N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide. Initial evaluation with an intravenous infusion of NAPA indicated a favorable antiarrhythmic response. The QTC interval was prolonged, but the 2.4 ms/microgram per ml incremental QTC interval lengthening caused by NAPA was not greater than usual. During subsequent oral therapy with NAPA, torsade de pointes developed at plasma levels of this drug that appeared to be well tolerated during the initial evaluation.
Ten patients with chronic premature ventricular contractions (PVCs) received short-term oral therapy with N-acetylprocainamide (NAPA) to determine its antiarrhythmic efficacy and side effects under the conditions of a placebo-controlled, dose-ranging trial. NAPA was effective in suppressing PVCs in 8 patients but caused a paradoxical increase in PVC frequency in one. Results were equivocal in the remaining patient because PVCs did not recur when NAPA therapy was withdrawn. Mean NAPA plasma levels as high as 41.1 microng/ml did not have untoward hypotensive or myocardial depressant effects, as judged by electrocardiographic and systolic time intervals. There was, in fact, a consistent reduction in PEP/LVET ratio, indicating that NAPA increases the force of myocardial contraction. The mean NAPA elimination half-life of 10.9 hr was longer than the 6.2 hr half-life reported for normal subjects, but its prolongation was predictably correlated with reductions in creatinine clearance. Gastrointestinal side effects experienced by 3 patients and insomnia noted by 2 patients are similar to known adverse reactions to procainamide.
T h i s paper p r e s e n t s t h e r e s u l t s of a s t u d y designed t o i n v e s t i g a t e t h e e f f e c t s o f s u b t r a c t i v e -t y p e n o i s e r e d u c t i o n a l g o r i t h m s on LPC based s p e c t r a l paramet e r e s t i m a t i o n as r e l a t e d t o t h e p e r f o rmance of speech p r o c e s s o r s o p e r a t i n g w i t h i n p u t SNRs o f 1 5 d8. and b e l o w . S u b t r a ct i v e n o i s e p r e -p r o c e s s i n g g r e a t l y i mp r o v e s t h e S N R b u t system performance improvement i s n o t commensurate. LPC s p e c t r a l e s t i m a t i o n i s a f f e c t e d by t h e c h a r a c t e r o f t h e r e s i d u a l n o i s e which e x h i b i t s g r e a t e r v a r i a n c e and s p e c t r a l g r a n u l a r i t y t h a n t h e o r i g i n a l broadband n o i s e . The s t u d y shows t h a t removing l e s s t h a n t h e f u l l amount o f n o i s e and w h i t e ni n g i t improve s p e c t r a l e s t i m a t i o n and speech d e v i c e performance. Techniques and Derformance r e s u l t s a r e p r e s e n t e d . 1. I n t r o d u c t i o n The performance o f most speech r e c o g n i t i o n and p a r a m e t r i c speech c o d i n g systems b e g i n s t o s u f f e r a t s i g n a l -t on o i s e r a t i o s o f 1 5 de. and below. N o i s e i n t e r f e r e s w i t h t h e a c c u r a t e e x t r a c t i o n and m o d e l i n g o f speech s p e c t r a l and t e m p o r a l f e a t u r e s n e c e s s a r y f o r a c c u r a t e r e c o g n i t i o n and c o d i n g . P a r t i c u l a r l y a f f e c t e d a r e p i t c h e x t r a c t i o n , spectrum and f o r m a n t e s t i m a t i o n , and word boundary d e t e c t i o n a l g o r i t h m s . P a t t e r n m a t c h i n g systems s u c h as speech r e c o g n i z e r s and VQ based c o d e r s t e n d t o be a d v e r s e l y a f f e c -. t e d because t h e i n p u t speech f e a t u r e v e c t o r p a t t e r n s a r e supposed t o c o r r e spond w i t h t h e s t o r e d t e m p l a t e s g e n e r a t e d under non-noisy c o n d i t i o n s . Performance g e n e r a l l y i s h i g h l y c o r r e l a t e d w i t h i n p u t SNR a t r a t i o s o f 1 5 d8. and below and u s u a l l y degrades p r e c i p i t o u s l y . I t s t a n d s t o reason t h a t i m p r o v i n g t h e SNR o f t h e i n p u t speech t o p a r a m e t r i c sDeech p r o c e s s o r s by means o f some n o i s e r e d u c t i o n p r e p r o c e s s o r s h o u l d improve d e v i c e performance. V a r i o u s c l a s s e s o f n o i s e r e d u c t i o n a l g o r i t h m s have been developed and implemented o v e r t h e y e a r s w i t h some success. One such c l a s s i s t h e s o e c t r a l / c e p s t r a l s u b t r a c t i o n t e c h n i q u e s and t h e i r v a r i a n t s . I t has been demons t r a t e d [ 1 . 2 , 3 . 4 ] t h a t s u b t r a c t i v e -t y p e broadband n o i s e r e d u c t i o n t e c h n i q u e s can s u b s t a n t i a l l y improve t h e SNR of n o i s y speech and t...
The effects of long-term NAPA therapy were evaluated in 6 patients with chronic PVCs known to respond to this drug during a previous placebo-controlled, dose-ranging trial. Underlying cardiac status was evaluated every six months by switching each patient from NAPA to placebo. Placebo period PVC frequency after one year of NAPA therapy was reduced, compared to baseline placebo values. Mean PEP/LVET, measured while the patients received placebo, was elevated at the beginning of the study but was normal after one year of NAPA therapy. Comparison of NAPA and placebo period observations indicated a reduction in PEP/LVET when NAPA therapy was begun. This effect, however, could not be demonstrated one year later when mean placebo period PEP/LVET was normal. The apparent dependence of this effect on underlying status of left ventricular function suggests that the initial reduction in PEP/LVET represents an an indirect effect of NAPA rather than a direct inotropic action. NAPA therapy was well tolerated by the 6 patients and ANA titers became abnormal in only one, in marked contrast to reported experience with procainamide.
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