Quinidine, “pure quinidine,” and hydroquinidine

Weisman, S. A.

doi:10.1016/s0002-8703(42)90971-2

Cited by 11 publications

(2 citation statements)

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“…The fact that it is structurally related to quinidine, led in the past to its being considered as one of the many quinidine salts employed as antiarrhythmic agents; however experimental and clinical studies (Hailey et 1945;Ueda and Makoid, 1979;Ueda et al, 1976;Weisman, 1942) have shown that the kinetics and bioavailability of DQ differ from those of quinidine; some other observations (Balazs et al, 1978;Dietman et al, 1977;Hollander and Besch, 1969) suggest that DQ has a different electrophysiologic action and that in some experimental settings DQ may be even more effective than quinidine (Alexander et Unlike quinidine, which is still widely used worldwide, purified DQ is commercially available in only a few countries. No controlled study of its antiarrhythmic efficacy has been reported to the present and its therapeutic range is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

“…Dihydroquinidine (DQ) is present as an impurity in variable amounts in quinidine preparations (Huynh-Ngoc and Sirois, 1974;Smith et al, 1973). The fact that it is structurally related to quinidine, led in the past to its being considered as one of the many quinidine salts employed as antiarrhythmic agents; however experimental and clinical studies (Hailey et al, 1981;Regazzi-Bonora et al, 1982;Scott el al., 1945;Ueda and Makoid, 1979;Ueda et al, 1976;Weisman, 1942) have shown that the kinetics and bioavailability of DQ differ from those of quinidine; some other observations (Balazs et al, 1978;Dietman et al, 1977;Hollander and Besch, 1969) suggest that DQ has a different electrophysiologic action and that in some experimental settings DQ may be even more effective than quinidine (Alexander et al, 1947;Lewis et al, 1922;Model er al., 1949).…”

Section: Introductionmentioning

confidence: 99%

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Dihydroquinidine versus disopyramide: Efficacy in patients with chronic stable ventricular ectopy

Chimienti

Panciroli

et al. 1984

Clinical Cardiology

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Summary: Dihydroquinidine (DQ) is contained in sub-stantial amounts in quinidine salts, but its direct antiarrhythmic action has not been studied. The efficacy of oral DQ (300 mg t.i.d.) compared to disopyramide (D) (200 mg t.i.d.) was thus investigated using a double-blind crossover placebo-controlled protocol in 12 patients, aged 13 to 67 years, with chronic stable high frequency premature ventricular beats (PVB), defined as > 100 PVB/h during 48-72-h control Holter monitoring. The protocol included three 72-h treatment periods: DQ, D, and placebo at random. On days 2 and 3 of each period a 24-h Holter recording was carried out; drug blood levels were determined at peak (days 2 and 3) and trough time (day 3). No significant difference in the mean PVB/h was found between control (735 +400) and placebo periods complex PVBs were abolished in 3 of 6 patients on both treatments. On day 3, DQ plasma levels were 1.3 1 f0.44 (peak) and 0.92f0.45 (trough) mg/l; D plasma levels were 2.88Ik0.64 (peak) and 2.02Ik0.31 (trough) mg/l; no significant difference was found between day 2 and day 3 samples. Side effects were cutaneous rashes in one patient on DQ and pyrosis in one patient on D. The conclusion is that DQ at the doses used is a very effective and well-tolerated antiarrhythmic agent. In this study it appeared to be superior to average doses of D for suppressing chronic ventricular arrhythmias.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dihydroquinidine versus disopyramide: Efficacy in patients with chronic stable ventricular ectopy

Chimienti

Panciroli

et al. 1984

Clinical Cardiology

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Studies on the Effects of Parenteral Quinidine Administration

Blinder¹

1950

Arch Intern Med

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Pharmacokinetics of dihydroquinidine in congestive heart failure patients after intravenous quinidine administration

Ueda

Dzindzio

1979

Eur J Clin Pharmacol

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The pharmacokinetics of dihydroquinidine were studied in 8 patients with congestive heart failure following a 22 min intravenous infusion of a quinidine preparation that contained 5.9% dihydroquinidine as an impurity. Using a thin layer chromatography-fluorometric assay procedure for dihydroquinidine, the post-infusion plasma dihydroquinidine concentrations declined biexponentially. The half-life of the fast and slow dispositional processes was 4.42 +/- 1.81 min and 6.52 +/- 2.40 h, respectively. The central compartment volume for dihydroquinidine in these patients was 0.44 +/- 0.11 l/kg with an overall apparent volume of distribution of 1.14 +/- 0.38 l/kg. The computed values of total body plasma clearance of dihydroquinidine ranged from 1.29 to 2.69 ml/min/kg with a mean value of 1.94 +/- 0.60 ml/min/kg. In these patients, approximately 16% of the administered dihydroquinidine dose was excreted intact into the urine in 48 h. The estimated value of renal clearance was 0.314 +/- 0.129 ml/min/kg. When compared to control cardiac patients, the data showed that the apparent volume of distribution for dihydroquinidine is smaller in patients with congestive heart failure and as a result of this diminished volume, the clearance rate of dihydroquinidine was slower. The net effect of these differences was the production of higher plasma concentrations of dihydroquinidine in the heart failure group.

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Quinidine, “pure quinidine,” and hydroquinidine

Cited by 11 publications

References 1 publication

Dihydroquinidine versus disopyramide: Efficacy in patients with chronic stable ventricular ectopy

Dihydroquinidine versus disopyramide: Efficacy in patients with chronic stable ventricular ectopy

Studies on the Effects of Parenteral Quinidine Administration

Pharmacokinetics of dihydroquinidine in congestive heart failure patients after intravenous quinidine administration

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