 7This study was intended to determine whether similar stimulating and inhibiting mechanisms would int/uence the sleeping times of rats receiving more recently introduced anaesthetics such as gamma hydroxybutyrate, 2-orthochlorophenyl, 2-methylaminocydohexanone (ci-581), and diazepam. To correlate our findings with previous reports, thiopental, pentobarbital, and the centrally acting muscle relaxant zoxazolamine were also tested. MATEt~ALS AND METHODSNineteen groups of ten rats each were divided into three allotments. Male albino Sprague-Dawley rats four to six weeks old and weighing 50 to 60 gm were used for all the studies. Intraperitoneal injections were given in the lower half of the abdomen in a dose corresponding to each animal's weight. The onset and duration of sleep were timed by the disappearance and return of the "righting reflex" (ability to turn spontaneously to the "on quarters" position when placed on the back). Animals that failed to show signs of anaesthesia were eliminated from the study.The sleep-time periods in minutes were added and mean-limes and standard devia6ons calculated. Statistical analysis of the results was conducted by the Student t-test.
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