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Comparison of two different loading doses of digoxin in severe renal impairment.

The correct loading dose of digoxin in patients with advanced renal failure is still a matter of discussion. The effects has been studied of loading doses of digoxin 0.625 mg or 1.25 mg given over 48 h according to randomized crossover design to healthy volunteers and to two different groups of patients with renal impairment and the same mean endogenous creatinine clearance of about 15 ml/min. The subsequent maintenance dose for 4 days was digoxin 0.25 mg in the volunteers and 0.125 mg in both groups of patients. The minimum plasma digoxin concentrations before each dose was measured by radioimmunoassay and the plasma levels in the different groups have been compared. In the healthy volunteers no significant difference was found during the study, despite wide variation in the plasma digoxin concentration. In contrast, in patients with renal failure, the group with the higher loading dose showed significantly higher plasma concentrations 24, 36 and 48 h after drug administration, reaching the highest mean value of 2.2 ng/ml at 48 h. However, after 120 h of maintenance therapy a mean digoxin concentration of 1.3 ng/ml was found in both groups. Thus, despite different loading doses identical plasma concentrations were reached during administration of the same maintenance therapy. The higher plasma digoxin concentration obtained during administration of a higher loading dose might be the cause of arrythmias in individual patients.

Adult↗

The pharmacokinetics of digoxin in newborn and adult sheep.

The pharmacokinetics of digoxin were determined in 12 ewes and 13 newborn sheep after bolus drug administration and under steady state drug conditions. After death, tissue distribution of digoxin was determined and normalized to plasma drug concentrations at steady state. Volume of distribution and total drug clearance were lower at steady state than the comparable variables calculated from bolus drug administration. No significant difference between ewes and newborns was shown for drug distribution half-life (0.72 vs. 0.76 hr), drug elimination half-life (15.2 vs. 13.7), or renal drug clearance (0.86 vs. 0.89 liters/kg/hr). Total drug clearance as well as the area derived and steady state volumes of distribution were higher in newborns than in ewes. Digoxin secretion into the urine was limited in newborns, as evidenced by a lower renal digoxin clearance to creatinine clearance ratio in newborns than in ewes (371 vs. 600%). The plasma concentration of digoxin at steady state correlated well with myocardial drug concentrations. Drug distribution was similar in both age groups; however, the tissue to plasma digoxin ratio in kidney was higher in newborns than in ewes (mean 469 vs. 263, respectively). Although age-related differences in drug clearance and distribution volume existed, intersubject variation was substantial, and the demonstrated variations were not large enough to account for the high doses of digoxin used to treat congestive heart failure in immature subjects.

Animals↗

Plasma digoxin levels in anuric patients and normal subjects taking digitoxin.

Plasma digoxin suspected to be elevated in anuric patients taking digitoxin was determined by radioimmunoassay in 15 anuric patients and 15 normal persons subjected to 0.1 mg digitoxin therapy per day. All plasma digoxin values from the anuric patients and the normal subjects were far below the lower limit of the therapeutic range of plasma digoxin. There existed no difference between the digoxin values determined in anuric patients and subjects with normal renal function; in both groups there was a scatter of digoxin values about the cross reaction line between digitoxin and digoxin antibody. It is concluded from the results that digoxin retention in anuric patients taking digitoxin plays an insignificant role; thus, the pharmacological effect is mediated by digitoxin itself.

Anuria↗

The digoxin-amiodarone interaction.

To assess the cause of the digoxin-amiodarone interaction, the systemic availability and renal excretion of digoxin were examined in 10 patients. Patients were studied before and after 1 week and 6 weeks of concurrent amiodarone therapy, and four were also studied after 4-8 months. Mean (+/- SD) peak plasma digoxin concentration rose from 1.55 +/- 0.6 microgram /1 prior to amiodarone therapy to 2.85 +/- 1.3 micrograms/1 after 1 week of combined therapy (p less than 0.01). Mean AUC also rose from 7.2 +/- 2.1 micrograms/1.h to 12.1 +/- 6.4 micrograms/1.h (p less than 0.01) during this period. Mean peak plasma digoxin concentration and AUC remained elevated after 6 weeks and, in the patients studied, at 4-8 months. Mean urinary digoxin clearance remained unchanged. Plasma amiodarone and desethylamiodarone concentrations were consistent with the prescribed doses. This study confirmed previous findings of raised plasma digoxin concentrations following the addition of amiodarone. It has also shown that this interaction is sustained for at least several months. The cause has not been fully elucidated but does not appear to be due to a change in the renal clearance of digoxin.

Aged↗

Digoxin and xamoterol in patients with moderate chronic heart failure. A double-blind, randomized, controlled study.

Xamoterol is a partial beta 1 adrenoceptor agonist with positive inotropic properties. Treatment with xamoterol and digoxin was compared in 19 patients with cardiac failure (NYHA class II-III). The study consisted of a short-term and a long-term phase. The former was a randomized, double-blind, crossover study with 6-week treatment periods. In the 15 patients who completed this phase, there was no significant difference between exercise duration on digoxin and on xamoterol. Exercise duration increased on digoxin by 27% and on xamoterol by 17% relative to baseline. Comparing digoxin and xamoterol, maximum exercise heart rate (p less than 0.001), blood pressure (p less than 0.01), and the pressure-rate product during maximum exercise were significantly lower on xamoterol treatment. The systolic time interval was shorter on digoxin than on xamoterol (p less than 0.001). No changes occurred in the echocardiographic parameters. After the short-term study, 13 patients were followed 3-6 months on the drug to which they had responded best (digoxin 7, xamoterol 6). The results of the short-term study were maintained during this period. In conclusion, we found that xamoterol may be an alternative to digoxin in patients with mild to moderate heart failure.

Adrenergic beta-Agonists↗

Clinical study on chronopharmacokinetics of digoxin in patients with congestive heart failure.

Fluorescence polarization immunoassay was used to study the chronopharmacokinetics of digoxin in 10 patients with congestive heart failure (CHF) who also served as self-controls. Our results showed that the serum digoxin concentration reached peak value 1 h after taking digoxin at 7:00 a.m., but the serum digoxin concentration reached the peak value 2 h after taking digoxin at 4:00 p.m. The average serum digoxin concentration area under curve was greater and the best maintainable time of serum concentration within 24 h after taking digoxin at 4 p.m. longer than those at 7:00 a.m. The heart rates were obviously lower and the cardiac function was significantly improved in 4:00 p.m. group.

Adult↗

Digoxin pharmacokinetics and MDR1 genetic polymorphisms.

BACKGROUND: The effect of MDR1 C3435T single nucleotide polymorphism (SNP) in exon 26 on digoxin pharmacokinetics has recently been challenged. OBJECTIVE. To clarify the relationships between MDR1 genetic polymorphisms in exon 26 (C3435T) and 21 (G2677T/A) and digoxin pharmacokinetics. MATERIALS AND METHODS: MDR1 genotypes for C3435T and G2677T/A SNPs were determined in 32 healthy subjects whose single oral dose digoxin pharmacokinetics had been measured over 48 h. RESULTS: A significant relationship was observed between C3435T SNP and digoxin AUCs ( p<0,05). Homozygous TT subjects had 20% higher digoxin plasma concentrations than CT and CC subjects and a trend for higher 48 h digoxin urinary recoveries (TT>CT>CC). Similar results, although not statistically significant, were observed from the MDR1 G2677T/A SNP. CONCLUSIONS: Our results confirm that the MDR1 C3435T single nucleotide polymorphism (SNP) significantly affects digoxin disposition kinetics, with homozygous TT subjects presenting the highest plasma concentrations.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Influence of carvedilol on serum digoxin levels in heart failure: is there any gender difference?

OBJECTIVE: The activity of the human cytochrome P450 and P-glycoprotein (P-gp) changes according to gender. The present study evaluated the effect of gender on the influence of carvedilol on serum digoxin levels in patients with heart failure. METHODS: Twenty-four patients (12 female and 12 male) with New York Heart Association class II-III heart failure were included in the study. Patients were taking oral digoxin (0.0625-0.25 mg, once a day) and were administered oral carvedilol (6.25 mg, two times daily) for 7 days. RESULTS: In the male group, carvedilol led to statistically significant increases in the area under the concentration time curve to 16 h (AUC(0-16h)) and the peak concentration (C(max)) for digoxin, with no change in time to peak (t(max))(AUC(0-16h)= 24.1+/-9.2 ng.h/ml vs. 15.4+/-5.8 ng.h/ml, p<0.001, C(max)=2.2+/-1.0 ng/ml vs. 1.6+/-0.6 ng/ml, p<0.01, t(max)=2.4+/-2.2 h vs. 2.1+/-1.0 h, p>0.05). In the female group, carvedilol administration did not cause statistically significant change in the AUC(0-16h), C(max), or t(max) for digoxin (p>0.05). In the male group, carvedilol resulted in a significant increase in the AUC(0-16h) and C(max) for digoxin compared with the female group (AUC(0-16h)=24.1+/- 9.2ng.h/ml vs. 17.0+/-6.8 ng.h/ml, C(max)=2.2+/-1.0 ng/ml vs. 1.5+/-0.6 ng/ml, p<0.05, respectively). CONCLUSION: Men seem to have a higher activity relative to women for the drug efflux transporter P-gp. Our results suggest that carvedilol will cause drug interaction with digoxin following the inhibition of P-gp-mediated transcellular transport of digoxin in males.

Aged↗

Tiagabine, a novel antiepileptic agent: lack of pharmacokinetic interaction with digoxin.

OBJECTIVE: To assess the possibility of any clinically relevant pharmacokinetic interactions between tiagabine, a novel antiepileptic drug, and digoxin. METHODS: Potential pharmacokinetic interactions between tiagabine and digoxin were investigated in an open-label, two-period cross-over study in healthy male volunteers. Thirteen volunteers, aged between 18 and 43 years, were randomised to receive digoxin (0.5 mg twice a day for 1 day, then 0.25 mg once a day for 8 days) either alone or co-administered with tiagabine (4 mg three times daily for 9 days). Following a 7-day washout period, volunteers crossed over to the other dosing regimen. Peak serum concentration, time to maximum serum, concentration, area under the serum concentration-time curve from zero to 24 h and steady state serum concentration were calculated for digoxin and compared between treatment groups. RESULTS: No statistically significant differences between treatment groups were observed for any of the derived digoxin pharmacokinetic parameters. The most common adverse events reported during digoxin alone and in combination with tiagabine were somnolence and headache; an overall greater frequency of adverse events was reported during combined treatment. Adverse events were generally mild in nature; no serious adverse events were reported. CONCLUSIONS: At the doses administered, there is no evidence of a pharmacokinetic interaction between digoxin and tiagabine in healthy male volunteers.

Adult↗

Re-entrant supraventricular tachycardia in infancy: current role of prophylactic digoxin treatment.

UNLABELLED: Re-entrant supraventricular tachycardia is the most common cardiac arrhythmia in infancy. Pharmacological prevention of recurrencies is a standard recommendation for infants less than 1 year of age. In view of the often benign spontaneous clinical course of the disease, the risk-benefit analysis of any antiarrhythmic agent given is important. It was the aim of this retrospective study, to assess the value of oral long-term digoxin given to paediatric patients with supraventricular tachycardia with onset in the first 4 months of life. Twenty-six newborns and infants fulfilled the inclusion criteria. Median age at first presentation of the patients was 7 days. Eight patients (31%) had structural heart disease, 9 patients had a pre-excitation syndrome, and the other 17 children had a concealed accessory atrioventricular pathway. Long-term prophylaxis with oral digoxin was considered successful in 17 children (65%). In 2 patients therapy with digoxin was considered partially effective and in 7 patients (27%) failure of digoxin to improve symptoms led to the introduction of other anti-arrhythmic agents. Serum digoxin levels were no different in the patients with successful therapy as compared to those with treatment failure. No side-effects due to digoxin were noted in all the patients treated. After a mean followup of 54 months (12-130 months), 19 children (73%) were free of recurrencies and on no medication, 5 children were free of recurrencies but had anti-arrhythmic therapy. Only 2 patients, both on anti-arrhythmic therapy, were still suffering from tachycardia. CONCLUSION: Digoxin remains an effective treatment option in infants with supraventricular tachycardia and it helped to avoid the long-term use of other anti-arrhythmic drugs with potentially more serious side-effects (pro-arrhythmia) in a considerable proportion of infants treated.

Anti-Arrhythmia Agents↗

Digoxin disposition in obesity: clinical pharmacokinetic investigation.

Digoxin pharmacokinetics were studied in 16 obese (mean +/- SD weight, 100.2 +/- 36.8 kg) and 13 control (64.6 +/- 10.5 kg) subjects. All subjects had normal renal function and no other coexisting disease. After administration of 0.75 mg digoxin by intravenous infusion, multiple plasma samples obtained over the 96 hours following infusion were analyzed for digoxin concentration by radioimmunoassay. Pharmacokinetic parameters were determined by weighted iterative nonlinear least squares regression analysis. Elimination half-life (t 1/2) was not different between obese and control groups (35.6 +/- 10.5 vs 41.2 +/- 16.7 hours). Absolute volume of distribution (Vd) also was not different (981 +/- 301 vs 937 +/- 397 liters), nor was total clearance of digoxin (328 +/- 82 vs 278 +/- 87 ml/min). Elimination t 1/2 was significantly negatively correlated with clearance among all subjects (r = -0.46; p less than 0.01). Using percent ideal body weight (IBW) as a measure of obesity, no correlation was found between percent IBW and Vd (r = 0.03). Thus digoxin is similarly distributed into IBW in obese and normal weight subjects, and there is no significant distribution of digoxin into excess body weight over IBV. In addition, there is no difference in total metabolic clearance or elimination half-life between obese and control subjects. Digoxin loading and maintenance dosage should be calculated on the basis of IBW, which reflects lean body mass, rather than TBW, which reflects adipose tissue weight in addition to lean body mass.

Adult↗

Acute effects of intravenous furosemide administration on serum digoxin concentration.

The effect of intravenous (IV) furosemide (2.5 mg/kg) on serum digoxin concentration, urine flow rate, and myocardial contractility and rhythm was studied in normal dogs and dogs treated with digoxin. Furosemide IV to animals which had not been receiving digoxin resulted in increased urine flow rate from 0.11 +/- 0.03 to 0.43 +/- 0.1 ml/min/kg, but had no effect on myocardial contractility, blood pressure, or cardiac rhythm. Furosemide IV to animals with steady-state therapeutic serum concentrations of digoxin (2.0 +/- 0.58 ng/ml) increased urine flow similarly but did not significantly alter serum digoxin concentration, blood pressure, myocardial contractility, or cardiac rhythm. Thus, contrary to some previous reports, furosemide does not interact with digoxin to produce an elevation in serum digoxin concentration or enhancement of the glycoside's myocardial action.

Animals↗

Inefficacy of "therapeutic" serum levels of digoxin in controlling the ventricular rate in atrial fibrillation.

Although therapeutic and toxic serum concentrations of digoxin have been established, there is sparse information permitting correlation of drug level with clinical effect. This study was undertaken to assess the radioimmunoassay serum digoxin levels in 30 patients with acute atrial fibrillation (38 determinations) and 30 patients with chronic atrial fibrillation (54 determinations). Those with chronic fibrillation were subdivided into those in clinically stable condition (14 patients), and those seriously ill and in clinically unstable condition (16 patients). Slowing of ventricular rate in patients with stable, chronic atrial fibrillation was accomplished in 10 of 16 instances by "therapeutic" and "subtherapeutic" levels of digoxin (less than 2 ng/ml). Ventricular rate was "controlled" (65 to 95 beats/min) with therapeutic levels of serum digoxin in only five instances of acute atrial fibrillation and seven of unstable chronic atrial fibrillation. In 43 studies (23 of acute atrial fibrillation, 20 of chronic atrial fibrillation), a rapid ventricular rate (95 to 140 beats/min) persisted in the presence of "therapeutic" or high levels of digoxin. Thirty-nine of these were in patients who were seriously ill with conditions such as infection, hypoxia or recent thoracotomy. Slowing of the ventricular rate required "toxic" concentrations of digoxin (2.5 to 6 ng/ml) in 15 instances. We conclude that sufficient amounts of digoxin to achieve "therapeutic" serum concentrations may fall to lower the ventricular rate in atrial fibrillation to less than 100 beats/min, especially when a serious, complicating illness coexists.

Atrial Fibrillation↗

Favorable effects of orally administered digoxin on left heart size and ventricular wall motion in patients with previous myocardial infarction.

The effects of maintenance oral digoxin therapy on segmental left ventricular wall motion (wall motion videotracking) and left heart size (radiographic left heart dimension) were evaluated in 14 patients with a prior myocardial infarction but without clinical signs or symptoms of congestive heart failure. The left heart dimension decreased in all six patients with cardiomegaly from an average of 55.0 +/- 1.6 (standard deviation) to 52.2 +/- 2.7 mm/m2 body surface area (P less than 0.01) during digoxin therapy. However, there was no significant change in the eight patients with normal heart size. In the resting state, the average extent of shortening in normal segments increased significantly from 3.1 +/- 0.8 to 4.2 +/- 1.2 mm during digoxin therapy. During submaximal handgrip exercise, the extent of shortening averaged 4.0 +/- 1.3 mm and increased further with digoxin therapy to 5.1 +/- 2.1 mm. The effects of digoxin therapy on the maximal velocity of shortening in normal segments at rest and during handgrip exercise were similar. In all 14 patients, there was a decrease in the number of segments with abnormal wall motion at rest or with handgrip exercise during digoxin therapy. With therapy, the number of abnormal sites decreased from 52 to 35 in the resting state and from 84 to 49 during handgrip exercise. Thus, in patients 6 or more months after transmural myocardial infarction, orally administered digoxin decreases cardiomegaly, increases the extent and maximal velocity of shortening in normal left ventricular segments and often reduces the extent of abnormal wall motion at rest or during isometric exercise.

Administration, Oral↗

Pharmacokinetics of digoxin in patients with acute myocardial infarction.

The effects of acute myocardial infarction on the pharmacokinetics of digoxin were studied. Digoxin, 0.75 mg, was given orally to 12 patients with left-sided cardiac failure due to acute myocardial infarction and to 9 healthy control subjects. Serum concentration of digoxin in the first 4 hours and the area under the serum concentration-time curve in the first 12 hours after administration of the drug were lower in patients with infarction than in control subjects (P less than 0.01). The 24 hour area under the concentration curve, the amount excreted in urine and the renal clearance did not differ between the groups. The 24 hour area under the concentration curve correlated with the predigoxin pulmonary capillary wedge pressure and with heart rate (P less than 0.01). The decrease of renal clearance of digoxin was related to the serum activity of MB isoenzyme of creatine kinase (P less than 0.001). Morphine reduced and delayed the peak serum concentrations of digoxin (P less than 0.001). Thus, the absorption of oral digoxin was slower and the peak concentrations remained lower in patients with acute myocardial infarction than in healthy control subjects. However, the total amount of digoxin absorbed was unchanged.

Administration, Oral↗

Pharmacokinetic interaction study with ramipril and digoxin in healthy volunteers.

Coadministration of captopril has been shown to increase serum digoxin concentration. The effects of ramipril, a new angiotensin converting enzyme inhibitor, on serum digoxin concentration after multiple dosing were studied in 12 healthy volunteers. All subjects were receiving steady-state digoxin medication (0.5 mg daily), and ramipril (5 mg daily) was coadministered for 14 days. Serum digoxin concentration was measured repeatedly before, during and up to 1 week after ramipril coadministration at 8 a.m. (trough values) and on selected trial days at 11 a.m., 3 hours after the morning medication. Simultaneously, blood levels of ramipril and its active metabolite diacid were determined. Volunteers were followed closely for side effects and for changes in blood pressure, heart rate and electrocardiogram. Safety pharmacology included serial determination of sodium, potassium, serum glutamic oxaloacetic transaminase, creatinine and a full blood count. Mean serum digoxin concentration was not significantly influenced by ramipril coadministration with trough levels of 0.90 +/- 0.24 before, 0.93 +/- 0.38 during and 0.82 +/- 0.33 ng/ml after ramipril medication. The increase in serum digoxin concentration 3 hours after the morning dose was also not significantly affected by ramipril. Serum levels of ramipril and its diacid showed a wide range of variation. Mean serum potassium increased by 0.3 mmol/liter during ramipril coadministration with development of symptomless hyperkalemia (6.0 mmol/liter) in 1 subject. The only other side effect possibly related to ramipril was a dry cough in 1 subject. Both drugs were well tolerated. Ramipril showed no significant influence on serum digoxin levels in healthy volunteers.

Adult↗

Urinary excretion of reduced metabolites of digoxin.

The urinary excretion of the relatively cardioinactive reduced metabolites of digoxin, dihydrodigoxin and related compounds was measured by radioimmunoassay in 131 normal subjects during studies of the bioavailability of digoxin preparations. Digoxin reduction products (DRP) constitute more than 5 percent of the excretion of digoxin and its metabolites in one-third of the volunteers after the administration of single or multiple doses of digoxin. There was little or no output of DRP during the first 8 hours after a single dose, with maximal excretion usually occurring on the second day. Most subjects who excreted more than 5 percent DRP on one occasion did so with each subsequent exposure to digoxin. Six volunteers, however, in whom substantial amounts of DRP had previously been found, failed to excrete detectable quantities after subsequent doses. In two, this change occurred shortly after they took erythromycin. Urinary DRP were less after the intravenous administration compared to the oral administration of digoxin. After oral doses, DRP excretion tended to vary inversely with the bioavailability of the preparation. The findings are consistent with the hypothesis that DRP are formed as the result of the activity of a variable component of the intestinal flora. Prospective studies will be necessary to prove this hypothesis.

Adult↗

Pharmacokinetic effects of fluvastatin in patients chronically receiving digoxin.

A double-blind, randomized, crossover study assessed the effects of a single 40-mg dose of fluvastatin on the steady-state pharmacokinetics of digoxin in chronically treated patients. After demonstrating consistent digoxin serum concentrations as part of the inclusion criteria, 18 patients received a single dose of either fluvastatin or placebo, with a 1-week washout period between crossover to the other treatment. For each patient, 14 serum samples were drawn and urine collected over 24 hours; all samples were assayed for digoxin using a fluorescence polarization immunoassay. The following pharmacokinetic parameters were determined using noncompartmental techniques: area under the curve for 24 hours (AUC24); time to maximum concentration after digoxin (tmax); maximum concentration after digoxin dosing (Cmax); concentration at 24 hours after fluvastatin or placebo (Cmin); total amount excreted in the urine over 24 hours (U24); and urinary clearance (Clren). The pharmacokinetic data were analyzed for sequence, patient nested with sequence, and period and treatment differences using ANOVA, Schuirmann's two one-sided testing approach, confidence intervals, and power analysis. The AUC24, Cmax, and tmax for digoxin were considered bioequivalent with the two treatments. The differences in Cmax, U24, and Clren were statistically significant but were not considered to be clinically relevant due to the low magnitude of the difference (< 20%). There were no clinically significant adverse reactions attributable to either digoxin or fluvastatin.

Aged↗