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PubMed1980

Subjective assessment of sexual dysfunction of patients on long-term administration of digoxin.

Various data suggest that male patients who have received digoxin on a longterm basis have increased levels of serum estrogen and decreased levels of plasma testosterone and luteinizing hormone (LH). This study was undertaken to investigate the links between the long-term administration of digoxin therapy and sexual behavior, and the effect of digoxin on plasma levels of estradiol, testosterone, and LH. The patients of the study and control group (without digoxin) were of similar cardiac functional capacity and age (25-40 years) and were randomly selected from the rheumatic heart disease patients. A subjective assessment of sexual behavior in the study and control groups was carried out, using parameters such as sexual desire, sexual excitement, and frequency of sexual relations. Personal interviews and a questionnaire were also used for the evaluation of sexual behavior. The findings support the reports concerning digoxin effect on plasma estradiol, testosterone, and LH. The differences in the means were significant. Tests used to evaluate the changes in sexual behavior showed a significant decrease in sexual desire, sexual excitement phase (erection), and frequency of sexual relations in the study group.

Adult↗
PubMed1981

Digoxin-quinidine interaction in patients with renal failure.

Investigations were performed in order to study whether or not quinidine would exert similar effects on the serum digoxin concentration in patients with renal failure as in normal subjects. Fourteen out of fifteen patients showed a significant increase of the serum digoxin level after four days of quinidine application. This indicates, that the quinidine effect is not solely caused by a decrease of the renal digoxin clearance, although nine patients, not being hemodialysed, revealed a correlation between their creatinine clearance and the rise of the serum digoxin concentration after quinidine. As however, the patients on hemodialysis did not show higher digoxin levels than those treated conservatively, it is suggested that the degree of the uremic intoxication might be responsible for the observed correlation.

Acetyldigoxins↗
PubMed1993

Evaluation of two prediction models for digoxin dosing.

The relationship between the digoxin elimination parameter (A%) and creatinine clearance (CLCr) was determined, from blood level data of 160 hospital patients receiving digoxin tablets. The linear regression equation obtained, which varied only slightly from that reported by Jelliffee previously, was used to predict serum digoxin concentrations in 140 patients of four age groups (50-60, 60-70, 70-80 and 80-90 years). The predictions made were found to be less biased and more precise, irrespective of the age of the patients, than those produced using another predictive method known as Dobbs method. However, correlation coefficients of predicted versus measured serum digoxin concentrations for each method did not differ significantly and frequency distribution analyses of prediction errors gave poor results (up to 63% only). Therefore, neither method can be considered to be superior to the other nor can they be said to ensure accurate predictions of serum digoxin concentrations.

Aged↗
PubMed1987

Delayed digoxin toxicity following discontinuance in acute renal failure.

A digitalized 75-year-old patient with postoperative renal failure demonstrated a progressive rise in serum digoxin concentration, peaking at 3.4 nmol X L-1 three days following discontinuance of the drug. This was accompanied by cardiac bradyarrhythmias. Although the serum digoxin concentration had already started to climb from a therapeutic level prior to the discontinuance of the drug, the unabated and substantial rise was consistent with a dramatic decrease in the apparent volume of distribution of digoxin accompanying acute renal failure. Serum digoxin levels were determined with fluorescence polarization immunoassay, which has an improved specificity when compared to the commonly used radioimmunoassays for digoxin.

Acute Kidney Injury↗
PubMed2001

A hypothalamic digoxin mediated model for conscious and subliminal perception.

The isoprenoid pathway and its metabolites--digoxin, dolichol and ubiquinone were assessed in schizophrenia. There was an upregulation of the isoprenoid pathway as evidenced by elevated HMG CoA reductase activity. Digoxin, an endogenous Na+-K+ ATPase inhibitor secreted by the hypothalamus was found to be elevated and RBC membrane Na+-K+ ATPase activity was found to be reduced in schizophrenia. Membrane Na+-K+ ATPase inhibition can result in increased intracellular Ca2+ and reduced magnesium levels. Hypothalamic digoxin can modulate conscious and subliminal perception and its dysfunction may lead on to schizophrenia. Digoxin can also preferentially upregulate tryptophan transport over tyrosine resulting in increased levels of depolarising tryptophan catabolites--serotonin and quinolinic acid (NMDA agonist), and decreased levels of hyperpolarising tyrosine catabolites--dopamine and noradrenaline contributing to membrane Na+-K+ ATPase inhibition. NMDA excitotoxicity could result from hypomagnesemia induced by membrane Na+-K+ ATPase inhibition and quinolinic acid, an NMDA agonist acting on the NMDA receptor. Hypomagnesemia and increased dolichol level can affect glycoconjugate metabolism and membranogenesis leading on to disordered synaptic connectivity in the limbic allocortex and defective presentation of viral antigens and neuronal antigens contributing to autoimmunity and viral persistance important in the pathogenesis. Membrane Na+-K+ ATPase inhibition can produce immune activation, a component of autoimmunity. Mitochondrial dysfunction consequent to altered calcium/magnesium ratios and reduced ubiquinone levels can result in increased free radical generation and reduced free radical scavenging & defective apoptosis leading on to abnormal synaptogenesis. Schizophrenia can thus be considered as a syndrome of hypothalamic digoxin hypersecretion consequent to an upregulated isoprenoid pathway.

Adult↗
PubMed2005

Modification of the P-glycoprotein dependent pharmacokinetics of digoxin in rats by human recombinant interferon-alpha.

PURPOSE: This study was conducted to investigate in vivo the impact of interferon-alpha (IFN)-alpha on P-glycoprotein (P-gp) activity in rats by studying how its administration modifies the bioavailability of digoxin, a fairly pure P-gp substrate. METHODS: Human recombinant IFN-alpha was given to rats (n = 5-7 per group) daily for 8 days at different doses (IntronA) 10(6), 2.10(6), or 4.10(6) IU kg(-1), s.c.), whereas pegylated-IFN-alpha (ViraferonPeg), 29 microg kg(-1)) was given s.c. three times a week. Rats were then given digoxin (32 microg kg(-1)) i.v. or orally. The pharmacokinetics of digoxin was studied. Intestinal P-gp expression was also examined. RESULTS: The pharmacokinetics of i.v. administered digoxin was not modified by IFN-alpha, but a dose-dependent increase in areas under the curve (AUCs) was observed in the orally administered digoxin parameters in rats (AUCs: 392 +/- 83 min microg L(-1), p < 0.01 and 550 +/- 97 min microg L(-1), p < 0.001, respectively, vs. 286 +/- 111 min microg L(-1) for control). A decrease in P-gp expression in the ileum (relative intensities: 0.70 +/- 0.19 for 4 Million International Unit (MIU) kg(-1) IFN-alpha-treated animals vs. 1.00 +/- 0.13 for controls, p < 0.05) and mainly in the jejunum (relative intensities: 0.46 +/- 0.13 for 4 MIU kg(-1) IFN-alpha-treated animals vs. 1.00 +/- 0.08 for controls, p < 0.001) was observed. CONCLUSION: IFN-alpha induces in vivo a significant dose-dependent inhibitory effect on intestinal P-gp activity related to a local decrease in its expression, thereby predicting important clinical consequences when IFN-alpha and other P-gp substrates are associated.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1978

Dose-independent pharmacokinetics of digoxin in humans.

Nine healthy male volunteers received single 0.5, 1.0, and 1.5 mg. doses of intravenous digoxin in a randomized three-way crossover study. Multiple venous blood samples were drawn during 35 hours after each dose, and all urine was collected for 6 consecutive days. Concentrations of digoxin in serum and urine were determined by radioimmunoassay. Over-all mean values for kinetic variables were: distribution half-life, 0.35 hours; elimination half-life, 27.9 hours; volume of distribution, 5.46 liters/Kg; total clearance, 2.51 ml./min./Kg. The mean projected cumulative urinary excretion of digoxin was 70.1% of the dose; mean renal clearance of digoxin was 1.71 ml./min./Kg., not significantly different from creatinine clearance (1.50 ml./min./Kg.). None of the identifiable pharmacokinetic variables was significantly influenced by dose, suggesting that digoxin disposition is dose-independent in healthy individuals.

Adult↗
PubMed1982

Postoperative supraventricular arrhythmias and the role of prophylactic digoxin in cardiac surgery.

A prospective study of 182 patients undergoing cardiac surgery was performed. The patients were divided into three groups. Group I consisted of 83 patients who had never been treated with digitalis. Group II comprised 59 patients who were taking digoxin before operation and had medication discontinued 24 to 48 hours prior to surgery; they did not receive maintenance digoxin in the postoperative periods. Group III was made up of 40 patients who were given prophylactic digoxin in the perioperative period; none had taken digoxin before. Sixty of 83 group I patients (72%) and two of the group III patients (5%) developed postoperative supraventricular tachyarrhythmia. Digoxin was reinstituted in 56 of group II patients (95%) for supraventricular arrhythmia and/or heart failure. Of the various factors evaluated, only valvular surgery and ECG evidence of myocardial infarction were associated with postoperative supraventricular tachyarrhythmias.

Adult↗
PubMed1984

Effects of chronic digoxin treatment on cardiac function, electrolytes, and sarcolemmal ATPase in the canine failing heart due to chronic mitral regurgitation.

This study was designed to determine whether digoxin therapy in the canine heart failing because of mitral regurgitation (MR) provides only hemodynamic benefit and accompanying subjective improvement or if it also reverses the changes in intracellular Ca++ and sarcolemmal Na+-K+-ATPase. The dogs were divided into four groups: control, MR of 3 months' duration, MR of 6 months', and digoxin treatment for 3 months after 3 months of MR. Six months of MR produced a marked decrease in the index of myocardial contractility and function associated with a decrease in intracellular Ca++ and Na+, and an increase in intracellular K+, extracellular space, sarcolemmal Na+-K+-ATPase, and Mg++-ATPase. Digoxin treatment tended to return the changes in the index of myocardial contractility and cardiac function, intracellular Ca++, Na+, K+, extracellular space, and sarcolemmal Na+-K+-ATPase of the failing heart toward control levels. Digoxin treatment did not affect Mg++-ATPase. The right ventricle, which did not fail, also did not show any significant changes in the parameters measured. The results showed that digoxin treatment not only improved the index of myocardial contractility and cardiac function of the failing heart but also tended to return the electrolytes and sarcolemmal Na+-K+-ATPase toward control levels.

Animals↗
PubMed1985

Hemodynamic effects of digoxin in acute myocardial infarction in man: a randomized controlled trial.

Hemodynamic effects of digoxin in acute myocardial infarction (AMI) have been acknowledged to depend on the basal cardiocirculatory state. In the present study, the effects of digoxin in patients with AMI were evaluated in four hemodynamic subsets, based on the relationship between mean pulmonary capillary wedge pressure (PCWP, in mm Hg) and left ventricular stroke work index (LVSWI, in g-m/m2): subset 1: normal (less than or equal to 15 mm Hg) PCWP and normal (greater than or equal to 35 g-m/m2) LVSWI; subset 2: elevated (greater than 15 mm Hg) PCWP and normal LVSWI; subset 3: reduced (less than 35 g-m/m2) LVSWI and normal PCWP; and subset 4: elevated PCWP and LVSWI moderately reduced to a range between 16 and 34 g-m/m2. Forty patients were admitted to the study and were randomly assigned to one of two groups in each subset: control group (19 patients) and treated group (21 patients). Five patients were randomized into each of the subsets 2, 3, and 4 in both the control and treated groups, while in subset 1 there were four control and six digoxin-treated patients. Control patients were administered a placebo saline solution and digoxin-treated patients received 0.50 mg of the drug intravenously in 20 minutes. The effects of the placebo and of the drug were evaluated at 30, 60, and 90 minutes from the end of the infusion. Hemodynamic data did not vary in the control group, and digoxin did not exert any relevant effect in subsets 1 and 2. After drug infusion, cardiac index (Cl, in L/min/m2) significantly increased in subset 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Effect of digoxin on sinus nodal reentry in the dog.

The effect of digoxin on sinus reentry was examined in 20 open chest mongrel dogs during infusion of digoxin at a rate of 2.5 mu g/kg per min. The extrinsic cardiac nerve supply was removed acutely in 10 dogs and was left intact in the remaining 10 dogs. Sinus nodal reentry was relatively unaffected by digoxin in 18 of 20 dogs. In these 18 dogs, digitalis toxicity developed before reentry was abolished and was manifested as increased atrial and ventricular automaticity in 14 and as advanced atrioventricular (A-V) block in four. In the remaining two dogs, sinus nodal reentry was relatively sensitive to digoxin and was abolished before toxicity became manifest as advanced A-V block. The knowledge of the relative insensitivity of sinus nodal reentry to digoxin, at least in this experimental model, contrasts with the previously reported sensitivity of sinus nodal reentry to quinidine, and may be important in the management of sinus nodal reentry in man.

Animals↗
PubMed1984

Interaction of flecainide with digoxin and propranolol.

The effect of flecainide, 200 mg twice daily for 5 days, on steady-state plasma digoxin levels was determined in 15 healthy male subjects who received 0.25 mg of digoxin per day. The predose mean plasma digoxin level before flecainide administration on days 9 and 10 was 0.46 ng/ml, compared with 0.57 ng/ml on day 13 (p less than 0.05) and 0.49 ng/ml on day 15 (difference not significant [NS]) when flecainide was given concurrently with digoxin. The 6-hour postdose mean level for days 9 and 10 was 0.58 ng/ml, compared with mean levels of 0.62 ng/ml on day 13 (NS) and 0.65 ng/ml on day 15 (p less than 0.05). On average, predose and 6-hour postdose digoxin levels increased by 24 +/- 35% and 13 +/- 19%, respectively, during co-administration. A significant prolongation of the electrocardiographic PR interval in 6 of 15 subjects was noted on the combined drug dosage. This reverted to normal after cessation of drug administration. Vital signs showed no significant clinical change during the course of the study. Ten other healthy male subjects were given propranolol, 80 mg 3 times daily, or flecainide, 200 mg twice daily, alone or in combination. Effects on vital signs, exercise heart rate, electrocardiographic interval, M-mode indexes of ventricular function and plasma drug levels were monitored to determine effects of the study drugs when given separately or concurrently. Both drugs caused a decrease in blood pressure, with the systolic pressure affected more than the diastolic; the effects of propranolol and flecainide were additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

A controlled trial of digoxin in congestive heart failure.

Because of conflicting results from studies examining the usefulness of digoxin in congestive heart failure (CHF) patients in sinus rhythm, a cross-over trial was conducted in which 20 patients received 7 weeks of digoxin titrated to a level of 1.54 to 2.56 nmol/liter and 7 weeks of matched placebo. The order of treatments was determined by random allocation and patients, clinicians and research staff were blind to allocation. In patients with deteriorating condition, the treatment period was terminated and outcome measures were obtained. If deterioration occurred during the first period, the patient was crossed over without the code being broken. Seven patients required premature termination of study periods because of increasing symptoms of CHF. All 7 were taking placebo at the time (p = 0.016). Small differences in dyspnea (p = 0.044), walking test score (p = 0.055), clinical assessment of CHF (p = 0.036) and ejection fraction (p = 0.004) favored the digoxin treatment group. Patients with more severe CHF were more likely to benefit from digoxin administration. It was concluded that oral digoxin, in doses titrated to produce a serum level of 1.54 to 2.56 nmol/liter, improved quality of life and functional exercise capacity in some patients with CHF in sinus rhythm.

Aged↗
PubMed1992

Redefining the role of digoxin in the treatment of atrial fibrillation.

Atrial fibrillation (AF) encompasses a variety of discrete clinical syndromes, including paroxysmal, chronic, acute, and postoperative. Digoxin, long considered the mainstay of therapy for rate control in all types of AF, appears to have only modest electrophysiologic effects, which are mediated primarily by the autonomic nervous system. Digoxin has less potency than the calcium antagonists or beta-blocking drugs with respect to atrioventricular nodal blockade. Although less potent than calcium antagonists or beta-blocking drugs on the atrioventricular node, digoxin provides positive inotropic support, whereas the other 2 agents can suppress left ventricular function. Thus, digoxin is the agent of choice in patients with AF in the setting of significant left ventricular dysfunction. However, in the absence of left ventricular dysfunction, digoxin should be considered second-line therapy for the treatment of all AF syndromes.

Acute Disease↗
PubMed1980

Bioavailability of digoxin tablets in patients with gastrointestinal dysfunction.

In 47 patients with disorders of the gastrointestinal tract, the bioavailability of digoxin tablets was assessed by measuring the area under the serum concentration-time curve (AUC) after the oral administration of single 0.5 mg doses. In 13 or 14 patients who had undergone a previous ileal resection, in 10 of 10 patients with sprue and in 14 of 14 patients with a variety of disorders of the gastrointestinal tract, digoxin absorption was normal despite marked steatorrhea in many. A patient with extensive jejunal and ileal resection, and inflammation of the remaining small bowel,was the sole exception. Impaired digoxin bioavailability was found in five of nine patients who had undergone jejunoileal bypass procedures (bypass patients. A strong correlation was noted between the length of jejunum remaining in continuity and the AUC (r = 0.86, p less than 0.01). Two of three bypass patients also showed decreased absorption of more rapidly dissolving tablets or an elixir. Digoxin bioavailability correlated significantly with and 2 hour serum xylose levels but not with urinary xylose excretion, fecal fat or the Schilling test result. The findings are consistent with the role of the upper small bowel as the predominant site of digoxin absorption as well as the reserve function of the ileum in the event of jejunal dysfunction or bypass.

Adult↗
PubMed1982

Is digoxin really important in treatment of compensated heart failure? A placebo-controlled crossover study in patients with sinus rhythm.

To assess the efficacy of digitalis in patients with chronic clinically compensated congestive heart failure and normal sinus rhythm, we performed a double-blind crossover study with digoxin and placebo in 30 consecutive outpatients fulfilling these criteria; serum digoxin levels, clinical symptoms and signs, and objective indexes of cardiac function were monitored. No patient's clinical condition deteriorated during three months of placebo administration. Discontinuation of digoxin resulted in a small increase in echocardiographically determined resting left ventricular end-diastolic dimension (1.8 +/- 0.6 mm, p less than 0.001) and a similar decrease in velocity of circumferential fiber shortening (-0.08 +/- 0.04 circ/sec, p less than 0.05) from the corresponding values of 55.8 +/- 2.3 mm and 0.90 +/- 0.08 circ/sec during digitalis therapy. Resting left ventricular ejection time and pre-ejection period were prolonged by digoxin withdrawal. Maximal exercise capacity was unchanged. No clinical exacerbation of heart failure attributable to digitalis withdrawal occurred over a follow-up period averaging 19 months. The results indicate that long-term digoxin therapy has only a minor effect on cardiac performance that is without apparent clinical importance in a representative population of ambulatory patients treated with cardiac glycosides.

Adult↗
PubMed1985

Color vision deficiencies in two cases of digoxin toxicity.

Color vision deficiencies are a common sign of digoxin intoxication and color vision testing can be used to diagnose digoxin toxicity. We tested two patients, a 79-year-old man and a 61-year-old man, with digoxin toxicity by means of the Farnsworth-Munsell 100-hue test, AOH-R-R plates, and Ishihara plates. Initial testing disclosed both red-green and blue-yellow color vision deficiencies. These improved when digoxin levels diminished. The deficiencies were superimposed on preexisting acquired and congenital deficits. As serum digoxin levels decreased, the color vision deficiencies lessened on all three tests. The Farnsworth-Munsell 100-hue test gave the best quantifiable measure of color vision deficiencies, but proved difficult to use for routine bedside testing.

Aged↗
PubMed1991

Prevention of arrhythmias after noncardiac thoracic operations: flecainide versus digoxin.

Cardiac arrhythmias are known complications of thoracic operations. The prophylactic value of flecainide administered as a constant-rate, intravenous infusion (0.15 mg.kg-1.h-1) after a loading dose (2 mg.kg-1) was compared with digoxin (10 micrograms.kg-1 for 12 hours, then 0.25 mg.24 h-1) in a randomized study in 30 patients using Holter monitoring during the first 72 hours after operation. Drug monitoring was performed every day to keep a serum level of flecainide of 200 to 600 ng.mL-1 and a digoxin level of 0.8 to 2 ng.mL-1. Failure, defined as the appearance of atrial fibrillation or flutter or the development of complex ventricular arrhythmias (Lown IVb and V), was observed in one patient in the flecainide group (7%) and in 7 patients in the digoxin group (47%) (p less than 0.05). It is concluded that flecainide is more efficient than digoxin in preventing and treating cardiac arrhythmias after thoracic operations. At the dosage used side effects related to flecainide or digoxin were not observed.

Arrhythmias, Cardiac↗